Purvalanol B (Synonyms: NG 95; NG95; NG-95) |
| Catalog No.GC16268 |
Purvalanol B(NG 95)는 cdc2-cyclin B, CDK2-cyclin A, CDK2-cyclin E에 대한 IC50이 6 nM, 6 nM, 9 nM, 6 nM인 강력하고 선택적이고 가역적이며 ATP 경쟁적인 억제제 CDK입니다. 각각 CDK5-p35.
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Cas No.: 212844-54-7
Sample solution is provided at 25 µL, 10mM.
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Purvalanol B is a selective inhibitor of CDK1, CDK2 and CDK4.
CDKs (cyclin-dependent kinases) family has the ability to regulate cell cycle.
Purvalanol B is reported as one of the most potent and selective CDK inhibitors. When tested with Chinese hamster lung fibroblast CCL39 cell line, treatment with Purvalanol B inhibited cells proliferate via targeting CKD1 which induced a G2/M block with a GI50 of 2.5 μM. In asynchronous cells, exposed to Purvalanol B led to an accumulation of cells in G2/M phase [1].
In a mouse model with NCI-H2228 subcutaneous xenograft, oral administration of ASP3026 caused significant reduction of phosphorylated ALK and tumor growth. 30 mg/kg/d ASP3026 for 2 weeks induced tumor regression by 78%. In mice injected with Karpas 299 cells, ASP3026 treatment caused remarkable lymphoma regression [2, 3].
Purvalanol B also interacts with p42/p44 MAPK proteins when tested with several mammalian cell lines including MCF-7 cell line [1].
References:
1.Kuromitsu S, Mori M, Shimada I, et al. Anti-tumor activity of ASP3026, a novel and selective ALK inhibitor of anaplastic lymphoma kinase (ALK). Annual Meeting of the American Association for Cancer Research (AACR), Orlando, FL. 2011.
2.Mori M, Ueno Y, Konagai S, et al. The Selective Anaplastic Lymphoma Receptor Tyrosine Kinase Inhibitor ASP3026 Induces Tumor Regression and Prolongs Survival in Non–Small Cell Lung Cancer Model Mice. Molecular cancer therapeutics, 2014, 13(2): 329-340.
3.George S K, Vishwamitra D, Manshouri R, et al. The ALK inhibitor ASP3026 eradicates NPM-ALK+ T-cell anaplastic large-cell lymphoma in vitro and in a systemic xenograft lymphoma model. Oncotarget, 2014, 5(14): 5750-5763.
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