SU-9516

Research use only, not for human use.

A selective CDK2 inhibitor with IC50 of 22 nM; shows less potent for CDK1/CDK4(IC50=40/200 nM), no inhibition on PKC, EGFR, p38MAPK; decreases the phosphorylation of pRb, and increases caspase-3 activation.

A selective CDK2 inhibitor with IC50 of 22 nM; shows less potent for CDK1/CDK4(IC50=40/200 nM), no inhibition on PKC, EGFR, p38MAPK; decreases the phosphorylation of pRb, and increases caspase-3 activation.

SU9516 shows slight activities against PKC, p38, PDGFr and EGFR, with IC50 of >10, >10, 18, and >100 μM. SU9516 (5 μM) decreases cdk2-specific Phosphorylation of pRB and inhibits cell cycle progression in RKO cells. SU9516 (5 μM) also induces apoptosis in RKO and SW480 Cells. SU9516 (5 μM) results in enhanced pRb/E2F complex formation in HT-29 cells. SU9516 enhances presence of E2F species in multiprotein complexes. SU9516 (5 μM) rapidly induces cytochrome crelease, Bax mitochondrial translocation, and apoptosis in association with pronounced down-regulation of the antiapoptotic protein Mcl-1. SU9516 causes down-regulation of Mcl-1 mRNA levels in human leukemia cells. Furthermore, SU9516 treatment results in a marked increase in reactive oxygen species production.

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SU9516 | SU 9516

Angiogenesis

CDK

CDK1|CDK2|CDK4|p38|PKC

Cancer

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377090-84-1

241.2453

C13H11N3O2

>98% (HPLC)

10 mM in DMSO

O=C1NC2=C(C=C(OC)C=C2)/C1=C/C3=CN=CN3

2H-Indol-2-one, 1,3-dihydro-3-(1H-imidazol-5-ylmethylene)-5-methoxy-, (3Z)-

(-20℃)

With Ice Pack

≥ 2 years