TP508 TFA

For research use only. Not for therapeutic Use.

  • CAT Number: I045906
  • Molecular Formula: C99H147N28F3O38S
  • Molecular Weight: 2426.46
  • Purity: ≥95%
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TP508 TFA is a 23-amino acid nonproteolytic thrombin peptide that represents a portion of the receptor-binding domain of thrombin molecule. TP508 TFA activates endothelial NO synthase (eNOS) and stimulates production of NO in human endothelial cells. TP508 TFA activates endothelial cells and stem cells to revascularize and regenerate tissues[1][2].
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[1].
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)[1].
TP508 acts as an antagonist for the effects of thrombin. TP508 peptide inhibits these thrombin-induced effects through a RGD and αvβ3-related mechanism[3].
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[1].


Catalog Number I045906
Molecular Formula C99H147N28F3O38S
Purity ≥95%
Reference

[1]. Olszewska-Pazdrak B, et al. Nuclear Countermeasure Activity of TP508 Linked to Restoration of Endothelial Function and Acceleration of DNA Repair. Radiat Res. 2016 Aug;186(2):162-74.
 [Content Brief]

[2]. Olszewska-Pazdrak B, et al. Systemic administration of thrombin peptide TP508 enhances VEGF-stimulated angiogenesis and attenuates effects of chronic hypoxia. J Vasc Res. 2013;50(3):186-9
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[3]. Tsopanoglou NE, et al. On the mode of action of thrombin-induced angiogenesis: thrombin peptide, TP508, mediates effects in endothelial cells via alphavbeta3 integrin. Thromb Haemost. 2004 Oct;92(4):846-57.
 [Content Brief]

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