research use only
Cat.No.S6501
| Related Targets | Bcl-2 PD-1/PD-L1 Ferroptosis p53 Apoptosis related Synthetic Lethality STAT TNF-alpha Ras KRas |
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| Other Caspase Inhibitors | Emricasan (IDN-6556) Z-VAD-FMK Q-VD-Oph Z-DEVD-FMK Belnacasan (VX-765) Z-IETD-FMK Ac-DEVD-CHO Z-LEHD-FMK TFA Z-VAD(OH)-FMK PAC-1 |
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In vitro |
DMSO
: 86 mg/mL
(199.28 mM)
Ethanol : 8 mg/mL Water : Insoluble |
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In vivo |
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Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)
Calculation results:
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.
| 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 |
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| Synonyms | N/A | Smiles | C1C2CC3CC1CC(C2)(C3)C(=O)NC4=CC5=C(C=C4)N=C(S5)NC(=O)C6=CC=CC=C6 | ||
| Targets/IC50/Ki |
CreK
(Cell-free assay) 12 nM
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| 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. |
References |
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