TP508

Research use only, not for human use.

TP508 is a 23 amino acid synthetic peptide representing residues 508-530 of human prothrombin which is identified as a potential receptor-binding domain based on competition for high-affinity thrombin binding to fibroblasts.TP508 (Chrysalin) is an investigational peptide drug that was developed for use in stimulating repair of dermal and musculoskeletal tissues.

TP508 is a 23 amino acid synthetic peptide representing residues 508-530 of human prothrombin which is identified as a potential receptor-binding domain based on competition for high-affinity thrombin binding to fibroblasts.TP508 (Chrysalin) is an investigational peptide drug that was developed for use in stimulating repair of dermal and musculoskeletal tissues.(In Vitro):TP508 treatment reverses radiation effects on NO signaling, restores tube formation and accelerates the repair of radiation-induced DSB in irradiated human endothelial cells. TP508 injection increases responsiveness of endothelial cells from aortic explants to VEGF-stimulated angiogenesis in vitro. TP508 stimulation does not significantly affect the VEGF mRNA levels in normoxic or hypoxic cells. TP508 acts as an antagonist for the effects of thrombin. TP508 peptide inhibits these thrombin-induced effects through a RGD and αvβ3-related mechanism.(In Vivo):TP508 (500 μg) in sham-irradiated animals significantly increases the amount of endothelial cell sprouting from aortic explants. TP508 significantly increases the sprouting in sham-irradiated and irradiated animals, more than doubling the amount of sprouting in explants from animals at all exposure doses. TP508 (10 mg/kg) given 24 h after 8.5 Gy gamma irradiation significantly increases 30-day survival in mice, from 26.7 to 73.3%. TP508 injection increases endothelial sprouting and potentiates VEGF-stimulated angiogenesis. In type I diabetic swine, TP508 (1 mg/kg, infusion) reduces infarct size after IR.

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 (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.

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Immunology/Inflammation

NOS

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121341-81-9

2312.44

C97H146N28O36S

>98% (HPLC)

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Sequence:Ala-Gly-Tyr-Lys-Pro-Asp-Glu-Gly-Lys-Arg-Gly-Asp-Ala-Cys-Glu-Gly-Asp-Ser-Gly-Gly-Pro-Phe-Val

(-20℃)

With Ice Pack

≥ 2 years