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编 号：F756182
分子式：C35H38FN7O2
分子量：607.72
分子式：C35H38FN7O2
分子量：607.72
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CAS No: 2821863-70-9
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生物活性：
KRAS G12C inhibitor 57 (Compound 50) is a potent, selective, covalent and orally active KRAS G12C inhibitor with an IC50 of 0.21 μM in KRAS G12C/SOS1 binding assay. KRAS G12C inhibitor 57 induces cancer cell apoptosis.
体内研究：
KRAS G12C inhibitor 57 (Compound 50) (10 and 30 mg/kg; p.o.; daily for 20 days) 对 H358异种移植模型小鼠有抗肿瘤作用。Pharmacokinetic data of KRAS G12C inhibitor 57 (Compound 50) in ICR mice. Parameteriv (3 mg/kg) Parameter po (30 mg/kg)
AUC(0?t) (h*ng/mL)801AUC(0?t) (h*ng/mL)600
AUC(0?∞) (h*ng/mL)804AUC(0?∞) (h*ng/mL)835
C0 (ng/mL)1964Cmax (ng/mL)316
T1/2 (h)0.930T1/2 (h)4.79
Vss (L/kg)4.98Tmax (h)0.083
CL (mL/h/kg)3739F (%)10.4
AUCo?inf (h*mg/mL)7060 ± 1020 (14.5%)21800 ± 2310 (10.6%)101000 ± 16700 (16.6%)
Animal Model:BALB/c-nu/nu mice, H358 xenograft model
Dosage:10 mg/kg and 30 mg/kg
Administration:Oral administration, daily for 20 days
Result:Significantly inhibited the tumor growth in a dose-dependent manner with remarkable tumor regression at the dose of 30 mg/kg (tumor growth inhibition, TGI = 84.0%). All dosage groups were well-tolerated with no loss of body weight and no morphological damage to viscera including the heart, spleen, and kidney. Significantly suppressed the phosphorylation of ERK and AKT in tumors of nude mice when dosing orally at 10 mg/kg and 30 mg/kg.
Animal Model:ICR mice
Dosage:3 mg/kg or 30 mg/kg
Administration:IV or PO (Pharmacokinetic Analysis)
Result:Displayed reasonable clearance and half-life by iv administration. Showed a moderate oral bioavailability (F) of 10.4%.
体外研究：
KRAS G12C inhibitor 57 (Compound 50) (0-10 μM; 3 days)对 KRAS 和 KRAS 驱动的细胞系有选择性抑制，以及对下游信号的强烈抑制。KRAS G12C inhibitor 57 (0.1-1 μM; 24 h) 诱导 H358 细胞凋亡。KRAS G12C inhibitor 57 (0.1-1 μM; 48 h)抑制 H358 细胞肿瘤转移。
KRAS G12C inhibitor 57 (Compound 50) is a potent, selective, covalent and orally active KRAS G12C inhibitor with an IC50 of 0.21 μM in KRAS G12C/SOS1 binding assay. KRAS G12C inhibitor 57 induces cancer cell apoptosis.
体内研究：
KRAS G12C inhibitor 57 (Compound 50) (10 and 30 mg/kg; p.o.; daily for 20 days) 对 H358异种移植模型小鼠有抗肿瘤作用。Pharmacokinetic data of KRAS G12C inhibitor 57 (Compound 50) in ICR mice. Parameteriv (3 mg/kg) Parameter po (30 mg/kg)
AUC(0?t) (h*ng/mL)801AUC(0?t) (h*ng/mL)600
AUC(0?∞) (h*ng/mL)804AUC(0?∞) (h*ng/mL)835
C0 (ng/mL)1964Cmax (ng/mL)316
T1/2 (h)0.930T1/2 (h)4.79
Vss (L/kg)4.98Tmax (h)0.083
CL (mL/h/kg)3739F (%)10.4
AUCo?inf (h*mg/mL)7060 ± 1020 (14.5%)21800 ± 2310 (10.6%)101000 ± 16700 (16.6%)
Animal Model:BALB/c-nu/nu mice, H358 xenograft model
Dosage:10 mg/kg and 30 mg/kg
Administration:Oral administration, daily for 20 days
Result:Significantly inhibited the tumor growth in a dose-dependent manner with remarkable tumor regression at the dose of 30 mg/kg (tumor growth inhibition, TGI = 84.0%). All dosage groups were well-tolerated with no loss of body weight and no morphological damage to viscera including the heart, spleen, and kidney. Significantly suppressed the phosphorylation of ERK and AKT in tumors of nude mice when dosing orally at 10 mg/kg and 30 mg/kg.
Animal Model:ICR mice
Dosage:3 mg/kg or 30 mg/kg
Administration:IV or PO (Pharmacokinetic Analysis)
Result:Displayed reasonable clearance and half-life by iv administration. Showed a moderate oral bioavailability (F) of 10.4%.
体外研究：
KRAS G12C inhibitor 57 (Compound 50) (0-10 μM; 3 days)对 KRAS 和 KRAS 驱动的细胞系有选择性抑制，以及对下游信号的强烈抑制。KRAS G12C inhibitor 57 (0.1-1 μM; 24 h) 诱导 H358 细胞凋亡。KRAS G12C inhibitor 57 (0.1-1 μM; 48 h)抑制 H358 细胞肿瘤转移。
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