JNJ-38877605 - CAS 1072116-03-0
Catalog number:
1072116-03-0
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
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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).
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Synonyms:
JNJ-38877605
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Current Developer:
Johnson & Johnson
1.Effectiveness of inhibitor rapamycin, saracatinib, linsitinib and JNJ-38877605 against human prostate cancer cells.
Li W1, Wang Z2, Wang L3, He X3, Wang G3, Liu H3, Guo F3, Wang Z4, Chen G2. Int J Clin Exp Med. 2015 Apr 15;8(4):6563-7. eCollection 2015.
To investigate the effect of different concentrations of inhibitors rapamycin, saracatinib, linsitinib and JNJ-38877605 on PC-3 cells with CCK-8 assay, respectively. PC-3 cells were incubated with different concentrations of rapamycin, saracatinib, linsitinib and JNJ-38877605, respectively, for 48 h at 37°C, the concentrations of rapamycin were 5 nM, 10 nM, 20 nM, 50 nM, 75 nM, 100 nM; Saracatinib: 0.125 nM, 0.25 nM, 0.5 nM, 1 nM, 2.5 nM, 5 nM; Linsitinib: 2 nM, 5 nM, 10 nM, 20 nM, 40 nM, 60 nM; JNJ-38877605: 0.125 nM, 0.5 nM, 1 nM, 2.5 nM, 5 nM, 10 nM. The proliferation of PC-3 cells was examined by CCK-8. Different concentrations of inhibitor rapamycin remarkably inhibited PC-3 cell proliferation after 48 h (P<0.05), inhibitory action did not change significantly from 5 nM-100 nM; different concentrations of saracatinib, linsitinib and JNJ-38877605 did not inhibit PC-3 cell proliferation after 48 h. Rapamycin treatment at low concentration can inhibit the proliferation of PC-3 cells, while saracatinib, linsitinib and JNJ-38877605 do not inhibit PC-3 cell proliferation.
2.The c-Met Tyrosine Kinase Inhibitor JNJ-38877605 Causes Renal Toxicity through Species-Specific Insoluble Metabolite Formation.
Lolkema MP1, Bohets HH2, Arkenau HT3, Lampo A2, Barale E2, de Jonge MJ4, van Doorn L4, Hellemans P2, de Bono JS3, Eskens FA4. Clin Cancer Res. 2015 May 15;21(10):2297-304. doi: 10.1158/1078-0432.CCR-14-3258. Epub 2015 Mar 5.
PURPOSE: The receptor tyrosine kinase c-Met plays an important role in tumorigenesis and is a novel target for anticancer treatment. This phase I, first-in-human trial, explored safety, pharmacokinetics, pharmacodynamics, and initial antitumor activity of JNJ-38877605, a potent and selective c-Met inhibitor.
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CAS 1072116-03-0 JNJ-38877605

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