KED: The Vascular Bioregulator

KED is a tripeptide vascular bioregulator with documented effects on endothelial cell function. Published research describes its role in connexin 43 gap junction restoration, endothelin-1 normalization, SIRT1 upregulation, and synergistic action with GHK on the endothelial nitric oxide synthase (eNOS) pathway.

Endothelial gap junction restoration

Published research documents KED's effect on connexin 43 expression in aging vascular endothelial cells. Gap junction restoration is a mechanism associated with improved cell-to-cell signaling and barrier integrity in the vascular wall.

SIRT1 upregulation

KED administration is associated with upregulation of SIRT1, a sirtuin family deacetylase implicated in cellular longevity, mitochondrial biogenesis, and metabolic regulation.

Synergy with GHK

Co-administration of KED and GHK in research models has demonstrated synergistic effects on the endothelial nitric oxide synthase pathway, supporting nitric oxide bioavailability and downstream vasodilation signaling.

Molecular weight and delivery

At 390 Daltons, KED falls below the 500 Dalton threshold for passive transdermal penetration. The compound is one of three actives in HelioMend formulations.

Citations

  1. Khavinson VKh et al. Vascular bioregulator peptide series. St. Petersburg Institute of Bioregulation and Gerontology.
  2. eNOS pathway and KED co-administration research. Khavinson Institute publications.
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