JNJ-38877618-DataSheet-生命科学试剂-MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEJNJ-38877618Cat. No.: HY-111050CAS No.: 943540-74-7分式: CHFN分量: 374.35作靶点: c-Met/HGFR作通路: Protein Tyrosine Kinase/RTK储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性数据体外实验 DMSO : 5 mg/mL (13.36 mM; Need u

2、ltrasonic)Mass Solvent1 mg 5 mg 10 mg Concentration制备储备液1 mM 2.6713 mL 13.3565 mL 26.7130 mL5 mM 0.5343 mL 2.6713 mL 5.3426 mL10 mM 0.2671 mL 1.3356 mL 2.6713 mL请根据产品在不同溶剂中的溶解度，选择合适的溶剂配制储备液，并请注意储备液的保存式和期限。体内实验 请根据您的实验动物和给药式选择适当的溶解案，配制前请先配制澄清的储备液，再依次添加助溶剂(为保证实验结果的可靠性，体内实验的作液，建议您现现配，当天使；澄清的储备液可以根据储存条件

3、，适当保存；以下溶剂前的百分 指该溶剂在您配制终溶液中的体积占)：1. 请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 0.5 mg/mL (1.34 mM); Clear solution2. 请依序添加每种溶剂： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 0.5 mg/mL (1.34 mM); Clear solution3. 请依序添加每种溶剂： 10% DMSO 90% corn oilSolubility: 0.5 mg/mL (1.34 mM);

4、Clear solution1/2 Master of Small Molecules 您边的抑制剂师www.MedChemEBIOLOGICAL ACTIVITY物活性 JNJ-38877618种有效的，选择性的，服可的 (Met) 激酶抑制剂，对于野型和突变体的 IC50 值分别为2和3 nM。IC50 & Target IC50: 2 nM (wt Met), 2 nM (mutant Met) 1体外研究 OMO-1 (formerly JNJ-38877618), is a potent, highly selective, orally bioavailable Met kinas

5、e inhibitor with nMbinding affinity (Kd=1.4 nM) and enzyme inhibitory activity against wt and M1268T mutant Met (2 and 3 nMIC50). Met inhibitory effects are assessed in proliferation, colony formation and motility assays. JNJ-38877618 displays nM potency against Met Ampl/mutant and therapy resistant

6、 models 1.体内研究 JNJ-38877618 induces complete inhibition of tumor growth in 3 models: the SNU5 Met amp gastric, U87-MGHGF autocrine glioblastoma and Hs746T Met exon 14 skipping mutant gastric cancer. JNJ-38877618induces regression of large Met amplified EBC-1 SqNSCLC where JNJ-38877618 leads to dose-

7、 and time-dependent inhibition of Met kinase activation, with the duration of target shut down considerably exceedingplasma exposure times. Combination treatments are well tolerated and improved EGFR targeted therapy 1.REFERENCES1. Libouban M, et al. OMO-1, a potent, highly selective, orally bioavai

8、lable, Met kinase inhibitor with a favorable preclinical toxicity profile,shows both monotherapy activity, against Met pathway-driven tumors, and EGFR TKI combination activity in acquired resistance modelsabstract. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL.Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4791.McePdfHeightCaution: Product has not been fully validated for medical applica