# GHK-Cu dosage as the studies recorded it, model by model and route by route > GHK-Cu Dosage in the Research Literature: Concentrations, Routes and Models — What concentrations and routes GHK-Cu studies actually used, model by model — fibroblast culture, rodent intranasal and IP, topical formulations — plus stability and the pharmacokinetic gap. **DOSING RECORD // BY MODEL** A log of study parameters, not a protocol. No human dose exists for this compound outside topical cosmetic formulation. ## The short version on doses This page lists what researchers gave to cells and animals, and at what strengths. It is a record of study parameters. It is not a protocol, and there is no human GHK-Cu dose to give — outside cosmetic creams, no health authority anywhere has approved this compound for anything. A few things are worth knowing up front. The amounts that work on cells in a dish are astonishingly small — a billionth of a mole per litre, not milligrams [1]. Skin creams sit in the 0.05% to 2% range by weight. Rodent brain studies used a nose-drop at 15 mg/kg of body weight [7][8]. And nobody has ever measured how long GHK-Cu lasts in a human body; the closest data is a rat study showing the bare peptide vanishing from blood quickly [11]. Community injection routines have no published basis at all. ## Concentrations and routes recorded across models The parameters below are what each cited or corpus-recorded study administered. Species and route are stated because they are not interchangeable. - **Human fibroblast culture (in vitro, medium):** 10^-12 to 10^-9 M. Collagen synthesis onset between 10^-12 and 10^-11 M, maximum near 10^-9 M [1]. - **Topical cosmetic and clinical formulations:** approximately 0.05% to 2% (w/w) in creams, serums and gels. - **Mouse pulmonary emphysema (intraperitoneal):** 0.2, 2 and 20 ug/g/day on alternate days. - **Mouse pulmonary fibrosis (intraperitoneal):** 2.6, 26 and 260 ug/mL/day. - **Mouse silicosis (intraperitoneal):** 2 and 20 mg/kg. - **Mouse DSS-colitis (oral gavage):** 20 mg/kg daily. - **Aging and Alzheimer mouse cognition (intranasal):** 15 mg/kg daily for eight weeks in 20-month-old mice [7]; 15 mg/kg three times weekly for twelve weeks in 5xFAD mice [8]. - **Rat behavioural studies (intraperitoneal):** approximately 0.5 ug/kg to 0.5 mg/kg, in the anxiolytic [10] and pain-induced aggression [12] models. - **Human hair-loss randomised trial (topical, combination formulation):** 50 mg/mL and 100 mg/mL of a 5-aminolevulinic acid plus GHK complex over six months [4]. - **In vitro CNS assays:** GHK applied directly to cultured neurons, microglia and astrocytes [15]; 0-30 uM for the biotinylated-GHK antioxidant and antiglycant work [9]. Routes represented across the record: topical in many vehicles — cream, serum, liposome, nano-lipid carrier, ionic-liquid microemulsion, wound dressing and hydrogel, nanofiber; intraperitoneal for rodent systemic work; intranasal for rodent cognition; oral gavage for rodent colitis; intravenous and subcutaneous for rodent pharmacokinetics; and intradermal or dermal infusion by microneedle in hair studies. The span from 10^-9 M in a dish to 15 mg/kg in a mouse is not a contradiction. They are different questions: the first is what concentration a fibroblast responds to at its membrane, the second is what body-weight-scaled amount has to be administered upstream to get some fraction of it to a target. ## The pharmacokinetic gap, stated plainly No rigorous human pharmacokinetic half-life has been published for GHK-Cu. That sentence is the most important one on this page. What exists is a rat HPLC study establishing that GHK is rapidly metabolised in plasma to the dipeptide histidyl-lysine after intravenous administration, with detection limits of 50 ng/mL for GHK and 15 ng/mL for HK [11]. That is consistent with rapid peptidase clearance of the free 340.38 Da tripeptide. Secondary literature cites a short systemic elimination half-life on the order of one to two hours, with the copper-chelated complex more stable than free GHK — but that is secondary literature, not a measured human value. Topical behaviour is better characterised, because it was directly measured: about 97 ug/cm^2 of copper retained in human skin as a dermal depot over 48 hours, with 136.2 ug/cm^2 permeated and a permeability coefficient of 2.43 x 10^-4 cm/h [5]. A depot means prolonged local availability, which is a formulation fact rather than a systemic one. The consequence is unavoidable: injectable or systemic protocols circulating in community contexts have no peer-reviewed human pharmacokinetic basis. There is no Cmax, no bioavailability figure, no tissue-distribution map. A protocol without those is a guess with units on it. ## Formulation and stability parameters Because this compound is a metal complex rather than a plain peptide, its handling conditions are part of its dosing record. The complex has a very high copper stability constant, log K around 16.4, far higher than free GHK, which limits pro-oxidant free-copper release. It is most stable near pH 5 to 6.5 at a 1:1 copper-to-peptide ratio. The blue-violet colour of a reconstituted solution is the expected Cu(II) d-orbital absorption and indicates an intact complex; brown or green shifts indicate oxidation or precipitation. Strong reducing agents break it. Ascorbic acid below about pH 3.5 reduces the Cu(II) and dismantles the complex, and AHAs, BHAs and other low-pH actives can destabilise it or compete for the copper [14]. Delivery enhancement is an active research problem rather than a solved one. Free GHK is highly hydrophilic at clogP -2.24, which limits passive stratum-corneum penetration; palmitoylation raises Pal-GHK to clogP 1.14, and liposomal encapsulation, ionic-liquid microemulsions and microneedle pretreatment have all been evaluated — microneedling moved roughly 134 nmol of GHK where intact skin passed none [14]. These are early-stage enhancement strategies, reported as such. ## What human clinical dosing does and does not exist Human evidence is predominantly topical and dermatologic. It consists of small placebo-controlled facial cream and serum trials with roughly 20 to 71 participants, reporting improved skin density, firmness, fine lines and wrinkle depth [3], and one six-month randomised hair-loss trial in 45 men using a combination 5-ALA plus GHK complex, which reported significant hair-count gains against placebo [4]. There are no completed Phase 2 or Phase 3 trials for systemic or injectable GHK-Cu. A topical wound-healing trial has been registered. There is no FDA- or EMA-approved therapeutic indication for GHK-Cu by any route; topical Copper Tripeptide-1 is a legal cosmetic ingredient in the US, EU and UK, and injectable or oral systemic formulations are unapproved research chemicals with no established regulatory pathway. On athletic-testing status: GHK-Cu is not currently listed on the WADA Prohibited List as of the 2024-2025 lists, which distinguishes it from BPC-157 and TB-500. WADA's catch-all S0 category can cover non-approved pharmacological substances, so the current list is the only reliable check. What this page cannot supply, and will not: a human dose, a schedule, a titration, or a route recommendation. The reported experiences and the [copper peptide side effects](/effects) are documented separately, without doses attached, exactly because attaching one would turn a record into instructions. --- A readout panel over the GHK-Cu literature: every figure pinned to the study that measured it, every preprint marked as one, and nothing here dosed, diagnosed, prescribed or sold.