| Bioactivity | N-Acetyl-Ser-Asp-Lys-Pro, an endogenous tetrapeptide secreted by bone marrow, is a specific substrate for the N-terminal site of ACE. |
| Invitro | 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]. |
| Name | N-Acetyl-Ser-Asp-Lys-Pro |
| CAS | 127103-11-1 |
| Sequence | Ac-Ser-Asp-Lys-Pro |
| Shortening | Ac-SDKP |
| Formula | C20H33N5O9 |
| Molar Mass | 487.50 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |