RM-018 is an inhibitor of the active state of KRASG12C. Rm-018 retains the ability to bind and inhibit KRASG12C/Y96D. Rm-018 combines with GTP-bound to activate the [" RAS(ON) "] state of KRASG12C.
Powder -20°C 3 years ; 4°C 2 years
In solvent -80°C 6 months ; -20°C 1 month
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.
 Noritaka Tanaka, et al. Cancer Discov. Clinical Acquired Resistance to KRAS G12C Inhibition through a Novel KRAS Switch-II Pocket Mutation and Polyclonal Alterations Converging on RAS-MAPK Reactivation
 Leslie A McSweeney, et al. Cell Microbiol. Nuclear localization of the Escherichia coli cytolethal distending toxin CdtB subunit
|Related Ras Products|
BI-0474 is a covalent KRASG12C inhibitor. The IC50 value for GDP-KRAS::SOS1 protein-protein interaction was 7.0 nM. BI-0474 also showed better antitumor activity in non-small cell lung cancer xenograft models.
MRTX849 acid can be used to synthesize PROTAC LC-2. LC-2 is a potent, first-in-class PROTAC capable of degrading endogenous KRAS G12C (DC50, between 0.25 and 0.76 μM).
BDP9066 is a potent and selective MRCK inhibitor, reducing substrate phosphorylation.
ASP2453 is a potent, selective and covalent inhibitor of KRAS G12C. ASP2453 inhibits Son of Sevenless (SOS)-mediated interactions between KRAS G12C and Raf with an IC50 value of 40 nM.
AZD4625 is a highly potent, selective, covalent and metabotropic inhibitor of the mutant GTPase KRASG12C. AZD4625 has high oral bioavailability. It is being developed to study advanced solid malignancies.
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