This is a working overview of Lactam bridge, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-06-24 and is reviewed periodically as new material appears.
Approved use is narrow and jurisdiction-specific. In the United States, the injectable product is authorised for premenopausal women with acquired, generalised hypoactive sexual desire disorder, a diagnosis that requires documented distress. It is not approved for men, for postmenopausal women, or for use alongside hormonal contraceptives under the approved labelling. Outside regulated markets, the same peptide is frequently sold as a research chemical, where identity, purity, and sterility are not independently verified.
Bremelanotide is a synthetic cyclic heptapeptide developed as an analogue of alpha-melanocyte-stimulating hormone, a naturally occurring peptide involved in pigmentation and appetite signalling. Its structure contains seven amino acid residues joined by a lactam bridge that closes the ring between two side chains. The molecular formula is C50H68N14O10 and the nominal molecular mass is near 1025 daltons. Much of the early laboratory literature refers to the same molecule by the development code PT-141.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H68N14O10 | Cyclic heptapeptide backbone |
| Molecular mass | Approximately 1025 Da | Nominal mass of the free peptide |
| Appearance | White to off-white lyophilised powder | Typical for purified synthetic peptides |
| Solubility class | Freely soluble in water | Organic solubility is limited |
| Typical storage temperature | −20 °C or below | Protect from moisture and light |
Bremelanotide is a cyclic heptapeptide that acts as an agonist at melanocortin receptors. It binds MC1R, MC3R, MC4R, and MC5R, with MC4R activation considered most relevant to sexual desire pathways in the central nervous system. The molecule is a synthetic analog of alpha-melanocyte-stimulating hormone, a naturally occurring peptide involved in pigmentation and energy regulation. Early research explored its use in tanning before attention shifted toward sexual dysfunction applications. Receptor binding affinity varies across these subtypes.
Activation of MC4R in the hypothalamus is thought to influence dopaminergic signaling, which in turn affects arousal and desire. This mechanism differs from that of phosphodiesterase type 5 inhibitors, which act primarily on vascular smooth muscle in the genital region. Because the pathway is central rather than peripheral, effects are not strictly dependent on local blood flow. The precise downstream cascade linking receptor binding to behavioral outcomes remains an area of ongoing investigation.
Bremelanotide acts as an agonist at melanocortin receptors, a family of five G-protein-coupled receptors labeled MC1 through MC5. Binding studies indicate activity at several of these subtypes rather than strict selectivity for one. Signalling proceeds mainly through Gs-mediated activation of adenylyl cyclase, raising intracellular cyclic AMP. The MC4 receptor, expressed in hypothalamic and limbic circuits, is widely regarded as the subtype most relevant to sexual response. Because the molecule is not subtype-selective, effects at other melanocortin receptors are expected and are used to explain some observed side effects.
The peptide contains seven amino acids arranged in a ring, closed by a lactam bridge between a side-chain acid and an amine. This cyclic constraint holds the backbone in a defined conformation and increases resistance to enzymatic breakdown relative to linear analogs. N-terminal acetylation and a C-terminal amide further protect the molecule from exopeptidases. The result is a compound with a comparatively long circulation time for a small peptide. Structural modification of the bridge alters receptor affinity, which is one reason analogs in this family differ in their subtype preferences.
Whether the behavioral effect originates centrally, peripherally, or through both remains an active question. Animal experiments using receptor antagonists and site-specific injections point toward hypothalamic melanocortin circuits as a key locus, but translating those findings to humans is not straightforward. Blood pressure changes observed in trials suggest a vascular component that may be peripherally mediated. The relationship between receptor occupancy and reported effect has not been mapped in humans, and no validated biomarker predicts response. This gap makes it difficult to explain individual variability on pharmacological grounds alone.
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.
Identity and purity are usually established with reversed-phase high-performance liquid chromatography combined with mass spectrometry. A gradient of water and acetonitrile containing trifluoroacetic acid is a common mobile phase, and ultraviolet detection near 214 nanometres responds to the peptide backbone. Mass spectrometry confirms the expected molecular mass and helps reveal truncation or oxidation products. Purity is reported as a peak-area percentage, a figure that depends on the wavelength and gradient used, so values from different laboratories are not always directly comparable. Peptide mapping and amino acid analysis provide additional confirmation when required.
Regulatory status varies by jurisdiction, where approved prescription products, compounded preparations and research-grade material are treated as distinct categories with different documentation requirements. Suppliers of research material commonly issue a certificate of analysis listing purity, identity and sometimes endotoxin content. Independent verification by a third-party laboratory is often recommended because self-reported figures are difficult to check. Literature discussions usually state the source, purity and storage conditions of the material used, since these details affect reproducibility. Analysts note that a reported purity figure does not by itself describe biological activity.
== Types == Types include those acting directly as membrane-bound receptors (Receptor protein serine/threonine kinase) and intracellular kinases participating in Signal transduction. Of the latter, types include:
== External links == Human ANG genome location and ANG gene details page in the UCSC Genome Browser. Human RNASE4 genome location and RNASE4 gene details page in the UCSC Genome Browser. Human AMOT genome location and AMOT gene details page in the UCSC Genome Browser. Overview of all the structural information available in the PDB for UniProt: P03950 (Human Angiogenin) at the PDBe-KB. Overview of all the structural information available in the PDB for UniProt: P21570 (Mouse Angiogenin) at the PDBe-KB.
== T == Koichi Tanaka (born 1959), Japanese electrical engineer, 2002 Nobel Prize in Chemistry Henry Taube (1915–2005), American chemist, (1983 Nobel Prize in Chemistry Louis Jacques Thénard (1777–1857), French chemist, discovered hydrogen peroxide and Thenard's Blue Sir Harold Warris Thompson (1908–1983), English physical chemist J. J. Thomson (1856–1940), British physicist, Known in chemistry for discovery of isotopes T. Don Tilley (born 1954), organometallic chemist Arne Tiselius (1902–1971), Swedish biochemist, 1948 Nobel Prize in Chemistry Max Tishler (1906–1989), American chemist, 1970 Priestley Medal Alexander R. Todd, Baron Todd (1907–1997), British biochemist, 1957 Nobel Prize in Chemistry Evangelista Torricelli (1608–1647), Italian physicist and chemist, invented the barometer, pupil of Galileo Roger Y. Tsien (1952–2016), American biochemist, 2008 Nobel Prize in Chemistry Mikhail Tsvet (1872–1919), Russian botanist, known for adsorption chromatography Kristy Turner, British chemist
== Pharmacokinetics == Unlike many laxative products, lubiprostone does not show signs of drug tolerance, chemical dependency, or altered serum electrolyte concentration. Minimal distribution of the drug occurs beyond the immediate gastrointestinal tissues. Lubiprostone is rapidly metabolized by reduction/oxidation, mediated by carbonyl reductase. There is no metabolic involvement of the hepatic cytochrome P450 system. The measurable metabolite, M3, exists in very low levels in plasma and makes up less than 10% of the total administered dose. Data indicate that metabolism occurs locally in the stomach and jejunum.
Sources: en.wikipedia.org
== Biography == He is a member of the editorial board of the journal Intelligence. His PhD was completed in 1994 at the University of Auckland (New Zealand) and integrated the Eysenckian dimensional model of psychosis with the categorical model of schizotypy proposed by Paul E. Meehl, using measures of personality, creativity, evoked potentials, and smooth pursuit eye movement dysfunction. The title of his doctoral thesis was Psychometric & psychophysiological measures for schizotypy, creativity & psychoticism. Subsequent academic publications include demonstrating the existence of two separate forms of dyslexia, underpinned by distinct genes, and, subsequently, demonstrating that the genes associated with dyslexia are also linked to normal variation in reading ability. This work lead to searches for specific genes involved in reading and language. In positive psychology, he showed (along with Alexander Weiss and Michelle Luciano) that the genes for happiness are genes for personality, suggesting that a general factor of genetic well-being and specific genetic influences from the five factor model traits of Extraversion, Neuroticism/Stability, and Conscientiousness completely explain the heritable component of differences in happiness. With Caroline Rae, Bates showed that creatine supports cognitive function – finding that creatine supplements in vegans substantially increased their cognitive ability and working memory by comparison with placebo. This supported a literal 'mental energy' model of intelligence, first postulated by Charles Spearman.
1993/1977) County Court (Pensions Ombudsman) (Enforcement of Directions and Determinations) Rules 1993 (S.I. 1993/1978) Education (School Inspection) (Wales) (No. 2) Regulations 1993 (S.I. 1993/1982) Education (National Curriculum) (Assessment Arrangements for the Core Subjects) (Key Stage 1) Order 1993 (S.I. 1993/1983) Education (National Curriculum) (Assessment Arrangements for the Core Subjects) (Key Stage 3) Order 1993 (S.I. 1993/1984) Social Security (Industrial Injuries) (Prescribed Diseases) Amendment (No. 2) Regulations 1993 (S.I. 1993/1985) Education (School Inspection) (No. 2) Regulations 1993 (S.I. 1993/1986) Education (Further Education in Schools) Regulations 1993 (S.I. 1993/1987) A27 Trunk Road (Polegate Bypass Slip Roads) Order 1993 (S.I. 1993/1990) A27 Trunk Road (Polegate Bypass De-Trunking)Order 1993 (S.I. 1993/1991) A259 Trunk Road Brookland Diversion Order 1993 (S.I. 1993/1992) Education (Further Education Institutions Information) (England) Regulations 1993 (S.I. 1993/1993) Merchant Shipping (Load Lines) Act 1967 (Unregistered Ships) Order 1993 (S.I. 1993/1994) Poultry Breeding Flocks, Hatcheries and Processed Animal Protein (Fees) Order 1993 (S.I. 1993/1998)
Clinicians use drug detoxification to reduce or relieve withdrawal symptoms while helping an addicted person adjust to living without drug use. Drug detoxification does not aim to treat addiction but rather represents an early step within long-term treatment. Detoxification may be achieved drug-free or may use medications as an aspect of treatment. Often drug detoxification and treatment will occur in a community program that lasts several months and takes place in a residential setting rather than in a medical center. Drug detoxification varies depending on the location of treatment, but most detox centers provide treatment to avoid the symptoms of physical withdrawal from alcohol and from other drugs. Most also incorporate counseling and therapy during detox to help with the consequences of withdrawal.
Sources: en.wikipedia.org
It is a synthetic cyclic peptide that acts as an agonist at melanocortin receptors. It is not a hormone replacement therapy and not a vasodilator in the usual clinical sense, although it does affect vascular tone. Chemically it belongs to the melanocortin analogue family.
PT-141 was the internal development code used during early research and it persists in older publications, conference abstracts, and informal listings. The code and the approved name refer to the same molecule. Its continued use reflects habit in the literature rather than any difference in substance.
No. The intranasal form was studied in trials but was never approved, and absorption through the nasal route varies considerably between individuals. Approved labelling covers a subcutaneous injection only. Any nasal product sold outside regulated channels falls outside verified manufacturing.
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.