产品
编 号：F285484
分子式：C32H35ClFN7O2
分子量：604.12
分子式：C32H35ClFN7O2
分子量：604.12
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规格
价格
是否有货
10mM*1mL in DMSO
询价
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 2326521-71-3
产品详情
生物活性：
Adagrasib (MRTX849) is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. Adagrasib covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction.
体内研究：
MRTX849 (1-100 mg/kg；口腔灌胃.；每日一次至第 16 天) 在耐受良好的剂量范围内显示剂量依赖性抗肿瘤疗效，MRTX849 的最大有效剂量在 30-100 mg/kg/天之间。Animal Model:MIA PaCa-2 model (6-8-week-old, female, athymic nude-Foxn1 nu mice)
Dosage:1, 3, 10, 30 and 100 mg/kg
Administration:Oral gavage; daily until Day 16
Result:Rapid tumor regression was observed at the earliest posttreatment tumor measurement and animals in the 30 and 100 mg/kg cohorts exhibited evidence of a complete response at study Day 15. Dosing was stopped at study Day 16 and all 4 mice in the 100 mg/kg cohort and 2 out of 7 mice in the 30 mg/kg cohort remained tumor-free through study Day 70.
体外研究：
MRTX849 (0.1-10000 nM; 3 天 /2D 条件，12 天 /3D 条件) 对绝大多数 KRAS G12C 突变体细胞系的生长有明显的抑制作用，其 IC50 在 2D 条件下为 10~973 nM，3D 条件为 0.2~1042 nM。 MRTX849 (0.24-1000nM; 24 小时) 抑制 KRAS 依赖的信号转导靶点，包括 ERK1/2 磷酸化 (Thr202/Tyr204 ERK1; pERK)、S6 磷酸化
Adagrasib (MRTX849) is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. Adagrasib covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction.
体内研究：
MRTX849 (1-100 mg/kg；口腔灌胃.；每日一次至第 16 天) 在耐受良好的剂量范围内显示剂量依赖性抗肿瘤疗效，MRTX849 的最大有效剂量在 30-100 mg/kg/天之间。Animal Model:MIA PaCa-2 model (6-8-week-old, female, athymic nude-Foxn1 nu mice)
Dosage:1, 3, 10, 30 and 100 mg/kg
Administration:Oral gavage; daily until Day 16
Result:Rapid tumor regression was observed at the earliest posttreatment tumor measurement and animals in the 30 and 100 mg/kg cohorts exhibited evidence of a complete response at study Day 15. Dosing was stopped at study Day 16 and all 4 mice in the 100 mg/kg cohort and 2 out of 7 mice in the 30 mg/kg cohort remained tumor-free through study Day 70.
体外研究：
MRTX849 (0.1-10000 nM; 3 天 /2D 条件，12 天 /3D 条件) 对绝大多数 KRAS G12C 突变体细胞系的生长有明显的抑制作用，其 IC50 在 2D 条件下为 10~973 nM，3D 条件为 0.2~1042 nM。 MRTX849 (0.24-1000nM; 24 小时) 抑制 KRAS 依赖的信号转导靶点，包括 ERK1/2 磷酸化 (Thr202/Tyr204 ERK1; pERK)、S6 磷酸化
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