N-Acetyl-Ser-Asp-Lys-Pro TFA

Research use only, not for human use.

N-Acetyl-Ser-Asp-Lys-Pro (TFA), an endogenous tetrapeptide secreted by bone marrow, is a specific substrate for the N-terminal site of ACE.

N-Acetyl-Ser-Asp-Lys-Pro (TFA), an endogenous tetrapeptide secreted by bone marrow, is a specific substrate for the N-terminal site of ACE. (In Vitro):N-Acetyl-Ser-Asp-Lys-Pro is degraded specifically by ACE, and its plasma level rises substantially during ACE inhibitor therapy. Flow cytometry of rat cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro shows significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle. Moreover, phosphorylation and nuclear translocation of Smad2 is decreased in cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro. N-acetyl-seryl-aspartyl-lysyl-proline appears to exert this function by blocking the action of a stem cell-specific proliferation stimulator and acts selectively on quiescent progenitors. N-Acetyl-Ser-Asp-Lys-Pro inhibits collagenase expression and activation is associated with increased expression of TIMP-1 and TIMP-2. N-Acetyl-Ser-Asp-Lys-Pro normalizes the IL-1β-mediated increase in MMP-2 and MMP-9 activities and MMP-13 expression.(In Vivo):N-Acetyl-Ser-Asp-Lys-Pro prevents hypertension-induced inflammatory cell infiltration, collagen deposition, nephrin downregulation and albuminuria, which could lead to renoprotection in hypertensive mice.

Others

Other Targets

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601.5

C22H34F3N5O11

>98% (HPLC)

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(-20℃)

With Ice Pack

≥ 2 years