您好,欢迎来到试剂信息网! [登录] [免费注册]
试剂信息网
位置:首页 > 产品库 > 6H05
立即咨询
咨询类型:
     
*姓名:
*电话:
*单位:
Email:
*留言内容:
请详细说明您的需求。
*验证码:
 
6H05
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
6H05图片
CAS NO:1469338-01-9
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
5mg电议
25mg电议

产品介绍
6H05 是致癌突变体 K-Ras(G12C) 的选择性变构抑制剂。
Cas No.1469338-01-9
别名6H05(6H零5)
化学名1-(2-((4-chlorophenyl)thio)acetyl)-N-(2-((2-(dimethylamino)ethyl)disulfanyl)ethyl)piperidine-4-carboxamide 2,2,2-trifluoroacetate
Canonical SMILESClC1=CC=C(SCC(N2CCC(C(NCCSSCCN(C)C)=O)CC2)=O)C=C1.OC(C(F)(F)F)=O
分子式C22H31ClF3N3O4S3
分子量590.14
溶解度≥ 29.5mg/mL in DMSO
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

6H05 is a selective inhibitorof the common oncogenic mutant K-Ras (G12C). 6H05 allosterically modifies and inhibits the oncogenic G12C mutant of highly homologous protein H-Ras, not affecting the wild-type K-Ras [1].

K-Ras plays an important role in human cancer, cause mutations in K-Ras are the most common activating lesions in human cancer[2]. 6H05 modifies the GDP-bound K-Ras (G12C) the most, which can be and be applied as the starting point for drug-discovery efforts targeting K-Ras (G12C) and eventually other alleles of K-Ras. 6H05 can be used as an intermediate for the synthesis of oncogenic K-Ras (G12C) inhibitors [3, 4].

Although it’s necessary to perform continued chemical optimization of 6H05 to be assessed in vivo, preliminary evaluation of 6H05 in lung cancer cell lines suggests that 6H05 shows allele-specific impairment of K-Ras function[1]. There are questions still need to be illustrated that the selectivity and efficiency of 6H05 in vivo, as well as its effects on the subcellular localization of other farnesylated GTPases should be assessed further[1, 3].

Questions still need to be answered surrounding the in vivo selectivity and efficacy of 6H05, including its effects on the subcellular localization of other farnesylated GTPases [3].

References:
[1] Ostrem JM, Peters U, Sos ML, et al.  K-Ras (G12C) inhibitors allosterically control GTP affinity and effector interactions[J]. Nature, 2013, 503(7477): 548-551.
[2] McCormick F.  KRAS as a Therapeutic Target[J]. Clinical Cancer Research, 2015, 21(8): 1797-1801.
[3] Milroy L-G,Ottmann C.  The Renaissance of Ras[J]. ACS chemical biology, 2014, 9(11): 2447-2458.
[4] Lu SY, Li S,Zhang J.  Harnessing Allostery: A Novel Approach to Drug Discovery[J]. Medicinal Research Reviews, 2014, 34(6): 1242-1285.