Molecular Formula | C14H21NO3S
|
Molar Mass | 283.39 |
Density | 1.137±0.06 g/cm3(Predicted) |
Melting Point | 103-105℃ |
Solubility | Soluble in DMSO (up to 100 mg/ml) or in Ethanol (up to 25 mg/ml) |
Appearance | solid |
Color | White |
pKa | 4.28±0.40(Predicted) |
Storage Condition | Sealed in dry,Room Temperature |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 3 months. |
In vitro study | Reparixins are noncompetitive allosteric inhibitors of CXCR1 and CXCR2 activation, inhibiting intracellular signaling pathways without affecting receptor binding. Reparixins can effectively and selectively inhibit many biological processes induced by CXCL8, such as leukocyte recruitment and functional inflammatory response. The Reparixin did not affect the activation of CXCR1/CXCR2 induced by other chemokines C5a, fMLP, cxcl12. Reparixins regulate the production of angiotensin II receptors, affecting Ang II-induced hypertension. In in vitro experiments, Reparaxin specifically prevented CXCR1/2-mediated migration of murine and human neutrophils without affecting other receptors. Reparixins inhibit cxcl8-mediated neutrophil activation and prevent phosphorylation of downstream signaling molecules. The Reparixin inhibited the increase of intracellular free calcium, the release of elastase and the production of reactive oxygen intermediates, and did not affect the phagocytosis of E. Coli. |
In vivo study | In a variety of injury models, reparixins attenuate the inflammatory response. Reparixin is effective in lowering systolic blood pressure and increasing blood flow. The thickness of the thoracic aortic wall in the primary hypertensive rats treated with Reparixin was significantly reduced compared to the normal primary hypertensive rats. |