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RU2473565C2 - АНТИТЕЛА, СВЯЗЫВАЮЩИЕ ТИРОЗИН ФОСФАТАЗУ БЕТА ЧЕЛОВЕКА (HPTPβ), И ИХ ИСПОЛЬЗОВАНИЕ - Google Patents

АНТИТЕЛА, СВЯЗЫВАЮЩИЕ ТИРОЗИН ФОСФАТАЗУ БЕТА ЧЕЛОВЕКА (HPTPβ), И ИХ ИСПОЛЬЗОВАНИЕ Download PDF

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RU2473565C2
RU2473565C2 RU2008138399/10A RU2008138399A RU2473565C2 RU 2473565 C2 RU2473565 C2 RU 2473565C2 RU 2008138399/10 A RU2008138399/10 A RU 2008138399/10A RU 2008138399 A RU2008138399 A RU 2008138399A RU 2473565 C2 RU2473565 C2 RU 2473565C2
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antibody
angiogenesis
antigen
disease
binding fragment
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Рокко Джейми РОТЕЛЛО
Кевин Джин ПЕТЕРС
Майкл Глен ДЭВИС
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Abstract

Изобретение относится к области иммунологии. Предложено антитело, полученное из гибридомы АТСС №РТА-7580, специфичное к человеческому белку тирозин фосфатазе бета (НРТРβ). Описан Fab вариант указанного антитела, а также варианты способов лечения и фармацевтические композиции, основанные на использовании антител. При связывании антитела с НРТРβ усиливается передача сигнала Tie-2 и таким образом увеличивается ангиогенез, тогда как при связывании Fab антиген-связывающего фрагмента антитела с НРТРβ ингибируется передача сигнала Tie-2, и таким образом уменьшается ангиогенез. Использование изобретения может найти применение в медицине для лечения заболеваний, связанных с нарушением ангиогенеза. 6 н. и 15 з.п. ф-лы, 12 ил., 1 табл., 5 пр.

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Claims (21)

1. Выделенное антитело, способное связываться с человеческим белком тирозин фосфатазой бета (НРТРβ), при этом упомянутое антитело произведено гибридомной клеточной линией АТСС №РТА-7580 и при связывании с НРТРβ усиливает передачу сигнала Tie-2 и таким образом увеличивает ангиогенез.
2. Выделенное антитело по п.1, отличающееся тем, что антитело способно связываться с N-концевой частью НРТРβ.
3. Выделенное антитело по п.2, отличающееся тем, что антитело способно связываться с первым FN3-повтором НРТРβ.
4. Выделенное антитело по п.3, отличающееся тем, что первый FN3-повтор НРТРβ включает последовательность, как показано в SEQ ID NO:11, или ее фрагмент.
5. Выделенное антитело по п.1, отличающееся тем, что антитело является моноклональным антителом.
6. Выделенное антитело по п.1, отличающееся тем, что антитело является гуманизированным.
7. Выделенный Fab антиген-связывающий фрагмент антитела, производимого гибридомной клеточной линией АТСС №РТА-7580, способный связываться с человеческим белком тирозин фосфатазой бета (НРТРβ), при этом упомянутый Fab антиген-связывающий фрагмент при связывании с НРТРβ ингибирует передачу сигнала Tie-2 и таким образом уменьшает ангиогенез.
8. Выделенный антиген-связывающий фрагмент по п.7, отличающийся тем, что антиген-связывающий фрагмент способен связываться с N-концевой частью НРТРβ.
9. Выделенный антиген-связывающий фрагмент по п.8, отличающийся тем, что антиген-связывающий фрагмент способен связываться с первым FN3-повтором НРТРβ.
10. Выделенный антиген-связывающий фрагмент по п.9, отличающийся тем, что первый FN3-повтор НРТРβ включает последовательность, как показано в SEQ ID NO:11, или ее фрагмент.
11. Выделенный антиген-связывающий фрагмент по п.7, отличающийся тем, что антитело является моноклональным антителом.
12. Выделенный антиген-связывающий фрагмент по п.7, отличающийся тем, что антиген-связывающий фрагмент является гуманизированным.
13. Способ лечения нарушения, при котором требуется увеличение ангиогенеза, у субъекта, содержащий этапы, на которых:
а) идентифицируют субъект, нуждающийся в увеличении ангиогенеза; и
б) вводят этому субъекту эффективное количество антитела по любому из пп.1-6.
14. Способ по п.13, отличающийся тем, что нарушение выбрано из группы, состоящей из: скелетно-мышечной или миокардиальной ишемии, инсульта, заболевания периферических сосудов и заболевания коронарной артерии.
15. Способ по п.13, отличающийся тем, что нарушение ангиогенеза является заболеванием периферических сосудов.
16. Способ по п.13, отличающийся тем, что нарушение ангиогенеза является заболеванием коронарной артерии.
17. Способ лечения нарушения, при котором требуется уменьшение ангиогенеза, у субъекта, содержащий этапы, на которых:
а) идентифицируют субъект, нуждающийся в уменьшении ангиогенеза; и
б) вводят этому субъекту эффективное количество антиген-связывающего фрагмента по любому из пп.7-12.
18. Способ по п.17, отличающийся тем, что нарушение выбрано из группы, состоящей из: диабетической ретинопатии, деградации желтого пятна сетчатки глаза, рака, серповидно-клеточной анемии, саркоида, сифилиса, псевдоксантомы эластикум, болезни Педжета, окклюзии вен, окклюзии артерий, обструктивного заболевания сонной артерии, хронического увеита/витрита, микобактериальной инфекции, болезни Лайма, системной волчанки, ретинопатии недоношенности, болезни Илза, болезни Бехчета, инфекций, вызванных ретинитом или хориоидитом, предполагаемого глазного гистоплазмоза, болезни Беста, миопии, глазных ямок, болезни Старгардта, pars planitis, хронического отслоения сетчатки, синдрома гипервязкости, токсоплазмоза, травмы и постлазерных осложнений, болезней, связанных с покраснением радужки, и пролиферативной витреоретинопатии.
19. Способ по п.17, отличающийся тем, что нарушение выбрано из группы, состоящей из воспалительных заболеваний кишечника, включающих болезнь Крона и язвенный колит, псориаза, саркоидоза, ревматоидного артрита, гемангиомы, болезни Рандю - Вебера - Ослера или наследственной геморрагической телангиектазии, твердых или переносимых кровью опухолей и синдрома приобретенного вируса иммунодефицита.
20. Фармацевтическая композиция для увеличения ангиогенеза, содержащая:
a) эффективное количество антитела по любому из пп.1-6; и
b) фармацевтически приемлемый носитель.
21. Фармацевтическая композиция для уменьшения ангиогенеза, содержащая:
a) эффективное количество антиген-связывающего фрагмента по любому из пп.7-12; и
b) фармацевтически приемлемый носитель.
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