N-Acetyl-Ser-Asp-Lys-Pro

CAS No. 127103-11-1

N-Acetyl-Ser-Asp-Lys-Pro ( —— )

Catalog No. M22966 CAS No. 127103-11-1

Acetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
Size Price / USD Stock Quantity
5MG 91 In Stock
10MG 156 In Stock
25MG 321 In Stock
50MG 482 In Stock
100MG 696 In Stock
200MG Get Quote In Stock
500MG Get Quote In Stock
1G Get Quote In Stock

Biological Information

  • Product Name
    N-Acetyl-Ser-Asp-Lys-Pro
  • Note
    Research use only, not for human use.
  • Brief Description
    Acetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?
  • Description
    Acetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?Flow cytometry of rat cardiac fibroblasts treated with AcSDKP showed significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle.?In cardiac fibroblasts transfected with a Smad-sensitive luciferase reporter construct, AcSDKP decreased luciferase activity by 55+/-9.7% (P=0.01).?Moreover, phosphorylation and nuclear translocation of Smad2 was decreased in cardiac fibroblasts treated with AcSDKP.?To conclude, AcSDKP inhibits the growth of cardiac fibroblasts and also inhibits TGFbeta1-stimulated phosphorylation of Smad2.?Because AcSDKP increases substantially during ACE inhibitor therapy, this suggests a novel pathway independent of angiotensin II, by which ACE inhibitors can inhibit cardiac fibrosis.
  • Synonyms
    ——
  • Pathway
    Endocrinology/Hormones
  • Target
    RAAS
  • Recptor
    ACE
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    127103-11-1
  • Formula Weight
    487.5
  • Molecular Formula
    C20H33N5O9
  • Purity
    >98% (HPLC)
  • Solubility
    ——
  • SMILES
    O=C([C@@H]1N(C([C@H](NC([C@@H](NC([C@H](NC(C)=O)CO)=O)CC(O)=O)=O)CCCCN)=O)CCC1)O
  • Chemical Name
    ——

Shipping & Storage Information

  • Storage
    (-20℃)
  • Shipping
    With Ice Pack
  • Stability
    ≥ 2 years

Reference

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.
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