RM-018

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

RM-018 

RM-018 是一种 KRASG12C 活性状态的抑制剂。RM-018 保留了结合和抑制 KRASG12C/Y96D 的能力。RM-018 与 GTP-bound 结合，激活 KRASG12C 的 [“RAS(ON)”] 状态。

RM-018

RM-018 Chemical Structure

CAS No. : 2641993-55-5

规格 价格 是否有货
5 mg ￥14500 询问价格 & 货期
10 mg ￥23500 询问价格 & 货期
25 mg ￥48000 询问价格 & 货期
50 mg ￥75000 询问价格 & 货期
100 mg ￥118000 询问价格 & 货期

* Please select Quantity before adding items.

生物活性

RM-018 is a potent, functionally distinct tricomplex KRASG12C active-state inhibitor. RM-018 retains the ability to bind and inhibit KRASG12C/Y96D and could overcome resistance. RM-018 binds specifically to the GTP-bound, active [“RAS(ON)”] state of KRASG12C[1].

IC50 & Target[1]

KRAS (G12C)

 

KRAS (G12C/Y96D)

 

体外研究
(In Vitro)

RM-018 is a “tricomplex” KRAS inhibitor, which exploits a highly abundant chaperone protein, cyclophilin A, to bind and inhibit KRASG12C[1].
RM-018 (0.01-1000 nM; 72 hours) has IC50s of 1.4-3.5 nM (KRASG12C) and 2.8-7.3 nM (KRASG12C/Y96D) in NCI-H358, MIA PaCa-2, Ba/F3, and MGH1138-1 cells[1].
RM-018 (0-100 nM; 4 hours) inhibits the expression of KRAS, pERK, and pRSK protein[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[1]

Cell Line: NCI-H358, MIA PaCa-2, Ba/F3, and MGH1138-1 cells, which stably infected with KRASG12C or KRASG12C/Y96D.
Concentration: 0.01-1000 nM
Incubation Time: 72 hours
Result: Inhibited the cell activity, but largely unaffected by KRASG12C/Y96D expression.

Western Blot Analysis[1]

Cell Line: MIA PaCa-2, HEK293T and MGH1138-1 cells, which expressing KRASG12C or KRASG12C/Y96D.
Concentration: 0-100 nM
Incubation Time: 4 hours
Result: Inhibited KRAS, pERK and pRSK levels with similar potency.

分子量

985.22

Formula

C56H72N8O8
CAS 号

2641993-55-5
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Tanaka N, et.al. Clinical Acquired Resistance to KRASG12C Inhibition through a Novel KRAS Switch-II Pocket Mutation and Polyclonal Alterations Converging on RAS-MAPK Reactivation. Cancer Discov. 2021 Aug;11(8):1913-1922.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务