| CAS NO: | 547756-93-4 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 250mg | 电议 |
| 500mg | 电议 |
| Molecular Weight (MW) | 408.29 |
|---|---|
| Formula | C17H19Cl2N7O |
| CAS No. | 547756-93-4 |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: 81 mg/mL (198.38 mM) |
| Water: <1 mg/mL | |
| Ethanol: 34 mg/mL (83.27 mM) | |
| Solubility (In vivo) | CC(C1=C2C(N(C)N=C2C)=NC(NNC(NC3=CC(Cl)=NC(Cl)=C3)=O)=C1)C |
| Synonyms | JTE-013; JTE 013; JTE013. |
| In Vitro | In vitro activity: JTE-013 reverses the inhibitory effects of S1P2 signaling on cell migration of vascular ECs and smooth muscle cells. It also regulates endothelial tight junctions and barrier function in vitro. Blockage of S1P2 signaling by JTE-013 significantly enhances the effects of S1P on the increase of TEER, an in vitro measurement of endothelial integrity, as well as the formation of TJs in senescent ECs Kinase Assay: JTE 013 is a novel potent and selective S1P2 (sphingosine-1-phosphate 2) antagonist with IC50 of 17.6 nM. It binds to the human and rat receptors with IC50 values of 17 and 22 nM, respectively, and with IC50 values>10 μM for human S1P1 and S1P3. It reverses the inhibitory effects of S1P2 signaling on cell migration of vascular ECs and smooth muscle cells. It also regulates endothelial tight junctions and barrier function in vitro. Blockage of S1P2 signaling by JTE-013 significantly enhances the effects of S1P on the increase of TEER, an in vitro measurement of endothelial integrity, as well as the formation of TJs in senescent ECs. Cell Assay: HUVECs preincubated with various concentrations of JTE-013 for 10 min are allowed to migrate for 4 h toward the lower chamber where the indicated concentrations of Sph-1-P are placed. The migrated cells on the lower side of the filter are fixed, stained, and counted. |
|---|---|
| In Vivo | JTE-013 inhibition of S1P2 significantly inhibits microvascular permeability in an in vivo animal model. It modulates the responses of brain endothelium by inhibiting cerebrovascular permeability, the development of intracerebral heamorrhage, and neurovascular injury in an experimental model of stroke. JTE-013 reduced mast cell activation, airway infiltration, and the serum levels of histamine and several cytokines in vitro and in vivo studies. In a murine model, JTE-013 suppresses streptozotocin-induced blood glucose increases, pancreatic b cell apoptosis, and the incidence of diabetes. In a New Zealand obese diabetic mouse model under high-fat diet conditions, it protected pancreatic b cells. Treatment with JTE-013 also reduces plasma levels of IL-1b and IL-18 (endotoxin-induced inflammatory cytokines) in ApoE–/– mice and S1P2 gene deficiency reduces atherosclerosis. The compound offers a novel means of treating inflammatory disorders, such as, atherosclerosis and sepsis. |
| Animal model | Mice(C57BL/6×129Sv genetic background) |
| Formulation & Dosage | 1.2 mg/kg; i.p |
| References | Biochem Biophys Res Commun. 2002 Dec 6;299(3):483-7;Am J Physiol Heart Circ Physiol. 2009 Jan;296(1): H33-42; Biomol Ther (Seoul). 2017 Jan 1;25(1):80-90; Arterioscler Thromb Vasc Biol. 2011 Jan;31(1):81-5. |
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