Angiotensin (1-7) vs Cortagen

Binds Mas receptor (MasR), activating nitric oxide synthase and reducing oxidative stress. Opposes TGF-β and angiotensin II signaling to reduce fibrosis. Enhances insulin sensitivity and provides cardiovascular protection.

Angiotensin-(1-7) [Ang-(1-7)] is an endogenous heptapeptide hormone generated primarily through cleavage of angiotensin II by ACE2, functioning as a counter-regulatory arm of the renin-angiotensin system (RAS) by binding the Mas receptor to promote vasodilation, anti-fibrotic, anti-inflammatory, and cardioprotective effects that oppose the vasoconstrictive actions of angiotensin II. Ang-(1-7) acts through the ACE2/Mas receptor axis to reduce oxidative stress, attenuate NF-kB-mediated inflammation, and suppress TGF-beta fibrosis signaling; the ACE2/Ang-(1-7)/Mas axis has emerged as a key regulatory pathway in cardiovascular and metabolic disease, and gained renewed research attention given ACE2's role as the SARS-CoV-2 entry receptor. A Phase 1-2 randomized clinical trial of Ang-(1-7) infusion in COVID-19 ICU patients reported preliminary safety, tolerability, and dose-response data, providing the primary indexed human pharmacokinetic evidence; broader cardiovascular protective applications are supported by preclinical data but have not been established by completed Phase 3 trials. Ang-(1-7) has no FDA approval and no approved therapeutic indication in any jurisdiction; it is an endogenous peptide under active clinical investigation as a candidate for cardiovascular, metabolic, and inflammatory conditions, with emerging human safety data but an incomplete evidence base for any specific approved clinical use.

Brain cortex-derived tetrapeptide that modulates gene expression in neural and cardiac tissue through chromatin regulatory mechanisms; microarray analysis demonstrates broad transcriptional effects following administration.

Cortagen is a synthetic tetrapeptide (Ala-Glu-Asp-Pro) classified as a Khavinson-class bioregulator derived from cerebral cortex tissue, investigated for gene expression regulatory effects in neural and cardiac tissue. As a Khavinson-class bioregulator, cortagen is proposed to modulate transcriptional activity in aging target tissue by interacting with gene regulatory elements; microarray analysis of cardiac gene expression following cortagen administration has demonstrated broad effects on transcriptional profiles across multiple functional gene categories, suggesting tissue-regulatory activity beyond its cortical tissue origin. Published research on Khavinson-class peptides has further characterized the systematic gene expression regulatory potential of short bioregulator peptides across tissue types, providing the mechanistic context within which cortagen's transcriptional effects are interpreted. Cortagen has no FDA approval or regulatory approval in any major Western jurisdiction; evidence derives from Khavinson-series preclinical studies with no independent clinical trials published in Western-indexed journals. Cortagen benefits investigated in preclinical research include neuroprotective effects in neural tissue, cardiovascular gene expression modulation, and support for vascular wall integrity in aged animal models. As a brain cortex-derived Khavinson bioregulator, cortagen is proposed to regulate transcription in neural and cardiac tissue through chromatin-level mechanisms, potentially preserving tissue-specific gene expression patterns that decline with aging. Research interest encompasses cortagen's role in neurological aging, post-ischemic brain tissue recovery in preclinical models, and combined bioregulator protocols that pair cortagen with cardiovascular and metabolic peptides for comprehensive longevity applications. Cortagen is a research compound with no regulatory approval in any jurisdiction; evidence is limited to preclinical studies and Russian clinical research literature, with no independent randomized trials published in Western peer-reviewed journals.