Purvalanol A CDK inhibitor

Cat.No.S7793

Purvalanol A is a potent, and cell-permeable CDK inhibitor with IC50 of 4 nM, 70 nM, 35 nM, and 850 nM for cdc2-cyclin B, cdk2-cyclin A, cdk2-cyclin E, and cdk4-cyclin D1, respectively. This compound induces endoplasmic reticulum stress-mediated apoptosis and autophagy.
Purvalanol A CDK inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 388.89

Quality Control

Batch: S779301 DMSO]60 mg/mL]false]Ethanol]13 mg/mL]false]Water]Insoluble]false Purity: 99.4%
99.4

Chemical Information, Storage & Stability

Molecular Weight 388.89 Formula

C19H25ClN6O

Storage (From the date of receipt)
CAS No. 212844-53-6 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles CC(C)C(CO)NC1=NC(=C2C(=N1)N(C=N2)C(C)C)NC3=CC(=CC=C3)Cl

Solubility

In vitro
Batch:

DMSO : 60 mg/mL (154.28 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 13 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
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Mechanism of Action

Targets/IC50/Ki
Cdc2/CyclinB [1]
4 nM
CDK2/CyclinE [1]
35 nM
CDK2/CyclinA [1]
70 nM
CDK4/CyclinD1 [1]
850 nM
In vitro
Purvalanol A decreases cell viability in dose-dependent manner in MCF-7 and MDA-MB-231 cell lines. This compound induces cell viability loss by 50 % in MCF-7 cells but MDA-MB-231 cells sre less sensitive to it (32 % decreases in cell viability). It induces mitochondria-mediated apoptosis in MCF-7 and MDA-MB-231 cells.[2] This chemical effectively prevents c-Src-mediated transformation by inhibiting both cell cycle progression and c-Src signaling, and effectively suppresses the anchorage independent growth of some human cancer cells in which c-Src is up-regulated. It has a stronger inhibitory effect on the anchorage-independent growth of HT29 and SW480 human colon cancer cells. [3]
References

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