CN105061600A - Rheumatoid factor IgA inhibitory polypeptide and application thereof - Google Patents
Rheumatoid factor IgA inhibitory polypeptide and application thereof Download PDFInfo
- Publication number
- CN105061600A CN105061600A CN201510556863.1A CN201510556863A CN105061600A CN 105061600 A CN105061600 A CN 105061600A CN 201510556863 A CN201510556863 A CN 201510556863A CN 105061600 A CN105061600 A CN 105061600A
- Authority
- CN
- China
- Prior art keywords
- polypeptide
- iga
- arthritis
- polyclonal
- rheumatoid factors
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Pending
Links
- 108090000765 processed proteins & peptides Proteins 0.000 title claims abstract description 44
- 229920001184 polypeptide Polymers 0.000 title claims abstract description 43
- 102000004196 processed proteins & peptides Human genes 0.000 title claims abstract description 43
- 230000002401 inhibitory effect Effects 0.000 title abstract 2
- 208000019069 chronic childhood arthritis Diseases 0.000 claims abstract description 16
- 208000003456 Juvenile Arthritis Diseases 0.000 claims abstract description 15
- 206010059176 Juvenile idiopathic arthritis Diseases 0.000 claims abstract description 15
- 201000002215 juvenile rheumatoid arthritis Diseases 0.000 claims abstract description 15
- 230000002265 prevention Effects 0.000 claims description 5
- 208000037265 diseases, disorders, signs and symptoms Diseases 0.000 claims description 3
- 239000002775 capsule Substances 0.000 claims 1
- 238000010255 intramuscular injection Methods 0.000 claims 1
- 239000007927 intramuscular injection Substances 0.000 claims 1
- 238000001990 intravenous administration Methods 0.000 claims 1
- 238000010253 intravenous injection Methods 0.000 claims 1
- 239000007922 nasal spray Substances 0.000 claims 1
- 229940097496 nasal spray Drugs 0.000 claims 1
- 239000006187 pill Substances 0.000 claims 1
- 238000010254 subcutaneous injection Methods 0.000 claims 1
- 239000007929 subcutaneous injection Substances 0.000 claims 1
- 230000001629 suppression Effects 0.000 claims 1
- 239000003814 drug Substances 0.000 abstract description 16
- 229940079593 drug Drugs 0.000 abstract description 10
- 230000000694 effects Effects 0.000 abstract description 4
- 238000011161 development Methods 0.000 abstract description 3
- 230000009286 beneficial effect Effects 0.000 abstract description 2
- 241000700159 Rattus Species 0.000 description 17
- 241000699666 Mus <mouse, genus> Species 0.000 description 11
- 102000008186 Collagen Human genes 0.000 description 10
- 108010035532 Collagen Proteins 0.000 description 10
- 206010003246 arthritis Diseases 0.000 description 10
- 229920001436 collagen Polymers 0.000 description 10
- 239000002671 adjuvant Substances 0.000 description 9
- 238000010171 animal model Methods 0.000 description 9
- 241001465754 Metazoa Species 0.000 description 6
- 210000003423 ankle Anatomy 0.000 description 6
- 230000002917 arthritic effect Effects 0.000 description 6
- 208000009386 Experimental Arthritis Diseases 0.000 description 5
- FBOZXECLQNJBKD-ZDUSSCGKSA-N L-methotrexate Chemical compound C=1N=C2N=C(N)N=C(N)C2=NC=1CN(C)C1=CC=C(C(=O)N[C@@H](CCC(O)=O)C(O)=O)C=C1 FBOZXECLQNJBKD-ZDUSSCGKSA-N 0.000 description 5
- 229960000485 methotrexate Drugs 0.000 description 4
- 239000013641 positive control Substances 0.000 description 4
- 206010039073 rheumatoid arthritis Diseases 0.000 description 4
- 230000008961 swelling Effects 0.000 description 4
- 230000001225 therapeutic effect Effects 0.000 description 4
- 102000002734 Collagen Type VI Human genes 0.000 description 3
- 108010043741 Collagen Type VI Proteins 0.000 description 3
- 206010039361 Sacroiliitis Diseases 0.000 description 3
- 230000000366 juvenile effect Effects 0.000 description 3
- 208000024891 symptom Diseases 0.000 description 3
- BSYNRYMUTXBXSQ-UHFFFAOYSA-N Aspirin Chemical compound CC(=O)OC1=CC=CC=C1C(O)=O BSYNRYMUTXBXSQ-UHFFFAOYSA-N 0.000 description 2
- 241000699670 Mus sp. Species 0.000 description 2
- 229960001138 acetylsalicylic acid Drugs 0.000 description 2
- 238000006243 chemical reaction Methods 0.000 description 2
- 208000018631 connective tissue disease Diseases 0.000 description 2
- 230000006378 damage Effects 0.000 description 2
- 238000013461 design Methods 0.000 description 2
- 238000001514 detection method Methods 0.000 description 2
- 239000003995 emulsifying agent Substances 0.000 description 2
- 230000003203 everyday effect Effects 0.000 description 2
- 238000002474 experimental method Methods 0.000 description 2
- 210000003414 extremity Anatomy 0.000 description 2
- 210000002683 foot Anatomy 0.000 description 2
- 238000000034 method Methods 0.000 description 2
- 229940021182 non-steroidal anti-inflammatory drug Drugs 0.000 description 2
- 239000002504 physiological saline solution Substances 0.000 description 2
- 238000011160 research Methods 0.000 description 2
- 239000000243 solution Substances 0.000 description 2
- 238000007920 subcutaneous administration Methods 0.000 description 2
- 230000001988 toxicity Effects 0.000 description 2
- 231100000419 toxicity Toxicity 0.000 description 2
- WHTVZRBIWZFKQO-AWEZNQCLSA-N (S)-chloroquine Chemical compound ClC1=CC=C2C(N[C@@H](C)CCCN(CC)CC)=CC=NC2=C1 WHTVZRBIWZFKQO-AWEZNQCLSA-N 0.000 description 1
- QTBSBXVTEAMEQO-UHFFFAOYSA-M Acetate Chemical compound CC([O-])=O QTBSBXVTEAMEQO-UHFFFAOYSA-M 0.000 description 1
- 206010002091 Anaesthesia Diseases 0.000 description 1
- 241000894006 Bacteria Species 0.000 description 1
- VVNCNSJFMMFHPL-VKHMYHEASA-N D-penicillamine Chemical compound CC(C)(S)[C@@H](N)C(O)=O VVNCNSJFMMFHPL-VKHMYHEASA-N 0.000 description 1
- 229940123907 Disease modifying antirheumatic drug Drugs 0.000 description 1
- 241000287828 Gallus gallus Species 0.000 description 1
- HEFNNWSXXWATRW-UHFFFAOYSA-N Ibuprofen Chemical compound CC(C)CC1=CC=C(C(C)C(O)=O)C=C1 HEFNNWSXXWATRW-UHFFFAOYSA-N 0.000 description 1
- 206010022941 Iridocyclitis Diseases 0.000 description 1
- 101000974353 Mus musculus Nuclear receptor coactivator 5 Proteins 0.000 description 1
- 241000187479 Mycobacterium tuberculosis Species 0.000 description 1
- CMWTZPSULFXXJA-UHFFFAOYSA-N Naproxen Natural products C1=C(C(C)C(O)=O)C=CC2=CC(OC)=CC=C21 CMWTZPSULFXXJA-UHFFFAOYSA-N 0.000 description 1
- 101710115512 Nuclear receptor coactivator 5 Proteins 0.000 description 1
- 208000001132 Osteoporosis Diseases 0.000 description 1
- -1 Salazopyrine Chemical compound 0.000 description 1
- 206010070834 Sensitisation Diseases 0.000 description 1
- 206010048873 Traumatic arthritis Diseases 0.000 description 1
- 241000700605 Viruses Species 0.000 description 1
- 230000037005 anaesthesia Effects 0.000 description 1
- 239000005557 antagonist Substances 0.000 description 1
- 201000004612 anterior uveitis Diseases 0.000 description 1
- 230000003356 anti-rheumatic effect Effects 0.000 description 1
- 239000000427 antigen Substances 0.000 description 1
- 102000036639 antigens Human genes 0.000 description 1
- 108091007433 antigens Proteins 0.000 description 1
- 239000003435 antirheumatic agent Substances 0.000 description 1
- 230000037396 body weight Effects 0.000 description 1
- 210000000988 bone and bone Anatomy 0.000 description 1
- 210000000845 cartilage Anatomy 0.000 description 1
- 229960003677 chloroquine Drugs 0.000 description 1
- WHTVZRBIWZFKQO-UHFFFAOYSA-N chloroquine Natural products ClC1=CC=C2C(NC(C)CCCN(CC)CC)=CC=NC2=C1 WHTVZRBIWZFKQO-UHFFFAOYSA-N 0.000 description 1
- 230000009849 deactivation Effects 0.000 description 1
- 229960003957 dexamethasone Drugs 0.000 description 1
- UREBDLICKHMUKA-CXSFZGCWSA-N dexamethasone Chemical compound C1CC2=CC(=O)C=C[C@]2(C)[C@]2(F)[C@@H]1[C@@H]1C[C@@H](C)[C@@](C(=O)CO)(O)[C@@]1(C)C[C@@H]2O UREBDLICKHMUKA-CXSFZGCWSA-N 0.000 description 1
- 229960001259 diclofenac Drugs 0.000 description 1
- DCOPUUMXTXDBNB-UHFFFAOYSA-N diclofenac Chemical compound OC(=O)CC1=CC=CC=C1NC1=C(Cl)C=CC=C1Cl DCOPUUMXTXDBNB-UHFFFAOYSA-N 0.000 description 1
- 229960001193 diclofenac sodium Drugs 0.000 description 1
- 201000010099 disease Diseases 0.000 description 1
- 238000004090 dissolution Methods 0.000 description 1
- 239000012634 fragment Substances 0.000 description 1
- 239000003862 glucocorticoid Substances 0.000 description 1
- 238000010438 heat treatment Methods 0.000 description 1
- 229960001680 ibuprofen Drugs 0.000 description 1
- 230000036039 immunity Effects 0.000 description 1
- 239000003018 immunosuppressive agent Substances 0.000 description 1
- 238000001727 in vivo Methods 0.000 description 1
- 230000005764 inhibitory process Effects 0.000 description 1
- 239000007924 injection Substances 0.000 description 1
- 238000002347 injection Methods 0.000 description 1
- 230000001788 irregular Effects 0.000 description 1
- 208000018934 joint symptom Diseases 0.000 description 1
- 210000004185 liver Anatomy 0.000 description 1
- 229960002009 naproxen Drugs 0.000 description 1
- CMWTZPSULFXXJA-VIFPVBQESA-N naproxen Chemical compound C1=C([C@H](C)C(O)=O)C=CC2=CC(OC)=CC=C21 CMWTZPSULFXXJA-VIFPVBQESA-N 0.000 description 1
- 239000000041 non-steroidal anti-inflammatory agent Substances 0.000 description 1
- 230000007170 pathology Effects 0.000 description 1
- 230000002688 persistence Effects 0.000 description 1
- 230000003863 physical function Effects 0.000 description 1
- 230000035479 physiological effects, processes and functions Effects 0.000 description 1
- 229960004618 prednisone Drugs 0.000 description 1
- XOFYZVNMUHMLCC-ZPOLXVRWSA-N prednisone Chemical compound O=C1C=C[C@]2(C)[C@H]3C(=O)C[C@](C)([C@@](CC4)(O)C(=O)CO)[C@@H]4[C@@H]3CCC2=C1 XOFYZVNMUHMLCC-ZPOLXVRWSA-N 0.000 description 1
- 238000002360 preparation method Methods 0.000 description 1
- 201000003068 rheumatic fever Diseases 0.000 description 1
- 229940061969 rheumatrex Drugs 0.000 description 1
- 230000008313 sensitization Effects 0.000 description 1
- 210000002966 serum Anatomy 0.000 description 1
- JGMJQSFLQWGYMQ-UHFFFAOYSA-M sodium;2,6-dichloro-n-phenylaniline;acetate Chemical compound [Na+].CC([O-])=O.ClC1=CC=CC(Cl)=C1NC1=CC=CC=C1 JGMJQSFLQWGYMQ-UHFFFAOYSA-M 0.000 description 1
- 210000000952 spleen Anatomy 0.000 description 1
- 238000002636 symptomatic treatment Methods 0.000 description 1
- 238000002560 therapeutic procedure Methods 0.000 description 1
- 231100000331 toxic Toxicity 0.000 description 1
- 230000002588 toxic effect Effects 0.000 description 1
Landscapes
- Medicines That Contain Protein Lipid Enzymes And Other Medicines (AREA)
Abstract
The invention relates to the field of medicines, and in particular to a polypeptide which has an effect of inhibiting a rheumatoid factor IgA, and can be used for preventing and treating juvenile rheumatoid arthritis. The sequence of the polypeptide is EFVFLLKGHEDLRQDERVMQ which is a brand-new sequence. The polypeptide provided by the invention has the beneficial effects that the polypeptide can be used for treating the juvenile rheumatoid arthritis and has a potential new medicine development value.
Description
Technical field:
The present invention relates to pharmaceutical field, be specifically related to the polypeptide being used for the treatment of or preventing juvenile rheumatoid arthritis.
Background technology:
Juvenile rheumatoid arthritis (juvenilerheumatoidarthritis, JRA) be a kind of common connective tissue disease (CTD) in children's's period, be its principal feature with chronic arthritis, and getting involved with whole body multisystem, comprise joint, skin, flesh, liver, spleen, lymphoglandula.Young infant often first has the irregular heating of persistence, and its constitutional symptom comparatively joint symptoms is more remarkable.
When the patient suffering from rheumatic arthritis for juvenile treats, except with except non-steroidal anti-inflammatory drugs symptomatic treatment, should start as early as possible with doing medication slowly.Immunosuppressor toxicity is comparatively large, only just careful use in severe case.For the patient that illness is lighter, acetylsalicylic acid etc. is selected to be suitable for the non-steroidal anti-inflammatory drug of children.Because children are easier, toxicity symptom is produced to acetylsalicylic acid.Other drug, as Ibuprofen BP/EP, Naproxen Base, Diclofenac Sodium (diclofenac), golden preparation, Trolovol, chloroquine, Salazopyrine, Rheumatrex etc., but the toxic side effect of this kind of medicine is also larger.In addition, for whole body type, there are multi-joint, Multisystem damage or pauciarthritis type to merge the severe juvenile patient with rheumatoid arthritis of iridocyclitis, select the glucocorticosteroid such as prednisone, dexamethasone.But these medicines can only play and improve symptom, act on osteoclasia without change, and have obstruction upgrowth and development of children, cause osteoporosis and reduce untoward reactions such as other diseases resistibilitys, therefore can not use in a large number as conventional medicine.In addition, due to each side such as physical functions, the untoward reaction of juvenile to some antirheumatics is more responsive than adult patient.Therefore, safer, the effective novel anti-juvenile rheumatoid arthritis medicine of exploitation is badly in need of.
Rheumatoid factors, polyclonal (rheumatoidfactor, RF) is the class autoantibody for epitope in IgGFC fragment in rheumatoid arthritis serum.Rheumatoid factors, polyclonal is because infectant (bacterium, virus etc.) causes a kind of antibody being antigen with sex change IgG (a kind of antibody) produced in body, therefore also known as anti-antibody.Common Rheumatoid factors, polyclonal has IgM type, IgG type, IgA type and IgE type.In human body, ubiquity Rheumatoid factors, polyclonal, and plays certain physiological action.IgA-RF is relevant with destruction of bone, and early stage IgA-RF raises normal prompting and is in a bad way.Therefore, IgA-RF can be used as the therapy target of the early stage morbidity of juvenile rheumatoid arthritis morbidity.Suppress IgA-RF effectively can treat juvenile rheumatoid arthritis, but the IgA-RF of unripe exploitation suppress polypeptide to come out.
Summary of the invention:
The present invention seeks to the feature for existing treatment juvenile rheumatoid arthritis, design a kind of IgA-RF polypeptide antagonist, be applicable to the application of clinical treatment juvenile rheumatoid arthritis.
Technical solution of the present invention is to provide a kind of Rheumatoid factors, polyclonal IgA and suppresses polypeptide, and its sequence is EFVFLLKGHEDLRQDERVMQ, and the application in treatment or prevention juvenile rheumatoid arthritis medicine.
Beneficial outcomes:
Rheumatoid factors, polyclonal IgA in the present invention suppresses peptide sequence EFVFLLKGHEDLRQDERVMQ, can targeted inhibition Rheumatoid factors, polyclonal IgA, the physiology suppressing Rheumatoid factors, polyclonal IgA acceptor to produce or the effect of pathology, reach the effect of prevention or treatment juvenile rheumatoid arthritis.
Through great many of experiments, contriver knows that Rheumatoid factors, polyclonal IgA suppresses polypeptide can suppress the development of adjuvant type infant rats rheumatoid arthritis and DBA/1 young mice collagen type rheumatoid arthritis, experiment in vivo proves to have the arthritic effect of significant treatment similar rheumatism type.Illustrate that the Rheumatoid factors, polyclonal IgA that the present invention designs suppresses polypeptide scientific, rational, feasible and effective, can as treatment or prevention juvenile rheumatoid arthritis medicine.
Embodiment
Polypeptide of the present invention is synthesized by Shanghai gill.
Embodiment 1
Rheumatoid factors, polyclonal IgA suppresses polypeptide immanoprotection action in collagen-induced mouse arthritis animal model
Build collagen type mouse arthritis animal model, research Rheumatoid factors, polyclonal IgA suppresses polypeptide to the therapeutic action of mouse collagen Induced Arthritis (collageninducedarthritis, CIA).Adopt mouse as animal subject, SPF level DBA/1 mouse 90 (is provided by Shanghai western pul-Bi Kai laboratory animal company limited (Sino-BritishSIPPRLab.AnimalLtd), animal productiong ticket number: SCXK (Shanghai) 2008-0016), male, 4-5 week age, be divided into 6 groups at random, Normal group respectively, model control group, low middle high 3 the dosage groups (0.4 of polypeptide, 0.8,1.6mg/kg) and positive drug control group (methotrexate 2mg/kg).Except normal group, within the 0th day, each experimental group sets up mouse CIA model, and method is chicken cartilage II Collagen Type VI (c II) becomes 4mg/ml solution with 0.1mol/l acetate dissolution, in 4 DEG C of refrigerator overnight.Experimental day is fully emulsified with complete Freund's adjuvant (CFA) equal-volume containing 4mg/mlMyeobaeteriumtuberculosisstrainH37Rv with II Collagen Type VI, after DBA/1 mouse anesthesia, often only inject emulsifying agent 50 μ l in its afterbody intracutaneous and carry out sensitization, after fully emulsified with II Collagen Type VI (c II) of 4mg/ml and incomplete Freund's adjuvant (IFA) equal-volume after 21d, carry out immunity again with the emulsifying agent of same dose in afterbody.Modeling 30d plays subcutaneous administrations: 3 dosage groups (0.4,0.8,1.6mg/kg) of polypeptide: every day twice, continuous 10 days; Positive drug control group (methotrexate 2mg/kg): every five days once, continuous 3 times; Normal group and model control group (physiological saline): continuous 10 days.Medicine is observed on the arthritic impact of mouse collagen type respectively at the 40th day Joint scores, detection left and right metapedes ankle diameter after modeling.
Rheumatoid factors, polyclonal IgA suppresses polypeptide immanoprotection action concrete outcome in collagen-induced mouse arthritis animal model as follows: Rheumatoid factors, polyclonal IgA suppresses polypeptide on the impact of mouse collagen type arthritis knuckle swelling rate; positive controls, Rheumatoid factors, polyclonal IgA suppress polypeptide high, medium and low dosage group Articular swelling rate to compare with model group, all have pole significant difference (P<0.01) experimental result to have statistical significance.Rheumatoid factors, polyclonal IgA suppresses polypeptide on the impact of mouse collagen type sacroiliitis foot pawl swelling rate, positive controls, Rheumatoid factors, polyclonal IgA suppress polypeptide high, medium and low dosage group foot pawl swelling rate to compare with model group, all have pole significant difference (P<0.01), experimental result has statistical significance.Polypeptide is on the impact of collagen type arthritic mice Joint scores, the scoring of polypeptide basic, normal, high dosage group four limbs is significantly lower than model control group (P < 0.01), compare pole significant difference with model control group, experimental result has statistical significance.
Table 1 Rheumatoid factors, polyclonal IgA suppresses polypeptide on the arthritic impact of collagen type (means ± SD) * P<0.05; * P<0.01 (comparing with model group)
Conclusion: Rheumatoid factors, polyclonal IgA suppresses polypeptide to have therapeutic action to mouse collagen type sacroiliitis.
Embodiment 2
Rheumatoid factors, polyclonal IgA suppresses polypeptide to immanoprotection action in adjuvant type rat arthritis animal model
Build adjuvant type rat arthritis animal model, research polypeptide is to the therapeutic action of adjuvant-induced arthritis (Adjuvantarthritis, AA) rat.Adopt rat as animal subject, SPF level SD rat (is provided by Shanghai western pul-Bi Kai laboratory animal company limited (Sino-BritishSIPPRLab.AnimalLtd), animal productiong ticket number: SCXK (Shanghai) 2008-0016), male, body weight is 100g-120g, be divided into 6 groups at random, Normal group respectively, model control group, Rheumatoid factors, polyclonal IgA suppresses low middle high 3 the dosage groups (0.2 of polypeptide, 0.4,0.8mg/kg) and positive drug control group (methotrexate 1mg/kg).Except normal group, within the 0th day, each experimental group sets up rat AA model, and method is that injection of wasting time fully afterwards in the left side of rat causes experimental animal model of CFA induced adjuvant arthritis in rats containing mycobacterium tuberculosis (H37RA, 10mg/ml) the complete Freund's adjuvant 0.1ml of deactivation.Modeling plays subcutaneous administrations on the 10th day: 3 dosage groups (0.2,0.4,0.8mg/kg) of polypeptide: every day twice, continuous 10 days; Positive drug control group (methotrexate 1mg/kg): every five days once, continuous 3 times; Normal group and model control group (physiological saline): continuous 10 days.Medicine is observed on the arthritic impact of rat adjuvant type respectively at the 21st day Joint scores, detection left and right metapedes ankle diameter after modeling.
Polypeptide is immanoprotection action in adjuvanticity rat arthritis animal model, concrete outcome is as follows: Rheumatoid factors, polyclonal IgA suppresses polypeptide on the impact of the left back ankle diameter of rat primary sacroiliitis, rat positive controls, Rheumatoid factors, polyclonal IgA suppress the left back ankle diameter of basic, normal, high dosage group of polypeptide to compare with model group, have pole significant difference (P<0.01); Rheumatoid factors, polyclonal IgA suppresses polypeptide on the impact of the right back ankle diameter of rat post-traumatic arthritis, rat positive controls, Rheumatoid factors, polyclonal IgA suppress the right back ankle diameter of polypeptide basic, normal, high dosage group to compare with model group, have significant difference (P<0.05).Rheumatoid factors, polyclonal IgA suppresses polypeptide on the impact of adjuvant type rats with arthritis Joint scores, the scoring of polypeptide basic, normal, high dosage group four limbs, significantly lower than model control group (P < 0.05), all has statistical significance with model control group comparing difference.
Table 2 Rheumatoid factors, polyclonal IgA suppresses polypeptide on the arthritic impact of adjuvant type (means ± SD)
* P<0.05; * P<0.01 (comparing with model group)
Conclusion: Rheumatoid factors, polyclonal IgA suppresses polypeptide to have therapeutic action to AA rat arthritis.
SEQUENCELISTING
Pu Luoda bio tech ltd, <110> Suzhou
<120> Rheumatoid factors, polyclonal IgA suppresses polypeptide and application thereof
<130>
<160>1
<170>PatentInversion3.5
<210>1
<211>20
<212>PRT
<213> artificial sequence
<400>1
GluPheValPheLeuLeuLysGlyHisGluAspLeuArgGlnAspGlu
151015
ArgValMetGln
20
Claims (3)
1. Rheumatoid factors, polyclonal IgA suppresses polypeptide, it is characterized in that its sequence is EFVFLLKGHEDLRQDERVMQ.
2. the application of suppression polypeptide in treatment and prevention juvenile rheumatoid arthritis disease of claim 1.
3. suppress the purposes of polypeptide according to claim 2, it is characterized in that: by multiple administering mode treatment and prevention juvenile rheumatoid arthritis disease, comprise subcutaneous or intramuscular injection, intravenous injection or intravenous drip, oral administration as pill, capsule etc., nasal spray etc.
Priority Applications (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN201510556863.1A CN105061600A (en) | 2015-09-05 | 2015-09-05 | Rheumatoid factor IgA inhibitory polypeptide and application thereof |
Applications Claiming Priority (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN201510556863.1A CN105061600A (en) | 2015-09-05 | 2015-09-05 | Rheumatoid factor IgA inhibitory polypeptide and application thereof |
Publications (1)
| Publication Number | Publication Date |
|---|---|
| CN105061600A true CN105061600A (en) | 2015-11-18 |
Family
ID=54491148
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| CN201510556863.1A Pending CN105061600A (en) | 2015-09-05 | 2015-09-05 | Rheumatoid factor IgA inhibitory polypeptide and application thereof |
Country Status (1)
| Country | Link |
|---|---|
| CN (1) | CN105061600A (en) |
Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| WO2018157807A1 (en) * | 2017-03-01 | 2018-09-07 | 成都惠泰生物医药有限公司 | Polypeptide, polypeptide fragment, derivative thereof, and applications thereof |
| CN119490598A (en) * | 2023-08-18 | 2025-02-21 | 重庆艾生斯生物工程有限公司 | An anti-RF antibody or its functional fragment and its application |
Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20080107668A1 (en) * | 2006-08-30 | 2008-05-08 | Immunotope, Inc. | Cytotoxic t-lymphocyte-inducing immunogens for prevention, treatment, and diagnosis of cancer |
| CN103159851A (en) * | 2011-12-19 | 2013-06-19 | 上海市第一人民医院 | Micromolecule polypeptide preventing and restraining inflammation and application thereof |
| CN103403030A (en) * | 2011-02-21 | 2013-11-20 | 菲布他丁有限合伙公司 | Methods of treating and diagnosing disease |
-
2015
- 2015-09-05 CN CN201510556863.1A patent/CN105061600A/en active Pending
Patent Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20080107668A1 (en) * | 2006-08-30 | 2008-05-08 | Immunotope, Inc. | Cytotoxic t-lymphocyte-inducing immunogens for prevention, treatment, and diagnosis of cancer |
| CN103403030A (en) * | 2011-02-21 | 2013-11-20 | 菲布他丁有限合伙公司 | Methods of treating and diagnosing disease |
| CN103159851A (en) * | 2011-12-19 | 2013-06-19 | 上海市第一人民医院 | Micromolecule polypeptide preventing and restraining inflammation and application thereof |
Non-Patent Citations (1)
| Title |
|---|
| ZHANG G等: "登录号:ELW68647.1", 《GENBANK》 * |
Cited By (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| WO2018157807A1 (en) * | 2017-03-01 | 2018-09-07 | 成都惠泰生物医药有限公司 | Polypeptide, polypeptide fragment, derivative thereof, and applications thereof |
| US12011475B2 (en) | 2017-03-01 | 2024-06-18 | Chengdu Huitai Biomedicine Co., Ltd. | Polypeptide, polypeptide fragment, derivative thereof, and applications thereof |
| CN119490598A (en) * | 2023-08-18 | 2025-02-21 | 重庆艾生斯生物工程有限公司 | An anti-RF antibody or its functional fragment and its application |
Similar Documents
| Publication | Publication Date | Title |
|---|---|---|
| Huang et al. | Skin manifestations of inflammatory bowel disease | |
| US8389479B2 (en) | Compositions and methods for treatment of multiple sclerosis | |
| KR101900520B1 (en) | A combination composition | |
| Van Vollenhoven et al. | Safety and efficacy of Atacicept in combination with rituximab for reducing the signs and symptoms of rheumatoid arthritis: a phase II, randomized, Double‐Blind, Placebo‐Controlled pilot trial | |
| Hisamatsu et al. | Treatment and outcomes: medical and surgical treatment for intestinal Behçet's disease | |
| Sagami et al. | Successful use of adalimumab for treating pyoderma gangrenosum with ulcerative colitis under corticosteroid-tapering conditions | |
| CN103739670A (en) | Polyethylene glycol modified polypeptide for inhibiting tumor necrosis factor-alpha and application of polypeptide | |
| CN105061600A (en) | Rheumatoid factor IgA inhibitory polypeptide and application thereof | |
| Saji et al. | Infliximab for Kawasaki syndrome | |
| CN103819540B (en) | Nf-KB peptide inhibitor and application thereof | |
| CN103772491B (en) | Nf-KB peptide inhibitor 3 and application thereof | |
| CN103254291B (en) | Tumor necrosis factor-alpha polypeptide inhibitors and application thereof | |
| CN105061583A (en) | Peripheral interleukin 35 polypeptide and application thereof | |
| CN103772489A (en) | Nuclear factor-KB polypeptide inhibitor 5 and application thereof | |
| CN103893161A (en) | Application of syringic acid-(4-hydroxyl-3,5-dimethoxybenzoic acid) in preparation of medicine for preventing and treating rheumatoid arthritis | |
| Korzenik | Crohn's disease: future anti–tumor necrosis factor therapies beyond infliximab | |
| CN113425723B (en) | Application of Pim1 small-molecule inhibitor in preparation of product for preventing and treating ankylosing spondylitis | |
| CN105111284A (en) | Tumor necrosis factor inhibitory polypeptide and application thereof | |
| CN105017388A (en) | NOD1 protein inhibiting polypeptide and application thereof | |
| CN103739669A (en) | Polypeptide capable of inhibiting interleukin-6 and application thereof | |
| CN103265619A (en) | Tumor necrosis factor-alpha polypeptide inhibitor and application thereof | |
| RU2401112C2 (en) | Pharmaceutical composition for treating autoimmune diseases associated with increased nucleic acid antibody formation | |
| CN105061565A (en) | Polypeptide inhibiting interferon regulation factor 5 and application thereof | |
| Atzeni et al. | Autoimmunity and the newer biopharmaceuticals | |
| Mandell | Trends in rheumatic disease: update on new diagnostic and treatment strategies |
Legal Events
| Date | Code | Title | Description |
|---|---|---|---|
| C06 | Publication | ||
| PB01 | Publication | ||
| C10 | Entry into substantive examination | ||
| SE01 | Entry into force of request for substantive examination | ||
| WD01 | Invention patent application deemed withdrawn after publication | ||
| WD01 | Invention patent application deemed withdrawn after publication |
Application publication date: 20151118 |