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6H05

6H05

Catalog No. A8902
Size Price Stock Qty
5mg $140.00 In stock
25mg $350.00 In stock

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Sample solution is provided at 25 µL, 10mM.

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Chemical structure

6H05

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Chemical Properties

Cas No. SDF Download SDF
Chemical Name 1-(2-((4-chlorophenyl)thio)acetyl)-N-(2-((2-(dimethylamino)ethyl)disulfanyl)ethyl)piperidine-4-carboxamide 2,2,2-trifluoroacetate
Canonical SMILES ClC1=CC=C(SCC(N2CCC(C(NCCSSCCN(C)C)=O)CC2)=O)C=C1.OC(C(F)(F)F)=O
Formula C22H31ClF3N3O4S3 M.Wt 590.14
Solubility Soluble in DMSO > 10 mM Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

Background

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.