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research use only
Cat.No.S2407
| Related Targets | EGFR STAT Pim |
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| Other JAK Products | BMS-986165 (Deucravacitinib) AZD1480 WP1066 Momelotinib (CYT387) Filgotinib (GLPG0634) AT9283 Gandotinib (LY2784544) TG101209 Cerdulatinib (PRT062070) hydrochloride Pacritinib |
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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 | 236.35 | Formula | C15H24O2 |
Storage (From the date of receipt) | |
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| CAS No. | 4871-97-0 | Download SDF | Storage of Stock Solutions |
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| Synonyms | N/A | Smiles | CC1CCC2C13CC(C(O3)(CC2=C)O)C(C)C | ||
| Targets/IC50/Ki |
JAK
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| In vitro |
Curcumol induced cell death in human lung adenocarcinoma (ASTC-a-1) cells by inducing G(2)/M phase arrest, nuclear fragmentation, phosphatidylserine externalization and a rapid translocation of Bax from cytosol into mitochondria. While, caspases are not involved in this compound-induced apoptosis. It also benefits rheumatoid arthritis treatment through suppressing the fibroblast-like synoviocytes (FLS) proliferation and DNA synthesis. This chemical attenuates PDGF-BB-induced Jak2 phosphorylation and downregulates STAT1 and STAT3 DNA-binding activities.
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References |
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