Bradykinin (1-5)

Research use only, not for human use.

Bradykinin (1-5) is a major stable metabolite of Bradykinin, formed by the proteolytic action of angiotensin-converting enzyme (ACE).The bradykinin (BK) fragment (1-5) (RPPGF) is among the most stable of naturally occurring metabolites. Bradykinin (1-5) may be used as a marker for BK production in vivo.

Bradykinin (1-5) is a major stable metabolite of Bradykinin, formed by the proteolytic action of angiotensin-converting enzyme (ACE).The bradykinin (BK) fragment (1-5) (RPPGF) is among the most stable of naturally occurring metabolites. Bradykinin (1-5) may be used as a marker for BK production in vivo.(In Vivo):Bradykinin is a short-lived vasoactive peptide, with a reported half-life in vivo of 17 s, that is rapidly metabolized in the circulation to Bradykinin (1-5). Bradykinin (1-5), the product of two sequential cleavages of Bradykinin by ACE at the Pro7-Phe8 and Phe5-Ser6bonds, has been identified as the major stable metabolite of Bradykinin in vivo in human subjects, with a terminal half-life of minutes. Both Bradykinin and Bradykinin (1-5) inhibit α- and γ-thrombin-induced platelet aggregation (P<0.01 versus baseline). Bradykinin (1-5) inhibits γ-thrombin-induced platelet aggregation 50% at a calculated dose of 183±3 pmol/min. Neither Bradykinin nor Bradykinin (1-5) affects thrombin receptor-activating peptide-induced platelet aggregation, consistent with the hypothesis that Bradykinin and Bradykinin 1-5 inhibit thrombin-induced platelet aggregation by preventing cleavage of the thrombin receptor and liberation of thrombin receptor-activating peptide. Bradykinin (1-5) significantly attenuates α-thrombin-induced platelet aggregation but not TRAP 1-6-induced platelet aggregation. Bradykinin (1-5) potently inhibits γ-thrombin (500 nM)-induced platelet aggregation with an ED50 of 183±2 pmol/min.

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Bradykinin is a short-lived vasoactive peptide, with a reported half-life in vivo of 17 s, that is rapidly metabolized in the circulation to Bradykinin (1-5). Bradykinin (1-5), the product of two sequential cleavages of Bradykinin by ACE at the Pro7-Phe8 and Phe5-Ser6bonds, has been identified as the major stable metabolite of Bradykinin in vivo in human subjects, with a terminal half-life of minutes. Both Bradykinin and Bradykinin (1-5) inhibit α- and γ-thrombin-induced platelet aggregation (P<0.01 versus baseline). Bradykinin (1-5) inhibits γ-thrombin-induced platelet aggregation 50% at a calculated dose of 183±3 pmol/min. Neither Bradykinin nor Bradykinin (1-5) affects thrombin receptor-activating peptide-induced platelet aggregation, consistent with the hypothesis that Bradykinin and Bradykinin 1-5 inhibit thrombin-induced platelet aggregation by preventing cleavage of the thrombin receptor and liberation of thrombin receptor-activating peptide. Bradykinin (1-5) significantly attenuates α-thrombin-induced platelet aggregation but not TRAP 1-6-induced platelet aggregation. Bradykinin (1-5) potently inhibits γ-thrombin (500 nM)-induced platelet aggregation with an ED50 of 183±2 pmol/min.

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GPCR/G Protein

Bradykinin Receptor

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23815-89-6

572.66

C27H40N8O6

>98% (HPLC)

In Vitro:?DMSO : 100 mg/mL (174.62 mM)

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Sequence:Arg-Pro-Pro-Gly-Phe

(-20℃)

With Ice Pack

≥ 2 years