Categories
Skin & Pigmentation Research
Compounds studied for dermatological outcomes and pigmentation biology.
This category groups compounds researched for effects on skin biology — cosmetic-dermatology endpoints, wound-associated skin remodelling, or melanocortin-driven pigmentation pathways.
Cosmetic-dermatology research does not translate to safety in prolonged unsupervised systemic use. Melanocortin agonists in particular have systemic effects beyond pigmentation, and unregulated supply chains carry additional risk. Read each compound's Safety card carefully.
Educational content only.
Compounds in this category
7 compounds in this category
Aura
Repair & RegenerationResearch BlendPreclinical EvidenceA three-component research blend combining GHK-Cu 50 mg, BPC-157 10 mg and KPV 10 mg in a single lyophilized vial (70 mg total). The three components address distinct but complementary layers of tissue repair: GHK-Cu modulates the expression of thousands of genes involved in ECM remodelling, collagen and elastin synthesis, angiogenesis and scarless healing; BPC-157 supports VEGF-driven angiogenesis, fibroblast migration and collagen production at the repair site; and KPV suppresses the NF-κB inflammatory pathway that would otherwise antagonise the ECM and vascular repair activities of the other two components. At the reference reconstitution (5 mL bacteriostatic water → 10 mg/mL GHK-Cu + 2 mg/mL BPC-157 + 2 mg/mL KPV) and 0.2 mL injection volume, all three components fall within their individually-established therapeutic ranges — a distinguishing feature of Aura relative to other multi-component repair blends. No blend-specific FDA authorisation exists; the individual components have their own regulatory profiles (see the component compound pages).
Learn moreGHK-Cu
Repair & RegenerationModerate Human EvidenceAn 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.
Learn moreGlow
Repair & RegenerationResearch BlendPreclinical EvidenceA three-component research blend combining GHK-Cu 50 mg, BPC-157 10 mg and TB-500 10 mg in a single lyophilized vial (70 mg total). Structural repair with skin rejuvenation: GHK-Cu at the gene-expression / ECM signalling layer, BPC-157 at the vascular / fibroblast layer, and TB-500 at the cellular migration and cytoskeletal-remodelling layer. The mechanism story is complementary rather than redundant — each component addresses a distinct rate-limiting step in tissue repair. Relative to Aura, Glow substitutes TB-500 for KPV, trading inflammatory-environment control for cellular-migration capacity. The trade-off worth being honest about: at the 0.2 mL reference injection, TB-500 is delivered at maintenance levels rather than acute-injury loading levels. No FDA blend authorisation exists; the individual components have their own regulatory profiles.
Learn moreGlutathione (GSH)
Cellular HealthEarly Human EvidenceGlutathione 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.
Learn moreKlow
Repair & RegenerationResearch BlendPreclinical EvidenceA four-component research blend that combines all three peptide families addressed by the other repair blends plus the anti-inflammatory KPV component. Composition: GHK-Cu 50 mg + TB-500 10 mg + BPC-157 10 mg + KPV 10 mg = 80 mg total. The mechanism story covers all four rate-limiting layers of tissue repair: GHK-Cu at the gene-level ECM signalling layer, TB-500 at the cellular migration and cytoskeletal remodelling layer, BPC-157 at the vascular supply and fibroblast layer, and KPV at the inflammatory-environment control layer. In effect, Klow is Glow plus KPV — adding NF-κB pathway suppression to the three mechanistic components of Glow — and Aura plus TB-500 — adding cellular migration to the three components of Aura. It is the most comprehensive of the repair blends when all four components are available and the intended use warrants their combined effect.
Learn moreMelanotan I
Skin & Pigmentation ResearchModerate Human EvidenceA 13-amino-acid linear α-MSH analogue with two stabilising substitutions (norleucine at position 4 and D-phenylalanine at position 7) that greatly extend its half-life relative to native α-MSH. It is a potent melanocortin receptor agonist, and its clinical effect is mediated principally through the MC1R on melanocytes: MC1R activation drives conversion of the light red/yellow pigment pheomelanin to the darker, more photoprotective eumelanin, producing a controlled skin darkening that in erythropoietic protoporphyria (EPP) increases tolerance to sunlight. As afamelanotide (Scenesse), the compound is delivered as a 16 mg controlled-release biodegradable subcutaneous implant. It is authorised by the EMA (2014) and FDA-approved on 2019-10-08 for the reduction of phototoxicity in adult EPP patients.
Learn moreMelanotan II
Skin & Pigmentation ResearchPreclinical EvidenceA synthetic cyclic heptapeptide α-MSH analogue with broad activity across all four peripheral melanocortin receptor subtypes: MC1R (skin darkening via eumelanin), MC3R and MC4R (central sexual-response circuitry and appetite regulation) and MC5R (sebaceous / exocrine gland activity). It has never been approved by any regulator. It circulates as a grey-market cosmetic tanning and sexual-response peptide via research-supply channels, and multiple national regulators — including the UK MHRA, Norwegian Medicines Agency, Irish HPRA, and Australian TGA — have issued specific warnings against its cosmetic use. Its historical significance is as the research tool whose accidental sexual-response observation launched the Palatin bremelanotide programme.
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