PT-141, also called bremelanotide, is a synthetic cyclic heptapeptide in the melanocortin analog family. FDA records characterize bremelanotide as a nonselective melanocortin receptor agonist, while the compound’s lineage traces to the University of Arizona melanocortin program rather than an MC4R-exclusive design. Apex Laboratory supplies PT-141 as a research-grade chemical reagent for in-vitro and preclinical research, distinct from the Vyleesi pharmaceutical formulation.
PT-141 is frequently reduced to the phrase “MC4R peptide.” That label is too narrow. The current evidence record spans a historical melanocortin analog program, multi-receptor pharmacology, preclinical model work, clinical development of a specific finished drug, and an FDA approval that belongs to Vyleesi—not to every material labeled PT-141.
- PT-141 and bremelanotide are names for the same active molecule, but a research reagent and Vyleesi are categorically different products.
- FDA review describes bremelanotide as a nonselective melanocortin receptor agonist, not an MC4R-selective agonist.
- MC4R-centered animal models can test one mechanistic hypothesis without proving exclusive receptor selectivity.
- The lineage begins with cyclic α-MSH analog work by Sawyer, Hruby, Hadley, and colleagues at the University of Arizona College of Medicine.
- Palatin Technologies licensed and developed bremelanotide; FDA approved AMAG Pharmaceuticals’ Vyleesi NDA 210557 on June 21, 2019 as a 1.75 mg/0.3 mL subcutaneous autoinjector.
- Reagent identity is fixed and checkable: CAS 189691-06-3, C50H68N14O10, 1025.18 Da free base, Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-OH.
- Research-grade PT-141 holds no FDA, EMA, NMPA or other regulatory approval anywhere globally; the approval attaches to the finished drug alone.
- Analytical identity and purity evidence does not transfer Vyleesi’s formulation, label, safety, efficacy, or approved indication to a research material.
PT-141 / Bremelanotide at a Glance
| Field | Evidence-based record | Interpretation boundary |
|---|---|---|
| Common names | PT-141; bremelanotide | These identify the same molecule, not every formulation or quality system |
| Material class | Synthetic cyclic heptapeptide melanocortin analog | Related to the Melanotan program but not interchangeable with Melanotan II or afamelanotide |
| Receptor description | FDA: nonselective melanocortin receptor agonist | MC4R may be mechanistically important without being the only receptor engaged |
| Research lineage | University of Arizona College of Medicine melanocortin program; later licensed and developed by Palatin Technologies | Historical lineage does not collapse distinct analogs into one compound |
| Approved finished drug | Vyleesi, NDA 210557; approved June 21, 2019; 1.75 mg/0.3 mL single-dose subcutaneous autoinjector | The approval belongs to the named drug, sponsor, formulation, evidence package, and label |
| Apex material | Research-grade chemical reagent for qualified in-vitro and preclinical work | No FDA, EMA, NMPA or other approval in any jurisdiction; not a finished drug, and not for human or veterinary use or consumption |
What Are PT-141 and Bremelanotide?
PT-141 is the development code commonly used for bremelanotide. The active molecule is a synthetic cyclic heptapeptide melanocortin analog. “PT-141,” “bremelanotide,” and the active ingredient named in Vyleesi therefore point to the same molecule, but they do not make all physical materials equivalent.
Reagent identity record
| Identity field | Recorded value |
|---|---|
| CAS Registry Number | 189691-06-3 |
| Molecular formula | C50H68N14O10 (free base) |
| Molecular weight | 1025.18 Da free base; salt form is lot-specific |
| Sequence | Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-OH — side-chain lactam from Asp to Lys, N-terminal norleucine |
| C-terminus | Free acid (–OH). Melanotan II carries the corresponding amide (C50H69N15O9, 1024.20 Da) and is a separate molecule |
| Apex material specification (supplier-reported) | 10 mg lyophilized powder; ≥99% chromatographic purity by HPLC with mass-spectrometry identity confirmation. Supplier-reported catalog specification, not a literature or regulatory value; the lot certificate of analysis is the governing record |
Sources for the table: CAS Registry Number 189691-06-3 is the public registry identifier for bremelanotide; the formula and mass are internally consistent, since C50H68N14O10 computes to 1025.18 Da from standard atomic weights and the Melanotan II amide C50H69N15O9 computes to 1024.20 Da — the two differ by exactly the acid-to-amide substitution, which is why the C-terminus assignment and the formula have to agree. Fill quantity and purity are supplier values verified per lot on the certificate of analysis, not published or regulatory figures.
Native α-melanocyte-stimulating hormone is a 13-residue linear peptide, Ac-Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2.[1] Bremelanotide compresses that scaffold into a constrained six-residue lactam ring; neither potency nor receptor behaviour reads across.
A research reagent is evaluated through its own identity, lot, analytical record, and intended research scope; Vyleesi is a finished drug evaluated under NDA 210557 with a controlled formulation, prescribing information, and approved indication. Same molecule; categorically distinct regulatory frameworks.
PT-141 is likewise distinct from Melanotan II and afamelanotide: shared melanocortin ancestry, separate structures, development records, and regulatory outcomes. The Melanotan II research guide owns MT-II-specific identity and early-study context.
The University of Arizona Melanocortin Lineage
The foundational program took shape at the University of Arizona College of Medicine. In 1982, Sawyer, Hruby, Hadley, and colleagues reported a conformationally restricted cyclic α-melanocyte-stimulating hormone analog with superagonist activity.[1] That disulfide-cyclized analog, [half-Cys4,half-Cys10]-α-MSH, was reported at more than 10,000-fold the potency of the native hormone in darkening frog (Rana pipiens) skin in vitro, about 30-fold in lizard (Anolis carolinensis) melanophores, and about 3-fold in a cell-free Cloudman S-91 mouse melanoma membrane adenylate-cyclase preparation. The work established a structure–activity precedent for potent cyclic melanocortin analogs; it was not itself the complete PT-141 finished-drug record.
Hadley, Hruby, Blanchard, Dorr, and colleagues documented the discovery and development of Melanotan I and II in a 1998 review.[2] Hadley and Dorr’s 2006 historical synthesis then followed melanocortin peptide research through clinical studies and commercialization, recording that PT-141, described there as a new MT-II analog from Palatin Technologies, had initial phase I/II trials and was scheduled to enter pivotal stage III trials.[3] Neither review is cited here for an effect size: the Melanotan figures stay with the dedicated Melanotan II guide, and the 2006 synthesis reports no quantitative endpoint of its own. Palatin Technologies licensed the Arizona program and developed bremelanotide.
Is PT-141 an MC4R-Selective Agonist?
No. FDA’s review record for NDA 210557 — the multidisciplinary review and the risk assessment review — describes bremelanotide as a nonselective melanocortin receptor agonist, and the published record agrees that more than one subtype is engaged: the 2006 clinical report calls bremelanotide an agonist at melanocortin receptors MC3R and MC4R,[7] and the 2021 structural work describes the family as high in sequence similarity and low in agonist selectivity (PMID 34433901). No subtype rank order or exposure-level affinity value is asserted here. The official description is incompatible with a categorical “MC4R-selective” label.
The melanocortin family contains five receptor subtypes, MC1R through MC5R. These receptors differ in tissue distribution, endogenous ligands, physiological roles, and assay behavior. Bremelanotide’s receptor profile must therefore be interpreted as multi-receptor pharmacology. “Nonselective” does not mean that every receptor has identical affinity, efficacy, exposure, or downstream consequences.
Why, then, does MC4R appear so often? Animal and mechanistic studies have used central melanocortin models to test behavioral and physiological hypotheses, and Cone’s 2005 anatomical review of the central melanocortin system describes those pathways narratively and reports no quantitative result.[5] The 2003 study most often quoted here dosed the related analog MT-II, not bremelanotide. In awake male rats, intracerebroventricular, intrathecal and intravenous MT-II produced dose-dependent penile erection; intrathecal delivery to the lumbosacral cord was more efficacious than the intracerebroventricular or intravenous route; and intrathecal SHU-9119 blocked the intrathecal response while intracerebroventricular SHU-9119 did not. In a separate anesthetized-rat arm, intracavernosal MT-II neither raised intracavernous pressure nor augmented neurostimulated erectile responses; the abstract reports no quantitative endpoint for either arm — no dose, no group size, no effect size.[4] A model can show that an MC4R-linked pathway contributes to an observation. It cannot, by itself, erase activity at other receptor subtypes or prove an exclusive molecular target, and a result obtained with MT-II is not a bremelanotide result.
Additional reported findings
Each result below is stated as its own source reports it, with model and species attached.
| Source · compound | Model / species | Reported result | PMID |
|---|---|---|---|
| Hadley & Haskell-Luevano 1999 · POMC melanocortins | Review; POMC in pituitary, brain, skin and other peripheral sites | 31 kDa POMC precursor yields α-MSH, ACTH and endorphins acting at MC1R–MC5R | PMID 10816638 |
| Schiöth et al. 2005 · receptor subtypes | Receptors cloned from fish; vertebrate comparison | MC4R and MC5R structure conserved across vertebrates; early receptors favoured ACTH over shorter MSH peptides. The review reports no quantitative endpoint | PMID 15985310 |
| Tao 2010 · MC4R | Review; human genetics | MC4R cloned in 1993; over 150 human mutations reported, the commonest monogenic obesity cause | PMID 20190196 |
| Zhang et al. 2021 · bremelanotide, afamelanotide, α-MSH, THIQ | Structural study; full-length MC4R–Gs protein complexes | Four high-resolution structures resolved; conserved peptidic-agonist binding mode; receptor family described as high in sequence similarity and low in agonist selectivity | PMID 34433901 |
| Pfaus et al. 2007 · bremelanotide | Ovariectomised, hormone-primed female rats | Solicitations rose after subcutaneous dosing and after lateral-ventricle or medial-preoptic infusion, not ventromedial; lordosis and pacing unchanged. The overview reports no quantitative endpoint | PMID 17958619 |
| Yuan & Tao 2022 · neural MCR ligands | Review | Over 100 years of ligand work since 1916; bremelanotide grouped with approved receptor ligands | PMID 36291616 |
What Does the Bremelanotide Evidence Record Show?
Receptor and animal-model evidence
Preclinical studies positioned melanocortin pathways as central regulators in specific model systems. In female rats, PT-141 selectively increased solicitational behaviours without altering lordosis, pacing, motor activity, or sexual reward perception; the authors framed that work against desire disorders affecting an estimated 30% of women in North America and Europe.[6] Such rat data can identify a mechanism worth testing. It does not establish human efficacy, a finished-drug protocol, or a favorable benefit–risk profile.
Early human development
Clinical development then evaluated bremelanotide in defined human populations and controlled protocols. A 2006 double-blind crossover study gave a single 20 mg intranasal dose to 18 premenopausal women with female sexual arousal disorder: more reported moderate or high desire than on placebo (P = 0.0114), more were satisfied with arousal among those attempting intercourse within 24 hours (P = 0.0256), and vaginal pulse amplitude did not change significantly while participants viewed erotic videos.[7] That record is historically relevant, but its intranasal route, small sample, terminology, and endpoints are not interchangeable with the later approved indication.
Phase 3 Vyleesi program
The two identical RECONNECT Phase 3 trials randomised n=1,267 premenopausal women with hypoactive sexual desire disorder 1:1 to 24 weeks of as-needed subcutaneous bremelanotide 1.75 mg or placebo (efficacy population 1,202; mean age 39 years). Against placebo the integrated desire-domain score rose 0.35 (P<.001) and desire-related distress fell 0.33 (P<.001); nausea, flushing and headache each occurred in 10% or more of treated participants in both studies.[8] That population, protocol, formulation, and analysis belong to the program. They do not validate a separate research reagent.
What Exactly Did FDA Approve?
FDA approved Vyleesi under NDA 210557 on June 21, 2019. The approval letter was addressed to AMAG Pharmaceuticals. The 2019 Vyleesi prescribing information identifies a narrow indication: premenopausal women with acquired, generalized hypoactive sexual desire disorder characterized by low sexual desire that causes marked distress or interpersonal difficulty and is not due to a co-existing medical or psychiatric condition, relationship problems, or the effects of a medication or drug substance.
The approval does not establish a broad indication for sexual performance, does not apply to every study population in the development history, and does not approve research-grade PT-141 materials. It covered the named finished drug, its sponsor, manufacturing controls, formulation, delivery presentation, labeled population, and post-approval obligations.
Regulatory status, stated per material
| Material | Regulatory status |
|---|---|
| Vyleesi, bremelanotide 1.75 mg/0.3 mL autoinjector | FDA-approved June 21, 2019, NDA 210557, AMAG Pharmaceuticals; indication limited to acquired, generalized HSDD in premenopausal women |
| Research-grade PT-141 / bremelanotide reagent | No FDA, EMA, NMPA or other regulatory approval anywhere globally; no investigational status |
| Melanotan II | No marketing authorization in any jurisdiction |
| Afamelanotide (Melanotan I) | Separately FDA-approved as Scenesse in October 2019 for erythropoietic protoporphyria — different molecule, sponsor, and dossier |
How Should a PT-141 Research Material Be Evaluated?
A research-material assessment starts with exact identity and lot traceability, connecting the material name and lot to analytical evidence: HPLC purity under a stated method, and a mass-spectrometry result read against the 1025.18 Da free-base mass. Neither establishes receptor activity, sterility, clinical performance, an approved formulation, or equivalence to a finished drug.
Published literature also requires identity control. A paper about MT-II is not automatically a PT-141 paper. A Vyleesi trial is evidence about the trial formulation and protocol, not a general-purpose research-material specification. The COA guide, HPLC guide, and mass-spectrometry guide provide the analytical framework for reviewing a lot-specific record.
The specialty research hub maps the broader research family. For the governing regulatory distinction, use research grade vs pharmaceutical grade.
Frequently Asked Questions
Are PT-141 and bremelanotide the same molecule?
Yes. PT-141 is the development name commonly used for bremelanotide. A research reagent and the Vyleesi finished drug can contain the same molecule while remaining categorically different products.
Is bremelanotide an MC4R-selective agonist?
No. FDA review describes bremelanotide as a nonselective melanocortin receptor agonist. MC4R-centered evidence does not establish exclusive receptor selectivity.
Is PT-141 the same as Melanotan II?
No. PT-141 and Melanotan II are related cyclic melanocortin analogs with a shared development lineage, but they are distinct molecules with separate evidence records.
What did FDA approve in 2019?
FDA approved Vyleesi under NDA 210557 on June 21, 2019 for a specified population of premenopausal women with acquired, generalized hypoactive sexual desire disorder.
Is an Apex PT-141 research material equivalent to Vyleesi?
No. The Apex material is a research-grade chemical reagent for qualified in-vitro and preclinical work. It does not inherit Vyleesi’s formulation, manufacturing system, label, indication, safety, efficacy, or approval.
References
- Sawyer TK, et al. [half-Cys4,half-Cys10]-alpha-Melanocyte-stimulating hormone: a cyclic alpha-melanotropin exhibiting superagonist biological activity. Proc Natl Acad Sci U S A. 1982;79(6):1751-5. PMID: PMID 6281785.
- Hadley ME, et al. Discovery and development of novel melanogenic drugs. Melanotan-I and -II. Pharm Biotechnol. 1998;11:575-95. PMID: PMID 9760697.
- Hadley ME, et al. Melanocortin peptide therapeutics: historical milestones, clinical studies and commercialization. Peptides. 2006;27(4):921-30. PMID: PMID 16412534.
- Wessells H, et al. Ac-Nle-c[Asp-His-DPhe-Arg-Trp-Lys]-NH2 induces penile erection via brain and spinal melanocortin receptors. Neuroscience. 2003;118(3):755-62. PMID: PMID 12710982.
- Cone RD. Anatomy and regulation of the central melanocortin system. Nat Neurosci. 2005;8(5):571-8. PMID: PMID 15856065.
- Pfaus JG, et al. Selective facilitation of sexual solicitation in the female rat by a melanocortin receptor agonist. Proc Natl Acad Sci U S A. 2004;101(27):10201-4. PMID: PMID 15226502.
- Diamond LE, et al. An effect on the subjective sexual response in premenopausal women with sexual arousal disorder by bremelanotide (PT-141), a melanocortin receptor agonist. J Sex Med. 2006;3(4):628-638. PMID: PMID 16839319.
- Kingsberg SA, et al. Bremelanotide for the Treatment of Hypoactive Sexual Desire Disorder: Two Randomized Phase 3 Trials. Obstet Gynecol. 2019;134(5):899-908. PMID: PMID 31599840.
