A practical reference on cyclic peptide: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2025-11-17 and is reviewed periodically as new material appears.
Across literature and commercial listings, the substance appears under several names, including bremelanotide, PT-141, and various brand designations. A CAS registry number provides a unique identifier for the compound, aiding retrieval from chemical databases. Synonym lists may also contain early development codes and descriptive chemical names. When consulting sources, researchers need to confirm that the cited names refer to the same molecular structure to avoid confusion. Naming consistency matters especially when comparing analytical data across publications.
PT-141 is a synthetic cyclic heptapeptide whose development code is bremelanotide. It belongs to the class of melanocortin receptor agonists and acts by mimicking endogenous peptide hormones. The compound originated from research on melanotan II, where investigators exploring derivatives found distinct pharmacological features. Unlike the parent compound, PT-141 showed effects on pathways related to sexual desire and function in early studies, prompting its development as a separate candidate. Its molecular design aimed to separate receptor activity from pigmentary effects.
The molecular backbone consists of seven amino acid residues joined into a ring through a disulfide bridge. This cyclic conformation is critical for receptor binding. The sequence includes an acetylated N-terminus and an amidated C-terminus, modifications that improve resistance to enzymatic breakdown. One residue is in the D-configuration, a feature that further stabilizes the peptide against protease activity. Together, the ring structure and specific stereochemistry determine selectivity among melanocortin receptor subtypes.
Development of the peptide passed through several delivery formats, including an intranasal version tested in early trials and an injectable version that entered later clinical study. Regulatory approval for a subcutaneous product in the United States was granted in 2019 after review of controlled trials in premenopausal women. Outside the clinic, the compound circulates in research and non-pharmaceutical markets under its code name, where identity and purity vary considerably between suppliers. Synonyms appearing across technical literature include bremelanotide, PT-141, and Palatin 141.
PT-141 is the research designation for bremelanotide, a synthetic cyclic heptapeptide developed as a melanocortin receptor agonist. The peptide contains seven amino acids with an internal lactam bridge that constrains the backbone into a stable ring. Cyclisation of this kind improves resistance to enzymatic degradation relative to linear analogues. The compound was first explored for effects on melanin production, because several melanocortin receptors influence pigmentation. Its later association with sexual desire emerged from observations made during that early work, and the molecule became the subject of a separate development programme.
Bremelanotide is a moderately large peptide with a molecular mass near 1025 daltons. In lyophilised form it appears as a white to off-white powder and is freely soluble in water and other polar solvents. The intact lactam ring is essential for receptor affinity, while linearised fragments bind far more weakly. Solutions are sensitive to extremes of pH and to prolonged exposure to light and heat, so handling typically involves buffered conditions and cold storage. Its short plasma half-life reflects rapid distribution and clearance rather than chemical breakdown inside the vial.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Cyclic peptide | Melanocortin receptor agonist family |
| Molecular weight | Approximately 1025 Da | Free base form |
| Appearance | White to off-white powder | Lyophilized product |
| Solubility | Soluble in water | Also dissolves in polar organic solvents |
| Storage temperature | -20 degrees Celsius | Dry and protected from light |
Handling procedures emphasize minimizing moisture uptake, since the dried solid is hygroscopic and can draw water when warmed to room temperature before a vial is opened. Laboratories record lot number, purity, counter-ion content, and residual solvent data supplied by the producer. Impurity profiles are compared run to run, and any shift in retention time or peak shape prompts re-verification against a reference standard. Certificates of analysis are treated as claims to be checked rather than accepted at face value.
Identity and purity testing for this peptide typically relies on reversed-phase high-performance liquid chromatography with ultraviolet detection, reported as area-percent purity. Mass spectrometry, usually in tandem mode, confirms molecular mass and supports quantification in biological matrices. Sequence confirmation may use peptide mapping after enzymatic digestion, while nuclear magnetic resonance and circular dichroism supply supplementary structural detail. No single technique establishes identity alone, so laboratories compare retention time, mass, and fragment pattern against a verified reference standard.
The lactam ring that closes the peptide backbone improves resistance to exopeptidase attack, but the molecule stays susceptible to hydrolysis and oxidation once dissolved. Degradation accelerates with temperature, extreme pH, and light exposure, and repeated freeze-thaw cycles promote aggregation and material loss. Lyophilized powder held desiccated at or below minus twenty degrees Celsius is the common way to keep reference material. Reconstituted solutions are generally kept cold and used within a short window because their stability is far lower than that of the dry solid.
Bremelanotide is a cyclic heptapeptide that binds several melanocortin receptors rather than one. In vitro assays report agonist activity at MC1R, MC3R, MC4R and MC5R, with MC4R generally treated as the subtype most relevant to sexual effects. MC4R is expressed in hypothalamic nuclei involved in appetite, energy balance and motivated behaviour, which provides a plausible route for central action. Selective MC4R agonists studied in animals produce comparable behavioural changes, supporting that interpretation.
How receptor activation translates into a change in desire is not established in detail. Proposed steps include modulation of dopaminergic signalling in reward circuits and downstream effects on autonomic tone. Human data consist mainly of clinical trials measuring self-reported outcomes rather than direct measurements of brain activity or transmitter release. The transient rise in blood pressure sometimes observed after administration is likewise reported consistently but explained only partly by known melanocortin pathways.
Melanocortin receptors form a family of five G-protein-coupled proteins, labelled MC1R through MC5R, that respond to peptides derived from pro-opiomelanocortin. Alpha-melanocyte-stimulating hormone and adrenocorticotropic hormone are the best-known endogenous ligands. The receptors are distributed differently across tissues, so a single agonist can produce effects in the brain, skin, adrenal gland and vasculature. This distribution explains why one peptide can influence both pigmentation and motivated behaviour.
PT-141 is the research code for bremelanotide, a cyclic heptapeptide derived from alpha-melanocyte-stimulating hormone. The molecule belongs to the melanocortin receptor agonist family and shows highest affinity for the MC4 receptor subtype, with weaker activity at MC1, MC3 and MC5. Its structure retains the core His-Phe-Arg-Trp sequence that defines melanocortin recognition, while cyclization and terminal modifications improve metabolic stability relative to the parent hormone. Early work classified the compound as a centrally acting agent rather than a peripherally acting vasodilator, which shaped subsequent development priorities.
Receptor activation in hypothalamic and limbic circuits is the mechanism most often cited for the observed effects on sexual desire. Signalling through MC4R couples to Gs proteins and raises intracellular cyclic AMP, which in turn modulates dopaminergic tone in reward-related pathways. Because the peptide reaches the central nervous system after subcutaneous administration, peripheral vascular changes are regarded as secondary rather than primary. The precise neural circuits that translate receptor occupancy into behavioural change remain incompletely mapped, and published accounts describe the pathway in general terms rather than as a fully resolved sequence.
Early research on PT-141 grew out of work on melanotan II, a related cyclic peptide studied for pigmentation. Investigators observed that centrally acting melanocortin agonists also influenced sexual behaviour in animal models, and the programme shifted toward that endpoint. A nasal formulation was evaluated in clinical trials but showed inconsistent absorption, and later studies used subcutaneous administration instead. Regulatory approval in the United States followed in 2019 for a defined population of premenopausal women with acquired, generalised hypoactive sexual desire disorder. That approval was specific to that group rather than a broad indication.
Bremelanotide acts as a non-selective agonist at melanocortin receptors, with reported activity at MC1R, MC3R, MC4R and MC5R. The proposed basis for its central effects is activation of MC4R populations in the hypothalamus, a region associated with appetite and reproductive signalling. Because the peptide carries a net positive charge and polar side chains, it does not cross biological membranes freely, which is one reason oral administration is not the standard route. Effects generally appear within an hour of parenteral administration and are described as centrally mediated rather than peripheral.
Bremelanotide, developed under the code PT-141, is a synthetic cyclic heptapeptide analogue of alpha-melanocyte-stimulating hormone. Its structure is Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-OH, with a lactam bridge joining the aspartate and lysine side chains. The molecule has the formula C50H68N14O10 and a monoisotopic mass near 1025 daltons. It is commonly prepared as the acetate salt and appears as a white to off-white lyophilised powder in solid form. The free acid is the pharmacologically relevant species, while the counter-ion improves handling and dissolution.
== North German Confederation (1867–1871) == The North German Confederation came into existence after the German Confederation was dissolved following the Prussian victory in the Austro-Prussian War of 1866. The chancellor was appointed by the Bundespräsidium, a position that was held constitutionally by the Prussian king. Political parties: None
== Regulation == Among the lipid-binding actin regulatory proteins, gelsolin (like cofilin) preferentially binds polyphosphoinositide (PPI). The binding sequences in gelsolin closely resemble the motifs in the other PPI-binding proteins. Gelsolin's activity is stimulated by calcium ions (Ca2+). Although the protein retains its overall structural integrity in both activated and deactivated states, the S6 helical tail moves like a latch depending on the concentration of calcium ions. The C-terminal end detects the calcium concentration within the cell. When there is no Ca2+ present, the tail of S6 shields the actin-binding sites on one of S2's helices. When a calcium ion attaches to the S6 tail, however, it straightens, exposing the S2 actin-binding sites. The N-terminal is directly involved in the severing of actin. S2 and S3 bind to the actin before the binding of S1 severs actin-actin bonds and caps the barbed end. Gelsolin can be inhibited by a local rise in the concentration of phosphatidylinositol (4,5)-bisphosphate (PIP2), a PPI. This is a two step process. Firstly, (PIP2) binds to S2 and S3, inhibiting gelsolin from actin side binding. Then, (PIP2) binds to gelsolin's S1, preventing gelsolin from severing actin, although (PIP2) does not bind directly to gelsolin's actin-binding site. Gelsolin's severing of actin, in contrast to the severing of microtubules by katanin, does not require any extra energy input.
== Adverse reactions == The common, adverse drug reactions (side effects) are the same as with other PDE5 inhibitors. The frequent vardenafil-specific side-effect is nausea; the infrequent side effects are abdominal pain, back pain, photosensitivity, abnormal vision, eye pain, facial edema, hypotension, palpitation, tachycardia, arthralgia, myalgia, rash, itch, and priapism. One possibly serious, but rare, side effect with vardenafil is heart attack. Also, in rare cases, vardenafil use may cause priapism, a very painful emergency condition that can cause impotence if left untreated. In October 2007, the U.S. Food and Drug Administration (FDA) announced that a warning about possible deafness (sudden hearing loss) would be added to the drug labels of vardenafil, and other PDE5 inhibitors.
The three substrates of this enzyme are salicylaldehyde, oxidised nicotinamide adenine dinucleotide (NAD+), and water. Its products are salicylic acid, reduced NADH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the aldehyde or oxo group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is salicylaldehyde:NAD+ oxidoreductase. This enzyme participates in naphthalene and anthracene degradation.
==== Split inteins ==== Sometimes, the intein of the precursor protein comes from two genes. In this case, the intein is said to be a split intein. For example, in cyanobacteria, DnaE, the catalytic subunit α of DNA polymerase III, is encoded by two separate genes, dnaE-n and dnaE-c. The dnaE-n product consists of an N-extein sequence followed by a 123-AA intein sequence, whereas the dnaE-c product consists of a 36-AA intein sequence followed by a C-extein sequence.
Sources: en.wikipedia.org
The a2 Corporation claims that milk containing A1 proteins is harmful, but a 2009 European Food Safety Authority (EFSA) review of scientific literature found there was insufficient evidence to prove that bioactive peptides in standard milk have a negative effect on health. A1 and A2 beta-casein are genetic variants of the beta-casein milk protein that differ by one amino acid. The A1 beta-casein type is the most common type found in cow's milk in Europe (excluding France), the US, Australia and New Zealand. A genetic test, developed by the A2 Milk Company, determines whether a cow produces the A2 or A1 type protein in its milk. The test allows the a2 Milk Company to license milk producers once proven their cows produce only A2 beta-casein protein in their milk, to the exclusion of the A1 beta-casein protein type.
Rice (1932–2024), physical chemist Ellen Swallow Richards (1842–1911), industrial and environmental chemist Theodore William Richards (1868–1928), 1914 Nobel Prize in Chemistry Wim Richter (1946–2019), South Africa Jeremias Benjamin Richter (1762–1807), German chemist, first used the term stoichiometry Nikolaus Riehl (1901–1990), German chemist Andrés Manuel del Río (1764–1849), Spanish-Mexican geochemist, discovered vanadium Robert Robinson (1886–1975), British chemist, 1947 Nobel Prize in Chemistry Pierre Jean Robiquet (1780–1840), French chemist, discovered caffeine, alizarin, cantharidin Hillar Rootare (1928–2008), Estonian-American physical chemist Irwin Rose (1926–2015), 2004 Nobel Prize in Chemistry Guillaume-François Rouelle (1703–1770), French chemist Hilaire-Marin Rouelle (1718–1779), French chemist Frank Sherwood Rowland (1927–2012), 1995 Nobel Prize in Chemistry Daniel Rutherford (1749–1819), Scottish chemist Ernest Rutherford (1871–1937), New Zealand born chemist and nuclear physicist. Discovered the proton. Nobel Prize in Chemistry 1908 Leopold Ruzicka (Lavoslav Ružička) (1887–1976), 1939 Nobel Prize in Chemistry
=== Ebola === After initial studies by the Centers for Disease Control and Prevention (CDC, Atlanta, Georgia, US) in cell culture models, on 6 October 2014, Chimerix received an FDA authorization for emergency investigational new drug applications of brincidofovir for the treatment of Ebola virus disease. Brincidofovir was administered to the first patient diagnosed in the Ebola virus disease outbreak in the US in 2014. The patient was given the drug starting six days after hospital admission when he was already critically ill; he died four days later. Brincidofovir was also given to Ebola patient Ashoka Mukpo at the Nebraska Medical Center, who had developed the disease and then was pronounced Ebola-free and released from the center on 22 October 2014. In October 2014, Chimerix reported it had been given approval by the FDA to start Phase 2 trials in patients infected with ebolaviruses for brincidofovir's safety, tolerability, and efficacy. Organised by a team of scientists at the University of Oxford, including Peter Horby, Jake Dunning, Laura Merson and Trudie Lang, a trial commenced during January 2015 in Liberia, but was subsequently discontinued. Because of a lack of suitable subjects in Liberia, Oxford University and Médecins Sans Frontières planned to extend the trial to Sierra Leone, where there were still Ebola cases; but on 30 January 2015, the manufacturer decided to withdraw support for the trial and end discussion of future trials.
Fibroblast growth factors comprise the largest family of growth factor ligands at 23 members. The natural alternate splicing of four fibroblast growth factor receptor (FGFR) genes results in the production of over 48 different isoforms of FGFR. These isoforms vary in their ligand binding properties and kinase domains; however, all share a common extracellular region composed of three immunoglobulin (Ig)-like domains (D1-D3), and thus belong to the immunoglobulin superfamily. Interactions with FGFs occur via FGFR domains D2 and D3. Each receptor can be activated by several FGFs. In many cases, the FGFs themselves can also activate more than one receptor. This is not the case with FGF-7, however, which can activate only FGFR2b. A gene for a fifth FGFR protein, FGFR5, has also been identified. In contrast to FGFRs 1-4, it lacks a cytoplasmic tyrosine kinase domain, and one isoform, FGFR5γ, only contains the extracellular domains D1 and D2.
=== Negotiated values === Results of an impact factor can change dramatically depending on which items are considered as "citable" and therefore included in the denominator. One notorious example of this occurred in 1988 when it was decided that meeting abstracts published in FASEB Journal would no longer be included in the denominator. The journal's impact factor jumped from 0.24 in 1988 to 18.3 in 1989. Publishers routinely discuss with Clarivate how to improve the "accuracy" of their journals' impact factor and therefore get higher scores. Such discussions routinely produce "negotiated values" which result in dramatic changes in the observed scores for dozens of journals, sometimes after unrelated events like the purchase by one of the larger publishers.
Sources: en.wikipedia.org
It belongs to the melanocortin receptor agonist family of peptides. Its cyclic structure distinguishes it from linear peptides and shapes its receptor binding profile.
It emerged from research on melanotan II. Investigators exploring derivatives observed distinct pharmacological features related to sexual function.
Common names include bremelanotide and PT-141. Chemical databases may also list early development codes and descriptive names.
PT-141 is a laboratory code for bremelanotide, a synthetic peptide that activates melanocortin receptors. It has been developed both as an injectable pharmaceutical product and as a research chemical. The two contexts differ sharply in how identity, purity, and dosing are controlled.