S-Ruxolitinib
Cat# M3030-5mg
Size : 5mg
Brand : AbMole Bioscience
All AbMole products are for research use only, cannot be used for human consumption.
Synonym:
S-Ruxolitinib; INCB18424
Quality Control & Documentation
Biological Activity
S-Ruxolitinib is the chirality of INCB018424, which is the first potent, selective, JAK1/2 inhibitor to enter the clinic with IC50 of 3.3 nM/2.8 nM, >130-fold selectivity for JAK1/2 versus JAK3.
Product Citations
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Blood Cancer J. 2016 Oct 7;6(10):e481.
Expression of CALR mutants causes mpl-dependent thrombocytosis in zebrafish.
S-Ruxolitinib purchased from AbMole -
Nature. 2014 Aug 7;512(7512):78-81.
Neuropathy of haematopoietic stem cell niche is essential for myeloproliferative neoplasms.
S-Ruxolitinib purchased from AbMole
Customer Product Validations & Biological Datas
Source | Blood cancer journal (2016) . Figure 4. ruxolitinib (Abmole Bioscience, Houston, TX, USA) and fedratinib (Abmole Bioscience) | |
Method | Western blotting | |
Cell Lines | Embroys of wild-type zebrafish | |
Concentrations | 1 μM ~ 8 μM | |
Incubation Time | 24 h | |
Results | The expression of CALRdel52 mRNA significantly increased stat5 phosphorylation (Figure 4a, lane 2). Furthermore, treatment with ruxolitinib and fedratinib significantly ameliorated the enhanced stat5 phosphorylation induced by CALR-del52 mRNA (Figure 4a, lane 3 and 4). In addition, treatment with ruxolitinib significantly decreased the numbers of CD41+ thrombocytes in uninjected control as well as CALR-del52-injected embryos in a dose-dependent manner (Figure 4b). Whereas treatment with fedratinib only had minimal inhibitory effect on the number of CD41+ thrombocytes in uninjected control embryos, and had a modest and significant dose-independent inhibitory effect on mutant CALR-induced thrombocytosis (Figure 4c). Our results demonstrated that mutant CALR-mediated pathogenic thrombopoiesis involves jak-stat activation that can be blocked by JAK inhibitors. |
Source | Nature (2014). Figure 1. The JAK inhibitor INCB018424 (S-ruxolitinib, Abmole Bioscience) | |
Method | automated blood counter, flowcytometry | |
Cell Lines | haematopoietic cell and BM MSCs | |
Concentrations | oral gavage (30mg/kg, twice per day separated 10–12h) | |
Incubation Time | 4 weeks | |
Results | Nestin1 MSC reduction was instead explained by a threefold increased apoptotic rate in mutant mice, and was not prevented by the JAK inhibitor ruxolitinib. Treatment with the JAK1/2 inhibitor ruxolitinib reduces haematopoietic cell expansion in MPN but it does not rescue BM MSCs. |
Protocol (for reference only)
Cell Experiment | |
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Cell lines | Ba/F3-EpoR-JAK2V617F or HEL cells |
Preparation method | Cells were seeded at 2000/well of white bottom 96-well plates, treated with compounds from DMSO stocks (0.2% final DMSO concentration), and incubated for 48 hours at 37°C with 5% CO2. Viability was measured by cellular ATP determination using the Cell-Titer Glo (Promega) luciferase reagent or viable cell counting. Values were transformed to percent inhibition relative to vehicle control, and IC50 curves were fitted according to nonlinear regression analysis of the data using PRISM GraphPad. |
Concentrations | 0~10µM |
Incubation time | 48h |
Animal Experiment | |
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Animal models | 6- to 8-week-old female BALB/c mice Ba/F3-JAK2V617F cells model |
Formulation | 5% dimethyl acetamide, 0.5% methocellulose |
Dosages | 180mg/kg, twice a day |
Administration | orally |
Chemical Information
Molecular Weight | 306.37 |
Formula | C17H18N6 |
CAS Number | 941685-37-6 |
Solubility (25°C) | DMSO 51 mg/mL |
Storage | Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |