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 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^[1]. 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^[2]. 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^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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^[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

601.53

C₂₂H₃₄F₃N₅O₁₁

Ac-Ser-Asp-Lys-Pro

Ac-SDKP

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

*In solvent : -80deg;C, 6 months; -20deg;C, 1 month (sealed storage, away from moisture)

H₂O

Peptide Solubility and Storage Guidelines:

1.;;Calculate the length of the peptide.

2.;;Calculate the overall charge of the entire peptide according to the following table:

3.;;Recommended solution:

• [1]. Rousseau A, et al. The hemoregulatory peptide N-acetyl-Ser-Asp-Lys-Pro is a natural and specificsubstrate of the N-terminal active site of human angiotensin-converting enzyme. J Biol Chem. 1995 Feb 24;270(8):3656-61.

  [2]. Pokharel S, et al. N-acetyl-Ser-Asp-Lys-Pro inhibits phosphorylation of Smad2 in cardiac fibroblasts. Hypertension. 2002 Aug;40(2):155-61.

  [3]. Rhaleb NE, et al. N-acetyl-Ser-Asp-Lys-Pro inhibits interleukin-1β-mediated matrix metalloproteinase activation in cardiac fibroblasts. Pflugers Arch. 2013 Oct;465(10):1487-95.

  [4]. Rhaleb NE, et al. Renal protective effects of N-acetyl-Ser-Asp-Lys-Pro in deoxycorticosterone acetate-salt hypertensive mice. J Hypertens. 2011 Feb;29(2):330-8.