ARS-1620 是一种阻转异构且有选择性的 KRAS^G12C 抑制剂，具有理想的药代动力学。

ARS-1620 is an atropisomeric selective KRAS inhibitor with desirable pharmacokinetics.

Solid

KRAS(G12C)

ARS-1620 is an atropisomeric selective KRAS inhibitor with desirable pharmacokinetics. ARS-1620 exhibits complete growth suppression of p.G12C cell lines (IC50=150 nM) with relatively benign effects on control cell lines. It is found that ARS-1620 significantly reduces expression of the gene set in p.G12C mutant cells in a time-dependent manner but not in the p.G12S mutant cells. Following a 5-day treatment period, only a minority of G12C mutant cell lines are sensitive to ARS-1620 under monolayer culture conditions, whereas in 3D-spheroid conditions, ARS-1620 elicits a robust response (p=0.0140). has not independently confirmed the accuracy of these methods. They are for reference only.

Following a single oral dose or 5 consecutive daily doses, ARS-1620 yields average peak tumor concentrations of 1.5 μM (50 mg/kg) and 5.5 μM (200 mg/kg), respectively, that enables significant KRAS target occupancy (>=70% G12C-TE at 200 mg/kg) for >24 hr. In MIAPaCa2 xenografts (p.G12C), ARS-1620 significantly inhibits tumor growth (p<0.001) in a dose-dependent manner with marked regression at a dose of 200 mg/kg, given once daily. Across all tumor models employed, ARS-1620 is well tolerated over the entire 3-week treatment period. Moreover, there are no observed clinical signs or toxicity of ARS-1620 in CD-1 mice even at oral doses up to 1,000 mg/kg administered daily over a 7-day period. has not independently confirmed the accuracy of these methods. They are for reference only.

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[1]. Janes MR, et al. Targeting KRAS Mutant Cancers with a Covalent G12C-Specific Inhibitor. Cell. 2018 Jan 25;172(3):578-589.e17.

In Vitro: DMSO : 125 mg/mL (290.13 mM; Need ultrasonic)H₂O : 11 mg/mL (25.53 mM; ultrasonic and adjust pH to 3 with HCl)配制储备液