Purvalanol A | CDK inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $50.00 | ||
| 25 mg | $200.00 |
Purvalanol A (212844-53-6) is a cyclin-dependent kinase inhibitor. IC50s= 4, 70, 35, 75 and 850 nM for cdc2/cyclin B, cdk2/cyclin A, cdk2/cyclin E, cdk5/p35 and cdk4/cyclin D1 and respectively.1 Reversibly arrests synchronized cells in G1 and G2 phase.2 Induces ER stress-mediated apoptosis and autophagy in colon cancer cells.3 Suppresses Src-mediated transformation by inhibiting both CDKs and c-Src.4 In cells transformed with MYC, purvalanol A rapidly down-regulates survivin expression and induces MYC-dependent apoptosis.5 Cell permeable.
References/Citations:
1) Gray et al. (1998), Exploiting chemical libraries, structure, and genomics in the search for kinase inhibitors; Science, 281 533
2) Villerbu et al. (2002), Cellular effects of purvalanol A: a specific inhibitor of cyclin-dependent kinase activities; Int. J. Cancer, 97 761
3) Coker-Gurkan et al. (2015), Purvalanol induces endoplasmic reticulum stress-mediated apoptosis and autophagy in a time dependent manner in HCT116 colon cancer cells; Oncol. Rep., 33 2761
4) Hikita et al. (2010), Purvalanol A, a CDK inhibitor, effectively suppresses Src-mediated transformation by inhibiting both CDKs and c-Src; Genes Cells, 15 1051
5) Goga et al. (2007), Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC; Nat. Med., 13 820
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
Purvalanol A (212844-53-6) is a cyclin-dependent kinase inhibitor. IC50s= 4, 70, 35, 75 and 850 nM for cdc2/cyclin B, cdk2/cyclin A, cdk2/cyclin E, cdk5/p35 and cdk4/cyclin D1 and respectively.1 Reversibly arrests synchronized cells in G1 and G2 phase.2 Induces ER stress-mediated apoptosis and autophagy in colon cancer cells.3 Suppresses Src-mediated transformation by inhibiting both CDKs and c-Src.4 In cells transformed with MYC, purvalanol A rapidly down-regulates survivin expression and induces MYC-dependent apoptosis.5 Cell permeable.
References/Citations:
1) Gray et al. (1998), Exploiting chemical libraries, structure, and genomics in the search for kinase inhibitors; Science, 281 533
2) Villerbu et al. (2002), Cellular effects of purvalanol A: a specific inhibitor of cyclin-dependent kinase activities; Int. J. Cancer, 97 761
3) Coker-Gurkan et al. (2015), Purvalanol induces endoplasmic reticulum stress-mediated apoptosis and autophagy in a time dependent manner in HCT116 colon cancer cells; Oncol. Rep., 33 2761
4) Hikita et al. (2010), Purvalanol A, a CDK inhibitor, effectively suppresses Src-mediated transformation by inhibiting both CDKs and c-Src; Genes Cells, 15 1051
5) Goga et al. (2007), Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC; Nat. Med., 13 820
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Focus Biomolecules • Plymouth Meeting, PA USA • 1-855-FOCUS21
Focus Biomolecules
Plymouth Meeting, PA USA
1-855-FOCUS21
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