Peptide Library

A "matrikine" — a fragment of a matrix protein that signals to fibroblasts to make more collagen, fibronectin and glycosaminoglycans, as if repairing a wound

pal-GHK is proposed to signal collagen and matrix rebuilding; pal-GQPR is proposed to damp the skin's production of the inflammatory messenger interleukin-6, which otherwise accelerates matrix breakdown

Proposed to compete with SNAP-25 in the SNARE complex that nerve endings use to release acetylcholine, slightly reducing the muscle signal that forms expression lines — a far milder, reversible version of what botulinum toxin does

Proposed to block the muscle-type nicotinic acetylcholine receptor on the muscle side of the junction, so the muscle responds less to nerve signals — the opposite side of the junction from Argireline-type peptides

Proposed to activate enkephalin (opioid) receptors on nerve endings, which lowers calcium entry and so reduces the amount of acetylcholine released at the neuromuscular junction

Reversibly inhibits tyrosinase, slowing production of new melanin so that existing pigment fades with normal skin turnover — without killing pigment cells

Blocks CXXC5 from binding Dishevelled, removing a natural brake on Wnt/β-catenin signalling in hair follicles and skin, which in mice re-activates follicle growth and wound-induced hair formation

A "matrikine" — a fragment that mimics a piece of broken-down collagen and signals fibroblasts to make new collagen, fibronectin and hyaluronic acid

Reported to dampen production of interleukin-6 (IL-6), an inflammatory messenger that rises with age and UV exposure and drives collagen breakdown

Designed to mimic the part of thrombospondin-1 that switches on latent TGF-β, the main growth factor that tells fibroblasts to make collagen; also claimed to inhibit collagen-degrading MMPs

Reported to inhibit angiotensin-converting enzyme (ACE) locally, improving microcirculation and fluid drainage under the eye, and to reduce glycation of collagen

GHK: signals fibroblast repair and binds copper already present in skin; GPO: acts as a collagen "building block" and matrikine signal to fibroblasts

Reported to delay cellular senescence in fibroblasts and keratinocytes and to increase firmness-related matrix proteins; marketed as a "firming" and "anti-ageing" peptide

Activates MC1R on melanocytes to increase melanin (especially the brown-black eumelanin) and, in the same pathway, dampens inflammatory signalling and supports DNA-repair responses

Both reduce melanin production upstream of tyrosinase: oligopeptide-68 by lowering MITF (the master pigment-gene switch); nonapeptide-1 by stopping α-MSH from binding its receptor

Peptides are meant to anchor and nourish the follicle (matrix proteins, microcirculation); the plant partners (apigenin, oleanolic acid; biochanin A) are meant to reduce DHT formation and inflammation around the follicle

EGF drives keratinocyte and fibroblast proliferation and migration via the EGF receptor; bFGF drives fibroblast proliferation, collagen synthesis and new blood-vessel growth via FGF receptors

Potently and selectively inhibits the neutrophil enzymes elastase and proteinase 3, limiting tissue destruction; also has antimicrobial, anti-inflammatory (NF-κB-dampening) and immune-modulating actions