包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
10mg | 电议 |
50mg | 电议 |
Cell lines | Naive T cell |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
Reaction Conditions | 16h; 50 nM |
Applications | A concentration of 100 nM. 50 nM, but not 10 nM, CP-690,550 suppressed IFN- c production 4 days after Th1 differentiation conditions were established, while both 10 nM and 50 nM CP-690,550 strongly suppressed IL-4 production under Th2 differentiation conditions. This suggests that CP-690,550 inhibits both Th1 and Th2 differentiation, and that Th2 is more sensitive than Th1 to this drug. We then examined the effect of CP-690,550 on Th17 and induced T regulatory (iTreg) cells. CP-690,550 enhanced IL-17 production while suppressing Foxp3 and IL-10 induction in a dose-dependent manner under Th17 differentiation conditions. These data indicate that<100 nM CP-690,550 efficiently inhibits Th1, Th2 and iTreg while promoting Th17, in vitro. |
Animal models | C57BL6/J mice and DBA/1J mice |
Dosage form | 30 nM; intraperitoneal injection |
Applications | Naive CD4+T cells isolated from mice were stimulated with various cytokines in the presence of various concentrations of CP-690,550. CP-690,550 selectively inhibited IFN c -induced STAT1, IL-4-induced STAT6, and IL-2-induced STAT5 at 3–30 nM, while 30 nM CP-690,550 did not suppress IL-6-induced STAT3 phosphorylation. A concentration greater than 100 nM was required for the partial suppression of STAT3 |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
产品描述 | Tofacitinib citrate is an orally available JAK1/2/3 inhibitor with IC50s of 1, 20, and 112 nM, respectively. Tofacitinib (CP-690550) citrate binds potentially at JAK3 and JAK2 as 2.2 nM and 5 nM (Kd). The report includes additional binding for Tofacitinib at Camk1 (Kd of 5,000 nM), DCamkL3 (Kd of 4.5 nM), Mst2 (Kd of 4,300 nM), Pkn1 (Kd of 200 nM), Rps6ka2 (Kin.Dom.2-C-terminal) (Kd of 1,400 nM), Rps6ka6 (Kin.Dom.2-C-terminal) (Kd of 1,200 nM), Snark (Kd of 420 nM), Tnk1 (Kd of 640 nM) and Tyk2 (Kd of 620 nM)[1]. K562, KCL22, and THP-1 cells are exposed to different doses of STI571 or JAK inhibitors for 72 h to quantify the effects of tyrosine kinase inhibitor (TKI) activity. Cell growth inhibition is then evaluated using the MTT assay. The proliferation of K562 and KCL22 cells, but not THP-1 cells, is inhibited by IMA in a concentration-dependent manner. The IC50 value of IMA is 0.28 μM for K562 and 0.17 μM for KCL22. Although treatment with Tofacitinib (TOF) or INCB018424 alone does not suppress cell proliferation, both Tofacitinib and INCB018424 make the K562 and KCL22 more sensitive to IMA[4]. Animals that are treated with Tofacitinib show a significantly lower production of anti-drug antibodies (ADAs) compare with PEG-treated control mice (for five weeks after initial immunization, p4 hours[3]. References: |