research use only

NVP 231 Caspase activator

Cat.No.S6501

NVP 231 is a novel CerK inhibitor that inhibits the catalytic activity of recombinant CerK in vitro with an IC50 of 12 nM. This compound induces cell apoptosis by increasing DNA fragmentation and caspase-3 and caspase-9 cleavage.
NVP 231 Caspase activator Chemical Structure

Chemical Structure

Molecular Weight: 431.55

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 431.55 Formula

C25H25N3O2S

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 362003-83-6 -- Storage of Stock Solutions

Synonyms N/A Smiles C1C2CC3CC1CC(C2)(C3)C(=O)NC4=CC5=C(C=C4)N=C(S5)NC(=O)C6=CC=CC=C6

Solubility

In vitro
Batch:

DMSO : 86 mg/mL ( (199.28 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 8 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Working concentration: mg/ml;

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.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Mechanism of Action

Targets/IC50/Ki
CreK [1]
(Cell-free assay)
12 nM
In vitro

NVP-231 reduces cell viability and DNA synthesis by triggering cell death of cancer cells. This compound-treated cells committed M phase arrest rather than arrest at the G2/M boundary. In MCF-7 and NCI-H358 cells, this chemical treatment causes a concentration-dependent up-regulation of cyclin B1 phosphorylation at Ser133 and a reduction of CDK1 phosphorylation at Tyr15. Wee1 is down-regulated by this compound in both NCI-H358 and MCF-7 cells. Upon this chemical treatment of cancer cells, CDK4 protein is concentration- and time-dependently down-regulated. This effect is even more pronounced in synchronized cells[2].

References

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