PT-141

PT-141, also known as bremelanotide, is a synthetic cyclic heptapeptide. It is an analog of alpha-melanocyte-stimulating hormone (α-MSH). Its sequence is N-acetyl-Nle-Asp-His-D-Phe-Arg-Trp-Lys. A lactam bond between Asp and Lys closes it into a ring. It ends in a free carboxylic acid (PubChem CID 9941379). It was created as an analog of melanotan II (Hadley and Dorr, 2006).

It is an agonist at melanocortin receptors, including MC3R and MC4R. These receptors are expressed mainly in the central nervous system (Molinoff et al., 2003). Published PT-141 peptide research covers receptor structure, plus rodent and primate behavior. It also covers clinical pharmacology and analytical chemistry.

It is not that drug product. It is not intended for that indication or any clinical use, and it is not for use in people.

The 10 mg size is the labeled amount shown there. Sequence and aliases come from PubChem (CID 9941379, which lists 1025.2 g/mol).

Published work on PT-141 falls into six areas. Each summary below states the model used. Human studies used drug products in clinical settings. They describe those products, not the research material sold here.

Receptor pharmacology and structure

A team solved high-resolution structures of full-length MC4R in complex with its G protein. Peptide agonists in these structures were α-MSH, afamelanotide and bremelanotide. A structure with a small-molecule agonist was solved as well. With pharmacological assays, they showed a conserved binding mode for the peptide agonists (Zhang et al., 2021). A neurobiology review notes that PT-141 activates several melanocortin receptor subtypes nonselectively. It also sums up animal work on where it acts.

That work suggests it acts on presynaptic MC4R in the medial preoptic area of the hypothalamus. The suggested effect is a rise in dopamine release (Pfaus et al., 2022). In human glioblastoma cell lines, the peptide reduced survivin expression. It also caused cell death at concentrations not toxic to normal human cells. An MC3R and MC4R antagonist blocked both effects (Suzuki et al., 2024).

Rodent and primate models

In rats and nonhuman primates, PT-141 produced penile erections. In rats given it systemically, c-Fos immunoreactivity rose in the hypothalamus. This protein is a marker of neuron activation (Molinoff et al., 2003). In female rats, it selectively increased solicitation behaviors. It did not change lordosis or pacing. It did not cause generalized motor activation. Nor did it alter measures of sexual reward (Pfaus et al., 2004).

Early clinical pharmacology

Early human studies included healthy men and men with erectile dysfunction. In both groups, PT-141 produced a rapid increase in erectile activity (Molinoff et al., 2003). A crossover study enrolled 18 premenopausal women with sexual arousal disorder. It compared PT-141, given once by the nasal route, with placebo. More women reported moderate or high sexual desire after PT-141.

Vaginal vasocongestion did not differ significantly (Diamond et al., 2006). Two phase 1 trials studied premenopausal women with obesity. They were set up to study MC4R effects on appetite. They reported lower calorie intake, by roughly 400 kcal per day in one trial. They also reported greater short-term weight reduction than placebo (Spana et al., 2022).

Phase 3 trials and reanalysis

Two identical 24-week phase 3 trials included 1,267 premenopausal women with hypoactive sexual desire disorder. The women were randomized to the drug product or placebo. The trials reported statistically significant differences in the coprimary desire and distress scores. Nausea, flushing and headache were more common than with placebo (Kingsberg et al., 2019). An independent reanalysis argued that most protocol-listed outcomes went unreported. It also argued that discontinuation due to adverse events was much higher with bremelanotide (Spielmans, 2021).

Safety and cardiovascular measurements

A study of 397 premenopausal women used ambulatory monitoring. It found small, transient rises in systolic blood pressure of 2.4 to 3.2 mmHg relative to placebo. These came during the first 4 hours. Peaks usually lasted under 15 minutes. Heart rate fell in the highest-exposure group (White et al., 2017). Pooled safety data span a clinical program of 43 studies and about 3,500 participants.

In the phase 3 double-blind period, the most common adverse events were nausea, flushing and headache. Nausea rates were 40.0 percent, versus 1.3 percent with placebo. Some participants received it daily for up to 16 days in a row. More than a third of them had focal hyperpigmentation (Clayton et al., 2022).

Analytical chemistry and stability

A validated UHPLC-MS/MS assay measured the peptide in 100 µL of plasma, down to 10 pg/mL. It was used to study oral exposure in beagle dogs (Sauter et al., 2020). Forced-degradation work used international guideline stress conditions. It found bremelanotide acetate more stable under acidic than basic conditions. It was also highly prone to oxidation. Heat and light caused further breakdown. Eight degradation products were found. They were traced to deacetylation, peptide-bond hydrolysis, oxidation and epimerization (Yuvaraaj and Sharma, 2026).