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AcSDKP ELISA

  • Regulatory status:RUO
  • Type:Competitive ELISA
  • Species:Multispecies
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Cat. No. Size Price


RA19007R 96 wells (1 kit)
PubMed Product Details
Technical Data

Type

Competitive ELISA

Applications

Serum, Urine, Plasma

Sample Requirements

50 µl/well

Storage/Expiration

Store the kit at –20°C. Under these conditions, the kit is stable until expiration date (see label on the box).

Limit of Detection

0,1 nM

Summary

Summary

AcSDKP is a new reliability marker of chronic ACE inhibition. The tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is an endogenous regulatory factor of hematopoiesis which reverses stem cells and normal early progenitors into S-phase. Angiotensin I-Converting Enzyme (ACE) has two homologous active NH2– and COOH-terminal domains and displays activity toward a broad range of substrates. The AcSDKP has been shown to be hydrolyzed by ACE and to be a preferential substrate for its NH2-terminal active site. In healthy subjects, the acute administration of the ACE inhibitor captopril increases the AcSDKP plasma levels. Several studies aimed to measure plasma or urine AcSDKP levels during treatment with various ACE inhibitors and to confirm its relevance as a marker of ACE inhibition.

References to Summary

References to acSDKP

  • Azizi M, Ezan E, Reny JL, Wdzieczak-Bakala J, Gerineau V, Menard J. Renal and metabolic clearance of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) during angiotensin-converting enzyme inhibition in humans. Hypertension. 1999 Mar;33 (3):879-86
  • Azizi M, Rousseau A, Ezan E, Guyene TT, Michelet S, Grognet JM, Lenfant M, Corvol P, Menard J. Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline. J Clin Invest. 1996 Feb 1;97 (3):839-44
  • Struthers AD, MacFadyen R, Fraser C, Robson J, Morton JJ, Junot C, Ezan E. Nonadherence with angiotensin-converting enzyme inhibitor therapy: a comparison of different ways of measuring it in patients with chronic heart failure. J Am Coll Cardiol. 1999 Dec;34 (7):2072-7
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