STF-62247|5mg|K1317-上海高创化学科技有限公司

STF-62247

参考价：¥836

供货周期：

一周

品牌：

规格：

5mg

货号：

K1317

CAS号：

315702-99-9

SKU:K1317		M. Wt:267.35
Formula:C15H13N3S		Solubility:No
Purity:>99%		Storage:2 years at -20 degrees centigrade
CAS No.:315702-99-9		Synonyms:N/A
Chemical NameN/A

Description	STF-62247
Targets
IC50	N/A
In vitro	STF-62247 specifically induces autophagic cell death in cells that have lost VHL, an essential mutation in the development of RCC. Treatment with STF-62247 did not alter cell cycle progression but when combined with radiation increased cell killing under oxic and hypoxic/physiological conditions. The cytotoxicity of STF-62247 is due to dysregulated autophagy. The reduction of protein levels of essential autophagy pathway components such as Atg5, Atg7 and Atg9 reduces sensitivity of VHL-deficient cells to killing by STF-62247. Loss of proteins involved in Golgi trafficking sensitized RCC with wild-type VHL to killing by STF-62247.
In vivo	In vivo mouse model, STF-62247 at a dose of 8 mg/kg byby intraperitoneal injection significantly reduces tumor growth of VHL-deficient SN12C tumor cells.
Clinical Trials	N/A
Features	N/A

Description

STF-62247

Targets

IC50

N/A

In vitro

STF-62247 specifically induces autophagic cell death in cells that have lost VHL, an essential mutation in the development of RCC. Treatment with STF-62247 did not alter cell cycle progression but when combined with radiation increased cell killing under oxic and hypoxic/physiological conditions. The cytotoxicity of STF-62247 is due to dysregulated autophagy. The reduction of protein levels of essential autophagy pathway components such as Atg5, Atg7 and Atg9 reduces sensitivity of VHL-deficient cells to killing by STF-62247. Loss of proteins involved in Golgi trafficking sensitized RCC with wild-type VHL to killing by STF-62247.

In vivo

In vivo mouse model, STF-62247 at a dose of 8 mg/kg byby intraperitoneal injection significantly reduces tumor growth of VHL-deficient SN12C tumor cells.

Clinical Trials

N/A

Features

N/A