Melanotan 1 Dosage Chart & MT-1 Protocols: What the Approved Afamelanotide Product Actually Doses

Melanotan I at a glance

What it is

Melanotan 1, also written MT-1 or MT-I, is afamelanotide — a synthetic analogue of alpha-melanocyte-stimulating hormone and a melanocortin-1 receptor (MC1-R) agonist. PubChem CID 16197727, molecular formula C78H111N21O19, molecular weight 1646.8 g/mol.

It is an approved drug

Afamelanotide is approved and marketed as SCENESSE (Clinuvel), indicated to increase pain-free light exposure in adult patients with a history of phototoxic reactions from erythropoietic protoporphyria (EPP). It is the only alpha-MSH analogue approved for any indication.

Approved dose

One 16 mg implant, repeated every 60 days in the pivotal trials — a solid, white to off-white, bioresorbable sterile rod approximately 1.7 cm long and 1.45 mm in diameter, inserted subcutaneously by a health care professional trained in the implantation procedure. It is not a solution, not a syringe, and not self-administered.

So what is the 'correct' MT-1 dose?

There is no published per-injection dose, because the tested product is not injected. A 16 mg implant releasing over roughly two months and a daily subcutaneous injection of a few hundred micrograms are different exposures by a different route on a different schedule. No dosage chart on any site derives from a trial.

Commonly reported figures

Community reports describe roughly 250-1000 mcg subcutaneously, often front-loaded then reduced. These are reported observations of practice, not trial-derived values, and no published human study establishes them.

What the trials measured

Two multicentre, randomised, double-blind, placebo-controlled trials of 16 mg implants every 60 days in EPP patients — 74 in the EU and 94 in the US — with hours of pain-free direct sunlight as the primary endpoint (PMID 26132941). Tanning was not the endpoint; photoprotection was.

Plasma half-life

No published figure for injected melanotan 1 — the compound was developed as a controlled-release implant, so the pharmacokinetics that were characterised belong to the implant, dosed every 60 days in the trials. Pigmentation also outlasts the drug: melanin turnover, not clearance, sets how long the visible effect persists.

Documented risk of the unregulated form

A review of unregulated melanotan I and II use records melanocytic changes in existing moles and new dysplastic naevi, and four case reports of melanoma arising from existing moles during or shortly after use (PMID 28266027). The review notes conclusive causal evidence is lacking — but this is the specific, documented concern, and it is dermatological rather than systemic.

Registered trials

23 studies list afamelanotide as an intervention on ClinicalTrials.gov — an unusually well-studied compound for this library, and all of it on the implant.

Reported ranges from research/community — examples, not recommendations.

What it is / mechanism

Melanotan 1 is an analogue of alpha-melanocyte-stimulating hormone, the endogenous peptide that drives pigmentation. It acts as an agonist at the melanocortin-1 receptor on melanocytes, and MC1-R activation shifts melanin synthesis toward eumelanin — the darker, more photoprotective pigment — rather than pheomelanin. Increased eumelanin in the epidermis absorbs and scatters ultraviolet and visible light before it reaches deeper structures, which is the basis of both the cosmetic effect people seek and the medical effect the approved product is licensed for. The distinction between those two effects is the whole clinical story. In erythropoietic protoporphyria, protoporphyrin IX accumulates and is activated by light in the visible violet range, producing severe phototoxic pain after minutes of exposure. Increasing epidermal eumelanin raises the threshold at which that reaction begins. The approved indication is therefore phrased as increasing pain-free light exposure — not as tanning, and not as protection against ultraviolet damage generally. The structural point that matters pharmacologically is why an analogue was needed at all. Native alpha-MSH is a short-lived peptide, and melanotan 1 is the substituted version designed to survive long enough to be useful. Its receptor selectivity is also more focused than its better-known relative: melanotan 2 is a cyclic, less selective melanocortin agonist that engages MC3-R and MC4-R appreciably, which is the source of the effects on appetite and sexual function that melanotan 2 is discussed for and melanotan 1 largely is not. Compounds sold under adjacent names here are genuinely different molecules with different receptor profiles, not strengths of one product. One consequence of the mechanism deserves stating because it is routinely inverted in marketing copy. Pigmentation is a threshold effect, not an armour: the trials measured how long patients could stay in direct sunlight before pain began, and the label's indication is written in those terms. A compound that raises a pain threshold in a photosensitivity disorder has not been shown to prevent photodamage in people without one.

Researched effects

The human evidence here is better than for almost anything else in this library, and it is all about photoprotection in a rare disease. The pivotal work is two multicentre, randomised, double-blind, placebo-controlled trials of subcutaneous implants containing 16 mg of afamelanotide, published together (PMID 26132941). Seventy-four patients in the European Union and ninety-four in the United States were randomised 1:1 to afamelanotide or placebo implants every 60 days — five implants in the EU study and three in the US study, across 180-day and 270-day study periods. The primary efficacy endpoint was the number of hours of direct sunlight exposure without pain. Type and duration of sun exposure, number and severity of phototoxic reactions and adverse events were recorded, quality of life was assessed with validated questionnaires, and a subgroup of US patients underwent photoprovocation testing. A later regulatory-focused review (PMID 26979527) summarises the same programme plus the phase III trial CUV039, in which afamelanotide improved light tolerance: patients spent more time in direct sunlight without pain compared with placebo, and took longer to develop the first symptoms of phototoxicity under a standardised light source. It was generally well tolerated with no drug-related serious adverse events reported in that trial; the commonly occurring adverse reactions were headache and implant-site reactions. The FDA label records that safety was evaluated across three randomised, multicentre, prospective, vehicle-controlled trials (CUV029, CUV030 and CUV039). What none of this establishes is the thing most people arrive looking for. No trial measured cosmetic tanning as an outcome, none studied people without EPP, and none administered the compound as a reconstituted subcutaneous injection. The evidence is real, substantial and specific — and it is evidence about a 16 mg implant in a photosensitivity disorder. On the unregulated form, the published record is not silent, and it is not reassuring. A 2017 review of unregulated alpha-MSH analogue use (PMID 28266027) notes that afamelanotide is the only alpha-MSH analogue approved for any medical indication and has been thoroughly tested, while the illegal melanotans are likely risky for several distinct reasons: uncertainty about preparation, administration and dosage, and an increasing number of case reports of cutaneous complications — particularly melanocytic changes in existing moles and newly emerging dysplastic naevi. Four case reports describe melanomas emerging from existing moles either during or shortly after melanotan use. The review is careful that conclusive evidence linking the two is lacking, and that caution should be reported alongside the finding rather than dropped from it.

Dosage — reported ranges (overview)

The arriving question is almost always some form of 'what is the MT-1 dosage chart', and the honest answer is more useful than a number: the only dose ever established for this compound belongs to a product that is not injected. The approved dose is one 16 mg implant, inserted subcutaneously, with the pivotal trials repeating it every 60 days. That is a controlled-release solid delivering its content over roughly two months. It is administered by a health care professional trained in the implantation procedure, not self-administered. There is no milligram-per-injection figure on the label because the label does not describe an injection. Community reports for the reconstituted product describe roughly 250-1000 mcg subcutaneously, frequently as a higher 'loading' period followed by less frequent maintenance. Those figures are reported practice. They are not derived from any published human study, and they cannot be reconciled with the implant by arithmetic: 16 mg released gradually over 60 days is not equivalent to 250 mcg injected as a bolus, because the route, the release profile and the resulting concentration curve all differ. Dividing one by the other produces a number with no pharmacological meaning. That is why the dosage charts circulating for MT-1 disagree with each other. They are not competing readings of a trial; there is no trial for them to read. One further point specific to this compound, because it changes what a 'beginner protocol' means. The endpoint that mattered in the trials was a threshold for phototoxic pain in a disease, reached with a defined, professionally administered implant, in patients under clinical supervision with dermatological monitoring. The documented concerns with unregulated use are dermatological — changes in existing moles and new dysplastic naevi (PMID 28266027) — which is exactly the kind of risk that a dose figure does not address and clinical skin monitoring does. Nothing here is a recommendation, a protocol, or an endorsement of any amount. The published dose is stated because it exists; the reported figures are stated because they are what circulates.

A printable protocol sheet with a reconstitution reference and an injection log comes with All-Access Lifetime.

Reconstitution — bac-water math

Reconstitution is only concentration math, not a personal dose. Add bacteriostatic water to the lyophilised vial and the concentration in mcg/mL equals total peptide (mcg) divided by the water volume (mL). On a U-100 insulin syringe, 100 units equals 1 mL, so units to draw = (amount in mcg / concentration in mcg/mL) x 100. The table uses a 10 mg (10,000 mcg) vial, the common presentation, with two reported example amounts. Every row has been checked against the 100-unit ceiling of a 1 mL U-100 syringe and all draw within it. Note what the arithmetic itself shows: even the largest row here is 30 units of a 3,333 mcg/mL solution — 1 mg — while the approved product contains 16 mg in a single implant. The table converts a vial; it does not convert a trial.

This is concentration math, not a dose recommendation.

Injection / administration basics

The approved product is not injected at all: SCENESSE is implanted subcutaneously above the anterior iliac crest by a trained health care professional using a cannula, as a solid bioresorbable rod. Anyone reasoning from the label should start there, because it is the only administration route with published human outcome data behind it. For the reconstituted vials sold for research use, community reports describe subcutaneous injection with a U-100 insulin syringe and rotation of sites. Reported practice also commonly describes taking the injection in the evening; no published study supports timing as a variable. The practical difference between the two is not a detail. A bioresorbable implant releases its content gradually over weeks — the trials repeated it every 60 days — whereas an injected bolus produces a peak and a decline. Effects, duration and the rate at which pigmentation develops all follow from that curve, so protocols built by converting the implant's milligrams into injections are converting between two things that behave differently. No route, dose or schedule is recommended here.

Half-life & frequency rationale

There is no widely published plasma half-life for melanotan 1 administered as an injection, and the reason is structural rather than accidental: the compound's clinical development went down the controlled-release path, so the pharmacokinetics that were characterised are the pharmacokinetics of the implant. What can be stated from the approved product is the duration that matters clinically. The implant contains 16 mg in a bioresorbable rod, and the pivotal trials dosed it every 60 days (PMID 26132941), which sets the practical interval of effect at about two months per implant. The compound is a substituted analogue of alpha-MSH, and the substitutions exist because native alpha-MSH is rapidly degraded — so the analogue is materially longer-lived than the endogenous peptide. That is a direction rather than a number, and it should be quoted as one. A second point matters more than the half-life for anyone reading a protocol. The visible effect of this compound is not a plasma concentration; it is melanin synthesis, which develops and then fades on the timescale of skin biology rather than of peptide clearance. Pigmentation persists well beyond the presence of the drug. Any half-life figure, if one existed, would tell you when the compound had gone and almost nothing about when its effect had.

Stacking — overview

Melanotan 1 is discussed alongside melanotan 2 more often than with anything else, and the comparison is more useful than a stack. They are not the same compound at different strengths: melanotan 2 is a cyclic, less selective melanocortin agonist with meaningful activity at MC3-R and MC4-R, which is why the effects reported for it extend to appetite and sexual function, and why its reported side-effect profile differs. Melanotan 1 is the more selective MC1-R agonist and the one with an approved product behind it. No human study has examined melanotan 1 in combination with any other compound in this library. Combination use is reported practice with no measurement behind it, and this page does not describe protocols for it.

For how combinations are grouped by research context, the named blends, and why a pre-mixed blend vial cannot be calculated from its total milligrams, see the peptide stacks guide.

Storage & handling

• Lyophilised vials are typically stored refrigerated and protected from light; light exposure is a routine degradation route for peptides and this one is handled in the context of light sensitivity.
• After reconstitution with bacteriostatic water, storage is refrigerated. The 0.9% benzyl alcohol in bacteriostatic water is the preservative that makes multiple withdrawals from a single vial possible; sterile water contains no preservative.
• Avoid repeated freeze-thaw cycles, which degrade peptides independently of the compound.
• Label the vial with the reconstitution date and the concentration in mcg/mL — the concentration cannot be recovered by looking at the vial, and it is the input every unit calculation depends on.

Evidence File

The Melanotan 1 Evidence File: Eleven Registered Trials That Never Reported

Melanotan 1 is the rare compound in this library with an approved product, a complete registry footprint and a thirty-year publication history behind it. That abundance is the problem. The most-quoted figures come from four different official sources that do not agree with one another, and several of them describe measurements that were never designed to be compared. This module rebuilds the public record from primary sources fetched directly on 2026-08-26: all twenty-three ClinicalTrials.gov records with their posted results tables, the current FDA prescribing information, and the origin pharmacology the modern implant programme replaced. It reports what each source holds, and names the exact search behind every stated absence.

• 23 registry records enumerated, every one filed by a single sponsor
• 11 of 23 registered trials carry no posted results
• 5 circulating figures traced to origin, 3 wrong as usually stated
• Published human injection doses run 22 to 59 times the reported low end

Sourcing File

The Melanotan 1 Sourcing File: The 17.96 Dalton Gap That Looks Like Water

This compound is easier to identify than almost anything else in the library and harder to quantify than most. Its approved label publishes the salt form and the exact free-base-to-salt ratio, which turns the usual guesswork about net peptide content into arithmetic that can be done line by line. Its nearest structural relative, meanwhile, sits a distance from it that a low-resolution instrument reads as an ordinary artefact rather than as the wrong molecule. This module works through the identity numbers, the substitution modes specific to the melanocortin family, the salt arithmetic, and a certificate read field by field.

• Neutral monoisotopic 1645.8365 Da against an average weight of 1646.8
• 17.96 Da separates this peptide from native alpha-MSH; water is 18.01
• The approved label puts 16 mg free base at 18 mg of acetate salt
• A nominal 250 mcg draw from an acetate-salt vial holds about 222 mcg

Benefit & Outcome Review

The Melanotan 1 Benefit and Outcome Review: Three of Eight Sites, and the Samples Underneath

The claims made for this compound divide cleanly into three groups: one that human measurement supports, one that human measurement supports only inside a rare disease, and one that belongs to a different molecule entirely. This module grades each on what was measured, in whom, against what comparator and for how long, keeping human, registry and label evidence separate and naming the sample size beside every effect size. It includes the decay curve that can be reconstructed from a registry results table, the non-response figures the source papers state about themselves, and the single most actionable line in the approved label's warnings.

• Tanning reached significance at 3 of 8 measured anatomic sites
• Forearm eumelanin rose 98 percent; the ratio shift itself was P = 0.054
• One implant's melanin gain had largely decayed by Day 120
• 0 human trials of this molecule for appetite or sexual function

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