BMS-599626 (AC480)|1mg|K1291-上海高创化学科技有限公司

BMS-599626 (AC480)

参考价：¥836

供货周期：

一周

品牌：

规格：

1mg

货号：

K1291

CAS号：

SKU:K1291		M. Wt:567.01
Formula:C27H27FN8O3.HCl		Solubility:No
Purity:>99%		Storage:2 years at -20 degrees centigrade
CAS No.:873837-23-1		Synonyms:N/A
Chemical NameN/A

Description	BMS-599626 (AC480)
Targets	HER1	HER2
IC50	20 nM	30 nM
In vitro	BMS-599626(AC480) inhibited HER1 and HER2 with IC50 of 20 and 30 nM. BMS-599626(AC480) is highly selective against a broad panel of diverse protein kinases. BMS-599626 abrogated HER1 and HER2 signaling and inhibited the proliferation of tumor cell lines that are dependent on these receptors, with IC50 in the range of 0.24 to 1 micromol/L. In tumor cells that are capable of forming HER1/HER2 heterodimers, BMS-599626 inhibited heterodimerization and downstream signaling. BMS-599626(AC480) significantly enhanced the radiosensitivity of HN-5 cells. In HN-5 cells, BMS-599626(AC480) inhibit the expression of pEGFR, pHER2, cyclins D and E, pRb, pAkt, pMAPK, pCDK1 and 2, CDK 6, and Ku70 proteins. BMS-599626(AC480) also induced accumulation of cells in the G1 cell cycle phase, inhibited cell growth, enhanced radiosensitivity, and prolonged the presence of gamma-H2AX foci up to 24 h after radiation.But BMS-599626(AC480) did not increase the percentage of cells undergoing radiation-induced apoptosis.
In vivo	BMS-599626 had antitumor activity in models that overexpress HER1 (GEO), as well as in models that have HER2 gene amplification (KPL4) or overexpression (Sal2), and there was good correlation between the inhibition of receptor signaling and antitumor activity. BMS-599626(AC480) was generally well tolerated, with disease stabilization across a range of tumor types and doses (100-660 mg/day).
Clinical Trials	N/A
Features	N/A

Description

BMS-599626 (AC480)

Targets

HER1

HER2

IC50

20 nM

30 nM

In vitro

BMS-599626(AC480) inhibited HER1 and HER2 with IC50 of 20 and 30 nM. BMS-599626(AC480) is highly selective against a broad panel of diverse protein kinases. BMS-599626 abrogated HER1 and HER2 signaling and inhibited the proliferation of tumor cell lines that are dependent on these receptors, with IC50 in the range of 0.24 to 1 micromol/L. In tumor cells that are capable of forming HER1/HER2 heterodimers, BMS-599626 inhibited heterodimerization and downstream signaling. BMS-599626(AC480) significantly enhanced the radiosensitivity of HN-5 cells. In HN-5 cells, BMS-599626(AC480) inhibit the expression of pEGFR, pHER2, cyclins D and E, pRb, pAkt, pMAPK, pCDK1 and 2, CDK 6, and Ku70 proteins. BMS-599626(AC480) also induced accumulation of cells in the G1 cell cycle phase, inhibited cell growth, enhanced radiosensitivity, and prolonged the presence of gamma-H2AX foci up to 24 h after radiation.But BMS-599626(AC480) did not increase the percentage of cells undergoing radiation-induced apoptosis.

In vivo

BMS-599626 had antitumor activity in models that overexpress HER1 (GEO), as well as in models that have HER2 gene amplification (KPL4) or overexpression (Sal2), and there was good correlation between the inhibition of receptor signaling and antitumor activity. BMS-599626(AC480) was generally well tolerated, with disease stabilization across a range of tumor types and doses (100-660 mg/day).

Clinical Trials

N/A

Features

N/A