ChemicalBook--->CAS DataBase List--->121341-81-9

121341-81-9

121341-81-9 Structure

121341-81-9 Structure
IdentificationBack Directory
[Name]

TP 508
[CAS]

121341-81-9
[Synonyms]

TP 508
[Molecular Formula]

C??H???N??O??S
[MDL Number]

MFCD11113617
[MOL File]

121341-81-9.mol
[Molecular Weight]

2312.46
Chemical PropertiesBack Directory
[density ]

1.56±0.1 g/cm3(Predicted)
[InChIKey]

MOZAQZCGIKWACU-BRMVNBHNNA-N
Hazard InformationBack Directory
[Biological Activity]

TP508 is a 23 amino acid non-proteolytic thrombin peptide representing part of the receptor binding domain of the thrombin molecule. It activates endothelial NO synthase (eNOS) and stimulates NO production in human endothelial cells. TP508 enables angiogenesis and tissue regeneration by activating endothelial cells and stem cells.
[in vitro]

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

< td class="col1"> 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.
[in vivo]

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. < /p>

< tr>
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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