Cellular Health

An endogenous copper-binding tripeptide (glycyl-L-histidyl-L-lysine complexed with copper(II)) first isolated from human plasma in 1973. GHK-Cu has the broadest gene-expression footprint characterised for any small research peptide — genome-wide microarray studies catalogue approximately 4200 human genes significantly modulated at physiological concentrations. Mechanistically, GHK-Cu functions as a copper-delivery vehicle: the tripeptide chelates and delivers copper into cells, where copper acts as an essential cofactor for enzymes involved in extracellular matrix synthesis, angiogenesis, antioxidant defense, and DNA repair. Approved and marketed for topical cosmetic use in many jurisdictions; not FDA-approved for systemic therapeutic indications.

Glutathione is a tripeptide of glutamate, cysteine and glycine, distinguished from most other peptides by a non-standard γ-carboxyl bond linking glutamate to cysteine that protects the molecule from routine peptidase degradation. It is present at millimolar concentrations in essentially every human cell, where it is the primary intracellular thiol antioxidant. Its cysteine thiol (-SH) group reduces reactive oxygen species directly; it conjugates with toxins and xenobiotics via glutathione S-transferase for hepatic Phase II export; it recycles oxidised vitamin C and vitamin E back to their active forms; it supports T-cell proliferation and NK-cell cytotoxicity; and it inhibits tyrosinase, the enzyme that catalyses the rate-limiting step of melanin synthesis — the mechanistic basis for glutathione's cosmetic skin-lightening effect at sustained doses. Oral glutathione has weak bioavailability; liposomal and sublingual formulations claim to improve absorption. Injectable IV or subcutaneous glutathione is used off-label for cosmetic skin lightening in several jurisdictions, a use that regulators including the Philippines FDA have specifically warned against for safety reasons.

A 16-amino-acid peptide encoded within a short open reading frame in the mitochondrial 12S ribosomal RNA gene — one of a small class of 'mitochondrial-derived peptides' whose defining feature is that they originate from the mitochondrial genome rather than the nuclear genome. First characterised by Lee, Cohen and colleagues at USC in 2015. Proposed to function as a mitochondrion-to-nucleus retrograde signal, with reported downstream activation of AMP-activated protein kinase (AMPK) and modulation of glucose metabolism and insulin sensitivity. Preclinical work in mice describes exercise-mimetic effects on skeletal muscle glucose handling and running capacity. Human data are dominated by circulating-level correlational studies (levels lower in aged, obese, and diabetic populations); no completed phase-2 or phase-3 interventional trial of exogenous MOTS-c in humans has been published.

NAD+ (nicotinamide adenine dinucleotide, oxidised form) is a pyridine-nucleotide coenzyme — chemically a dinucleotide, not a peptide. It sits at the centre of cellular redox biology: NAD+ / NADH cycling drives ATP production through the electron transport chain, and NAD+ is the required substrate for the sirtuin family of deacetylases (SIRT1–7) that regulate gene expression, mitochondrial biogenesis (via PGC-1α), inflammation and DNA-damage responses. NAD+ is also consumed by PARP-1 during DNA-strand-break repair and by CD38 during immune-cell signalling. Endogenous NAD+ levels decline with age, and this decline is thought to contribute to reduced sirtuin activity, mitochondrial dysfunction and impaired DNA repair. Injectable NAD+ has no FDA-approved therapeutic indication; its metabolic precursors (nicotinamide riboside — NR, nicotinamide mononucleotide — NMN) are widely sold as oral supplements. The compound is included in this catalog because the Healthy Mango PDF covers it alongside peptides, not because it is one.

A synthetic aromatic-cationic tetrapeptide originally developed by Hazel Szeto and Peter Schiller at Cornell University. Unlike most peptides, elamipretide concentrates in the inner mitochondrial membrane at 1,000-fold higher levels than in cytoplasm, where it binds cardiolipin — the phospholipid that stabilises cristae architecture and holds the electron-transport-chain complexes together. Cardiolipin binding stabilises cristae structure, preserves supercomplex assembly, restores efficient ATP synthesis and reduces reactive-oxygen-species leakage. Licensed to Stealth BioTherapeutics, elamipretide has been developed through a phase-3 randomised placebo-controlled trial (TAZPOWER) in Barth syndrome — a rare X-linked disorder of the cardiolipin remodelling enzyme tafazzin — and subsequently received FDA approval as Forzinity for that indication.