K-0066(K-0066) - 在研适应症：视网膜疾患_专利_临床

概要

基本信息

药物类型

小分子化药

别名

靶点-

作用机制-

治疗领域

眼部疾病

在研适应症

视网膜疾患

非在研适应症-

原研机构

KALA BIO, Inc.

在研机构

KALA BIO, Inc.

非在研机构-

最高研发阶段临床前

首次获批日期-

最高研发阶段(中国)-

特殊审评-

关联

100 项与 K-0066 相关的临床结果

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100 项与 K-0066 相关的转化医学

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100 项与 K-0066 相关的专利（医药）

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1

项与 K-0066 相关的文献（医药）

2017-12-01·Vascular Pharmacology3区 · 医学

Protein kinase CK2 inhibition suppresses neointima formation via a proline-rich homeodomain-dependent mechanism

3区 · 医学

Article

作者: Jayaraman, P-S ; George, S J ; Gaston, K ; Sala-Newby, G B ; Wadey, K S ; Brown, B A

Neointimal hyperplasia is a product of VSMC replication and consequent accumulation within the blood vessel wall. In this study, we determined whether inhibition of protein kinase CK2 and the resultant stabilisation of proline-rich homeodomain (PRH) could suppress VSMC proliferation. Both silencing and pharmacological inhibition of CK2 with K66 antagonised replication of isolated VSMCs. SiRNA-induced knockdown as well as ectopic overexpression of proline-rich homeodomain indicated that PRH disrupts cell cycle progression. Mutation of CK2 phosphorylation sites Ser¹⁶³ and Ser¹⁷⁷ within the PRH homeodomain enabled prolonged cell cycle arrest by PRH. Concomitant knockdown of PRH and inhibition of CK2 with K66 indicated that the anti-proliferative action of K66 required the presence of PRH. Both K66 and adenovirus-mediated gene transfer of S163C:S177C PRH impaired neointima formation in human saphenous vein organ cultures. Importantly, neither intervention had notable effects on cell cycle progression, cell survival or migration in cultured endothelial cells.

100 项与 K-0066 相关的药物交易

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