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Chemical Compound Review:

PubChem16670 N-[5-[(5-tert-butyl-1,3- oxazol-2...

Synonyms: SNS-032, Kinome_3820, S1145_Selleck, AC1MHGD4, SNS032, ...

Kamath, A.V. et al., Mukhopadhyay, P. et al., Ma, Y. et al., Caponigro, F. et al., Senderowicz, A.M., et al.

Caponigro, Basile, de Rosa, Normanno, Kamath, Chong, Chang, Marathe, Senderowicz,

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Disease relevance of BMS-387072

SNS-032 may have potential in treating hematologic malignancy by abrogating oncogene addiction [1].

High impact information on BMS-387072

Third, results from in vitro kinase assays clearly show that IL-1beta induces CDK2 activity in H358 cells and this activity is significantly inhibited by BMS-387032 [2].
First, we show that BMS-387032, a potent CDK2 inhibitor, blocks IL-1beta-induced expression as well as steady-state mRNA levels of COX-2 [2].
Taken together, the data suggest that CDK2 activity may play an important event in the IL-1beta-induced COX-2 expression and prostaglandin E(2) synthesis and might represent a novel target for BMS-387032 [2].
Direct cdk modulators are small molecules that specifically target the ATP binding site of cdk's. Examples for this group include flavopiridol, roscovitine and BMS-387032 [3].
To determine if BMS-387032 was a P-glycoprotein substrate, brain uptake studies were conducted in P-glycoprotein knockout versus wildtype mice [4].

Biological context of BMS-387072

The oral bioavailability of BMS-387032 has been found to be about 31% in rats [4].
Cell cycle inhibitors, such as CYC-202 and BMS-387032, represent a class of interesting compounds which are in the early phase of development and whose clinical results are eagerly awaited [5].

Anatomical context of BMS-387072

The rate of metabolism of BMS-387032 was investigated in liver microsomes [4].
The Caco-2 cell permeability of BMS-387032 was <15 nm/s in the apical to basolateral direction, and 161 nm/s in the basolateral to apical direction, indicating that it may be a substrate for an intestinal efflux transporter [4].
The permeability of BMS-387032 was evaluated using Caco-2 cells, an in vitro model of the intestinal epithelium [4].

Associations of BMS-387072 with other chemical compounds

We find that E2F4 levels are diminished following treatment with cyclin dependent kinase inhibitors (flavopiridol, roscovitine and BMS-387032) or with DNA damaging drugs (cisplatin and VP16) [6].

Gene context of BMS-387072

P-glycoprotein plays a role in the oral absorption of BMS-387032, a potent cyclin-dependent kinase 2 inhibitor, in rats [4].

Analytical, diagnostic and therapeutic context of BMS-387072

PURPOSE: BMS-387032, a novel cyclin-dependent kinase 2 inhibitor, is currently in phase I clinical trials for anticancer therapy [4].

References

Cyclin-dependent kinase 7/9 inhibitor SNS-032 abrogates FIP1-like-1 platelet-derived growth factor receptor α and bcr-abl oncogene addiction in malignant hematologic cells. Wu, Y., Chen, C., Sun, X., Shi, X., Jin, B., Ding, K., Yeung, S.C., Pan, J. Clin. Cancer Res. (2012) [Pubmed]
The cyclin-dependent kinase 2 inhibitor down-regulates interleukin-1beta-mediated induction of cyclooxygenase-2 expression in human lung carcinoma cells. Mukhopadhyay, P., Ali, M.A., Nandi, A., Carreon, P., Choy, H., Saha, D. Cancer Res. (2006) [Pubmed]
Small-molecule cyclin-dependent kinase modulators. Senderowicz, A.M. Oncogene (2003) [Pubmed]
P-glycoprotein plays a role in the oral absorption of BMS-387032, a potent cyclin-dependent kinase 2 inhibitor, in rats. Kamath, A.V., Chong, S., Chang, M., Marathe, P.H. Cancer Chemother. Pharmacol. (2005) [Pubmed]
New drugs in cancer therapy, National Tumor Institute, Naples, 17-18 June 2004. Caponigro, F., Basile, M., de Rosa, V., Normanno, N. Anticancer Drugs (2005) [Pubmed]
E2F4 deficiency promotes drug-induced apoptosis. Ma, Y., Freeman, S.N., Cress, W.D. Cancer Biol. Ther. (2004) [Pubmed]

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