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Cat. No. M3030
S-Ruxolitinib  Structure

S-Ruxolitinib; INCB18424

Size Price Availability Quantity
2mg USD 45  USD45 In stock
5mg USD 70  USD70 In stock
10mg USD 100  USD100 In stock
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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
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
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
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
Conversion of different model animals based on BSA (PMID: 27057123)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

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Keywords: S-Ruxolitinib , S-Ruxolitinib; INCB18424 supplier, JAK, inhibitors, activators

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