product name JNJ-38877605
Description: JNJ-38877605 is an orally bioavailable, ATP-competitive small-molecule inhibitor of c-Met with IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases. JNJ-38877605 has 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).
References: J Natl Cancer Inst. 2011 Apr 20;103(8):645-61; Int J Cancer. 2012 Mar 15;130(6):1357-66.
377.35
Formula
C19H13F2N7
CAS No.
943540-75-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 37 mg/mL (98.1 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
30% propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19402908
| In Vitro |
In vitro activity: JNJ-38877605 shows more than 600-fold selectivity for c-Met compared with more than 200 other diverse tyrosine and serine-threonine kinases and also potently inhibits HGF-stimulated and constitutively activated c-Met phosphorylation in vitro. In EBC1, GTL16, NCI-H1993, and MKN45 cells, JNJ-38877605 (500 nM) leads to a significant reduction of phosphorylation of Met and RON, another key player in invasive growth. A recent study shows that JNJ-38877605 is involved in modulating secretion of IL-8, GROa, uPAR and IL-6 in GTL16 cells. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | In mice bearing established GTL16 xenografts, JNJ-38877605, dosed orally with 40 mg/kg/day for 72 hours, results in a statistically significant decrease in the plasma levels of human IL-8 (from 0.150 ng/mL to 0.050 ng/mL) and GROα (from 0.080 ng/mL to 0.030 ng/mL). While concentrations of uPAR in the blood become reduced to more than 50% at the same dose. |
| Animal model | GTL16 cells are inoculated subcutaneously into the right posterior flank (or both right and left posterior flanks, for determination of uPAR and IL-6) of 6-week-old immunodeficient nu/nu female mice on Swiss CD1 background. |
| Formulation & Dosage | Dissolved in PBS; ≤40mg/kg; p.o. |
| References | J Natl Cancer Inst. 2011 Apr 20;103(8):645-61; Int J Cancer. 2012 Mar 15;130(6):1357-66. |
Related Posts
product name JNJ-38877605
Description: JNJ-38877605 is an orally bioavailable, ATP-competitive small-molecule inhibitor of c-Met with IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases. JNJ-38877605 has 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).
References: J Natl Cancer Inst. 2011 Apr 20;103(8):645-61; Int J Cancer. 2012 Mar 15;130(6):1357-66.
377.35
Formula
C19H13F2N7
CAS No.
943540-75-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 37 mg/mL (98.1 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
30% propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19402908
| In Vitro |
In vitro activity: JNJ-38877605 shows more than 600-fold selectivity for c-Met compared with more than 200 other diverse tyrosine and serine-threonine kinases and also potently inhibits HGF-stimulated and constitutively activated c-Met phosphorylation in vitro. In EBC1, GTL16, NCI-H1993, and MKN45 cells, JNJ-38877605 (500 nM) leads to a significant reduction of phosphorylation of Met and RON, another key player in invasive growth. A recent study shows that JNJ-38877605 is involved in modulating secretion of IL-8, GROa, uPAR and IL-6 in GTL16 cells. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | In mice bearing established GTL16 xenografts, JNJ-38877605, dosed orally with 40 mg/kg/day for 72 hours, results in a statistically significant decrease in the plasma levels of human IL-8 (from 0.150 ng/mL to 0.050 ng/mL) and GROα (from 0.080 ng/mL to 0.030 ng/mL). While concentrations of uPAR in the blood become reduced to more than 50% at the same dose. |
| Animal model | GTL16 cells are inoculated subcutaneously into the right posterior flank (or both right and left posterior flanks, for determination of uPAR and IL-6) of 6-week-old immunodeficient nu/nu female mice on Swiss CD1 background. |
| Formulation & Dosage | Dissolved in PBS; ≤40mg/kg; p.o. |
| References | J Natl Cancer Inst. 2011 Apr 20;103(8):645-61; Int J Cancer. 2012 Mar 15;130(6):1357-66. |