TP508 (10 mg/kg; intravenous injection; male CD-1 mice) treatment mitigates radiation-induced endothelial cell damage, also significantly increases survival of CD-1 mice when injected 24 h after 8.5 Gy exposure. Animal Model: Male CD-1 mice (12-15-week old) with γ irradiation Dosage: 10 mg/kg Administration: Intravenous injection Result: Mitigated radiation-induced endothelial cell damage, also significantly increased survival of CD-1 mice.

TP508 (50 μg/mL; 24 hours; HCAEC) treatment reverses radiation-induced endothelial dysfunction (ED) and loss of NO signaling by attenuating the downregulation of eNOS expression. TP508 treatment is able to stimulate NO production in the irradiated cells. TP508 mitigates effects of nuclear radiation on human endothelial cells in culture restoring endothelial NO production, tube formation and accelerating repair of radiation-induced DNA double-strand breaks (DSB). TP508 acts as an antagonist for the effects of thrombin. TP508 peptide inhibits these thrombin-induced effects through a RGD and αvβ3-related mechanism. Western Blot Analysis Cell Line: Primary human coronary artery endothelial cells (HCAEC) Concentration: 50 μg/mL Incubation Time: 24 hours Result: Prevented the radiation-induced downregulation of eNOS.

TP508 是一种 23 个氨基酸的非蛋白水解凝血酶肽，代表凝血酶分子受体结合结构域的一部分。TP508 可激活内皮 NO synthase (eNOS) 并刺激人内皮细胞中 NO 的产生。TP508 通过激活内皮细胞和干细胞以使血管再生和组织再生。