Independent · non-commercial · publishes on a quarterly cycle|Current cycle 2026 Q3
Compound Evidence InstituteEvidence synthesis · established 2023Graded assessments of compounds, trials, methods and supply
Document set current to 30 July 2026
Compound monograph · §2

PT-141 (bremelanotide) — pharmacology

Molecular targets, mechanism of action, pharmacokinetics and interactions as characterised in humans.

Document identifier
CEI-MN-048/2
Series
Compound monograph
Version
4.1
Published
15 May 2023
Last reviewed
15 Aug 2024
Next review
15 Aug 2026
Identifier
10.71829/cei.mono.48
Certainty
Moderate
Cycle
2023 Q2

§2Pharmacology

§2.1Molecular targets

Table 2. Molecular targets recorded for PT-141 (bremelanotide), with the character of the interaction and the potency where the Institute holds it.

TargetInteractionNote
Melanocortin-4 receptor (MC4R)AgonistThe receptor mediating the sexual-desire effect
Melanocortin-1 receptor (MC1R)AgonistMediates pigmentary effects; hyperpigmentation is a recognised adverse effect
Melanocortin-3 and -5 receptorsAgonistNon-selective across the family

§2.2Mechanism of action

Bremelanotide activates central melanocortin-4 receptors, acting on hypothalamic and limbic circuits regulating sexual desire. Unlike phosphodiesterase-5 inhibitors it does not act on the peripheral vasculature. Its non-selectivity across the melanocortin family accounts for the pigmentary and cardiovascular effects seen in the class.[1,2]

§2.3Pharmacokinetics

Terminal half-life
≈2.7 h
Time to maximum concentration
≈1 h
Volume of distribution
≈25.0 L
Plasma protein binding
≈21 %
Clearance
≈6.5 L/h
Bioavailability
≈100 % (subcutaneous)

Hydrolysis to peptide fragments with renal and faecal excretion. Not a cytochrome P450 substrate.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.00.20.40.60.80246810Time after first dose (hours)Relative concentrationt max ≈ 1 ht½ ≈ 3 h
Modelled profileSimulated observationsDose administration
Figure 2. Illustrative. Plasma concentration–time profile reconstructed by the Institute from the published half-life and time-to-maximum-concentration parameters using a one-compartment model with first-order absorption. The curve is not digitised from a published figure and its vertical scale is relative. It is published to convey the shape of the profile and the approach to steady state, not to supply a concentration at any time point.

§2.4Interactions

  • Naltrexone — oral naltrexone exposure is reduced by delayed gastric emptying
  • Oral medicines requiring rapid absorption may be affected

References cited on this page

References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.

  1. Clayton AH, Althof SE, Kingsberg S, DeRogatis LR, Kroll R, Goldstein I, Kaminetsky J, Spana C, Lucas J, Jordan R, Portman DJ. Bremelanotide for female sexual dysfunctions in premenopausal women: a randomized, placebo-controlled dose-finding trial. Women’s Health 2016;12(3):325–337. doi:10.2217/whe-2016-0018 · PMID 27638896
  2. D’Hondt M, Bracke N, Taevernier L, Gevaert B, Verbeke F, Wynendaele E, De Spiegeleer B. Related impurities in peptide medicines. Journal of Pharmaceutical and Biomedical Analysis 2014;101:2–30. doi:10.1016/j.jpba.2014.06.012 · PMID 25044089

Identifiers are reproduced only where the Institute holds them. Where a digital object identifier or PubMed identifier is not shown, the Institute has recorded the journal and year and has not constructed an identifier.

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