WO2022051323A1

WO2022051323A1 - Fixed dose combinations of chs-131 and a ppar agonist

Info

Publication number: WO2022051323A1
Application number: PCT/US2021/048596
Authority: WO
Inventors: Charles M. Cook
Original assignee: Coherus Biosciences Inc
Current assignee: Coherus Oncology Inc
Priority date: 2020-09-03
Filing date: 2021-09-01
Publication date: 2022-03-10
Anticipated expiration: 2023-03-03

Abstract

Provided herein are fixed dose combination formulations useful for the treatment of PPARΥ-mediated diseases or disorders. In particular, provided herein are fixed dose combinations comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. Also provided are methods of making and methods of using the fixed dose combination formulations.

Description

FIXED DOSE COMBINATIONS OF CHS-131 AND A PPAR AGONIST TECHNICAL FIELD The present disclosure in some embodiments relates to fixed dose combination formulations comprising a PPARγ inhibitor that is the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, that are used for treating PPARγ-mediated diseases or disorders. BACKGROUND The peroxisome proliferator-activated receptors (PPARs) are transducer proteins belonging to the steroid/thyroid/retinoid receptor superfamily. The PPARs were originally identified as orphan receptors, without known ligands, but were named for their ability to mediate the pleiotropic effects of fatty acid peroxisome proliferators. These receptors function as ligand- regulated transcription factors that control the expression of target genes by binding to their responsive DNA sequence as heterodimers with the retinoid X receptor (“RXR”). The target genes encode enzymes involved in lipid metabolism and differentiation of adipocytes. Accordingly, the discovery of transcription factors involved in controlling lipid metabolism has provided insight into regulation of energy homeostasis in vertebrates, and further provided targets for the development of therapeutic agents for disorders such as obesity, diabetes and dyslipidemia. Peroxisome proliferator-activated receptor γ (“PPARγ”) is one member of the nuclear receptor superfamily of ligand-activated transcription factors and has been shown to be expressed in an adipose tissue-specific manner. Its expression is induced early during the course of differentiation of several preadipocyte cell lines. Additional research has now demonstrated that PPARγ plays a pivotal role in the adipogenic signaling cascade. PPARγ also regulates the ob/leptin gene which is involved in regulating energy homeostasis and adipocyte differentiation, which has been shown to be a critical step to be targeted for anti-obesity and diabetic conditions. The compound of Formula (I):

is a selective peroxisome proliferator-activated receptor (PPAR) γ modulator. The compound of Formula (I) is under development as a treatment for NASH. The peroxisome proliferator-activated receptor (PPAR)-alpha subtype (herein PPAR-α) is a ligand-activated transcriptional factor that regulates the expression of genes involved in fatty acid beta-oxidation, and is a major regulator of energy homeostasis. PPAR-alpha agonists have been used to treat dyslipidemia because of their triglyceride (TG) lowering and high-density lipoprotein cholesterol (HDL-C) elevating effects. More recent research has demonstrated anti- inflammatory and anti-thrombotic actions of PPAR-alpha agonists in the vessel wall as well. Thus, PPAR-alpha agonists decrease the progression of atherosclerosis by modulating metabolic risk factors and by their anti-inflammatory actions on the level of the vascular wall. See van Raalte, D.H., Pharm Res. 2004 Sep;21(9):1531-8. PPARα is primarily expressed in the liver, heart, kidney, and muscle, and is involved in lipid metabolism. See Cox, R.L., PNAS March 28, 2017 114 (13) 3284-3285. The PPAR-delta subtype (herein PPAR-δ) is ubiquitously expressed, and activation in animal models improves lipid homeostasis and insulin sensitivity. These regulatory roles make the PPAR nuclear receptors attractive targets for treating dyslipidemia and type II diabetes. While fibrates and thiazolidinediones (TZDs) are used to treat these conditions by selectively activating PPARα and PPARγ, respectively, there are health issues caused by long-term use of these drugs, and thus a safe compound that specifically targets PPARδ could potentially aid in treatment of both hyperlipidemia and type II diabetes. See Cox, R.L., PNAS March 28, 2017114 (13) 3284- 3285. Elafibranor is a dual PPAR-α and PPAR-δ agonist that improves insulin sensitivity, glucose homeostasis, and lipid metabolism and reduces inflammation. The safety and efficacy of elafibranor has been assessed in a randomized, double-blind placebo-controlled trial of patients with nonalcoholic steatohepatitis (NASH). See Ratziu et al., Gastroenterology, Volume 150, Issue 5, May 2016, Pages 1147-1159.e5 There is an unmet need to provide patients with a single fixed- dose composition comprising the compound of Formula (I) and a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist as a convenient oral medication. For the fixed-dose composition to provide the intended therapeutic effect, it must be formulated so that the compound of Formula (I) and the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist each have the desired pharmacokinetic characteristics (e.g. absorption, bioavailability, Cmax, Tmax, AUC, half-life) even though each drug product in the composition has different properties (e.g. solubility, permeability, total dose, dose proportionality). Combining the compound of Formula (I) and a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, into a single therapeutic composition poses significant challenges. For instance, the compound of Formula (I) is poorly soluble (less than 2 µg dissolves in 1mL of water at pH 1 and less than 0.1 ^g dissolves in 1 mL of water at pH 3 to 8). Many PPAR-α agonists, PPAR-δ agonists, or dual PPAR-α/δ agonists, have variable solubility or low solubility (for example, elafibranor has a predicted solubility of approximately 0.3 µg/mL at pH 1 to 7). Further, the total dose of the compound of Formula (I) is relatively low (e.g. 1 to 10 mg) which poses challenges in creating a formulation with even distribution to achieve a desired dissolution profile and pharmacokinetic characteristics for that drug product. These characteristics present challenges in identifying suitable excipients for a fixed dose composition and the manufacturing techniques that will result in a stable drug product. Thus, creating a fixed-dose formulation comprising the compound of Formula (I) and a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist is unique to the properties of each drug substance. This makes the art of creating fixed dose formulations unpredictable. Accordingly, formulation chemists do not have a single universal set of rules or additives that enhance any given drug substance’s pharmacodynamic or physical properties. SUMMARY Some embodiments provide a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients. Some embodiments provide a process for preparing a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; and (j) applying the fourth blend obtained in step (i) to the surface of the tablet core, forming the outer layer. Some embodiments provide a process for preparing a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) applying the fourth blend obtained in step (i) to the surface of the tablet core, forming the outer layer; and (k) applying an immediate release coating to the outer layer. Some embodiments provide a process for preparing, a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules and drying the wet granules to obtain dry granules; (c) milling the dry granules obtained in step (b); (d) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a second blend; (e) forming dry granules comprising the second blend, or optionally mixing a granulating solution with the second blend obtained in step (d) to form wet granules, then drying the wet granules to form dry granules; (f) milling the dry granules obtained in step (e); (g) mixing the milled dry granules obtained in steps (c) and (f) with one or more excipients to form a third blend; and (h) compressing the third blend to form a tablet. Some embodiments provide a process for preparing a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) compressing the dry granules from step (b) or step (c) to form the tablet core; and (e) applying the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, to the surface of the tablet core, forming an outer layer. Some embodiments provide a process for preparing, a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) mixing the dry granules obtained in step (b) or step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; and (f) applying the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, to the surface of the tablet core, forming an outer layer. Some embodiments provide a process for preparing, a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules; (c) drying the wet granules obtained in step (b) to form dry granules; (d) milling the dry granules obtained in step (c); (e) mixing the milled dry granules obtained in step (d) with one or more excipients to form a second blend; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution to the third blend obtained in step (f), and mixing the solution and third blend to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the second blend obtained in step (e) and the fourth blend obtained in step (i); and (k) filling a capsule with the mixture obtained in step (j). Some embodiments provide a process for preparing, a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a capsule fill; and (j) filling a capsule with the tablet core and the capsule fill. Some embodiments provide a method of treating a PPARγ-mediated disease or disorder, comprising administering a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, to a subject in need thereof. In some embodiments, the PPARγ-mediated disease or disorder is type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), or a combination of any of the foregoing. Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. Methods and materials are described herein for use in the present invention; other, suitable methods and materials known in the art can also be used. The materials, methods, and examples are illustrative only and not intended to be limiting. All publications, patent applications, patents, sequences, database entries, and other references mentioned herein are incorporated by reference in their entirety. In case of conflict, the present specification, including definitions, will control. Other features and advantages of the invention will be apparent from the following detailed description and figures, and from the claims. DETAILED DESCRIPTION Definitions Reference to the term “about” has its usual meaning in the context of pharmaceutical compositions to allow for reasonable variations in amounts that can achieve the same effect and also refers herein to a value of plus or minus 10% of the provided value. For example, "about 20" means or includes amounts from 18 to and including 22. The term “administration” or “administering” refers to a method of giving a dosage of a compound or pharmaceutical composition to a vertebrate or invertebrate, including a mammal, a bird, a fish, or an amphibian. The preferred method of administration can vary depending on various factors, e.g., the components of the pharmaceutical composition, the site of the disease, and the severity of the disease. The term “CHS-131” as used herein refers to a compound of Formula (I):

or a pharmaceutically acceptable salt or solvate thereof. The compound of Formula (I) is a selective peroxisome proliferator-activated receptor (PPAR) γ modulator. The compound of Formula (I) is disclosed in, for example, U.S. Patent Nos.7,041,691; 6,200,995; 6,583,157; 6,653,332; and U.S. Publication Application No. 2016/0260398, the contents of each of which are incorporated by reference herein in their entireties. The compound of Formula (I) can be prepared, for example, by the methods described in U.S. Patent No.6,583,157 or US Patent No.6,200,995, each of which is incorporated by reference in its entirety herein. In some embodiments, different salts, e.g., besylate, tosylate HCl, or HBr salts, and/or polymorphs of the compound of Formula (I) are used within the methods and compositions described herein. Salts and polymorphs of the compound of Formula (I), such as those provided herein, can be prepared according to the methods described in U.S. Patent. Nos. 6,583,157 and 7,223,761, the contents of each of which are incorporated by reference in their entireties. As used herein, “PPAR-α agonist” refers to a compound that activates PPAR-α to produce a biological response. Examples of PPAR-α agonists include, but are not limited to, amphipathic carboxylic acids, such as seladelpar, ciprofibrate, bezafibrate, and fenofibrate. As used herein, “PPAR-δ agonist” refers to a compound that activates PPAR-δ to produce a biological response. Examples of PPAR-δ agonists include, but are not limited to, GW501516. As used herein, “dual PPAR-α and PPAR-δ agonist” refers to a compound that activates both PPAR-α and PPAR-δ to produce a biological response. Examples of dual PPAR-α and PPAR-δ agonists include, but are not limited to elafibranor. The term “SGLT-2 inhibitor” as used herein refers to a compound that inhibits the Sodium Glucose Co-Transporter-2 (SGLT-2). SGLT-2 inhibitors disrupt reabsorption of glucose by the kidneys and thus exert a glucose-lowering effect. By enhancing glucosuria, independently of insulin, SLGT-2 inhibitors have been shown to treat type 2 diabetes and improve cardiovascular outcomes. See, Wright, 2001, Am J Physiol Renal Physiol 280:F10; and Scheen, 2018, Circ Res 122:1439. SGLT2 inhibitors include a class of drugs known as gliflozins. The term “SGLT-2 inhibitor” is not limited to compounds that only inhibit SGLT-2, thus includes compounds that have other activities in addition to SGLT-2 inhibition. Examples of SGLT-2 inhibitors include, but are not limited to, bexagliflozin, canagliflozin (INVOKANA®), dapagliflozin (FARXIGA®), empagliflozin (JARDIANCE®), ertugliflozin (STEGLATRO™), ipragliflozin (SUGLAT®), luseogliflozin (LUSEFI®), remogliflozin, serfliflozin, licofliglozin, sotagliflozin (ZYNQUISTA^TM), and tofogliflozin. As used herein, the term “amorphous” refers to a solid material having no long range order in the position of its molecules. The molecules in an amorphous solid are arranged in a random manner so that there is no well-defined arrangement, e.g., molecular packing, and no long range order. Amorphous solids are generally isotropic, i.e. exhibit similar properties in all directions and do not have definite melting points. For example, an amorphous material is a solid material having no sharp characteristic crystalline peak(s) in its X-ray power diffraction (XRPD) pattern (i.e., is not crystalline as determined by XRPD). Instead, one or several broad peaks (e.g., halos) appear in its XRPD pattern. Broad peaks are characteristic of an amorphous solid. As used herein, the term “substantially amorphous” refers to a solid material having little or no long range order in the position of its molecules. For example, substantially amorphous materials have less than about 15% crystallinity (e.g., less than about 10% crystallinity or less than about 5% crystallinity). Moreover, ‘substantially amorphous’ includes the descriptor, ‘amorphous’, which refers to materials having no (0%) crystallinity (e.g., no detectable crystallinity under standard XRPD conditions). The term “excipient,” as used herein, refers to an inactive substance that serves as the vehicle or medium for an active substance. Excipients include, but are not limited to fillers (e.g., lactose, microcrystalline cellulose, dextrose, sucrose, mannitol, sorbitol, starch, dibasic calcium carbonate, and magnesium stearate), disintegrants (e.g., starch, microcrystalline cellulose, sodium starch glycolate, crosscarmellose sodium, crospovidone, gums, and alginates), lubricants (magnesium or calcium stearate, PEG 4000, and PEG 6000), granulating agents (starch, pregelatinized starch, polyvinylpyrrolidone, hydroxypropylmethylcellulose, methyl cellulose, and acacia), and glidants (colloidal silicon dioxide, talc, and magnesium carbonate). As used herein, the term “granulating solution” refers to a solvent, such as a volatile solvent, or a solution that wets a blend, which upon agitation forms wet granules. Granulating solutions include, for example, solvents such as water, ethanol, and isopropanol, or combinations thereof, as well as solutions of one or more excipients in water, ethanol, isopropanol, or combinations thereof, for example, a solution of povidone in water. As used herein, the term “tablet core” refers to the innermost portion of a tablet that contains drug substance, i.e., the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof and/or the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. As used herein, the term “outer layer” refers to the outermost portion of a tablet that contains drug substance, i.e., the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof and/or the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the outer layer is in contact with a coating and/or seal. As used herein, the term “intermediate layer” refers to a separating layer in contact with both the tablet core and the outer layer. Exemplary intermediate layers include, but are not limited to carbopols, hydroxypropylmethylcellulose, and other polymers. As used herein, “solvate” means a physical association of a compound with one or more solvent molecules. The solvate may comprise either a stoichiometric or nonstoichiometric amount of the solvent molecules. For example, a solvate with a nonstoichiometric amount of solvent molecules may result from partial loss of solvent from the solvate. Exemplary solvates include, but are not limited to hydrates, ethanolates, propylene glycol hydrates, and hemihydrates. Moreover, as used herein, the phrase “pharmaceutically acceptable salt or solvate,” refers to salts of a compound, solvates of a compound, as well as salts of solvates of a compound. For example, a pharmaceutically acceptable salt or solvate of the compound of Formula (I) includes the besylate salt of Formula (I), the hydrate of Formula (I), and the Formula (I) besylate hydrate. The terms “fixed combination” and “fixed dose combination,” used interchangeably herein, refer to a single composition or single dosage form comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In contrast, for example, a non-fixed combination or non-fixed dose combination refer to combination therapy where each active agent is formulated as a separate composition or dosage form, such that they may be administered concurrently or sequentially with variable intervening time limits. A “therapeutically effective amount” of a compound as provided herein is an amount that is sufficient to achieve the desired therapeutic effect and can vary according to the nature and severity of the disease condition, and the potency of the compound. A therapeutic effect is the relief, to some extent, of one or more of the symptoms of the disease, and can include curing a disease. “Curing” means that the symptoms of active disease are eliminated. However, certain long-term or permanent effects of the disease can exist even after a cure is obtained (such as, e.g., extensive tissue damage). In some embodiments, a “therapeutically effective amount” of a compound as provided herein refers to an amount of the compound that is effective as a monotherapy. In some embodiments, the amount of each compound as provided herein is a therapeutically effective amount. In such embodiments, the amount of each compound is effective in treating a PPARγ-mediated disease or disorder. In some embodiments, the amounts of the two compounds as provided herein together are effective in treating a PPARγ-mediated disease or disorder (e.g., the amounts of the compound of Formula (I) and a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist together are effective in treating a PPARγ-mediated disease or disorder). In such embodiments, the amount of each agent is also referred to as a “jointly therapeutically effective amount.” In some embodiments, the amounts of the two compounds as provided herein together are effective in treating a PPARγ- mediated disease or disorder (e.g., the amounts of the compound of Formula (I) and a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist together are effective in treating a PPARγ- mediated disease or disorder). In such embodiments, the amount of each agent is also referred to as a “jointly therapeutically effective amount.” The term “synergy” or “synergistic” is used herein to mean that the effect of the combination of the two or more therapeutic agents of the combination therapy is greater than the sum of the effect of each agent when administered alone. A “synergistic amount” or "synergistically effective amount" is an amount of the combination of the two combination partners that results in a synergistic effect, as “synergistic” is defined herein. Determining a synergistic interaction between two or more combination partners, the optimum range for the effect and absolute dose ranges of each component for the effect may be definitively measured by administration of the combination partners over different w/w (weight per weight) ratio ranges and doses to patients in need of treatment. However, the observation of synergy in in vitro models or in vivo models can be predictive of the effect in humans and other species and in vitro models or in vivo models exist to measure a synergistic effect and the results of such studies can also be used to predict effective dose and plasma concentration ratio ranges and the absolute doses and plasma concentrations required in humans and other species by the application of pharmacokinetic/pharmacodynamic methods. Exemplary synergistic effects includes, but are not limited to, enhanced therapeutic efficacy, decreased dosage at equal or increased level of efficacy, reduced or delayed development of drug resistance, reduction of unwanted drug effects (e.g. side effects and adverse events) of at least one of the therapeutic agents, and both simultaneous enhancement or equal therapeutic actions (e.g., the same therapeutic effect as at least one of the therapeutic agents) and reduction of unwanted drug effects of at least one of the therapeutic agents. For example, synergistic effects can include, but are not limited to reducing the risk of developing end-stage kidney disease (ESRD), reducing serum creatinine, reducing cardiovascular death and hospitalization for heart failure, reducing cardiovascular death and hospitalization for heart failure in subject with cardiovascular disease or multiple cardiac risk factors, reducing weight gain, improved cardiovascular function, and reducing diabetic nephropathy with albuminuria. As used herein, the terms “treat” or “treatment” refer to therapeutic or palliative measures. Beneficial or desired clinical results include, but are not limited to, alleviation, in whole or in part, of symptoms associated with a disease or disorder or condition, diminishment of the extent of disease, stabilized (i.e., not worsening) state of disease, delay or slowing of disease progression, amelioration or palliation of the disease state (e.g., one or more symptoms of the disease), and remission (whether partial or total), whether detectable or undetectable. “Treatment” can also mean prolonging survival as compared to expected survival if not receiving treatment. As used herein, “subject” refers to any subject, particularly a mammalian subject, for whom diagnosis, prognosis, or therapy is desired, for example, a human. As used herein, a “PPARγ-mediated disease or disorder” is a condition that results, directly or indirectly, from dysregulation of PPARγ, for example, protein expression above or below normal levels, or protein activity above or below normal levels. PPARγ-mediated diseases or disorders include, but are not limited to diabetes (including type 1 diabetes and type 2 diabetes), hypercholesterolemia, hyperlipidemia, rheumatoid arthritis, atherosclerosis, nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), chronic kidney disease (CKD), or pulmonary arterial hypertension (PAH). In some embodiments, the subject has NAFLD with attendant liver fibrosis. In some embodiments, the subject has NASH with attendant liver fibrosis. In some embodiments, the subject has NAFLD and type 2 diabetes. In some embodiments, the subject has NASH and type 2 diabetes. In some embodiments, the subject has type 2 diabetes and cardiovascular disease. In some embodiments, the subject has NAFLD and cardiovascular disease. In some embodiments, the subject has NASH and cardiovascular disease. In some embodiments, the subject has type 2 diabetes, cardiovascular disease, and NAFLD. In some embodiments, the subject has type 2 diabetes, cardiovascular disease, and NASH. Some embodiments provide a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients. In some embodiments, the compound of Formula (I) is provided in the form of a free base. In other embodiments, the compound of Formula (I) is provided as a pharmaceutically acceptable salt. Non-limiting examples of pharmaceutically acceptable salts include 2,2-dichloroacetic acid, 2-hydroxyethanesulfonic acid, 2-oxoglutaric acid, 4-acetamidobenzoic acid, 4-aminosalicylic acid, acetic acid, adipic acid, ascorbic acid (L), aspartic acid (L), benzenesulfonic acid (besylate), benzoic acid, camphoric acid (+), camphor-10-sulfonic acid (+), capric acid (decanoic acid), caproic acid (hexanoic acid), caprylic acid (octanoic acid), carbonic acid, cinnamic acid, citric acid, cyclamic acid, dodecylsulfuric acid, ethane-1,2-disulfonic acid, ethanesulfonic acid, fumaric acid, galactaric acid, gentisic acid, glucoheptonic acid (D), gluconic acid (D), glucuronic acid (D), glutamic acid, glutaric acid, glycerophosphoric acid, glycolic acid, hippuric acid, hydrobromic acid, hydrochloric acid, isobutyric acid, lactic acid (DL), lactobionic acid, lauric acid, maleic acid, malic acid (-L), malonic acid, mandelic acid (DL), methanesulfonic acid, nicotinic acid, nitric acid, oleic acid, oxalic acid, palmitic acid, pamoic acid, phosphoric acid, proprionic acid, pyroglutamic acid (-L), salicylic acid, sebacic acid, stearic acid, succinic acid, sulfuric acid, tartaric acid (+L), thiocyanic acid, p-toluenesulfonic acid, andundecylenic acid, or a combination of any of the foregoing. In some embodiments, the compound of Formula (I) is in the form of a besylate salt. In some embodiments, the compound of Formula (I) is in the form of an HCl salt. In some embodiments, the compound of Formula (I) is in the form of an HBr salt. In some embodiments, the compound of Formula (I) is in the form of a tosylate salt. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is seladelpar, ciprofibrate, bezafibrate, fenofibrate, GW5101516, or elafibranor, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is a free base. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is a pharmaceutically acceptable salt. In some embodiments, the PPAR-α agonist, PPAR- δ agonist, or dual PPAR-α/δ agonist is a pharmaceutically acceptable solvate. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is a pharmaceutically acceptable salt of a pharmaceutically acceptable solvate. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is a pharmaceutically acceptable solvate of a free base. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in an amount from about 40 mg to about 300 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in an amount from about 40 mg to about 60 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in an amount from about 50 mg to about 100 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in an amount from about 100 mg to about 200 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in an amount from about 150 mg to about 250 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in an amount from about 200 mg to about 300 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in an amount of about 40 mg, about 50 mg, about 60 mg, about 100 mg, about 200 mg, or about 300 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is fenofibrate. In some embodiments, the fenofibrate is present in an amount of about 40 mg or about 120 mg. In some embodiments, the fenofibrate is present in an amount of about 50 mg or about 160 mg. In some other embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is ciprofibrate. In some embodiments, the ciprofibrate is present in an amount of about 100 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is bezafibrate. In some embodiments, the bezafibrate is present in an amount of about 200 mg. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is elafibranor. In some embodiments, the elafibranor is present in an amount of about 300 mg. In some embodiments, the dose is a therapeutically effective amount. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is seladelpar. In some embodiments, the seladelpar is present in an amount of about 5 mg or about 10 mg. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 0.1 mg to about 10 mg. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 0.5 mg to about 5 mg. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 1 mg to about 3 mg. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount of 1.5 mg or 3 mg. In some embodiments, the amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 0.5 to about 4 milligrams (mg). For example, from about 0.5 to about 3.5 mg, about 1 to about 3 mg, or about 1.5 to about 2.5 mg. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is administered at a dose from about 0.5 to about 1.5 mg, about 1 to about 2 mg, about 1.5 to about 2.5 mg, about 2 to about 3 mg, or about any value in between. In some embodiments, the dose is a therapeutically effective amount. In some embodiments, the composition is formulated for administration twice a day or daily. In some embodiments, the composition is formulated for administration daily. In some embodiments, the composition comprises particles comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the particles are in the form of a powder. In some embodiments, the particles comprise the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and one or more excipients. In some embodiments, the particles consist essentially of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the particles are micronized. In some embodiments, 90% of the mass of the micronized particles have a size (d90) of about 2 μm to about 10 μm, or any value in between. For example, about 2 μm, about 2.5 μm, about 3 μm, about 3.5 μm, about 4 μm, about 4.5 μm, about 5 μm, about 5.5 μm, about 6 μm, about 6.5 μm, about 7 μm, about 7.5 μm, about 8 μm, about 8.5 μm, about 9 μm, about 9.5 μm, about 10 μm, or any value in between. In some embodiments, 50% of the mass of the micronized particles have a size (d50) of less than or equal to about 6 μm, or any value not exceeding about 6 μm. In some embodiments, 50% of the mass of the micronized particles have a size (d50) of about 2 μm to about 6 μm, or any value in between. For example, about 0.5 μm, about 1 μm, about 1.5 μm, about 2 μm, about 2.25 μm, about 2.5 μm, about 2.75 μm, about 3 μm, about 3.25 μm, about 3.5 μm, about 3.75 μm, about 4 μm, about 4.25 μm, about 4.5 μm, about 4.75 μm, about 5 μm, about 5.25 μm, about 5.5 μm, about 5.75 μm, about 6 μm, or any value in between. In some embodiments, the size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof. Direct imaging provides the volume distribution of particles, removing the grouping of particle sizes which is characteristic of sieve analyses by determining the full range of particle sizes in the sample and hence drawing the true volumetric distribution. In direct imaging particles are illuminated and imaged from the same side. Direct imaging of particles also allows morphology information to be measured as well as size distribution data, for example, aspect ratio of particles (maximum and minimum diameter measurements), surface quality, and roughness. Laser diffraction relies on detectors that measure the light-scattering effect caused by the interaction of a laser beam with particles. Similar to sieve analysis particle characteristics other than size cannot be measured. In some embodiments, the composition comprises granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the composition comprises grains comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the composition comprises particles comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the particles are in the form of a powder. In some embodiments, the particles comprise the PPAR-α agonist, PPAR-δ agonist, or dual PPAR- α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, and one or more excipients. In some embodiments, the particles consist essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the particles are micronized. In some embodiments, 90% of the mass of the micronized particles have a size (d90) of less than or equal to about 250 μm. In some embodiments, 90% of the mass of the micronized particles have a size (d90) of about 2 μm to about 10 μm, or any value in between. For example, about 2 μm, about 2.5 μm, about 3 μm, about 3.5 μm, about 4 μm, about 4.5 μm, about 5 μm, about 5.5 μm, about 6 μm, about 6.5 μm, about 7 μm, about 7.5 μm, about 8 μm, about 8.5 μm, about 9 μm, about 9.5 μm, about 10 μm, or any value in between. In some embodiments, 50% of the mass of the micronized particles have a size (d50) of less than or equal to about 100 μm. In some embodiments, 50% of the mass of the micronized particles have a size (d50) of less than or equal to about 100 μm. For example, about 2 μm, about 2.25 μm, about 2.5 μm, about 2.75 μm, about 3 μm, about 3.25 μm, about 3.5 μm, about 3.75 μm, about 4 μm, about 4.25 μm, about 4.5 μm, about 4.75 μm, about 5 μm, about 5.25 μm, about 5.5 μm, about 5.75 μm, about 6 μm, or any value in between. In some embodiments, the size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof. In some embodiments, the size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof. In some embodiments, the composition comprises granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the composition comprises grains comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the composition is in the form of a tablet. In some embodiments, the composition is in the form of a capsule. In some embodiments, the capsule is a gelatin capsule or a hydroxypropylmethylcellulose (HPMC) capsule. In some embodiments, the tablet comprises a tablet core and an outer layer; wherein the tablet core comprises the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof; and wherein the outer layer comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the tablet core contacts the outer layer. In some embodiments, the composition further comprises an intermediate layer between the tablet core and the outer layer and contacting the tablet core and outer layer. In some embodiments, the intermediate layer comprises one or more excipients. In some embodiments, the intermediate layer comprises one excipient. Exemplary intermediate layers include, but are not limited to a carbopol or hydroxypropylmethylcellulose. In some embodiments, the dissolution rate of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is about the same in a composition with an intermediate layer as in a reference composition lacking the intermediate layer. In some embodiments, the dissolution rate of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is about the same in a composition with an intermediate layer as in a reference composition lacking the intermediate layer. In some embodiments, the composition further comprises an immediate release coating around the outer layer. Exemplary immediate release coatings include, but are not limited to film coatings. In some embodiments, the outer layer consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the outer layer comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, and one or more excipients. In some embodiments, the outer layer comprises granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the tablet core further comprises one or more excipients. In some embodiments, the one or more excipients are selected from Acrylates Copolymer, Adipic Acid, Agar, Alginic Acid, Alkyl Aryl Sodium Sulfonate, Allantoin, Aluminum Acetate, Aluminum Hydroxide, Aluminum Monostearate, Aluminum Oxide, Aluminum Polyester, Aluminum Silicate, Aluminum Silicate Pentahydrate, Aluminum Starch Octenylsuccinate, Aluminum Stearate, Aluminum Sulfate Anhydrous, Aminobenzoate Sodium, Ammonio Methacrylate Copolymer, Ammonio Methacrylate Copolymer Type A, Ammonio Methacrylate Copolymer Type B, Ammonium Acetate, Ammonium Calcium Alginate, Ammonium Chloride, Ammonium Lauryl Sulfate, Ammonium Phosphate Dibasic, Ammonium Sulfate, Anhydrous Citric Acid, Anhydrous Dextrose, Anhydrous Dibasic Calcium Phosphate, Anhydrous Lactose, Anhydrous Trisodium Citrate, Anidrisorb 85/70, Arginine, Ascorbic Acid, Ascorbyl Palmitate, Aseptoform M, Aspartame, Aspartic Acid, Barium Sulfate, Benzensulfonic Acid, Benezethonium Chloride, Benzocaine, Benzododecinium Bromide, Benzoic Acid, Benzoin Resin, Butyl Ester Of Methyl Vinyl Ether/Maleic Anhydride Copolymer (125000 MW), Butyl Methacrylate And Methyl Methacrylate Copolymer (3:1; 150000 MW), Butyl Stearate, Butylated Hydroxyanisole, Butylated Hydroxytoluene, Butylene Glycol, Butylparaben, C13-14 Isoparaffin/Laureth-7/Polyacrylamide, Calcium, Calcium Acetate, Calcium Alginate And Ammonium Alginate, Calcium Carbonate, Calcium Chloride, Calcium Citrate, Calcium Hydroxide, Calcium Lactate, Calcium Phosphate, Calcium Phosphate, dibasic monohydrate, Calcium Phosphate, monobasic, anhydrous, Calcium Polycarbophil, Calcium Pyrophosphate, Calcium Saccharate, Calcium Silicate, Calcium Stearate, Calcium Sulfate, Calcium Sulfate Anhydrous, Calcium Sulfate Dihydrate, Caldiamide Sodium, Caprylic/Capric/Succinic Triglyceride, Caprylocaproyl Polyoxylglycerides 8,, Carbomer 1382, Carbomer Copolymer Type A (Allyl Pentaerythritol Crosslinked), Carbomer Copolymer Type B (Allyl Pentaerythritol Crosslinked), Carbomer Homopolymer Type A (Allyl Pentaerythritol Crosslinked), Carbomer Homopolymer Type B (Allyl Pentaerythritol Crosslinked), Carbomer Homopolymer Type B (Allyl Sucrose Crosslinked), Carbomer Homopolymer Type C (Allyl Pentaerythritol Crosslinked), Carbon Dioxide, Carboxymethyl Starch, Carboxymethylcellulose, Carboxymethylcellulose Calcium, Carboxymethylcellulose Sodium, Carboxypolymethylene, Carnauba Wax, Carrageenan, Carrageenan Calcium, Carrageenan Sodium, Cellulose Acetate, Cellulose Acetate CA-320S, Cellulose Acetate CA-398-10, Cellulose Microcrystalline/Carboxymethylcellulose Sodium, Cellulose, oxidized, Cellulosic Polymers, Citric Acid Monohydrate, Copovidone K25-31, Coriander Oil, Corn Glycerides, Corn Oil, Corn Oil Mono-And Di-Glycerides, C18, Corn Starch, partially hydrolyzed, Corn Syrup, Cottonseed Oil, Creatinine, Croscarmellose, Croscarmellose Sodium, Crospovidone, Cupric Sulfate, Cutina, Cyanocobalamin, Cyclomethicone, Cyclomethicone 5, Cyclomethicone/Dimethicone Copolyol, Dehydag Wax Sx, Dehydroacetic Acid, Dehymuls E, Denatonium Benzoate, Detosu/Triethylene Glycol/Triethylene Glycol Polyglycolide Copolymer, Dextran, Dextran 40, Dextrins Modified, Dextrose, Dextrose Monohydrate, Diacetylated Monoglycerides, Diatomaceous Earth, Diazolidinyl Urea, Dibasic Calcium Phosphate Dihydrate, Dibasic Potassium Phosphate, Dibutyl Sebacate, Dichlorobenzyl Alcohol, Diethanolamine, Diethyl Phthlate, Diethyl Sebacate, Diethylene Glycol Monoethyl Ether, Dihydroxyaluminum Aminoacetate, Dihydroxyaluminum Sodium Carbonate, Diisopropanolamine, Diisopropyl Adipate, Diisproplybenzothiazyl-2- suflenamide, Dimethicone 100, Dimethicone 350, Dimethiconol/Trimethylsiloxysilicate Crosspolymer (40/60 W/E; 1000000 PA.S), Dimethoxane, Dimethyl Isosorbide, Dimethyl Sulfoxide, Dimethylaminoethyl Methacrylate – Butyl Methacrylate –Methyl Methacrylate Copolymer, Dinoseb-Ammonium, Dipalmitoylphosphatidylglycerol, DL-Dipropylebe Glycol, Disodium Citrate Sesquihydrate, Disodium Cocoamphodiacetate, Disodium Hydrogen Citrate, Disodium Laureth Sulfosuccinate, Disodium Lauryl Sulfosuccinate, Distearoylphosphatidylcholine, DL-DMDM Hydantoin, Docusate Sodium, Docusate Sodium/Sodium Benzoate, Edetate Calcium Disodium, Edetate Disodium, Edetate Disodium Anhydrous, Edetate Sodium, Edetate Trisodium, Edetic Acid, Ethyl Acrylate and Methyl Methacrylate Copolymer (2:1; 600000 MW), Ethyl Acrylate and Methyl Methacrylate Copolymer (2:1; 750000 MW), Ethylcellulose, Ethylcellulose (10 MPA.S), Ethylcellulose (100 MPA.S), Ethylcellulose (20 MPA.S), Ethylcellulose (4 MPA.S), Ethylcellulose (45 MPA.S), Ethylcellulose (50 MPA.S), Ethylcellulose (7 MPA.S), Ethylene-Propylene Copolymer, Ethylene-Vinyl Acetate Copolymer (28% Vinyl Acetate), Ethylene-Vinyl Acetate Copolymers, Ethylhexyl Hydroxystearate, Ethylparaben, Ethylparaben Sodium, Fructose, Fumaric Acid, Fumaryl Diketopiperazine, Galactose, Galactose Monohydrate, Gelatin, Gelatin Capsule, hard, Gelatin Hydrolysate, Gelatin Type A Porcine (160 Bloom), Gelatin Type B Bovine (160 Bloom), Gelatin Type B Bovine (200 Bloom), Gelatin Type B Bovine (230 Bloom), Gluceptate Sodium, Gluconic Acid, Gluconolactone, Glucose Syrup, hydrogenated, Glumatic Acid Hydrochloride, Glutaral, Glycerin, Glycerin Polymer Solutions I-137, Glycerin Polymer Solutions IM-137, Glyceryl 1- Stearate, Glyceryl Behenate/Eicosadioate, Glyceryl Dibehenate, Glyceryl Distearate, Glyceryl Isostearate, Glyceryl Laurate, Glyceryl Mono and Dicaprylocaprate, Glyceryl Mono and Dipalmitostearate, Glyceryl Monoprylate, Glyceryl Monocaprylocaprate, Glyceryl Monocitrate, Glyceryl Monostearate, Glyceryl Oleate, Glyceryl Oleate/Propylene Glycol, Glyceryl Palmitate, Glyceryl Palmitostearate, Glyceryl Ricinoleate, Glyceryl Stearate SE, Glyceryl Stearate/Peg Stearate, Glyceryl Stearate/Peg-100 Stearate, Glyceryl Stearate/Peg-40 Stearate, Glyceryl Tristearate, Glycine, Glycine Hydrochloride, Glycol Stearate, Guanidine Hydrochloride, Guar Gum, Histidine, Hydrogenated Starch Hydrolysate, Hydroxyethyl Cellulose (140 MPA.S AT 5%), Hydroxyethyl Cellulose (2000 MPA.S AT 1%), Hydroxyethyl Cellulose (280 MPA.S AT 2%), Hydroxyethyl Cellulose (4000 MPA.S AT 1%), Hydroxyethyl Cellulose, unspecified, Hydroxyethyl Ethylcellulose, Hydroxyethylpiperazine Ethane Sulfonic Acid, Hydroxyethyl Cellulose, Hydropropyl Betadex, Hydropropyl Cellulose, Hydropropyl Cellulose (110000 WAMW), Hydropropyl Cellulose (1600000 WAMW), Hydropropyl Cellulose (20000 WAMW), Hydropropyl Cellulose (430000 WAMW), Hydropropyl Cellulose (45000 WAMW), Hydropropyl Cellulose (70000 WAMW), Hydropropyl Cellulose (90000 WAMW), Hymetellose (50 MPA.S), Hypromellose 2208 (100 MPA.S), Hypromellose 2208 (100000 MPA.S), Hypromellose 2208 (15000 MPA.S), Hypromellose 2208 (3 MPA.S), Hypromellose 2208 (4 MPA.S), Hypromellose 2208 (4000 MPA.S), Hypromellose 2906 (4000 MPA.S), Hypromellose 2906 (50 MPA.S), Hypromellose 2910 (10000 MPA.S), Hypromellose 2910 (15 MPA.S), Hypromellose 2910 (15000 MPA.S), Hypromellose 2910 (3 MPA.S), Hypromellose 2910 (4000 MPA.S), Hypromellose 2910 (5 MPA.S), Hypromellose 2910 (6 MPA.S), Hypromellose Acetate Succinate, Hypromellose Acetate Succinate 06081224 (3 MM2/S), Hypromellose Phthalate, Hypromellose Phthalate (24% PHTHALATE, 55 CST), Hypromellose Phthalate (31% PHTHALATE, 40 CST), Hypromelloses, Hystrene, Isoleucine, Isooctyl Acrylate/Acrylamide/Vinyl Acetate Copolymer, kollidon VA 64 polymer, Isopropyl Alcohol, Isopropyl Isostearate, Isopropyl Myristate, Isopropyl Palmitate, Isostearic Acid, Isostearyl Alcohol, Isotonic Sodium Chloride Solution, Kollidon SR, Lactic Acid, Lactic Acid, dl-, Lactic Acid, l-, Lactitol Monohydrate, Lactobionic Acid, Lactose, Lactose Monohydrate, Lactose Monohydrate-Cellulose, microcrystalline, Laneth, Lauramine Oxide, Laureth Sulfate, Laureth-2, Laureth-23, Laureth-4, Lauric Diethanolamide, Lauric Myristic Monoethanolamide, Lauric/Myristic Diethanolamide, Lauroyl Peg-32 Glycerides, Lauroyl Polyoxylglycerides, Lauryl Sulfate, Lecithin, Lecithin, soybean, Leucine, Levulinic Acid, Low- Substituted Hydroxypropyl Cellulose (11% Hydroxypropyl; 100000 MW), Low-Substituted Hydroxypropyl Cellulose (11% Hydroxypropyl; 120000 MW), Low-Substituted Hydroxypropyl Cellulose (11% Hydroxypropyl; 130000 MW), Low-Substituted Hydroxypropyl Cellulose, unspecified ludipress, Lysine, Lysine Acetate, Lysine Monohydrate, Magnesium Aluminometasilocate Type IA, , Magnesium Aluminum Silicate, Magnesium Carbonate, Magnesium Chloride, Magnesium Hydroxide, Magnesium Nitrate, Magnesium Oxide, Magnesium Palmitostearate, Magnesium Silicate, Magnesium Stearate, Magnesium Sulfate, Magnesium Sulfate Anhydrous, Magnesium Trisilicate, Maleic Acid, Malic Acid, Malic Acid, l-, Maltitol, Maltose Anhydrous, Maltose Monohydrate, Mannitol, Metaphosphoric Acid, Methacrylic Acid – Ethyl Acrylate Copolymer (1:1) Type A, Methacrylic Acid – Methyl Merhacrylate Copolymer (1:1), Methacrylic Acid – Methyl Merhacrylate Copolymer (1:2), Methacrylic Acid Copolymer, Methansulfonic Acid, Methionine, Methyl Acrylate – Methyl Methacrylate, Methylcellulose, Methylcellulose (15 MPA.S), Methylcellulose (1500 MPA.S), Methylcellulose (400 MPA.S), Methylchloroisothiazolinone, Methylchloroisothiazolinone/Methylisothiazolinone Mixture, Methylparaben, Methylparaben Sodium, Methylpyrrolidone, Mica, Microcrystalline Cellulose, Modified Corn Starch (1-Octenyl Succinic Anhydride), Mono and Diglyceride, Monoethanolamine, Monoglycerides, Monosodium Citrate, Monosodium Glutamate, Monothioglycerol, Parabens, Paraffin, Pectin, Pectin, cirtrus, Peg 6-32 Stearate/Glycol Stearate, Peg/Ppg-18/18 Dimethicone, Peg-100 Stearate, Peg-120 Glyceryl Stearate, Peg-120 Methyl Glucose Dioleate, Peg-2 Stearate, Peg-20 Methyl Glucose Sesquistearate, Peg-20 Sorbitan Isostearate, Peg-25 Propylene Glycol Stearate, Peg-40 Castor Oil. Peg-40 Sorbitan Diisostearate, Peg-5 Oleate, Peg-6 Isostearate, Peg-60 Hydrogenated Castor Oil, Peg-7 Methyl Ether, Peg-75 Lanolin, Peg-8 Laurate, Peg-8 Stearate, Pegoxol 7 Stearate, Phenylalanine, Phenylethyl Alcohol, Phenylmercuric Acetate, Phenylmercuric Nitrate, Phospholid, Phosphoric Acid, Pigment Blend PB-2417 Pink, Pigmented Polyethylene/Polyester 1501 Film, Poloxamer 124, Poloxamer 182, Poloxamer 188, Poloxamer 331, Poloxamer 407, Poly(DL-Lactic-Co-Glycolic Acid), (50:50; 12000 MW), Poly(Methyl Acrylate-Co-Methyl Metharylate-Co-Methacrylic Acid 7:3:1; 280000 MW), Polyacrylic Acid (250000 MW), Polybutene (1400 MW), Polycarbophil, Polydextrose, Polydextrose K, Polyethylene Glycol 1000, Polyethylene Glycol 1450, Polyethylene Glycol 1600, Polyethylene Glycol 200, Polyethylene Glycol 20000, Polyethylene Glycol 300, Polyethylene Glycol 3000, Polyethylene Glycol 3350, Polyethylene Glycol 400, Polyethylene Glycol 4000, Polyethylene Glycol 4500, Polyethylene Glycol 540, Polyethylene Glycol 600, Polyethylene Glycol 6000, Polyethylene Glycol 800, Polyethylene Glycol 8000, Polyethylene Glycol 900, Polyethylene Oxide 100000, Polyethylene Oxide 1000000, Polyethylene Oxide 200000, Polyethylene Oxide 2000000, Polyethylene Oxide 7000000, Polyethylene Oxide 900000, Polyglactin, Polyglyceryl-3 Oleate, Polyisobutylene, Polyisobutylene/Polybutene Adhesive, Polyactide, Polyoxyethylene-Polyoxypropylene 1800, Polyoxyethylene Alcohols, Polyoxyethylene Fatty Acid Esters, Polyoxyl 15 Hydroxystearate, Polyoxyl 20 Cetostearyl Ether, Polyoxyl 35 Castor Oil, Polyoxyl 40 Hydrogenated Castor Oil, Polyoxyl 40 Stearate, Polyoxyl 6 and Polyoxyl 32 Palmitostearate, Polyoxyl Distearate, Polyoxyl Glyceryl Stearate, Polyoxyl Stearate, Polypropylene, Polypropylene Glycol, Polyquaternium-10, Polysaccharides Soy, Polysiloxane, Polysorbate 20, Polysorbate 40, Polysorbate 60, Polysorbate 80, Polyvinyl Acetate, Polyvinyl Alcohol, Polyvinyl Alcohol (108000 MW), Polyvinyl Alcohol (94000 MW), Polyvinyl Alcohol Graft Polyethylene Glycol Copolymer (3:1; 45000 MW), Polyvinylacetal, Ponceau 3R, Ponceau Xylidine, Potassium Acetate, Potassium Alum, Potassium Bicarbonate, Potassium Bitartrate, Potassium Chloride, Potassium Citrate, Potassium Hydroxide, Potassium Metabisulfite, Potassium Metaphosphate, Potassium Phosphate, monobasic, Potassium Soap, Potassium Sorbate, Potassium Sulfate, Povidone K12, Povidone K17, Povidone K25, Povidone K27, Povidone K30, Povidone K90, Povidone/Eicosene Copolymer, Povidones, Powdered Cellulose, PPG-12/SZmDI Copolymer, PPG-15 Stearyl Ether, PPG-20 Methyl Glucose Ether Distearate, PPG-26 Oleate, Proline, Propylene Glycol, Propylene Glycol – Lecithin, Propylene Glycol Alginate, Propylene Glycol Diacetate, Propylene Glycol Dicaprylate, Propylene Glycol Monolaurate, Propylene Glycol Monopalmitostearate, Propylene Glycol Monostearate, Propylparaben, Propylparaben Sodium, Serine, Silicon Dioxide, Silicone, Silicone Adhesive 4302, Silicone Emulsion, Silicone/Polyester Film Strip, Silodrate, Simethicone, Sodium 1,2- Ethanedisulfonate, Sodium Acetate, Sodium Acetate Anhydrous, Sodium Alginate, Sodium Alkyl Sulfate, Sodium Aluminosilicate, Sodium Ascorbate, Sodium Benzoate, Sodium Bicarbonate, Sodium Bisulfate, Sodium Bisulfate Acetone, Sodium Bisulfite, Sodium Bitartrate, Sodium Borate, Sodium Carbonate, Sodium Carbonate Monohydrate, Sodium Cellulose, Sodium Cetostearyl Sulfate, Sodium Chlorate, Sodium Chloride, Sodium Cocomonoglyceride Sulfonate, Sodium Cocoyl Isethionate, Sodium Dithionate, Sodium Dithionite, Sodium Formaldehyde Sulfoxylate, Sodium Gluconate, Sodium Hydroxide, Sodium Hypochlorite, Sodium Iodide, Sodium Lactate, Sodium Lactate, l-, Sodium Laureth-2 Sulfate, Sodium Laureth-3 Sulfate, Sodium Laureth-5 Sulfate, Sodium Lauroyl Sarcosinate, Sodium Lauryl Sulfate, Sodium Lauryl Sulfoacetate, Sodium Metabisulfite, Sodium Metaphosphate, insoluble, Sodium Methyl Cocoyl Taurate, Sodium N-(Carbonyl-Methoxypolyethylene Glycol 2000)-1,2-Distearoyl-SN-Glycero-3- Phosphoethanolamine, Sodium Nitrate, Sodium Oleate, Sodium Phosphate, Sodium Polyacrylate, Sodium Polymetaphosphate, Sodium Polystyrene Sulfonate, Sodium Propionate, Sodium Pyrophosphate, Sodium Pyrrolidone Carboxylate, Sodium Salicylate, Sodium Silicate, Sodium Stearate, Sodium Stearyl Fumarate, Sodium Sulfate, Sodium Sulfate Anhydrous, Sodium Sulfite, Sodium Tartrate, Sodium Tartrate Dihydrate, Sodium Tripolyphosphate, Sorbic Acid, Sorbitan, Sorbitan Monolaurate, Sorbitan Monooleate, Sorbitan Monopalmitate, Sorbitan Monostearate, Sorbitan Sesquioleate, Sorbitan Trioleate, Sorbitan Tristearate, Sorbitol, Sorbitol Special Polyol Solution, Sorbito-Glycerin Blend, Starch, Starch, pregelatinized, Stearic Acid, Succinic Acid, Sucrose, Sucrose Palmitate, Sucrose Stearate, Sugar/Starch Insert Granules, Talc, Tartaric Acid, Tartaric Acid, dl-, Threonine, Titanium Dioxide, Tocopherol, Tocophersolan, Tragacanth, Triacetin, Tribasic Calcium Phosphate, Tricaprilin, Trichloroethane, Trichloromonofluoromethane, Trideceth-10, Triethanolamine Lauryl Sulfate, Triethyl Citrate, Trihydroxystearin, Trimethylsilyl Treated Dimethiconol/Trimethylsiloxysilicate Crosspolymer (40/60 W/W; 5000000 PA.S), Trimethylsilyl Treated Dimethiconol/Trimethylsiloxysilicate Crosspolymer (45/55 W/W; 100000 PA.S), Trisodium Citrate Dihydrate, Trisodium Hedta, Trolamine, Tromethamine, Tryptophan, Valine, Xanthan Gum, Xylitol, Xylitol 300, Zinc Acetate, Zinc Chloride, Zinc Oxide, Zinc Stearate, Zinc Sulfate. In some embodiments, the one or more excipients are selected from crospovidone, croscarmellose sodium, sodium starch glycolate, povidone, colloidal silicon dioxide, silicon dioxide, colloidal anhydrous silica, hydroxypropylcellulose, sodium stearoyl fumarate, maize starch, lactose monohydrate, anhydrous lactose, dextrose, sucrose, sorbitol, calcium carbonate, calcium stearate, PEG, microcrystalline cellulose, pregelatinized starch, talc, magnesium carbonate, mannitol, hydroxypropylmethylcellulose, and magnesium stearate. In some embodiments, the tablet core comprises granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the capsule comprises a tablet core and capsule fill. In some embodiments, the tablet core comprises the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof; and wherein the capsule fill comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. The skilled artisan would understand that after forming the tablet core, it can be placed in a capsule, with capsule fill including one or more excipients and/or drug substance, such that the final dosage form is a capsule (despite containing a “tablet” core). In some embodiments, the tablet core further comprises one or more excipients; and wherein the capsule fill further comprises one or more excipients. In some embodiments, the composition further comprises an outer layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, and an intermediate layer between the tablet core and the outer layer and contacting the tablet core and outer layer. In some embodiments, the composition further comprises an outer layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing wherein the tablet core is in contact with the outer layer. In some embodiments, the outer layer consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the outer layer comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, and one or more excipients, as described herein. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is ciprofibrate, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is bezafibrate, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is fenofibrate, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, GW5101516, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is elafibranor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is seladelpar, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the tablet core comprises granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, wherein the granules are coated with a layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the granules further comprise one or more excipients, as described herein. In some embodiments, the granules consisting essentially of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, further comprises one or more excipients. In some embodiments, the layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the composition comprises (i) granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and (ii) granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the composition comprises (i) granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and (ii) the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, in powder form. In some embodiments, the granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, further comprise one or more excipients. In some embodiments, the granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, consist essentially of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, further comprise one or more excipients. In some embodiments, the granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, consist essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, (i) and (ii) are blended. In some embodiments, the particles comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, have a mean diameter from about 100 nm to about 2 µm, or any value in between, for example, about 100 nm to about 500 nm, about 250 nm to about 750 nm, about 500 nm to about 1 µm, about 750 nm to about 1.25 µm, about 1 µm to about 1.5 µm, about 1.25 µm to about 1.75 µm, about 1.5 µm to about 2 µm, or any value in between. In some embodiments, the particles comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, have a mean diameter of about 100 nm, about 200 nm, about 300 nm, about 400 nm, about 500 nm, about 600 nm, about 700 nm, about 800 nm, about 900 nm, about 1 µm, about 1.1 µm, about 1.2 µm, about 1.3 µm, about 1.4 µm, about 1.5 µm, about 1.6 µm, about 1.7 µm, about 1.8 µm, about 1.9 µm, or about 2 µm. In some embodiments, the particles comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, have a mean diameter from about 100 nm to about 1 µm, or any value in between, for example, about 100 nm, about 200 nm, about 300 nm, about 400 nm, about 500 nm, about 600 nm, about 700 nm, about 800 nm, about 900 nm, or about 1 µm, or any value in between. In some embodiments, the particles comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, have a mean diameter from 100 nm to about 2 µm, or any value in between, for example, about 100 nm to about 500 nm, about 250 nm to about 750 nm, about 500 nm to about 1 µm, about 750 nm to about 1.25 µm, about 1 µm to about 1.5 µm, about 1.25 µm to about 1.75 µm, about 1.5 µm to about 2 µm, or any value in between. In some embodiments, the particles comprising the PPAR- α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, have a mean diameter of about 100 nm, about 200 nm, about 300 nm, about 400 nm, about 500 nm, about 600 nm, about 700 nm, about 800 nm, about 900 nm, about 1 µm, about 1.1 µm, about 1.2 µm, about 1.3 µm, about 1.4 µm, about 1.5 µm, about 1.6 µm, about 1.7 µm, about 1.8 µm, about 1.9 µm, or about 2 µm. In some embodiments, the particles comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, have a mean diameter from about 100 nm to about 1 µm, or any value in between, for example, about 100 nm, about 200 nm, about 300 nm, about 400 nm, about 500 nm, about 600 nm, about 700 nm, about 800 nm, about 900 nm, or about 1 µm, or any value in between. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in substantially amorphous form. In some embodiments, the substantially amorphous compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is prepared by spray drying, spray drying with one or more excipients, hot-melt extrusion, dissolution followed by lyophilization, evaporation vacuum drying, tray drying, microwave drying or other processes that are known to a skilled person to result in solvent evaporation, thereby resulting in the formation of solid dispersion or dissolution followed by precipitation onto an amorphous substrate. In some embodiments, the amorphous substrate is amorphous silica or fumed silica. Hot melt extrusion (HME) is the processing of a material above its glass transition temperature (Tg), combining melting and mechanical energy followed by expulsion through an extruder to provide an amorphous material. All components are sheared, heated, plastified, mixed and dispersed, and finally shaped by pressing them through a die opening. For example, the material to be processed (e.g., a compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and/or a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing) can be optionally mixed with one or more excipients, and heated above the melting point of the compound of mixture while being processed in an extruder, such as a twin-screw extruder. Spray drying is another method for manufacturing amorphous solid materials. Fast solvent evaporation that leads to a rapid transformation of solution to a solid state. For example, a solution or slurry of a compound is formed (e.g., a compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and/or a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR- α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing), optionally including one or more excipients, and the solution or slurry is passed through an atomizer or spray nozzle to disperse the liquid into a stream of hot gas (e.g., nitrogen or air) which rapidly evaporates the solvent. Dissolution followed by precipitation onto an amorphous substrate involves dissolving material (e.g., a compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and/or a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing) in a suitable solvent, and optionally also dissolving one or more excipients in the solvent, to form a solution. The solution may be passed over the amorphous substrate and treated with a hot gas stream (e.g., nitrogen) to aid in solvent removal. As the concentration of the compound (and optionally, one or more excipients) in the solution increases, material begins to precipitate onto the amorphous substrate. In some embodiments, the amorphous substrate is amorphous silica. In some embodiments, the amorphous substrate is fumed silica. The hot drying gas can be passed in as a co-current, same direction as sprayed liquid atomizer, or counter-current, where the hot air flows against the flow from the atomizer. With co- current flow, particles spend less time in the system and the particle separator (typically a cyclone device). With counter-current flow, particles spend more time in the system and is usually paired with a fluidized bed system. Co-current flow generally allows the system to operate more efficiently. In lyophilization (freeze drying), dissolution (e.g., a compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and/or a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing) in a suitable solvent (and/or water) with or without excipients, is followed by freezing the solution during a freezing cycle to form a frozen mixture; evacuating (vacuum) the lyophilization chamber; and drying the frozen mixture during a primary drying cycle which comprises at least one primary drying stage. The process may further comprise further drying using a secondary drying cycle comprising at least one secondary drying stage. Near the end, or upon completion, of the freezing cycle, the frozen mixtures are exposed to a vacuum sufficient to remove the water or solvent (which may exist in a liquid and/or solid phase) at the average temperature of the primary drying cycle. The primary drying cycle is optionally followed by a secondary drying cycle, during which residual water or solvent is removed. Completion of the lyophilization process yields a stable amorphous solid. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is present in crystalline form. In some embodiments, the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, further comprises an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the SGLT-2 inhibitor is empagliflozin, canagliflozin, or dapagliflozin, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the SGLT-2 inhibitor is canagliflozin hemihydrate. In some embodiments, the SGLT-2 inhibitor is empagliflozin. In some embodiments, the SGLT-2 inhibitor is dapagliflozin propylene glycol hydrate. In some embodiments, the SGLT-2 inhibitor is a free base. In some embodiments, the SGLT-2 inhibitor is a pharmaceutically acceptable salt. In some embodiments, the SGLT-2 inhibitor is a pharmaceutically acceptable solvate. In some embodiments, the SGLT-2 inhibitor is a pharmaceutically acceptable salt of a pharmaceutically acceptable solvate. In some embodiments, the SGLT-2 inhibitor is a pharmaceutically acceptable solvate of a free base. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 300 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 200 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 100 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 50 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 25 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 20 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 15 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 10 mg. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount of about 5 mg, about 10 mg, or about 25 mg. In some embodiments, the SGLT-2 inhibitor is canagliflozin. In some embodiments, the canagliflozin is present in an amount of about 100 mg or about 300 mg. In some embodiments, the canagliflozin is present in an amount of about 100 mg or about 300 mg of canagliflozin hemihydrate. In some other embodiments, the SGLT-2 inhibitor is dapagliflozin. In still other embodiments, the SGLT-2 inhibitor is dapagliflozin propylene glycol hydrate. In some embodiments, the dapagliflozin is present in an amount of about 5 mg or about 10 mg. In still other embodiments, the dapagliflozin is present in an amount of about 5 mg or about 10 mg of dapagliflozin propylene glycol hydrate. In some embodiments, the SGLT-2 inhibitor is empagliflozin. In some embodiments, the empagliflozin is present in an amount of about 10 mg or about 25 mg. In some embodiments, the dose is a therapeutically effective amount. In some embodiments, the composition comprises particles comprising the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the particles are in the form of a powder. In some embodiments, the particles comprise the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, and one or more excipients. In some embodiments, the particles consist essentially of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the particles are micronized. In some embodiments, 90% of the mass of the micronized particles have a size (d90) of less than or equal to about 250 μm. In some embodiments, 90% of the mass of the micronized particles have a size (d90) of about 2 μm to about 10 μm, or any value in between. For example, about 2 μm, about 2.5 μm, about 3 μm, about 3.5 μm, about 4 μm, about 4.5 μm, about 5 μm, about 5.5 μm, about 6 μm, about 6.5 μm, about 7 μm, about 7.5 μm, about 8 μm, about 8.5 μm, about 9 μm, about 9.5 μm, about 10 μm, or any value in between. In some embodiments, 50% of the mass of the micronized particles have a size (d50) of less than or equal to about 100 μm. In some embodiments, 50% of the mass of the micronized particles have a size (d50) of less than or equal to about 100 μm. For example, about 2 μm, about 2.25 μm, about 2.5 μm, about 2.75 μm, about 3 μm, about 3.25 μm, about 3.5 μm, about 3.75 μm, about 4 μm, about 4.25 μm, about 4.5 μm, about 4.75 μm, about 5 μm, about 5.25 μm, about 5.5 μm, about 5.75 μm, about 6 μm, or any value in between. In some embodiments, the size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof. In some embodiments, the size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof. In some embodiments, the composition comprises granules comprising the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, the composition comprises grains comprising the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. As used herein, the term “buffer” refers to an aqueous solution that resists a change in pH. Exemplary buffers include, but are not limited to, phosphate, acetate, and citrate. In some embodiments, the composition exhibits a dissolution profile in about 900 mL of water, containing about 0.5% sodium dodecyl sulfate (SDS) at about pH 1.5, at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 rpm; wherein from about 70 to about 80 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. In some embodiments, about 75 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. See, for example, https://www.usp.org/sites/default/files/usp/document/harmonization/gen- method/stage_6_monograph_25_feb_2011.pdf, which is hereby incorporated by reference in its entirety. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. See, for example, https://www.usp.org/sites/default/files/usp/document/harmonization/gen- method/stage_6_monograph_25_feb_2011.pdf, which is hereby incorporated by reference in its entirety. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 60 to about 80 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 1 to about pH 2 at 37° C.±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 60 to about 80 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 60 to about 80 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 1 to about pH 2 at 37° C.±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 60 to about 80 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes. In some embodiments, the composition exhibits a dissolution profile in about 1,000 mL of acetate buffer at about pH 4.5, at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 60 rpm; wherein from about 50 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, about 75 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is dapagliflozin propylene glycol hydrate. In some embodiments, the composition exhibits a dissolution profile in about 900 mL of 0.05M phosphate buffer at about pH 6.8 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 75 rpm; wherein from about 50 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, about 75 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is empagliflozin. In some embodiments, the composition exhibits a dissolution profile in about 1,000 mL of water with 0.75% wt sodium lauryl sulfate (SLS) at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 75 rpm; wherein from about 50 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 20 minutes. In some embodiments, about 75 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 20 minutes. In some embodiments, the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is canagliflozin hemihydrate. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 25 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 25 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, the composition exhibits a dissolution profile in about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes. In some embodiments, about 50% to about 99 wt %, or any value in between, of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is released after about 45 minutes. For example, about 50% to about 75%, about 60% to about 85%, about 70% to about 95%, or about 80% to about 99%, or any value in between, is released after about 45 minutes. In some embodiments, about 75 to about 99% of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is released after about 45 minutes, for example, about 75%, about 76%, about 77%, about 78%, about 79%, about 80%, about 81%, about 82%, about 83%, about 84%, about 85%, about 86%, about 87%, about 88%, about 89%, about 90%, about 91%, about 92%, about 93%, about 94%, about 95%, about 96%, about 97%, about 98%, about 99%, or any value in between. In some embodiments, about 25% to about 99 wt %, or any value in between, of the PPAR- α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is released after about 15 minutes. In some embodiments, about 50% to about 99 wt %, or any value in between, of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is released after about 15 minutes. For example, about 50% to about 75%, about 60% to about 85%, about 70% to about 95%, or about 80% to about 99%, or any value in between, is released after about 15 minutes. In some embodiments, about 75 to about 99% of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is released after about 15 minutes, for example, about 75%, about 76%, about 77%, about 78%, about 79%, about 80%, about 81%, about 82%, about 83%, about 84%, about 85%, about 86%, about 87%, about 88%, about 89%, about 90%, about 91%, about 92%, about 93%, about 94%, about 95%, about 96%, about 97%, about 98%, about 99%, or any value in between. In some embodiments, about 25% to about 99 wt %, or any value in between, of the SGLT- 2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is released after about 15 minutes. In some embodiments, about 50% to about 99 wt %, or any value in between, of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is released after about 15 minutes. For example, about 50% to about 75%, about 60% to about 85%, about 70% to about 95%, or about 80% to about 99%, or any value in between, is released after about 15 minutes. In some embodiments, about 75 to about 99% of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is released after about 15 minutes, for example, about 75%, about 76%, about 77%, about 78%, about 79%, about 80%, about 81%, about 82%, about 83%, about 84%, about 85%, about 86%, about 87%, about 88%, about 89%, about 90%, about 91%, about 92%, about 93%, about 94%, about 95%, about 96%, about 97%, about 98%, about 99%, or any value in between. In some embodiments, the compositions described herein provide a Cmax of the compound of Formula (I) of from about 50 to about 60 ng/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Cmax of the compound of Formula (I) of about 54 ng/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Tmax of the compound of Formula (I) of from about 3 hours to about 6 hours, when administered to a subject, for example, about 3 hours, about 4 hours, about 5 hours, or about 6 hours. In some embodiments, the subject is in a fasted state. In some embodiments, the subject is in a fed state. In some embodiments, the he compositions described herein provide a Tmax of the compound of Formula (I) of from about 3 hours to about 4 hours, when administered to a subject in a fasted state. In some embodiments, the he compositions described herein provide a T^max of the compound of Formula (I) of from about 4 hours to about 5 hours, when administered to a subject in a fed state. In some embodiments, the compositions described herein provide an AUC of the compound of Formula (I) of from about 700 to about 1,000 ng·hr/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide an AUC of the compound of Formula (I) of from about 750 to about 900 ng·hr/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Cmax of the compound of Formula (I) of from about 50 to about 60 ng/mL/mg, a Tmax of the compound of Formula (I) of from about 3 hours to about 6 hours, and an AUC of the compound of Formula (I) of from about 700 to about 1,000 ng·hr/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Cmax of the SGLT-2 inhibitor of from about 5 to about 150 ng/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Cmax of the SGLT-2 inhibitor of about 10 to about 15 ng/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Cmax of empagliflozin of from about 75 to about 125 ng/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Cmax of canagliflozin of from about 5 to about 15 ng/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide a Tmax of the SGLT-2 inhibitor of from about 0.5 hours to about 2.5 hours, when administered to a subject, for example, about 0.5 hours, about 0.75 hours, about 1 hour, about 1.25 hours, about 1.5 hours, about 1.75 hours, about 2 hours, or about 2.5 hours. In some embodiments, the subject is in a fasted state. In some embodiments, the subject is in a fed state. In some embodiments, the compositions described herein provide a Tmax of the SGLT-2 inhibitor of from about 1 to about 2 hours, when administered to a subject. In some embodiments, the compositions described herein provide a Tmax of dapagliflozin of about 2 hours, when administered to a subject. In some embodiments, the compositions described herein provide a Tmax of empagliflozin of about 1 hour, when administered to a subject. In some embodiments, the compositions described herein provide a Tmax of canagliflozin of about 1.5 hours, when administered to a subject. In some embodiments, the compositions described herein provide an AUC of the SGLT-2 inhibitor of from about 30 to about 80 ng·hr/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide an AUC of the SGLT-2 inhibitor of from about 30 to about 50 ng·hr/mL/mg, about 40 to about 60 ng·hr/mL/mg, about 50 to about 70 ng·hr/mL/mg, or about 60 to about 80 ng·hr/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide an AUC of dapagliflozin of from about 35 to about 55 ng·hr/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide an AUC of empagliflozin of from about 30 to about 40 ng·hr/mL/mg, when administered to a subject. In some embodiments, the compositions described herein provide an AUC of canagliflozin of from about 60 to about 80 ng·hr/mL/mg, when administered to a subject. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) mixing the dry granules obtained in step (b) with one or more excipients to form a second blend; (d) compressing the second blend to form the tablet core; (e) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (f) forming dry granules comprising the third blend; (g) mixing the dry granules obtained in step (h) with one or more excipients to form a fourth blend; and (h) applying the fourth blend obtained in step (i) to the surface of the tablet core, forming the outer layer. In some embodiments, the dry granules obtained in steps (b) and/or (f) are milled prior to the mixing with one or more excipients in steps (c) and/or (g). In some embodiments, the third blend of step (e) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (e)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; and (j) applying the fourth blend obtained in step (i) to the surface of the tablet core, forming the outer layer. In some embodiments, the third blend of step (f) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (b)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) applying the fourth blend obtained in step (i) to the surface of the tablet core, forming the outer layer; and (k) applying an immediate release coating to the outer layer. In some embodiments, the third blend of step (f) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (b)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a second blend; (d) forming dry granules comprising the second blend; (e) mixing the milled dry granules obtained in steps (c) and (f) with one or more excipients to form a third blend; and (f) compressing the third blend to form a tablet. In some embodiments, the dry granules obtained in steps (b) and/or (d) are milled prior to the mixing with one or more excipients in steps (c) and/or (e). In some embodiments, the second blend of step (c) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (d)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules and drying the wet granules to obtain dry granules; (c) milling the dry granules obtained in step (b); (d) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a second blend; (e) forming dry granules comprising the second blend, or optionally mixing a granulating solution with the second blend obtained in step (d) to form wet granules, then drying the wet granules to form dry granules; (f) milling the dry granules obtained in step (e); (g) mixing the milled dry granules obtained in steps (c) and (f) with one or more excipients to form a third blend; and (h) compressing the third blend to form a tablet. In some embodiments, the second blend of step (d) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (d)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) compressing the dry granules from step (b) or step (c) to form the tablet core; and (e) applying the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, to the surface of the tablet core, forming an outer layer. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (b)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) mixing the dry granules obtained in step (b) or step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; and (f) applying the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, to the surface of the tablet core, forming an outer layer. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (b)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules; (c) drying the wet granules obtained in step (b) to form dry granules; (d) milling the dry granules obtained in step (c); (e) mixing the milled dry granules obtained in step (d) with one or more excipients to form a second blend; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution to the third blend obtained in step (f), and mixing the solution and third blend to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the second blend obtained in step (e) and the fourth blend obtained in step (i); and (k) filling a capsule with the mixture obtained in step (j). Some embodiments provide a process for preparing the composition, comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a capsule fill; and (j) filling a capsule with the tablet core and the capsule fill. Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) optionally forming dry granules comprising the first blend; (c) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, optionally with one or more excipients, to form a second blend; (d) optionally forming dry granules comprising the second blend; (e) mixing the first blend with the second blend, and optionally one or more excipients, to form a third blend; (f) compressing the third blending into the tablet; and (g) optionally applying a film coating to the tablet. In some embodiments, the dry granules obtained in steps (b) and/or (d) are milled prior to the mixing in step (e). In some embodiments, the second blend of step (c) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (b)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) mixing the dry granules obtained in step (b) with one or more excipients to form a second blend; (d) compressing the second blend to form the tablet core; (e) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (f) forming dry granules comprising the third blend; (g) mixing the dry granules obtained in step (f) with one or more excipients to form a fourth blend; (h) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fifth blend; (i) forming dry granules comprising the fifth blend; (j) mixing the dry granules obtained in step (i) with one or more excipients to form a sixth blend; (k) mixing the fourth blend of step (g) with the sixth blend of step (j), optionally with one or more excipients, to form a seventh blend; and (l) applying the seventh blend obtained in step (k) to the surface of the tablet core, forming the outer layer. In some embodiments, the dry granules obtained in steps (b) and/or (f) and/or (i) are milled prior to the mixing with one or more excipients in steps (c) and/or (g) and/or (j). In some embodiments, the third blend of step (e) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the fifth blend of step (h) consists essentially of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (e)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fifth blend; (k) forming dry granules comprising the fifth blend; (l) milling the dry granules obtained in step (k); (m) mixing the milled dry granules obtained in step (l) with one or more excipients to form a sixth blend; (n) mixing the fourth blend of step (i) with the sixth blend of step (m), optionally with one or more excipients, to form a seventh blend; and (o) applying the seventh blend obtained in step (n) to the surface of the tablet core, forming the outer layer. In some embodiments, the third blend of step (f) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the fifth blend of step (j) consists essentially of the SGLT- 2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (g)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fifth blend; (k) forming dry granules comprising the fifth blend; (l) milling the dry granules obtained in step (k); (m) mixing the milled dry granules obtained in step (l) with one or more excipients to form a sixth blend; (n) mixing the fourth blend of step (i) with the sixth blend of step (m), optionally with one or more excipients, to form a seventh blend; (o) applying the seventh blend obtained in step (n) to the surface of the tablet core, forming the outer layer; and (p) applying an immediate release coating to the outer layer. In some embodiments, the third blend of step (f) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the fifth blend of step (j) consists essentially of the SGLT- 2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. In some embodiments, forming dry granules comprises mixing a granulating solution with a blend, as described herein (for example, in step (g)), to form wet granules, and drying the wet granules to form dry granules. Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules and drying the wet granules to obtain dry granules; (c) milling the dry granules obtained in step (b); (d) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a second blend; (e) forming dry granules comprising the second blend, or optionally mixing a granulating solution with the second blend obtained in step (d) to form wet granules, then drying the wet granules to form dry granules; (f) milling the dry granules obtained in step (e); (g) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (h) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (g) to form wet granules and drying the wet granules to obtain dry granules; (i) milling the dry granules obtained in step (h); (j) mixing the milled dry granules obtained in steps (c), (f), and (i) with one or more excipients to form a fourth blend; and (k) compressing the fourth blend to form a tablet. In some embodiments, the third blend of step (g) consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, the fifth blend of step (h) consists essentially of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof. Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) compressing the dry granules from step (b) or step (c) to form the tablet core; and (e) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, and the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, optionally with one or more excipients, to form a second blend; and (f) applying the second blend to the surface of the tablet core, forming an outer layer. In some embodiments, the dry granules obtained in step (b) are milled prior to step (d). In some embodiments, the dry granules obtained in step (b) are not milled prior to step (d). A process for preparing the composition of any one of Claims 1-52 or 63-90, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) mixing the dry granules obtained in step (b) or step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; and (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, and the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, optionally with one or more excipients, to form a third blend; and (g) applying the third blend to the surface of the tablet core, forming an outer layer. In some embodiments, the dry granules obtained in step (b) are milled prior to step (d). In some embodiments, the dry granules obtained in step (b) are not milled prior to step (d). Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules; (c) drying the wet granules obtained in step (b) to form dry granules; (d) milling the dry granules obtained in step (c); (e) mixing the milled dry granules obtained in step (d) with one or more excipients to form a second blend; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution to the third blend obtained in step (f), and mixing the solution and third blend to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fifth blend; (k) forming dry granules comprising the fifth blend, or optionally mixing a granulating solution to the fifth blend obtained in step (j), and mixing the solution and fifth blend to form wet granules, then drying the wet granules to form dry granules; (l) milling the dry granules obtained in step (k); (m) mixing the milled dry granules obtained in step (l) with one or more excipients to form a sixth blend; (n) mixing the second blend obtained in step (e), the fourth blend obtained in step (i), and the sixth blend obtained in step (m); and (o) filling a capsule with the mixture obtained in step (n). Some embodiments provide a process for preparing the composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof; and one or more excipients, the process comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fourth blend; (j) forming dry granules comprising the fourth blend, or optionally mixing a granulating solution with the fourth blend obtained in step (i) to form wet granules, then drying the wet granules to form dry granules; (k) milling the dry granules obtained in step (j); (l) mixing the milled dry granules obtained in step (h), the milled dry granules obtained in step (k), and one or more excipients to form a capsule fill; and filling a capsule with the tablet core and the capsule fill. In some embodiments, milling further comprises screen sieving. In some embodiments, forming dry granules comprises roller compaction. In some embodiments, forming wet granules comprises contacting a fluidized bed with a blend, as described herein. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, of step (a) is present in substantially amorphous form. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, of step (a) is prepared by spray drying, spray drying with one or more excipients, hot-melt extrusion, or dissolution followed by precipitation onto an amorphous substrate, as described herein. In some embodiments, the amorphous substrate is amorphous silica or fumed silica. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, of step (a) is milled prior to step (a). In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, of step (a) is micronized prior to step (a). In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, of steps (d), (e), or (f), is present in crystalline form. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is milled prior to use in the processes described herein. In some embodiments, the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, is micronized prior to use in the processes described herein. In some embodiments, micronizing comprises forming particles having a mean diameter of from about 2 µm to about 10 µm, or any value in between. For example, about 2 µm, about 2.5 µm, about 3 µm, about 3.5 µm, about 4 µm, about 4.5 µm, about 5 µm, about 5.5 µm, about 6 µm, about 6.5 µm, about 7 µm, about 7.5 µm, about 8 µm, about 8.5 µm, about 9 µm, about 9.5 µm, about 10 µm, or any value in between. Some embodiments provide a method of treating a PPARγ-mediated disease or disorder, comprising administering a composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients, to a subject in need thereof. In some embodiments, the PPARγ-mediated disease or disorder is type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), or a combination of any of the foregoing. In some embodiments, the PPARγ-mediated disease or disorder is type 2 diabetes and NASH. In some embodiments, the type 2 diabetes and NASH are treated. In some embodiments, the NASH is treated. In some embodiments, the subject has been previously diagnosed with NASH. In some embodiments, the subject has been previously diagnosed with type 2 diabetes. In some embodiments, the subject has been previously diagnosed with NASH and type 2 diabetes. In some embodiments, the subject has been previously diagnosed with NASH and type 2 diabetes, wherein administration composition described herein treats the NASH. In some embodiments, the subject has one or more cardiac risk factors, for example, high blood pressure, high cholesterol, a history (previous or current) of smoking, a family history of cardiovascular disease, obesity, and previous myocardial infarction or stroke. In some embodiments, the desired therapeutic effect is the same therapeutic effect observed in monotherapy of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, e.g., any of the beneficial or desired results including clinical results as described herein, for example slowing the symptomatic progression of a PPARγ-mediated disease or disorder, or symptoms thereof. In other embodiments, the desired therapeutic effect is the same therapeutic effect observed in monotherapy of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, a PPAR-α agonist, a PPAR- δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing, e.g., any of the beneficial or desired results including clinical results as described herein, for example slowing the symptomatic progression of a PPARγ-mediated disease or disorder, or symptoms thereof. In some embodiments, an unwanted drug effect, side effect, or adverse event is associated with or observed in monotherapy of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof and/or PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing. In some embodiments, an unwanted drug effect, side effect, or adverse event includes, but is not limited to edema, weight gain, hypertension, cardiovascular disease, and cardiovascular events (e.g. cardiovascular death, nonfatal myocardial infarction and nonfatal stroke). Diabetes, in particular type 2 diabetes, is an increasingly prevalent disease that due to a high frequency of complications leads to a significant reduction of life expectancy. Because of diabetes-associated microvascular complications, type 2 diabetes is currently the most frequent cause of adult-onset loss of vision, renal failure, and amputations in the industrialized world. In addition, the presence of type 2 diabetes is associated with a two to five fold increase in cardiovascular disease risk. After long duration of disease, most patients with type 2 diabetes will eventually fail on oral therapy and become insulin dependent with the necessity for daily injections and multiple daily glucose measurements. The UKPDS (United Kingdom Prospective Diabetes Study) demonstrated that intensive treatment with metformin, sulfonylureas or insulin resulted in only a limited improvement of glycemic control (difference in HbA1c ~0.9%). In addition, even in patients within the intensive treatment arm glycemic control deteriorated significantly over time and this was attributed to deterioration of β-cell function. Importantly, intensive treatment was not associated with a significant reduction in macrovascular complications, i.e. cardiovascular events. Therefore many patients with type 2 diabetes remain inadequately treated, partly because of limitations in long term efficacy, tolerability and dosing inconvenience of existing anti-hyperglycemic therapies. The high incidence of therapeutic failure is a major contributor to the high rate of long-term hyperglycemia-associated complications or chronic damages (including micro- and macrovascular complications such as diabetic nephropathy, retinopathy or neuropathy, and/or cardiovascular complications) in patients with type 2 diabetes. The World Health Organization diagnostic criteria for diabetes are shown below. Table 1. World Health Organization Diabetes Diagnostic Criteria

In some embodiments, the treatment of diabetes comprises one or more of a reduction in fasting glucose levels, improved glucose tolerance, and a decrease in HbA1c. NAFLD is characterized by hepatic steatosis with no secondary causes of hepatic steatosis including excessive alcohol consumption, other known liver diseases, or long-term use of a steatogenic medication (Chalasani et al., Hepatology. 2018, 67(1):328-357, which is hereby incorporated by reference in its entirety). NAFLD can be categorized into non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH). According to Chalasani et al., NAFL is defined as the presence of ≥ 5% hepatic steatosis without evidence of hepatocellular injury in the form of hepatocyte ballooning. NASH is defined as the presence of ≥ 5% hepatic steatosis and inflammation with hepatocyte injury (e.g., ballooning), with or without any liver fibrosis. Additionally, NASH is commonly associated with hepatic inflammation and liver fibrosis, which can progress to cirrhosis, end-stage liver disease, and hepatocellular carcinoma. However, liver fibrosis is not always present in NASH, but the severity of fibrosis can be linked to long-term outcomes. There are many approaches used to assess and evaluate whether a subject has NAFLD and if so, the severity of the disease including differentiating whether the NAFLD is NAFL or NASH. For example, these approaches include determining one or more of hepatic steatosis (e.g., accumulation of fat in the liver); the NAFLD Activity Score (NAS); hepatic inflammation; biomarkers indicative of one or more of liver damage, hepatic inflammation, liver fibrosis, and/or liver cirrhosis (e.g., serum markers and panels); and liver fibrosis and/or cirrhosis. Further examples of physiological indicators of NAFLD can include liver morphology, liver stiffness, and the size or weight of the subject’s liver. In some embodiments, NAFLD in the subject is evidenced by an accumulation of hepatic fat and detection of a biomarker indicative of liver damage. For example, elevated serum ferritin and low titers of serum autoantibodies can be common features of NAFLD. In some embodiments, methods to assess NAFLD include magnetic resonance imaging, either by spectroscopy or by proton density fat fraction (MRI-PDFF) to quantify steatosis, transient elastography (FIBROSCAN®), hepatic venous pressure gradient (HPVG), hepatic stiffness measurement with MRE for diagnosing significant liver fibrosis and/or cirrhosis, and assessing histological features of liver biopsy. In some embodiments, magnetic resonance imaging is used to detect one or more of steatohepatitis (NASH-MRI), liver fibrosis (Fibro-MRI), and steatosis see, for example, U.S. Application Publication Nos. 2016/146715 and 2005/0215882, each of which are incorporated herein by reference in their entireties. In some embodiments, treatment of NAFLD comprises one or more of a decrease in symptoms; a reduction in the amount of hepatic steatosis; a decrease in the NAS; a decrease in hepatic inflammation; a decrease in the level of biomarkers indicative of one or more of liver damage, inflammation, liver fibrosis, and/or liver cirrhosis; and a reduction in fibrosis and/or cirrhosis, a lack of further progression of fibrosis and/or cirrhosis, or a slowing of the progression of fibrosis and/or cirrhosis. In some embodiments, the severity of NALFD can be assessed using the NAS. In some embodiments, treatment of NAFLD can be assessed using the NAS. In some embodiments, treatment of NAFLD comprises a reduction in the NAS following administration of one or more compounds described herein. In some embodiments, the NAS can be determined as described in Kleiner et al., Hepatology.2005, 41(6):1313-1321, which is hereby incorporated by reference in its entirety. See, for example, Table 2 for a simplified NAS scheme adapted from Kleiner. Table 2. Example of the NAFLD Activity Score (NAS) with Fibrosis Stage

In some embodiments, the NAS is determined non-invasively, for example, as described in U.S. Application Publication No.2018/0140219, which is incorporated by reference herein in its entirety. In some embodiments, the presence of hepatic inflammation is determined by one or more methods selected from the group consisting of biomarkers indicative of hepatic inflammation and a liver biopsy sample(s) from the subject. In some embodiments, the severity of hepatic inflammation is determined from a liver biopsy sample(s) from the subject. For example, hepatic inflammation in a liver biopsy sample can be assessed as described in Kleiner et al., Hepatology. 2005, 41(6):1313-1321 and Brunt et al., Am J Gastroenterol 1999, 94:2467-2474, each of which are hereby incorporated by reference in their entireties. In some embodiments, treatment of NAFLD comprises treatment of fibrosis and/or cirrhosis, e.g., a decrease in the severity of fibrosis, a lack of further progression of fibrosis and/or cirrhosis, or a slowing of the progression of fibrosis and/or cirrhosis. In some embodiments, the presence of fibrosis and/or cirrhosis is determined by one or more methods selected from the group consisting of transient elastography (e.g., FIBROSCAN®), non-invasive markers of hepatic fibrosis, and histological features of a liver biopsy. In some embodiments, the severity (e.g., stage) of fibrosis is determined by one or more methods selected from the group consisting of transient elastography (e.g., FIBROSCAN®), a fibrosis-scoring system, biomarkers of hepatic fibrosis (e.g., non-invasive biomarkers), and hepatic venous pressure gradient (HVPG). Non-limiting examples of fibrosis scoring systems include the NAFLD fibrosis scoring system (see, e.g., Angulo, et al., Hepatology.2007; 45(4):846-54), the fibrosis scoring system in Brunt et al., Am J Gastroenterol. 1999, 94:2467-2474, the fibrosis scoring system in Kleiner et al., Hepatology.2005, 41(6):1313- 1321, and the ISHAK fibrosis scoring system (see Ishak et al., J Hepatol. 1995;22:696-9), the contents of each of which are incorporated by reference herein in their entireties. In some embodiments, the presence of NAFLD is determined by one or more biomarkers indicative of one or more of liver damage, inflammation, liver fibrosis, and/or liver cirrhosis or scoring systems thereof. In some embodiments, the severity of NAFLD is determined by one or more biomarkers indicative of one or more of liver damage, inflammation, liver fibrosis, and/or liver cirrhosis or scoring systems thereof. The level of the biomarker can be determined by, for example, measuring, quantifying, and monitoring the expression level of the gene or mRNA encoding the biomarker and/or the peptide or protein of the biomarker. Non-limiting examples of biomarkers indicative of one or more of liver damage, inflammation, liver fibrosis, and/or liver cirrhosis and/or scoring systems thereof include the aspartate aminotransferase (AST) to platelet ratio index (APRI); the aspartate aminotransferase (AST) and alanine aminotransferase (ALT) ratio (AAR); the FIB-4 score, which is based on the APRI, alanine aminotransferase (ALT) levels, and age of the subject (see, e.g., McPherson et al., Gut. 2010 Sep;59(9):1265-9, which is incorporated by reference herein in its entirety); hyaluronic acid; pro-inflammatory cytokines; a panel of biomarkers consisting of α2-macroglobulin, haptoglobin, apolipoprotein A1, bilirubin, gamma glutamyl transpeptidase (GGT) combined with a subject’s age and gender to generate a measure of fibrosis and necroinflammatory activity in the liver (e.g., FIBROTEST®, FIBROSURE®), a panel of biomarkers consisting of bilirubin, gamma-glutamyltransferase, hyaluronic acid, α2-macroglobulin combined with the subject’s age and sex (e.g., HEPASCORE®; see, e.g., Adams et al., Clin Chem.2005 Oct;51(10):1867-73), and a panel of biomarkers consisting of tissue inhibitor of metalloproteinase-1, hyaluronic acid, and α2-macroglobulin (e.g., FIBROSPECT®); a panel of biomarkers consisting of tissue inhibitor of metalloproteinases 1 (TIMP-1), amino-terminal propeptide of type III procollagen (PIIINP) and hyaluronic acid (HA) (e.g., the Enhanced Liver Fibrosis (ELF) score, see, e.g., Lichtinghagen R, et al., J Hepatol.2013 Aug;59(2):236-42, which is incorporated by reference herein in its entirety). In some embodiments, the presence of fibrosis is determined by one or more of the FIB-4 score, a panel of biomarkers consisting of α2-macroglobulin, haptoglobin, apolipoprotein A1, bilirubin, gamma glutamyl transpeptidase (GGT) combined with a subject’s age and gender to generate a measure of fibrosis and necroinflammatory activity in the liver (e.g., FIBROTEST®, FIBROSURE®), a panel of biomarkers consisting of bilirubin, gamma-glutamyltransferase, hyaluronic acid, α2- macroglobulin combined with the subject’s age and sex (e.g., HEPASCORE®; see, e.g., Adams et al., Clin Chem.2005 Oct;51(10):1867-73), and a panel of biomarkers consisting of tissue inhibitor of metalloproteinase-1, hyaluronic acid, and α2-macroglobulin (e.g., FIBROSPECT®); and a panel of biomarkers consisting of tissue inhibitor of metalloproteinases 1 (TIMP-1), amino- terminal propeptide of type III procollagen (PIIINP) and hyaluronic acid (HA) (e.g., the Enhanced Liver Fibrosis (ELF) score). In some embodiments, the level of aspartate aminotransferase (AST) does not increase. In some embodiments, the level of aspartate aminotransferase (AST) decreases. In some embodiments, the level of alanine aminotransferase (ALT) does not increase. In some embodiments, the level of alanine aminotransferase (ALT) decreases. In some embodiments, the “level” of an enzyme refers to the concentration of the enzyme, e.g., within blood. For example, the level of AST or ALT can be expressed as Units/L. In some embodiments, the severity of fibrosis is determined by one or more of the FIB-4 score, a panel of biomarkers consisting of α2-macroglobulin, haptoglobin, apolipoprotein A1, bilirubin, gamma glutamyl transpeptidase (GGT) combined with a subject’s age and gender to generate a measure of fibrosis and necroinflammatory activity in the liver (e.g., FIBROTEST®, FIBROSURE®), a panel of biomarkers consisting of bilirubin, gamma-glutamyltransferase, hyaluronic acid, α2-macroglobulin combined with the subject’s age and sex (e.g., HEPASCORE®; see, e.g., Adams et al., Clin Chem.2005 Oct;51(10):1867-73, which is incorporated by reference herein in its entirety), and a panel of biomarkers consisting of tissue inhibitor of metalloproteinase- 1, hyaluronic acid, and α2-macroglobulin (e.g., FIBROSPECT®); and a panel of biomarkers consisting of tissue inhibitor of metalloproteinases 1 (TIMP-1), amino-terminal propeptide of type III procollagen (PIIINP) and hyaluronic acid (HA) (e.g., the Enhanced Liver Fibrosis (ELF) score). In some embodiments, hepatic inflammation is determined by the level of liver inflammation biomarkers, e.g., pro-inflammatory cytokines. Non-limiting examples of biomarkers indicative of liver inflammation include interleukin-(IL) 6, interleukin-(IL) 1β, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, monocyte chemotactic protein (MCP)-1, C- reactive protein (CRP), PAI-1, and collagen isoforms such as Col1a1, Col1a2, and Col4a1 (see, e.g., Neuman, et al., Can J Gastroenterol Hepatol. 2014 Dec; 28(11): 607–618 and U.S. Patent No. 9,872,844, each of which are incorporated by reference herein in their entireties). Liver inflammation can also be assessed by change of macrophage infiltration, e.g., measuring a change of CD68 expression level. In some embodiments, liver inflammation can be determined by measuring or monitoring serum levels or circulating levels of one or more of interleukin-(IL) 6, interleukin-(IL) 1β, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, monocyte chemotactic protein (MCP)-1, and C-reactive protein In some embodiments, the NAFLD is NAFLD with attendant cholestasis. In cholestasis, the release of bile, including bile acids, from the liver is blocked. Bile acids can cause hepatocyte damage (see, e.g., Perez MJ, Briz O. World J Gastroenterol. 2009 Apr 14;15(14):1677-89) likely leading to or increasing the progression of fibrosis (e.g., cirrhosis) and increasing the risk of hepatocellular carcinoma (see, e.g., Sorrentino P et al.. Dig Dis Sci. 2005 Jun;50(6):1130-5 and Satapathy SK and Sanyal AJ. Semin Liver Dis. 2015, 35(3):221-35, each of which are incorporated by reference herein in their entireties). In some embodiments, the NAFLD with attendant cholestasis is NASH with attendant cholestasis. In some embodiments, the treatment of NAFLD comprises treatment of pruritus. In some embodiments, the treatment of NAFLD with attendant cholestasis comprises treatment of pruritus. In some embodiments, a subject with NAFLD with attendant cholestasis has pruritus. In some embodiments, treatment of NAFLD comprises an increase in adiponectin. It is thought that the compound of Formula (I) may be a selective activator of a highly limited number of PPARy pathways including pathways regulated by adiponectin. Adiponectin is an anti-fibrotic and anti-inflammatory adipokine in the liver (see e.g., Park et al., Curr Pathobiol Rep.2015 Dec 1; 3(4): 243–252.). In some embodiments, the level of adiponectin is determined by, for example, an ELISA enzymatic assay. (CRP). In some embodiments, treatment of NAFLD comprises a decrease of one or more symptoms associated with NAFLD in the subject. Exemplary symptoms can include one or more of an enlarged liver, fatigue, pain in the upper right abdomen, abdominal swelling, enlarged blood vessels just beneath the skin's surface, enlarged breasts in men, enlarged spleen, red palms, jaundice, and pruritus. In some embodiments, the subject is asymptomatic. In some embodiments, the treatment of NAFLD, e.g., NAFL or NASH, comprises a reduction in hepatic steatosis. For example, hepatic steatosis is decreased by at least 2%, 3%, 4%, 5%, 6%, 7%, 8%.9%, 10%, 11%, 12%, 13%, 14%, 15%, 16%, 17%, 18%, 19%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 96%, 97%, 98%, 99%, or more than 99% following administration of (a) and (b) for a period of time. In some embodiments, the treatment of NAFLD, e.g., NAFL or NASH, is assessed using the NAFLD Activity Score (NAS). In some embodiments, treatment of NAFLD comprises a decrease in the NAS. In some embodiments, the NAS for a sample from the subject following administration is 7 or less. In some embodiments, the NAS for a sample from the subject following administration is 5 or less, 4 or less, 3 or less, or 2 or less. In some embodiments, the NAFLD activity score (NAS) for a sample from the subject following administration during the period of time is 7 or less. In some embodiments, the NAS for a sample from the subject following administration during the period of time is 5 or less, 4 or less, 3 or less, or 2 or less. In some embodiments, the sample from the subject is from a liver biopsy. In some embodiments, the treatment of NAFLD, e.g., NAFL or NASH, can be assessed using the NAFLD Activity Score (NAS). In some embodiments, the NAS for a sample from the subject following administration is reduced by 1 or more, 2 or more, 3 or more, 4 or more, 5 or more, or 6 or more. In some embodiments, the NAS for a sample from the subject following administration is reduced by 1, 2, 3, 4, 5, or 6. In some embodiments, the NAFLD activity score (NAS) for a sample from the subject following administration during the period of time is reduced by 1 or more, 2 or more, 3 or more, 4 or more, 5 or more, or 6 or more. In some embodiments, the NAS for a sample from the subject following administration during the period of time is reduced by 1, 2, 3, 4, 5, or 6. In some embodiments, the sample from the subject is from a liver biopsy. In some embodiments, the treatment of NAFLD, e.g., NAFL or NASH, comprises treatment of hepatic inflammation. In some embodiments, the severity of the hepatic inflammation is decreased by about 1% to about 50%, about 25% to about 75%, or about 50% to about 100%. In some embodiments, the severity of hepatic inflammation is decreased by about 5%, about 10%, about 15%, about 20%, about 25%, about 30%, about 35%, about 40%, about 45%, about 50%, about 55%, about 60%, about 65%, about 70%, about 75%, about 80%, about 85%, about 90%, or about 95%. In some embodiments, the treatment of NAFLD, e.g., NAFL or NASH, comprises treatment of fibrosis. In some embodiments, the treatment of the NAFLD comprises treatment of cirrhosis (e.g., stage 4 of fibrosis). In some embodiments, treatment of fibrosis comprises a decrease in the stage of fibrosis, for example, from stage 4 to stage 3, from stage 4 to stage 2, from stage 4 to stage 1, from stage 4 to stage 0, from stage 3 to stage 2, from stage 3 to stage 1, from stage 3 to stage 0, from stage 2 to stage 1, from stage 2 to stage 0, or from stage 1 to stage 0. In some embodiments, the adiponectin level in the subject is increased by at least about 30%, at least about 68%, at least about 175%, or at least about 200%. In some embodiments, the increase is by at least about 175%. In some embodiments, the level of aspartate aminotransferase (AST) in the subject does not increase. In some embodiments, the level of aspartate aminotransferase (AST) in the subject decreases. In some embodiments, the level of alanine aminotransferase (ALT) in the subject does not increase. In some embodiments, the level of alanine aminotransferase (ALT) in the subject decreases. In some embodiments, the total body weight of the subject does not increase. In some embodiments, the total body weight of the subject decreases. In some embodiments, the body mass index (BMI) of the subject does not increase. In some embodiments, the body mass index (BMI) of the subject decreases. In some embodiments, the waist and hip (WTH) ratio of the subject does not increase. In some embodiments, the waist and hip (WTH) ratio of the subject decreases. In some embodiments, a non-invasive liver fibrosis marker does not increase or decreases. In some embodiments, the non-invasive liver fibrosis marker is Enhanced Liver Fibrosis (ELF) panel. In some embodiments, treatment of NAFLD comprises a decrease in the level of one or more biomarkers indicative of one or more of liver damage, inflammation, fibrosis, and/or cirrhosis, e.g., any of the biomarkers as described herein. In some embodiments, treatment of NAFLD comprises a decrease in the level of one or more biomarkers indicative of one or more of liver damage, inflammation, fibrosis, and/or cirrhosis by at least about 5%, at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 99%. In some embodiments, the treatment of NAFLD decreases the level of serum bile acids in the subject. In some embodiments, the treatment of NAFLD comprises treatment of pruritus. In some embodiments, the subject has liver fibrosis associated with the NAFLD. In some embodiments, the subject has hepatic cirrhosis (e.g., stage 4 fibrosis) associated with the NAFLD. In some embodiments, the subject has liver fibrosis as a comorbidity. In some embodiments, the subject has hepatic cirrhosis (e.g., stage 4 fibrosis) as a comorbidity. In some embodiments, the subject has liver fibrosis caused by the NAFLD. In some embodiments, the subject has hepatic cirrhosis (e.g., stage 4 fibrosis) caused by the NAFLD. In some embodiments, the NAFLD is simple nonalcoholic fatty liver (NAFL). In some embodiments, the NAFLD is NAFL with attendant liver fibrosis. In some embodiments, the NAFLD is NAFL with attendant liver cirrhosis. In some embodiments, the NAFLD is nonalcoholic steatohepatitis (NASH). In some embodiments, the NAFLD is NASH with attendant liver fibrosis. In some embodiments, the NAFLD is NASH with attendant liver cirrhosis. In some embodiments, the method further comprises performing a liver biopsy to determine the NAFLD activity score of the biopsy sample obtained from the subject. Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by a progressive pulmonary vasculopathy leading to right ventricular hypertrophy. Right heart failure occurs if left untreated. The hemodynamic definition of PAH is an average resting pulmonary artery pressure greater than or equal to 25 mmHg in the presence of a pulmonary capillary wedge pressure less than or equal to 15 mmHg. For comparison, the normal average pulmonary artery pressure is 12- 16 mmHg and normal wedge pressure is 6-12 mmHg . If left untreated, it carries a high rate of mortality. In the pediatric population, familial or idiopathic IPAH disease is the most common type (~55%), followed by PH secondary to congenital heart disease (~35%) and chronic respiratory disorders (~15%) Pathologies involved in PAH include one or more of vasoconstriction, vascular proliferation and remodeling, thrombosis and inflammation. Features of PAH may include reduction in peripheral PAs vascular pruning, thickening of the pulmonary adventitia, venous hypertrophy, and increased expression of TGF-β; matrix proteins such as elastin, fibronectin, and tenascin-C; and glycosaminoglycans. In addition to macrophages, B and T cells may be found in abundance in the perivascular space and may be seen invading the vessel wall. An additional feature that may be observed in severe forms of PAH is a complex vascular lesion known as plexiform lesion. Dysfunctional EPCs, which are hyperproliferative with impaired ability to form vascular networks, may also be implicated in the vascular remodeling in PAH. Factors that increase the rapidity of development of pulmonary vascular disease may include increased MPAP, increased pulmonary blood flow, and the presence of hypoxia or hypercapnia. The events that drive heart failure in PAH may include maladaptive RV hypertrophy (RVH) and dilation, capillary rarefication, cardiac fibrosis, in some cases myocardial ischemia/ hypoxia, and ultimately, RV failure. Cardiovascular remodeling in pulmonary vascular disease (PVD), PAH, and RV failure may relate to increased growth factor–mediated cell proliferation, activation and recruitment of myofibroblasts, DNA damage/resistance to apoptosis, extracellular matrix remodeling and fibrosis, and inflammation and endothelial dysfunction, with a smaller contribution from vasoconstriction. Abnormalities in glucose and lipid metabolism and epigenetic dysregulation [microRNAs (miRNAs) may be observed. Histone deacetylases (HDACs) may be involved in both PAH/PVD and RV failure. In some embodiments, the subject that has been identified, selected, or diagnosed as having PAH through the use of histological analysis and/or a regulatory agency-approved, e.g., FDA- approved test or assay for identifying PAH in a subject or a biopsy sample from the subject or by performing any of the non-limiting examples of assays described herein. In some embodiments, the PAH is selected from idiopathic PAH; familial PAH; PAH associated with a collagen vascular disease selected from: scleroderma, CREST syndrome, systemic lupus erythematosus (SLE), rheumatoid arthritis, Takayasu's arteritis, polymyositis, and dermatomyositis; PAH associated with a congenital heart disease selected from: atrial septic defect (ASD), ventricular septic defect (VSD) and patent ductusarteriosus; PAH associated with portal hypertension; PAH associated with HIV infection; PAH associated with ingestion of a drug or toxin; PAH associated with hereditary hemorrhagic telangiectasia; PAH associated with splenectomy; PAH associated with significant venous or capillary involvement; PAH associated with pulmonary veno-occlusive disease (PVOD); and PAH associated with pulmonary capillary hemangiomatosis (PCH).. In some embodiments, the PAH is idiopathic PAH. In some embodiments, the PAH is familial PAH. In some embodiments, the PAH is PAH associated with a collagen vascular disease selected from: scleroderma, CREST syndrome, systemic lupus erythematosus (SLE), rheumatoid arthritis, Takayasu's arteritis, polymyositis, and dermatomyositis. In some embodiments, the PAH is PAH associated with a congenital heart disease selected from: atrial septic defect (ASD), ventricular septic defect (VSD) and patent ductusarteriosus. In some embodiments, the PAH is PAH associated with portal hypertension. In some embodiments, the PAH is PAH associated with HIV infection. In some embodiments, the PAH is PAH associated with ingestion of a drug or toxin. In some embodiments, the PAH is PAH associated with hereditary hemorrhagic telangiectasia. In some embodiments, the PAH is PAH associated with splenectomy. In some embodiments, the PAH is PAH associated with significant venous or capillary involvement. In some embodiments, the PAH is PAH associated with pulmonary veno-occlusive disease (PVOD). In some embodiments, the PAH is PAH associated with pulmonary capillary hemangiomatosis (PCH). In some embodiments, the treatment of PAH comprises relieving at least to some extent one or more signs or symptoms associated with PAH. In some embodiments, the symptoms are one or more of the following: dyspnea, angina, syncope and edema. EXAMPLES The following example further illustrates the invention. Example 1. Preparation of a fixed dose combination tablet comprising a tablet core and a coating. 3 mg of the besylate salt of the compound of Formula (I) are mixed with MCC, crosspovidone, colloidal silicon dioxide, lactose monohydrate, povidone and magnesium stearate to form a powder blend. Wet granulation with ethanol provides granules containing the besylate salt of the compound of Formula (I). The granules are then compressed in a tablet core. The tablet core is then coated with a mixture of 120 mg of elafibrinor, croscarmellose sodium, microcrystalline cellulose, lactose, and magnesium stearate. A PVA coating may be added if desired. Example 2. Preparation of a fixed dose combination tablet. 3 mg of the besylate salt of the compound of Formula (I) are mixed with MCC, crosspovidone, colloidal silicon dioxide, lactose monohydrate, povidone and magnesium stearate to form a powder blend. Wet granulation with ethanol provides granules containing the besylate salt of the compound of Formula (I). Separately, 120 mg of elafibrinor are wet granulated with ethanol with croscarmellose sodium, microcrystalline cellulose, lactose, and magnesium stearate to provide granules containing the elabirinor. The granules containing the besylate salt of the compound of Formula (I) and the granules containing the elafibrinor are then blended with each other and with additional excipients. The resulting blend is compressed in a tablet core. The tablet core is then coated with a mixture of elafibrinor, croscarmellose sodium, microcrystalline cellulose, lactose, and magnesium stearate. A PVA coating may be added if desired. Example 3. Dissolution of a fixed dose combination tablet. A comparison of the dissolution profile of (A) a tablet containing the besylate salt of the compound of formula (I) as the only active agent (tablet (A)), and (B) the fixed dose combination tablet according to Example 1 (tablet (B)), is performed as follows. Tablet (A) is prepared as follows: 3 mg of the besylate salt of the compound of Formula (I) are mixed with MCC, crospovidone, colloidal silicon dioxide, lactose monohydrate, povidone and magnesium stearate to form a powder blend. Wet granulation with ethanol provides granules containing the besylate salt of the compound of Formula (I). The granules are then compressed in a tablet. The dissolution rate of tablet (A) is then determined in about 900 mL of water, containing about 0.5% sodium dodecyl sulfate (SDS) at about pH 1.5, at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 rpm. The dissolution rate of tablet (B) is then determined under the same conditions as described above for tablet (A).

Claims

WHAT IS CLAIMED IS: 1. A composition comprising a fixed dose combination of a compound of Formula (I)

or a pharmaceutically acceptable salt or solvate thereof; a PPAR-α agonist, a PPAR-δ agonist, or a dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate of any of the foregoing; and one or more excipients.

2. The composition Claim 1, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is seladelpar ciprofibrate, bezafibrate, fenofibrate, GW5101516, or elafibranor, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

3. The composition of Claim 1 or 2, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is seladelpar, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

4. The composition of Claim 1 or 2, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is bezafibrate, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

5. The composition of Claim 1 or 2, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is fenofibrate, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

6. The composition of Claim 1 or 2, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is GW5101516, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

7. The composition of Claim 1 or 2, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist is elafibranor, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

8. The composition of any one of Claims 1-7, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 40 mg to about 300 mg.

9. The composition of any one of Claims 1-8, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 50 mg to about 100 mg.

10. The composition of any one of Claims 1-8, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 100 mg to about 200 mg.

11. The composition of any one of Claims 1-8, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount of about 40 mg, about 50 mg, about 60 mg, about 100 mg, about 200 mg, or about 300 mg.

12. The composition of any one of Claims 1-11, wherein the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 0.1 mg to about 10 mg.

13. The composition of any one of Claims 1-12, wherein the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 0.5 mg to about 5 mg.

14. The composition of any one of Claims 1-13, wherein the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 1 mg to about 3 mg.

15. The composition of any one of Claims 1-14, wherein the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in an amount of 1.5 mg or 3 mg.

16. The composition of any one of Claims 1-15, wherein the compound of Formula (I) is present as a pharmaceutically acceptable salt.

17. The composition of any one of Claims 1-16, wherein the compound of Formula (I) is present as a besylate salt.

18. The composition of any one of Claims 1-15, wherein the compound of Formula (I) is present as a free base.

19. The composition of any one of Claims 1-18, wherein the composition is formulated for administration twice a day or daily.

20. The composition of any one of Claims 1-19, wherein the composition is formulated for administration daily.

21. The composition of any one of Claims 1-20, further comprising an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof.

22. The composition Claim 21, wherein the SGLT-2 inhibitor is selected from the group consisting of: empagliflozin, canagliflozin, dapagliflozin, ertugliflozin, ipragliflozin, luseogliflozin, remogliflozin etabonate, serfliflozin etabonate, sotagliflozin, tofogliflozin, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

23. The composition of Claim 22, wherein the SGLT-2 inhibitor is empagliflozin, canagliflozin, or dapagliflozin, or a pharmaceutically acceptable salt or solvate of any of the foregoing.

24. The composition of Claim 22 or 23, wherein the SGLT-2 inhibitor is canagliflozin hemihydrate.

25. The composition of Claim 22 or 23, wherein the SGLT-2 inhibitor is empagliflozin.

26. The composition of Claim 22 or 23, wherein the SGLT-2 inhibitor is dapagliflozin propylene glycol hydrate.

27. The composition of any one of Claims 22-26, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 300 mg.

28. The composition of any one of Claims 22-26, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 200 mg.

29. The composition of any one of Claims 22-26, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 100 mg.

30. The composition of any one of Claims 22-26, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 50 mg.

31. The composition of any one of Claims 22-30, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 25 mg.

32. The composition of any one of Claims 22-31, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 20 mg.

33. The composition of any one of Claims 22-32, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 15 mg.

34. The composition of any one of Claims 22-33, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount from about 5 mg to about 10 mg.

35. The composition of any one of Claims 22-31, wherein the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, is present in an amount of about 5 mg, about 10 mg, or about 25 mg.

36. The composition of any one of Claims 1-35, comprising particles comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof.

37. The composition of Claim 36, wherein the particles comprise the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and one or more excipients.

38. The composition of Claim 36, wherein the particles consist essentially of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof.

39. The composition of any one of Claims 36-38, wherein the particles are micronized.

40. The composition of Claim 39, wherein 90% of the mass of the micronized particles have a size (d90) of about 2 μm to about 10 μm.

41. The composition of Claim 39 or 40, wherein 50% of the mass of the micronized particles have a size (d50) of about 2 μm to about 6 μm.

42. The composition of Claim 40 or 41, wherein size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof.

43. The composition of any one of Claims 1-42, comprising granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof.

44. The composition of any one of Claims 1-42, comprising grains comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof.

45. The composition of any one of Claims 1-44, comprising particles comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

46. The composition of Claim 45, wherein the particles comprise the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, and one or more excipients.

47. The composition of Claim 45, wherein the particles consist essentially of the PPAR- α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

48. The composition of any one of Claims 45-47, wherein the particles are micronized.

49. The composition of Claim 48, wherein 90% of the mass of the micronized particles have a size (d90) of about 3 μm to about 300 μm.

50. The composition of Claim 49, wherein 50% of the mass of the micronized particles have a size (d50) of about 1 μm about 100 μm.

51. The composition of Claim 49 or 50, wherein size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof.

52. The composition of any one of Claims 1-46, comprising granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

53. The composition of any one of Claims 1-46, comprising grains comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

54. The composition of any one of Claims 1-53, further comprising particles comprising an SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof.

55. The composition of Claim 54, wherein the particles comprise the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, and one or more excipients.

56. The composition of Claim 54, wherein the particles consist essentially of the SGLT- 2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof.

57. The composition of any one of Claims 54-56, wherein the particles are micronized.

58. The composition of Claim 57, wherein 90% of the mass of the micronized particles have a size (d90) of about 10 μm to about 250 μm.

59. The composition of Claim 58, wherein 50% of the mass of the micronized particles have a size (d50) of about 10 μm about 100 μm.

60. The composition of Claim 58 or 59, wherein size of the micronized particles is determined by direct imaging, laser diffraction, or a combination thereof.

61. The composition of any one of Claims 1-54, comprising granules comprising the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof.

62. The composition of any one of Claims 1-54, comprising grains comprising the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof.

63. The composition of any one of Claims 1-62, wherein the composition is in the form of a tablet.

64. The composition of Claim 63, wherein the tablet comprises a tablet core and an outer layer; wherein the tablet core comprises the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof; and wherein the outer layer comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

65. The composition of Claim 64, further comprising an intermediate layer between the tablet core and the outer layer and contacting the tablet core and outer layer.

66. The composition of Claim 64, wherein the tablet core is in contact with the outer layer.

67. The composition of any one of Claims 64-66, further comprising an immediate release coating around the outer layer.

68. The composition any one of Claims 64-67, wherein the outer layer consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

69. The composition any one of Claims 64-68, wherein the outer layer comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, and one or more excipients.

70. The composition of any one of Claims 64-69, wherein the outer layer comprises granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

71. The composition of any one of Claims 64-70, wherein the tablet core further comprises one or more excipients.

72. The composition of any one of Claims 64-71, wherein the tablet core comprises granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof.

73. The composition of any one of Claims 64-72, further comprising an outer layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, and an intermediate layer between the tablet core and the outer layer and contacting the tablet core and outer layer.

74. The composition of any one of Claims 64-72, further comprising an outer layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof wherein the tablet core is in contact with the outer layer.

75. The composition of Claim 73 or 74, wherein the outer layer consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

76. The composition of any one of Claims 73-75, wherein the outer layer comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, and one or more excipients.

77. The composition of any one of Claims 73-76, wherein the outer layer comprises granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

78. The composition of any one of Claims 73-77, wherein the outer layer further comprises an SGLT-2 inhibitor, or a pharmaceutically acceptable salt thereof.

79. The composition of any one of Claims 73-78, wherein the outer layer further comprises granules comprising the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof.

80. The composition of any one of Claims 1-62, wherein the composition is in the form of a capsule.

81. The composition of Claim 80, wherein the capsule is a gelatin capsule or a hydroxypropylmethylcellulose capsule.

82. The composition of Claim 80 or 81, wherein the capsule comprises a tablet core and capsule fill.

83. The composition of Claim 82, wherein the tablet core comprises the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof; and wherein the capsule fill comprises the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

84. The composition of Claim 83, wherein the tablet core further comprises one or more excipients; and wherein the capsule fill further comprises one or more excipients.

85. The composition of any one of Claims 1-63, 80, or 81, comprising granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, wherein the granules are coated with a layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

86. The composition of Claim 85, wherein the granules further comprise one or more excipients.

87. The composition of Claims 1-63, 80, or 81, wherein the granules consist essentially of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof.

88. The composition of any one of Claims 64-79, wherein the layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, further comprises one or more excipients.

89. The composition of any one of Claims 64-79, wherein the layer comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, consists essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

90. The composition of Claim 63, comprising (i) granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and (ii) granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

91. The composition of Claim 63, comprising (i) granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, and (ii) the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, in powder form.

92. The composition of Claim 90 or 91, wherein the granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, further comprise one or more excipients.

93. The composition of Claim 90, wherein the granules comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, consist essentially of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof.

94. The composition of any one of Claims 90-93, wherein the granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, further comprise one or more excipients.

95. The composition of any one of Claims 90-93, wherein the granules comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, consist essentially of the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof.

96. The composition any one of Claims 90-95, wherein (i) and (ii) are blended.

97. The composition of any one of Claims 1-96, wherein the particles comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, have a mean diameter from about 100 nm to about 2 mm.

98. The composition of any one of Claims 1-97, wherein the particles comprising the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, have a mean diameter from about 100 nm to about 1 mm.

99. The composition of any one of Claims 1-98, wherein the particles comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, have a mean diameter from 100 nm to about 2 mm.

100. The composition of any one of Claims 1-99, wherein the particles comprising the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, have a mean diameter from about 100 nm to about 1 mm.

101. The composition of any one of Claims 1-100, wherein the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in substantially amorphous form.

102. The composition of Claim 101, wherein the substantially amorphous compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is prepared by spray drying, spray drying with one or more excipients, hot-melt extrusion, or dissolution followed by precipitation onto an amorphous substrate.

103. The composition of Claim 102, wherein the amorphous substrate is amorphous silica or fumed silica.

104. The composition of any one of Claims 1-103, wherein the PPAR-α agonist, PPAR- δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, is present in crystalline form.

105. The composition of any one of Claims 1-104, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes.

106. The composition of any one of Claims 1-105, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 60 to about 80 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes.

107. The composition of any one of Claims 1-106, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 1 to about pH 2 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes.

108. The composition of any one of Claims 1-107, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 1 to about pH 2 at 37° C.±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 60 to about 80 wt % of the total amount of the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof is released after about 45 minutes.

109. The composition of any one of Claims 21-108, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 25 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes.

110. The composition of any one of Claims 21-109, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 1 (basket) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes.

111. The composition of any one of Claims 21-110, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 25 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes.

112. The composition of any one of Claims 21-111, wherein the composition exhibits a dissolution profile after combining the composition with about 900 mL buffer at from about pH 4 to about pH 7.5 at 37° C ±0.5° C according to USP 28 <711> test method 2 (paddle) at a speed of about 50 to about 100 rpm; wherein from about 50 to about 99 wt % of the total amount of the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof is released after about 15 minutes.

113. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; and (j) applying the fourth blend obtained in step (i) to the surface of the tablet core, forming the outer layer.

114. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) applying the fourth blend obtained in step (i) to the surface of the tablet core, forming the outer layer; and (k) applying an immediate release coating to the outer layer.

115. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules and drying the wet granules to obtain dry granules; (c) milling the dry granules obtained in step (b); (d) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a second blend; (e) forming dry granules comprising the second blend, or optionally mixing a granulating solution with the second blend obtained in step (d) to form wet granules, then drying the wet granules to form dry granules; (f) milling the dry granules obtained in step (e); (g) mixing the milled dry granules obtained in steps (c) and (f) with one or more excipients to form a third blend; and (h) compressing the third blend to form a tablet.

116. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) compressing the dry granules from step (b) or step (c) to form the tablet core; and (e) applying the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, to the surface of the tablet core, forming an outer layer.

117. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) mixing the dry granules obtained in step (b) or step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; and (f) applying the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, to the surface of the tablet core, forming an outer layer.

118. A process for preparing the composition of any one of Claims 1-62, 80-87, or 97- 112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules; (c) drying the wet granules obtained in step (b) to form dry granules; (d) milling the dry granules obtained in step (c); (e) mixing the milled dry granules obtained in step (d) with one or more excipients to form a second blend; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution to the third blend obtained in step (f), and mixing the solution and third blend to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the second blend obtained in step (e) and the fourth blend obtained in step (i); and (k) filling a capsule with the mixture obtained in step (j).

119. A process for preparing the composition of any one of Claims 1-62, 80-87, or 97- 112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a capsule fill; and (j) filling a capsule with the tablet core and the capsule fill.

120. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fifth blend; (k) forming dry granules comprising the fifth blend; (l) milling the dry granules obtained in step (k); (m) mixing the milled dry granules obtained in step (l) with one or more excipients to form a sixth blend; (n) mixing the fourth blend of step (i) with the sixth blend of step (m), optionally with one or more excipients, to form a seventh blend; and (o) applying the seventh blend obtained in step (n) to the surface of the tablet core, forming the outer layer.

121. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fifth blend; (k) forming dry granules comprising the fifth blend; (l) milling the dry granules obtained in step (k); (m) mixing the milled dry granules obtained in step (l) with one or more excipients to form a sixth blend; (n) mixing the fourth blend of step (i) with the sixth blend of step (m), optionally with one or more excipients, to form a seventh blend; (o) applying the seventh blend obtained in step (n) to the surface of the tablet core, forming the outer layer; and (p) applying an immediate release coating to the outer layer.

122. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules and drying the wet granules to obtain dry granules; (c) milling the dry granules obtained in step (b); (d) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a second blend; (e) forming dry granules comprising the second blend, or optionally mixing a granulating solution with the second blend obtained in step (d) to form wet granules, then drying the wet granules to form dry granules; (f) milling the dry granules obtained in step (e); (g) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (h) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (g) to form wet granules and drying the wet granules to obtain dry granules; (i) milling the dry granules obtained in step (h); (j) mixing the milled dry granules obtained in steps (c), (f), and (i) with one or more excipients to form a fourth blend; and (k) compressing the fourth blend to form a tablet.

123. A process for preparing the composition of any one of Claims 1-79 or 88-112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) compressing the dry granules from step (b) or step (c) to form the tablet core; and (e) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, and the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, optionally with one or more excipients, to form a second blend; and (f) applying the second blend to the surface of the tablet core, forming an outer layer.

124. A process for preparing the composition of any one of Claims 1-52 or 63-90, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) optionally milling the dry granules obtained in step (b); (d) mixing the dry granules obtained in step (b) or step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; and (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, and the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, optionally with one or more excipients, to form a third blend; and (g) applying the third blend to the surface of the tablet core, forming an outer layer.

125. A process for preparing the composition of any one of Claims 1-62, 80-87, or 97- 112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend, or optionally mixing a granulating solution with the first blend obtained in step (a) to form wet granules; (c) drying the wet granules obtained in step (b) to form dry granules; (d) milling the dry granules obtained in step (c); (e) mixing the milled dry granules obtained in step (d) with one or more excipients to form a second blend; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution to the third blend obtained in step (f), and mixing the solution and third blend to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the milled dry granules obtained in step (h) with one or more excipients to form a fourth blend; (j) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fifth blend; (k) forming dry granules comprising the fifth blend, or optionally mixing a granulating solution to the fifth blend obtained in step (j), and mixing the solution and fifth blend to form wet granules, then drying the wet granules to form dry granules; (l) milling the dry granules obtained in step (k); (m) mixing the milled dry granules obtained in step (l) with one or more excipients to form a sixth blend; (n) mixing the second blend obtained in step (e), the fourth blend obtained in step (i), and the sixth blend obtained in step (m); and (o) filling a capsule with the mixture obtained in step (n).

126. A process for preparing the composition of any one of Claims 1-62, 80-87, or 97- 112, comprising: (a) mixing the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a first blend; (b) forming dry granules comprising the first blend; (c) milling the dry granules obtained in step (b); (d) mixing the milled dry granules obtained in step (c) with one or more excipients to form a second blend; (e) compressing the second blend to form the tablet core; (f) mixing the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a third blend; (g) forming dry granules comprising the third blend, or optionally mixing a granulating solution with the third blend obtained in step (f) to form wet granules, then drying the wet granules to form dry granules; (h) milling the dry granules obtained in step (g); (i) mixing the SGLT-2 inhibitor, or a pharmaceutically acceptable salt or solvate thereof, with one or more excipients to form a fourth blend; (j) forming dry granules comprising the fourth blend, or optionally mixing a granulating solution with the fourth blend obtained in step (i) to form wet granules, then drying the wet granules to form dry granules; (k) milling the dry granules obtained in step (j); (l) mixing the milled dry granules obtained in step (h), the milled dry granules obtained in step (k), and one or more excipients to form a capsule fill; and (m) filling a capsule with the tablet core and the capsule fill.

127. The process of any one of Claims 113-126, wherein the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is present in substantially amorphous form.

128. The process of any one of Claims 113-127, wherein the compound of Formula (I), or a pharmaceutically acceptable salt or solvate thereof, is prepared by spray drying, spray drying with one or more excipients, hot-melt extrusion, or dissolution followed by precipitation onto an amorphous substrate.

129. The process of Claim 128, wherein the amorphous substrate is amorphous silica or fumed silica.

130. The process of any one of Claims 113-129, wherein the PPAR-α agonist, PPAR-δ agonist, or dual PPAR-α/δ agonist, or a pharmaceutically acceptable salt or solvate thereof, is present in crystalline form.

131. A method of treating a PPARγ-mediated disease or disorder, comprising administering the composition of any one of Claims 1-112 to a subject in need thereof.

132. The method of Claim 131, wherein the PPARγ-mediated disease or disorder is type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), or a combination of any of the foregoing.

133. The method of Claim 131 or 132, wherein the PPARγ-mediated disease or disorder is type 2 diabetes and NASH.

134. The method of Claim 133, wherein type 2 diabetes and NASH are treated.

135. The method of Claim 133, wherein NASH is treated.