WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#: 201615
Description: JNJ-38877605 is an orally bioavailable, small-molecule receptor tyrosine kinase inhibitor with potential antineoplastic activity. c-Met inhibitor JNJ-38877605 selectively inhibits c-Met (mesenchymal-epithelial transition), a receptor tyrosine kinase (RTK) involved in cancer cell survival and invasiveness, and tumor angiogenesis. c-Met is also known as hepatocyte growth factor receptor (HGFR).
MedKoo Cat#: 201615
Chemical Formula: C19H13F2N7
Exact Mass: 377.12005
Molecular Weight: 377.35023
Elemental Analysis: C, 60.48; H, 3.47; F, 10.07; N, 25.98
Synonym: JNJ-38877605; JNJ38877605; JNJ 38877605.
IUPAC/Chemical Name: 6-(difluoro(6-(1-methyl-1H-pyrazol-3-yl)-[1,2,4]triazolo[4,3-b]pyridazin-3-yl)methyl)quinoline
InChi Key: HUWHDIWESZXGII-UHFFFAOYSA-N
InChi Code: InChI=1S/C19H13F2N7/c1-27-10-8-16(25-27)15-6-7-17-23-24-18(28(17)26-15)19(20,21)13-4-5-14-12(11-13)3-2-9-22-14/h2-11H,1H3
SMILES Code: CN1N=C(C2=NN3C(C=C2)=NN=C3C(C4=CC=C5N=CC=CC5=C4)(F)F)C=C1
JNJ-38877605 is a small-molecule, ATP-competitive inhibitor of the catalytic activity of c-Met. 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. (source: Clin Cancer Res April 1, 2009 15; 2207 ).
1: De Bacco F, Luraghi P, Medico E, Reato G, Girolami F, Perera T, Gabriele P, Comoglio PM, Boccaccio C. Induction of MET by ionizing radiation and its role in radioresistance and invasive growth of cancer. J Natl Cancer Inst. 2011 Apr 20;103(8):645-61. Epub 2011 Apr 4. PubMed PMID: 21464397.
2: Galimi F, Torti D, Sassi F, Isella C, CorÃ D, Gastaldi S, Ribero D, Muratore A, Massucco P, Siatis D, Paraluppi G, Gonella F, Maione F, Pisacane A, David E, Torchio B, Risio M, Salizzoni M, Capussotti L, Perera T, Medico E, Di Renzo MF, Comoglio PM, Trusolino L, Bertotti A. Genetic and expression analysis of MET, MACC1, and HGF in metastatic colorectal cancer: response to met inhibition in patient xenografts and pathologic correlations. Clin Cancer Res. 2011 May 15;17(10):3146-56. Epub 2011 Mar 29. PubMed PMID: 21447729.
3: Benvenuti S, Lazzari L, Arnesano A, Li Chiavi G, Gentile A, Comoglio PM. Ron kinase transphosphorylation sustains MET oncogene addiction. Cancer Res. 2011 Mar 1;71(5):1945-55. Epub 2011 Jan 6. PubMed PMID: 21212418.