[CAS NO. 383150-41-2]  JTE 013

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PRODUCTS SPECIFICATIONS [383150-41-2]

Catalog
SLK-S7182
Brand
Selleck
CAS
383150-41-2

DESCRIPTION [383150-41-2]

Overview

MDLMFCD09878275
Molecular Weight408.29
Molecular FormulaC17H19Cl2N7O
SMILESCC(C1=C2C(N(C)N=C2C)=NC(NNC(NC3=CC(Cl)=NC(Cl)=C3)=O)=C1)C

For research use only.

Storage

3 years,-20°C,powder
1 years,-80°C,in solvent

Shipping

Room temperature shipping(Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

1 mg5 mg10 mg
1 mM2.4492 mL12.2462 mL24.4924 mL
5 mM0.4898 mL2.4492 mL4.8985 mL
10 mM0.2449 mL1.2246 mL2.4492 mL
50 mM0.0490 mL0.2449 mL0.4898 mL

Description

JTE 013 is a potent and selective antagonist with of 17.6 nM.

Targets

S1PR2(human) [1]
(in CHO cells)
S1PR2(rat) [1]
(in CHO cells)
17 nM22 nM

In vitro

JTE-013 reverses the inhibitory effects of S1P2 signaling on cell migration of vascular ECs and smooth muscle cells. It 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.

In vivo

JTE-013 inhibition of S1P2 significantly inhibits microvascular permeability in an in vivo animal model. JTE-013 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.