N-Acetyl-Ser-Asp-Lys-Pro(Synonyms: Ac-SDKP)

N-Acetyl-Ser-Asp-Lys-Pro;(Synonyms: Ac-SDKP)

N-Acetyl-Ser-Asp-Lys-Pro 是来自骨髓的内源性四肽,是 ACE 的N-末端位点的特异性底物。

N-Acetyl-Ser-Asp-Lys-Proamp;;(Synonyms: Ac-SDKP)

N-Acetyl-Ser-Asp-Lys-Pro Chemical Structure

CAS No. : 127103-11-1

规格 是否有货
100 mg ; 询价 ;
250 mg ; 询价 ;
500 mg ; 询价 ;

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N-Acetyl-Ser-Asp-Lys-Pro 的其他形式现货产品:

N-Acetyl-Ser-Asp-Lys-Pro acetate


N-Acetyl-Ser-Asp-Lys-Pro, 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[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.

(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[4].

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









Sequence Shortening



Room temperature in continental US; may vary elsewhere.


Please store the product under the recommended conditions in the Certificate of Analysis.

  • [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.