JNJ-38877605

JNJ-38877605 is an orally active ATP-competitive inhibitor of c-Met with an IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases[1][2]. JNJ-38877605 inhibits c-Met phosphorylation and regulates lipid accumulation. JNJ-38877605 can be used for tumor and metabolic disease reseach[3][4][5].

Product Specifications

CAS Number

[943540-75-8]

UNSPSC

12352005

Hazard Statement

H315, H319, H320

Target

C-Met/HGFR

Type

Reference compound

Related Pathways

Protein Tyrosine Kinase/RTK

Applications

Cancer-Kinase/protease

Field of Research

Cancer; Metabolic Disease

Assay Protocol

https://www.medchemexpress.com/JNJ-38877605.html

Purity

99.95

Solubility

DMSO : 25 mg/mL (ultrasonic)

Smiles

FC(F)(C1=NN=C2C=CC(C3=CN(C)N=C3)=NN21)C4=CC5=C(N=CC=C5)C=C4

Molecular Formula

C19H13F2N7

Molecular Weight

377.35

Precautions

H315, H319, H320

References & Citations

[1]Perera T, 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|[2]Wang A, et.al. CPNE1 promotes non-small cell lung cancer progression by interacting with RACK1 via the MET signaling pathway. Cell Commun Signal. 2022 Jan 31;20 (1) :16.|[3]Park YK, et.al. The Receptor Tyrosine Kinase c-Met Promotes Lipid Accumulation in 3T3-L1 Adipocytes. Int J Mol Sci. 2023 Apr 29;24 (9) :8086. |[4]De Bacco F, et al. Induction of MET by ionizing radiation and its role in radioresistance and invasive growth of cancer. J Natl Cancer Inst. 2011 Apr, 103 (8), 645-661.|[5]Torti D, et al. A preclinical algorithm of soluble surrogate biomarkers that correlate with therapeutic inhibition of the MET oncogene in gastric tumors. Int J Cancer. 2012, 130 (6), 1357-1366.