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RU2013103027A - Введение гипоксически активируемых пролекарств и средств, препятствующих ангиогенезу, для лечения рака - Google Patents

Введение гипоксически активируемых пролекарств и средств, препятствующих ангиогенезу, для лечения рака Download PDF

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RU2013103027A
RU2013103027A RU2013103027/15A RU2013103027A RU2013103027A RU 2013103027 A RU2013103027 A RU 2013103027A RU 2013103027/15 A RU2013103027/15 A RU 2013103027/15A RU 2013103027 A RU2013103027 A RU 2013103027A RU 2013103027 A RU2013103027 A RU 2013103027A
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angiogenesis
inhibitor
agent
activated prodrug
group
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RU2013103027/15A
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RU2597844C2 (ru
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Чарльз ХАРТ
Джон КУРД
Стюарт КРОЛЛ
Джессика САН
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Тресхолд Фармасьютикалз, Инк.
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Abstract

1. Способ лечения пациента с онкологическим заболеванием, которому необходимо такое лечение, при этом указанный способ включает введение средства, препятствующего ангиогенезу, и введение гипоксически активируемого пролекарства указанному пациенту.2. Способ по п.1, где первое введение гипоксически активируемого пролекарства происходит только после того, как введение средства, препятствующего ангиогенезу, привело к увеличению гипоксической фракции онкологического образования.3. Способ по п.2, где первое введение гипоксически активируемого пролекарства происходит по меньшей мере через 7 дней после первого введения средства, препятствующего ангиогенезу.4. Способ по любому из пп.1-3, где гипоксически активируемое пролекарство выбрано из группы, состоящей из ТН-281, ТН-302 и ТН-308.5. Способ по п.1, где средство, препятствующее ангиогенезу, выбрано из группы, состоящей из антитела против VEGF, ловушки для VEGF, антитела против VEGFR, ингибитора VEGFR, талидомида, ингибитора D114-Notch, нацеленного на тубулин разрушающего сосуды средства (VDA), ингибитора взаимодействия ангиопоэтина и Tie2, ингибитора синтазы оксида азота (NOS), дендримера из катионных полиаминокислот, рапамицина, эверолимуса, темсиролимуса, низкомолекулярного гепарина, пептида SPARC (остеонектина), бевацизумаба, ранибизумаба, рамуцирумаба, афлиберсепта, интерлейкина 17 (IL-17), DC101, сунитиниба; сорафениба, пазопаниба, AMG706, цедираниба, вандетаниба, варгатефа, бриваниба, XL-184, акситиниба, тивозаниба, талидомида, леналидомида, DMXAA, надропарина, 2,5-диметилцелекоксиба, циклофосфамида, НВС и тасквинимода.6. Способ по п.4, где средство, препятствующее ангиогенезу, выбрано из группы, состоящей �

Claims (15)

1. Способ лечения пациента с онкологическим заболеванием, которому необходимо такое лечение, при этом указанный способ включает введение средства, препятствующего ангиогенезу, и введение гипоксически активируемого пролекарства указанному пациенту.
2. Способ по п.1, где первое введение гипоксически активируемого пролекарства происходит только после того, как введение средства, препятствующего ангиогенезу, привело к увеличению гипоксической фракции онкологического образования.
3. Способ по п.2, где первое введение гипоксически активируемого пролекарства происходит по меньшей мере через 7 дней после первого введения средства, препятствующего ангиогенезу.
4. Способ по любому из пп.1-3, где гипоксически активируемое пролекарство выбрано из группы, состоящей из ТН-281, ТН-302 и ТН-308.
5. Способ по п.1, где средство, препятствующее ангиогенезу, выбрано из группы, состоящей из антитела против VEGF, ловушки для VEGF, антитела против VEGFR, ингибитора VEGFR, талидомида, ингибитора D114-Notch, нацеленного на тубулин разрушающего сосуды средства (VDA), ингибитора взаимодействия ангиопоэтина и Tie2, ингибитора синтазы оксида азота (NOS), дендримера из катионных полиаминокислот, рапамицина, эверолимуса, темсиролимуса, низкомолекулярного гепарина, пептида SPARC (остеонектина), бевацизумаба, ранибизумаба, рамуцирумаба, афлиберсепта, интерлейкина 17 (IL-17), DC101, сунитиниба; сорафениба, пазопаниба, AMG706, цедираниба, вандетаниба, варгатефа, бриваниба, XL-184, акситиниба, тивозаниба, талидомида, леналидомида, DMXAA, надропарина, 2,5-диметилцелекоксиба, циклофосфамида, НВС и тасквинимода.
6. Способ по п.4, где средство, препятствующее ангиогенезу, выбрано из группы, состоящей из бевацизумаба, пазопаниба, сорафениба и сунитиниба.
7. Способ по п.6, где средство, препятствующее ангиогенезу, является бевацизумабом, а гипоксически активируемое пролекарство является ТН-302.
8. Способ по п.7, где онкологическое заболевание выбрано из группы, состоящей из рака груди, колоректального рака, глиобластомы, несквамозного немелкоклеточного рака легких и почечноклеточной карциномы.
9. Способ по п.6, где средство, препятствующее ангиогенезу, является пазопанибом, а гипоксически активируемое пролекарство является ТН-302.
10. Способ по п.9, где онкологическое заболевание выбрано из группы, состоящей из рака поджелудочной железы, почечнокпеточной карциномы и саркомы.
11. Способ по п.6, где средство, препятствующее ангиогенезу, является сорафенибом, а гипоксически активируемое пролекарство является ТН-302.
12. Способ по п.11, где онкологическое заболевание выбрано из группы, состоящей из гепатоклеточной карциномы и почечноклеточной карциномы.
13. Способ по п.6, где средство, препятствующее ангиогенезу, является сунитинибом, а гипоксически активируемое пролекарство является ТН-302.
14. Способ по п.13, где онкологическое заболевание выбрано из группы, состоящей из стромальной опухоли желудочно-кишечного тракта, почечноклеточной карциномы и нейроэндокринной опухоли поджелудочной железы.
15. Способ по любому из пп.1 и 6-14, где гипоксическую фракцию онкологического образования измеряют перед первым введением средства, препятствующего ангиогенезу, или после него.
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