Parstatin (mouse)

Research use only, not for human use.

Cell-permeable peptide cleaved from protease-activated receptor 1 (PAR1) upon receptor activation. Attenuates endothelial cell migration and proliferation (IC50 ~ 20 μM), and induces cell cycle arrest. Promotes activation of caspase-3 and exhibits pro-apoptotic activity in vitro. Inhibits angiogenesis and exhibits cardioprotective activity in vivo.

Cell-permeable peptide cleaved from protease-activated receptor 1 (PAR1) upon receptor activation. Attenuates endothelial cell migration and proliferation (IC50 ~ 20 μM), and induces cell cycle arrest. Promotes activation of caspase-3 and exhibits pro-apoptotic activity in vitro. Inhibits angiogenesis and exhibits cardioprotective activity in vivo.

Parstatin (0-10 μM) increases recovery of LVDP in a concentration-dependent manner. The optimal concentration was 1 μM which produced a 23% recovery of LVDP.

Parstatin (single dose, 1-25 μg/kg, iv) administered prior to ischaemia confers immediate cardioprotection by recruiting the Gi-protein activation pathway including p38 MAPK, ERK1/2, NOS, and KATP channels. Parstatin exerts effects on both the cardiomyocytes and the coronary circulation to induce cardioprotection. This suggests a potential therapeutic role of parstatin in the treatment of cardiac injury resulting from ischaemia and reperfusion. Animal Model:Male Sprague–Dawley rats at 8 weeks of age (250-300 g).Dosage:1-25 μg/kg.Administration:IV injected 15 min prior to ischaemia.Result:A significant decrease in infarct size was detected with the 5-15 μg/kg doses with 10 μg/kg as the optimal dose. These hearts had an infarct size of 46 ± 3% of the area at risk, which is a 26% reduction in infarct size compared with the control.

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GPCR/G Protein

PAR

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1065756-01-5

4419.19

C189H326N58O57S3

>98% (HPLC)

water:1 mg/mL

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(-20℃)

With Ice Pack

≥ 2 years