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JNJ-38877605
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
JNJ-38877605图片
CAS NO:943540-75-8
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
5mg电议
25mg电议
100mg电议

产品介绍
JNJ-38877605 是一种 ATP 竞争性的 c-Met 抑制剂,IC50 为 4 nM,对 c-Met 的选择性是 200 种其他酪氨酸和丝氨酸-苏氨酸激酶的 600 倍。
Cas No.943540-75-8
别名6-[二氟[6-(1-甲基-1H-吡唑-4-基)-1,2,4-噻唑并[4,3-B]吡嗪-3-基]甲基]-喹啉
化学名6-[difluoro-[6-(1-methylpyrazol-4-yl)-[1,2,4]triazolo[4,3-b]pyridazin-3-yl]methyl]quinoline
Canonical SMILESCN1C=C(C=N1)C2=NN3C(=NN=C3C(C4=CC5=C(C=C4)N=CC=C5)(F)F)C=C2
分子式C19H13F2N7
分子量377.35
溶解度≥ 18.85mg/mL in DMSO, ≥ 3.25 mg/mL in EtOH with ultrasonic
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

JNJ-38877605 is a small-molecule ATP-competitive inhibitor of the catalytic activity of c-Met.

Extensive evidence that c-Met signaling is involved in the progression and spread of several cancers and an enhanced understanding of its role in disease have generated considerable interest in c-Met and HGF asmajor targets in anti-cancer drug development.

In vitro: JNJ-38877605 showed ~600-fold selectivity for c-Met compared with a panel of ~250 diverse tyrosine and serine-threonine kinases and was found to potently inhibit HGF-stimulated and constitutively activated c-Met phosphorylation in vitro [1].

In vivo: JNJ-38877605 showed excellent oral bioavailability approaching 100% in all examined species. In addition, JNJ-38877605 in a single dose was observed toinhibit Met phosphorylation in tumor xenografts for up to16 h. Inhibition of Met phosphorylation was associated withdose-dependent tumor growth inhibition using a range of oral dosing regimens [2].

Clinical trial: A Safety and Dose-finding Study of JNJ-38877605 in Patients With Advanced or Refractory Solid Tumors.

Reference:
[1] PereraT, L avrijssenT, Janssens B, et al.  JNJ-38877605: a selective Met kinase inhibitor inducing
regression of Met-driven tumor models.  Presented at the 99th AACR Annual Meeting; 2008 Apr 12 -16;