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AC1903

CAS No. : 831234-13-0

MCE 站：AC1903

产品活性：AC1903 是 TRPC5 的特异性选择性抑制剂，具有足细胞保护特性。AC1903 对 TRPC4 或 TRPC6 current 没有影响，并且在激酶谱分析中没有显示出脱靶效应。在局灶节段性肾小球硬化 (FSGS) 大鼠模型中，AC1903 抑制严重蛋白尿，并且防止足细胞丢失。

研究领域：Membrane Transporter/Ion Channel  |  Neuronal Signaling

作用靶点：TRP Channel

In Vitro: TRPC5 is a Ca²⁺?permeable nonselective cation channel highly expressed in brain and kidney.
AC1903 (0-100 ?M) blocks riluzole-activated TRPC5 whole-cell current, but fails to block carbachol (CCh)–induced TRPC4 and OAG-induced TRPC6 currents, even at high micromolar concentrations in Patch-clamp electrophysiology experiments. The ICIC₅₀ values of ML204 (HY-12949) (IC₅₀=13.6 μM) and AC1903 (IC₅₀=14.7 μM) are nearly equipotent in human embryonic kidney 293 (HEK-293) cells expressing TRPC5.
AC1903 (30 ?M) inhibits angiotensin II-induced production of reactive oxygen species (ROS) in wild-type podocytes and podocytes expressing a mutant angiotensin II type 1 (AT1) receptor that cannot be inactivated and endocytosed.
AC1903 (30 ?M) blocks caAT1R-induced ROS generation. Increased podocyte cell death within 36 hours of caAT1R expression?is observed, but AC1903 ?protects podocyte cells from cell death.

In Vivo: AC1903 (intraperitoneal injection; 50 mg/kg; twice per day; 7 days) significantly suppresses proteinuria as well as reduces pseudocyst formation and podocyte loss in an AT1?receptor transgenic rat model of kidney disease.
AC1903 (intraperitoneal injection; 50 mg/kg; twice per day; initiated on day 7 and treated for 1 week until day 14) initiatation on day 7 exhibits significant suppression of proteinuria with preserved podocyte numbers. Besides, AC1903 does not affect the mean arterial pressure (MAP) and exhibits no effect on body weight, blood urea nitrogen, or creatinine in Dahl S rats.

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