Evidence context
Preclinical research
Evidence is preclinical and expression/proliferation-readout level only, for exact Vesugen (Lys-Glu-Asp/KED). Supported-indirect in this record means Vesugen/KED was experimentally administered/exposed and Ki-67 (MKI67) expression/proliferation-associated readouts changed, without any physical molecular target engagement being shown. The primary source (PMID 25051766, Khavinson et al. 2014, Advances in Gerontology) reported that in tissue-specific cell cultures and dissociated vascular endothelial cell cultures, exact Vesugen/KED, studied alongside D-7, stimulated the aging-reduced proliferation-associated protein Ki-67; this finding is specific to Vesugen/KED and must never be read as transferring D-7's effects to Vesugen. The same publication used molecular docking to model a possible interaction of Vesugen/D-7 with the MKI67 promoter; this docking result is computational/modeling only and does not establish physical promoter binding, DNA occupancy, direct genomic target engagement, or chromatin occupancy. The supporting source (PMID 27259496, Linkova et al. 2016, Bulletin of Experimental Biology and Medicine) studied aging skin fibroblast cultures by immunofluorescent confocal microscopy and reported that KE, KED, AED, and AEDG all increased Ki-67 and CD98hc expression and reduced MMP-9 synthesis; KED is legitimately included in this group-wide Ki-67 result, but caspase-dependent apoptosis suppression was reported only for AED and AEDG and must never be attributed to KED, nor may any other KE/AED/AEDG-specific finding be transferred to KED. Both core studies share overlapping authorship and institutional lineage (Khavinson and the broader St. Petersburg bioregulator research program) and represent two distinct preclinical cultured-cell contexts from the same broader research lineage, not independent replication across unrelated laboratories. No direct Vesugen-Ki-67 protein binding, direct Vesugen-MKI67 promoter binding, promoter occupancy, direct Vesugen-DNA binding, or chromatin occupancy is established by either source. No human vascular-rejuvenation, atherosclerosis-treatment/prevention, restenosis-treatment, erectile-dysfunction-treatment, improved-human-circulation, anti-aging/longevity, neuroprotection/Alzheimer's-treatment, clinical-endothelial-restoration, safety, or approved-treatment claim is established by this record.
