产品
编 号：F741709
分子式：C29H28ClN7O
分子量：526.03
分子式：C29H28ClN7O
分子量：526.03
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
询价
5mg
询价
询价
10mg
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询价
结构图
CAS No: 2653994-08-0
产品详情
生物活性：
Opnurasib (JDQ-443) (NVP-JDQ443) is an orally active, potent, selective, and covalent KRAS G12C inhibitor (extracted from patent WO2021120890A1). Opnurasib shows antitumor activity.
体内研究：
Opnurasib (10-100 mg/kg, Orally, daily for 14 days) shows antitumor activity in KRAS G12C-mutated CDX models. ?Opnurasib (Orally, 100 mg/kg, daily (JDQ443) + 7.5 mg/kg, twice daily (TNO155), for 36 days) shows greater cell growth inhibition or cell killing compared with single-agent JDQ443 when combined with TNO155. ?Opnurasib generates categorical antitumor responses in PDX models of NSCLC and colorectal tumors that are improved by combination treatment with other agents.Animal Model:KRAS G12C tumor-bearing nude mice (MIA PaCa-2 (PDAC); NCIH2122, LU99, HCC44, NCI-H2030 (NSCLC); and KYSE410 (esophageal cancer))
Dosage:10, 30, 100 mg/kg
Administration:Orally, daily for 14 days
Result:Inhibited the growth of all models in a dose-dependent manner.
Animal Model:Three KRAS G12C-mutated CDX models (LU99, NCI-H2030, and KYSE410)
Dosage:100 mg/kg (JDQ443) + 7.5 mg/kg (TNO155)
Administration: Orally, daily (JDQ443) or twice daily (TNO155), for 36 days
Result:Combined with TNO155, showed either greater tumor efficacy compared with each agent alone (H2030, KYSE410) or a delayed time to tumor progression (LU99).
体外研究：
Opnurasib (NVP-JDQ443) traps the GDP-bound inactive conformation of KRAS.?Opnurasib promotes dose-dependent reductions of phosphorylated ERK (pERK) levels and the proliferation of the KRASG12C-mutated cell lines NCI-H358 and NCI-H2122, with IC50 values of 0.018 and 0.063 μM, respectively.?Opnurasib covalently and selectively binds and inhibits GDP-bound KRASG12C with low reversible binding affinity to the RAS switch II pocket, and also inhibits proliferation of KRASG12C-mutated and KRAS G12C/H95, G12C/R68S, and G12C/Y96 double-mutant cell lines.
Opnurasib (JDQ-443) (NVP-JDQ443) is an orally active, potent, selective, and covalent KRAS G12C inhibitor (extracted from patent WO2021120890A1). Opnurasib shows antitumor activity.
体内研究：
Opnurasib (10-100 mg/kg, Orally, daily for 14 days) shows antitumor activity in KRAS G12C-mutated CDX models. ?Opnurasib (Orally, 100 mg/kg, daily (JDQ443) + 7.5 mg/kg, twice daily (TNO155), for 36 days) shows greater cell growth inhibition or cell killing compared with single-agent JDQ443 when combined with TNO155. ?Opnurasib generates categorical antitumor responses in PDX models of NSCLC and colorectal tumors that are improved by combination treatment with other agents.Animal Model:KRAS G12C tumor-bearing nude mice (MIA PaCa-2 (PDAC); NCIH2122, LU99, HCC44, NCI-H2030 (NSCLC); and KYSE410 (esophageal cancer))
Dosage:10, 30, 100 mg/kg
Administration:Orally, daily for 14 days
Result:Inhibited the growth of all models in a dose-dependent manner.
Animal Model:Three KRAS G12C-mutated CDX models (LU99, NCI-H2030, and KYSE410)
Dosage:100 mg/kg (JDQ443) + 7.5 mg/kg (TNO155)
Administration: Orally, daily (JDQ443) or twice daily (TNO155), for 36 days
Result:Combined with TNO155, showed either greater tumor efficacy compared with each agent alone (H2030, KYSE410) or a delayed time to tumor progression (LU99).
体外研究：
Opnurasib (NVP-JDQ443) traps the GDP-bound inactive conformation of KRAS.?Opnurasib promotes dose-dependent reductions of phosphorylated ERK (pERK) levels and the proliferation of the KRASG12C-mutated cell lines NCI-H358 and NCI-H2122, with IC50 values of 0.018 and 0.063 μM, respectively.?Opnurasib covalently and selectively binds and inhibits GDP-bound KRASG12C with low reversible binding affinity to the RAS switch II pocket, and also inhibits proliferation of KRASG12C-mutated and KRAS G12C/H95, G12C/R68S, and G12C/Y96 double-mutant cell lines.
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