WARNING: This product is for research use only, not for human or veterinary use.

MedKoo CAT#: 201615

CAS#: 943540-75-8

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).

Chemical Structure

CAS# 943540-75-8

Theoretical Analysis

MedKoo Cat#: 201615
Name: JNJ-38877605
CAS#: 943540-75-8
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

Price and Availability

Size Price Availability Quantity
10.0mg USD 150.0 Same day
25.0mg USD 250.0 Same day
50.0mg USD 450.0 Same day
100.0mg USD 850.0 Same day
200.0mg USD 1450.0 Same day
500.0mg USD 2050.0 Same day
1.0g USD 3450.0 2 Weeks
2.0g USD 5450.0 2 Weeks
5.0g USD 9850.0 2 Weeks
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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 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

Appearance: Solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years)

Solubility: Soluble in DMSO, not soluble in water.

Shelf Life: >5 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001

Biological target: JNJ-38877605 is an ATP-competitive inhibitor of c-Met with IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases.
In vitro activity: To investigate the effect of different concentrations of inhibitor JNJ-38877605 on PC-3 cells with CCK-8 assay, PC-3 cells were incubated with different concentrations (0.125 nM, 0.5 nM, 1 nM, 2.5 nM, 5 nM, 10 nM) of JNJ-38877605 for 48 h at 37°C. The proliferation of PC-3 cells was examined by CCK-8. Different concentrations of JNJ-38877605 did not inhibit PC-3 cell proliferation after 48 h. Reference: Int J Clin Exp Med. 2015 Apr 15;8(4):6563-7.
In vivo activity: To study their ability to metastasize to bone, renal CSCs were injected in NOD/SCID mice implanted with a human bone and the effect of a c-MET inhibitor (JNJ-38877605) was tested on bone metastasis development. JNJ-38877605 inhibited the formation of metastases at bone implant site. It was shown that JNJ-38877605 inhibited the activation of osteoclasts induced by RCC stem cells and it stimulated osteoblast activity, finally resulting in a reduction of bone turnover consistent with the inhibition of bone metastases. The circulating levels of osteotropic factors induced by RCC stem cells in the sera of mice treated with c-Met inhibitor was measured, showing that IL-11 and CCL20 were reduced in mice treated with JNJ-38877605, strongly supporting the involvement of c-MET in the regulation of this process. Reference: Oncotarget. 2016 Jul 19;7(29):45525-45537.

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
DMSO 30.0 79.5

Preparing Stock Solutions

The following data is based on the product molecular weight 377.35023 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
In vitro protocol: 1. Li W, Wang Z, Wang L, He X, Wang G, Liu H, Guo F, Wang Z, Chen G. Effectiveness of inhibitor rapamycin, saracatinib, linsitinib and JNJ-38877605 against human prostate cancer cells. Int J Clin Exp Med. 2015 Apr 15;8(4):6563-7. PMID: 26131286; PMCID: PMC4483836.
In vivo protocol: 1. D'Amico L, Belisario D, Migliardi G, Grange C, Bussolati B, D'Amelio P, Perera T, Dalmasso E, Dalle Carbonare L, Godio L, Comoglio P, Trusolino L, Ferracini R, Roato I. C-met inhibition blocks bone metastasis development induced by renal cancer stem cells. Oncotarget. 2016 Jul 19;7(29):45525-45537. doi: 10.18632/oncotarget.9997. PMID: 27322553; PMCID: PMC5216739.

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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, Corà 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.

Additional Information

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 ).