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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
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 inducingregression of Met-driven tumor models. Presented at the 99th AACR Annual Meeting; 2008 Apr 12 -16;