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.
|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
|Related Ras Products|
CCG-222740 is an inhibitor of the Rho/MRTF pathway. CCG-222740 is also an effective α -smooth muscle actin protein expression inhibitor. CCG-222740 effectively reduces skin fibrosis and prevents melanoma metastasis.
MRTX0902 is an effective SOS1 inhibitor with an IC50 of 46 nM.
Gdc-6036 (compound 17A) is an oral covalently mutated KRAS G12C inhibitor with IC50<0.01 μM against K-Ras G12C. The EC50 of GDC-6036 in K-Ras G12C-alkylated HCC1171 cells was 2 nM.
HJC0197 is a potent antagonist of Epac1 (the exchange protein directly activated by cAMP 1) and Epac2 (IC50=5.9 μM for Epac2). HJC0197 selectively blocked camp-induced Epac activation. HJC0197 inhibited epAC1-mediated RAP1-GDP exchange activity in the presence of isoconcentration of cAMP.
SAH-SOS1A TFA is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A TFA binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM) and directly and independently blocks nucleotide association.
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