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Oxytocin receptor

From Wikipedia, the free encyclopedia
(Redirected from OXTR)

OXTR
Identifiers
AliasesOXTR, OT-R, oxytocin receptor
External IDsOMIM: 167055; MGI: 109147; HomoloGene: 20255; GeneCards: OXTR; OMA:OXTR - orthologs
Orthologs
SpeciesHumanMouse
Entrez

5021

18430

Ensembl

ENSG00000180914

ENSMUSG00000049112

UniProt

P30559

P97926

RefSeq (mRNA)

NM_000916

NM_001081147

RefSeq (protein)

NP_000907
NP_001341582
NP_001341583
NP_001341584
NP_001341585

NP_001074616

Location (UCSC)n/aChr 6: 112.45 – 112.47 Mb
PubMed search[2][3]
Wikidata
View/Edit HumanView/Edit Mouse

The oxytocin receptor, also known as OXTR, is a protein which functions as receptor for the hormone and neurotransmitter oxytocin.[4][5] In humans, the oxytocin receptor is encoded by the OXTR gene[6][7] which has been localized to human chromosome 3p25.[8]

Evolutionary tree of the oxytocin, vasotocin, mesotocin, and isotocin receptors and their ligands. From Koechbach et al.[9]

Function and location

[edit]

The OXTR protein belongs to the G protein-coupled receptor (GPCR) family, specifically Gq,[4] and acts as a receptor for oxytocin. Its activity is mediated by G proteins that activate several different second messenger systems.[10][11]

Oxytocin receptors are expressed by the myoepithelial cells of the mammary gland, and in both the myometrium and endometrium of the uterus at the end of pregnancy. The oxytocin receptor system plays an important role as an inducer of uterine contractions during parturition and of milk ejection.

OXTR is also associated with the central nervous system. The gene is believed to play a major role in social, cognitive, and emotional behavior.[12] A decrease in OXTR expression by methylation of the OXTR gene is associated with callous and unemotional traits in adolescence, rigid thinking in anorexia nervosa, problems with facial and emotional recognition, and difficulties in the affect regulation. A reduction in this gene is believed to lead to prenatal stress, postnatal depression, and social anxiety.[12] Studies on OXTR methylation—which downregulates oxytocin mechanisms—suggest this process is associated with increased gray matter density in the amygdala, implicating OXTR regulation in stress and parasympathetic regulation.[13]

Social isolation has been found to decrease oxytocin receptor levels in rodents, whereas levels of oxytocin were unchanged.[14] The decreased oxytocin receptor levels were associated with behavioral changes including increased aggression and anxiety-like behavior, hyperactivity, and diminished social behaviors and memory.[14] Exogenous administration of oxytocin receptor agonists like oxytocin or TGOT was able to partially reverse the behavioral changes.[14]

Fecal microbiota transplant from people with social anxiety disorder into rodents caused selective social anxiety-like symptoms in the rodents.[15][16][17][18][19] This was associated with brain oxytocinergic abnormalities, including decreased expression of the oxytocin receptor.[15][16][18] Lactobacillus reuteri has been found to increase oxytocinergic signaling in rodents, with its metabolite ergothioneine reducing social avoidance behavior.[20][17] Conversely, propionic acid (propionate), which is produced by certain gut bacteria and is increased by social isolation, has been found to induce social deficits and anxiety in rodents, with this being associated with decreased oxytocin receptor expression.[20][21][22]

In some mammals, oxytocin receptors are also found in the kidney and heart.

Mesolimbic dopamine pathways

[edit]

The oxytocinergic circuit projecting from the paraventricular hypothalamic nucleus (PVN) innervates the ventral tegmental area (VTA) dopaminergic neurons that project to the nucleus accumbens, i.e., the mesolimbic pathway.[23] Activation of the PVN→VTA projection by oxytocin affects sexual, social, and addictive behavior via this link to the mesolimbic pathway;[23] specifically, oxytocin exerts a prosexual and prosocial effect in this region.[23]

Polymorphism

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The receptors for oxytocin (OXTR) have genetic differences with varied effects on individual behavior. The polymorphism (rs53576) occurs on the third intron of OXTR in three types: GG, AG, AA. The GG allele is connected with oxytocin levels in humans.[citation needed] A-allele carriers are associated with more sensitivity to stress, lower social proficiency, and more mental health issues than the GG carriers.[24][qualify evidence]

In a study looking at empathy and stress, individuals with the allele GG scored higher than A-carrier individuals in a "Reading the Mind in the Eyes" test. GG carriers, with their naturally higher levels of oxytocin, were better able to distinguish between emotions.[citation needed] A-allele carriers responded with more stress to stressful situations than GG-allele carriers.[25][further explanation needed] A-allele carriers had lower scores on psychological resources, like optimism, mastery, and self-esteem, than GG individuals when measured with factor analysis for depressive symptomology and psychological resources, along with the Beck Depression Inventory. A-allele carriers had higher depressive symptomology and lower psychological resources than GG individuals.[24][qualify evidence] A-allele individuals scored lower in human sociality than GG people on a Tridimensional Personality Questionnaire. AA individuals had the lowest amygdala activation while processing emotionally salient information and those with GG had the highest activity when tested using BOLD during an fMRI.[26] On the other hand, variations at the CD38 rs3796863 and OXTR rs53576 loci were not associated with psychosocial characteristics of adolescents assessed with the Strengths and Difficulties Questionnaire (SDQ); in studies with a similar design, authors recommend replication with larger samples and greater power to detect small effects, especially in age–sex subgroups of adolescents.[27]

The frequency of the A allele varies among ethnic groups, being significantly more common among East Asians than Europeans.[28][quantify][additional citation(s) needed]

Some evidence suggests an association between OXTR gene polymorphism, IQ, and autism spectrum disorder (ASD).[29] Studies have done research focusing on variants in the third intron of the gene, a region that is strongly correlated with personality traits and ASD. OXTR knockout mice have shown abnormal behaviors such as social impairments and aggressiveness. These abnormalities can be reduced with oxytocin or oxytocin receptor agonist administration. Overall, the study suggests that rare variants are considerably more abundant in individuals with ASD compared to that of healthy individuals, however further research with larger sample sizes is needed.[30]

Ligands

[edit]

Several selective ligands for the oxytocin receptor have been developed, but close similarity between the oxytocin and related vasopressin receptors make it difficult to achieve high selectivity with peptide derivatives.[31][32] However the search for a druggable, non-peptide template has led to several potent, highly selective, orally bioavailable oxytocin receptor antagonists.[33] Oxytocin receptor agonists have also been developed.[34][35]

Agonists

[edit]

Peptide

[edit]

Non-peptide

[edit]
  • CA7 – among smallest-known oxytocin receptor agonists; considerable selectivity over the vasopressin V1A receptor[34][36]
  • KNX-200 (KNX200) – series; chemical structure(s) not yet disclosed[37][38]
  • LIT-001 — improved social deficits in mice; non-selective over vasopressin receptors
  • LIT-002 – extremely potent; improved social deficits in mice; non-selective over vasopressin receptors
  • TC OT 39 – non-selective over vasopressin receptors
  • WAY-267,464 – anxiolytic in mice; possibly non-selective over vasopressin receptors[32][39][40]
  • WJ0679 – among smallest-known oxytocin receptor agonists; produces prosocial effects in rodents[34][36]

Unknown

[edit]

Antagonists

[edit]

Peptide

[edit]

Non-peptide

[edit]

Positive allosteric modulators

[edit]

Indirect agonists

[edit]

See also

[edit]

References

[edit]
  1. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000049112 – Ensembl, May 2017
  2. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. 1 2 Gimpl G, Fahrenholz F (April 2001). "The oxytocin receptor system: structure, function, and regulation". Physiological Reviews. 81 (2): 629–83. Bibcode:2001PhyRv..81..629G. doi:10.1152/physrev.2001.81.2.629. PMID 11274341. S2CID 13265083.
  5. ↑ Zingg HH, Laporte SA (July 2003). "The oxytocin receptor". Trends in Endocrinology and Metabolism. 14 (5): 222–7. doi:10.1016/S1043-2760(03)00080-8. PMID 12826328. S2CID 21540056.
  6. ↑ EntrezGene 5021
  7. ↑ Kimura T, Tanizawa O, Mori K, Brownstein MJ, Okayama H (April 1992). "Structure and expression of a human oxytocin receptor" (PDF). Nature. 356 (6369): 526–9. Bibcode:1992Natur.356..526K. doi:10.1038/356526a0. PMID 1313946. S2CID 4273722. Archived from the original (PDF) on 2017-09-21. Retrieved 2021-05-29.
  8. ↑ Simmons CF, Clancy TE, Quan R, Knoll JH (April 1995). "The oxytocin receptor gene (OXTR) localizes to human chromosome 3p25 by fluorescence in situ hybridization and PCR analysis of somatic cell hybrids". Genomics. 26 (3): 623–5. doi:10.1016/0888-7543(95)80188-R. PMID 7607693.
  9. ↑ Koehbach J, Stockner T, Bergmayr C, Muttenthaler M, Gruber CW (February 2013). "Insights into the molecular evolution of oxytocin receptor ligand binding". Biochemical Society Transactions. 41 (1): 197–204. doi:10.1042/BST20120256. PMC 3634130. PMID 23356283.
  10. ↑ Devost D, Wrzal P, Zingg HH (2008). "Oxytocin receptor signalling". Advances in Vasopressin and Oxytocin — from Genes to Behaviour to Disease. Progress in Brain Research. Vol. 170. pp. 167–76. doi:10.1016/S0079-6123(08)00415-9. ISBN 978-0-444-53201-5. PMID 18655881.
  11. ↑ Gimpl G, Reitz J, Brauer S, Trossen C (2008). "Oxytocin receptors: ligand binding, signalling and cholesterol dependence". Advances in Vasopressin and Oxytocin — from Genes to Behaviour to Disease. Progress in Brain Research. Vol. 170. pp. 193–204. doi:10.1016/S0079-6123(08)00417-2. ISBN 978-0-444-53201-5. PMID 18655883.
  12. 1 2 Maud C, Ryan J, McIntosh JE, Olsson CA (May 2018). "The role of oxytocin receptor gene (OXTR) DNA methylation (DNAm) in human social and emotional functioning: a systematic narrative review". BMC Psychiatry. 18 (1) 154. doi:10.1186/s12888-018-1740-9. PMC 5975530. PMID 29843655.
  13. ↑ Lancaster K, Goldbeck L, Puglia MH, Morris JP, Connelly JJ (November 2018). "DNA methylation of OXTR is associated with parasympathetic nervous system activity and amygdala morphology". Social Cognitive and Affective Neuroscience. 13 (11): 1155–1162. doi:10.1093/scan/nsy086. PMC 6234329. PMID 30257007.
  14. 1 2 3 Krimberg JS, Lumertz FS, Orso R, Viola TW, de Almeida RM (March 2022). "Impact of social isolation on the oxytocinergic system: A systematic review and meta-analysis of rodent data". Neurosci Biobehav Rev. 134 104549. doi:10.1016/j.neubiorev.2022.104549. hdl:10923/25707. PMID 35074312.
  15. 1 2 Butler MI, Kittel-Schneider S, Wagner-Skacel J, Mörkl S, Clarke G (May 2025). "The Gut Microbiome in Anxiety Disorders". Curr Psychiatry Rep. 27 (5): 347–361. doi:10.1007/s11920-025-01604-w. PMC 12003441. PMID 40221592. In order to test the hypothesis that the microbiota plays a causal role in SAD, we subsequently used faecal microbiota transplantation (FMT), a method used to assess potential causality and mechanisms [52, 53]. This involved the transfer of the microbiota from patients with SAD to antibioticdepleted mice recipients and assessment of the behavioural and biological impact of such microbiota alteration [54]. Interestingly, the mice who received the SAD microbiome demonstrated a specific heightened social fear response, a validated mouse model of SAD [55]. They performed normally across other tests evaluating general anxiety-like and depression-like behaviours, an important feature of the study highlighting specificity for social fear responses. Additionally, changes in central and peripheral immune function and oxytocin expression in the bed nucleus of the stria terminalis were evident in the SAD-FMT-recipient mice.
  16. 1 2 O'Riordan KJ, Moloney GM, Keane L, Clarke G, Cryan JF (March 2025). "The gut microbiota-immune-brain axis: Therapeutic implications". Cell Rep Med. 6 (3) 101982. doi:10.1016/j.xcrm.2025.101982. PMC 11970326. PMID 40054458. FMT from individuals with SAD into mice revealed that gut microbiota can induce heightened sensitivity to social fear, mirroring symptoms of SAD.70 This response was accompanied by notable changes in both central and peripheral immune functions and a reduction in oxytocin expression within the bed nucleus of the stria terminalis.
  17. 1 2 Griffiths JA, Nirmalkar K, Wu WL, Krajmalnik-Brown R, Mazmanian SK (May 2026). "The gut microbiome shapes social behaviour across animal species". Nat Rev Microbiol. 24 (5): 328–343. doi:10.1038/s41579-025-01262-y. PMID 41238755. Microbiome transfers from adult humans with social anxiety disorder into mice increases sensitivity to social fear compared with microbiome transfers from healthy control individuals39. The fact that microbiome composition is sufficient to modulate social stress responses, at least in rodent models, suggests that targeted microbial interventions might be a feasible approach to reduce the negative outcomes of stress. [...] In a mouse model where mothers are fed a high-fat diet (MHFD), offspring exhibit social deficits and an altered microbiome with reduced diversity and decreased abundance of beneficial microorganisms from the Lactobacillus and Bifidobacterium genera58. Treatment with Lactobacillus reuteri upregulates oxytocinergic neurons in the paraventricular nucleus of the hypothalamus and rescues altered social behaviour in offspring of MHFD dams and several ASD models via vagus nerve signalling (Fig. 1) and/or the involvement of ventral tegmental area dopaminergic neurons57–59
  18. 1 2 Ritz NL, Brocka M, Butler MI, Cowan CS, Barrera-Bugueño C, Turkington CJ, et al. (January 2024). "Social anxiety disorder-associated gut microbiota increases social fear". Proc Natl Acad Sci U S A. 121 (1) e2308706120. doi:10.1073/pnas.2308706120. PMC 10769841. PMID 38147649.
  19. ↑ Feng YC, Liu XX, Yu H, Liu R, Pang TS, Wang HN, et al. (June 2026). "Fecal Microbiota Transplantation From Patients With Social Anxiety Disorder Is Associated With General Anxiety-Like Behavior and Gut Microbiota Alterations in Mice". Brain Behav. 16 (6) e71561. doi:10.1002/brb3.71561. PMC 13272884. PMID 42304699.
  20. 1 2 Ntiri ES, Chun Nin Wong A (December 2025). "Microbial metabolites as engines of behavioral variation across animals". Gut Microbes. 17 (1) 2501191. doi:10.1080/19490976.2025.2501191. PMC 12077453. PMID 40357979.
  21. ↑ Prescott SL, Logan AC (2025). "Propionic Acid-Producing Bacteria as Provocateurs of Anxiety and Depression? [Letter]". Neuropsychiatr Dis Treat. 21: 257–258. doi:10.2147/NDT.S516386. PMC 11809391. PMID 39931199. [...] multiple preclinical studies demonstrate that propionic acid is a potential neurotoxin. Propionic acid can cross the blood-brain barrier and induce inflammation, oxidative stress, mitochondrial dysfunction, while influencing and neurotransmission and gene expression.3 Indeed, propionic acid has been linked to increased anxiety and impairments in typical social behavior among animals.4,5
  22. ↑ Huang L, Duan C, Xia X, Wang H, Wang Y, Zhong Z, et al. (January 2021). "Commensal microbe-derived propionic acid mediates juvenile social isolation-induced social deficits and anxiety-like behaviors". Brain Res Bull. 166: 161–171. doi:10.1016/j.brainresbull.2020.12.001. PMID 33279588. [...] juvenile social isolation decreases the expression of oxytocin receptor (OXTR) in the medial prefrontal cortex (mPFC), and increases the amounts of fecal propionic acid (PA), a short-chain fatty acid derived from gut micobiota. Accordingly, infusion with an OXTR antagonist (OXTR-A, l-368,899) specifically in the mPFC or supplementation of PA both can cause social deficits and anxiety-like behaviors in group housed mice. Collectively, our findings reveal that juvenile social experience regulates prefrontal cortical OXTR expression through gut microbiota-produced PA and that is essential for normal social and emotional behaviors, [...]
  23. 1 2 3 McGregor IS, Callaghan PD, Hunt GE (May 2008). "From ultrasocial to antisocial: a role for oxytocin in the acute reinforcing effects and long-term adverse consequences of drug use?". British Journal of Pharmacology. 154 (2): 358–68. doi:10.1038/bjp.2008.132. PMC 2442436. PMID 18475254. Recent studies also highlight remarkable anxiolytic and prosocial effects of intranasally administered OT in humans, including increased 'trust', decreased amygdala activation towards fear-inducing stimuli, improved recognition of social cues and increased gaze directed towards the eye regions of others (Kirsch et al., 2005; Kosfeld et al., 2005; Domes et al., 2006; Guastella et al., 2008).
  24. 1 2 Saphire-Bernstein S, Way BM, Kim HS, Sherman DK, Taylor SE (September 2011). "Oxytocin receptor gene (OXTR) is related to psychological resources". Proceedings of the National Academy of Sciences of the United States of America. 108 (37): 15118–22. Bibcode:2011PNAS..10815118S. doi:10.1073/pnas.1113137108. PMC 3174632. PMID 21896752.
  25. ↑ Rodrigues SM, Saslow LR, Garcia N, John OP, Keltner D (December 2009). "Oxytocin receptor genetic variation relates to empathy and stress reactivity in humans". Proceedings of the National Academy of Sciences of the United States of America. 106 (50): 21437–41. Bibcode:2009PNAS..10621437R. doi:10.1073/pnas.0909579106. PMC 2795557. PMID 19934046.
  26. ↑ Tost H, Kolachana B, Hakimi S, Lemaitre H, Verchinski BA, Mattay VS, et al. (August 2010). "A common allele in the oxytocin receptor gene (OXTR) impacts prosocial temperament and human hypothalamic-limbic structure and function". Proceedings of the National Academy of Sciences of the United States of America. 107 (31): 13936–41. Bibcode:2010PNAS..10713936T. doi:10.1073/pnas.1003296107. PMC 2922278. PMID 20647384.
  27. ↑ Tereshchenko S, Kasparov E, Zobova S, Smolnikova M, Evert L, Semenova N, et al. (2021). "Oxytocin Pathway Gene (CD38, OXTR) Variants Are Not Related to Psychosocial Characteristics Defined by Strengths and Difficulties Questionnaire in Adolescents: A Field School-Based Study". Frontiers in Psychiatry. 12 714093. doi:10.3389/fpsyt.2021.714093. PMC 8380924. PMID 34434131.
  28. ↑ Sasaki JY, Kim HS, Xu J (July 2011). "Religion and Well-being: The Moderating Role of Culture and the Oxytocin Receptor (OXTR) Gene" (PDF). Journal of Cross-Cultural Psychology. 42 (8): 1394–1405. doi:10.1177/0022022111412526. S2CID 145567198.
  29. ↑ Lerer, E., Levi, S., Salomon, S. et al. Association between the oxytocin receptor (OXTR) gene and autism: relationship to Vineland Adaptive Behavior Scales and cognition. Mol Psychiatry 13, 980–988 (2008). https://doi.org/10.1038/sj.mp.4002087
  30. ↑ de Oliveira Pereira Ribeiro L, Vargas-Pinilla P, Kappel DB, Longo D, Ranzan J, Becker MM, et al. (June 2018). "Evidence for Association Between OXTR Gene and ASD Clinical Phenotypes". Journal of Molecular Neuroscience. 65 (2): 213–221. doi:10.1007/s12031-018-1088-0. PMID 29858823. S2CID 46924606.
  31. ↑ Chini B, Manning M (August 2007). "Agonist selectivity in the oxytocin/vasopressin receptor family: new insights and challenges". Biochemical Society Transactions. 35 (Pt 4): 737–41. doi:10.1042/BST0350737. PMID 17635137.
  32. 1 2 Manning M, Stoev S, Chini B, Durroux T, Mouillac B, Guillon G (2008). "Peptide and non-peptide agonists and antagonists for the vasopressin and oxytocin V1a, V1b, V2 and OT receptors: Research tools and potential therapeutic agents☆". Peptide and non-peptide agonists and antagonists for the vasopressin and oxytocin V1a, V1b, V2 and OT receptors: research tools and potential therapeutic agents. Progress in Brain Research. Vol. 170. pp. 473–512. doi:10.1016/S0079-6123(08)00437-8. ISBN 978-0-444-53201-5. PMID 18655903.
  33. ↑ Borthwick AD (September 2010). "Oral oxytocin antagonists". Journal of Medicinal Chemistry. 53 (18): 6525–38. doi:10.1021/jm901812z. PMID 20550119.
  34. 1 2 3 Nashar PE, Whitfield AA, Mikusek J, Reekie TA (2022). "The Current Status of Drug Discovery for the Oxytocin Receptor". Oxytocin. Methods Mol Biol. Vol. 2384. pp. 153–174. doi:10.1007/978-1-0716-1759-5_10. ISBN 978-1-0716-1758-8. PMID 34550574. S2CID 239090096.
  35. ↑ Gulliver D, Werry E, Reekie TA, Katte TA, Jorgensen W, Kassiou M (January 2019). "Targeting the Oxytocin System: New Pharmacotherapeutic Approaches". Trends Pharmacol Sci. 40 (1): 22–37. doi:10.1016/j.tips.2018.11.001. hdl:1959.4/unsworks_81554. PMID 30509888. S2CID 54559394.
  36. 1 2 "Non-peptide oxytocin receptor agonists". Google Patents. 12 December 2017. Retrieved 17 July 2026.
  37. 1 2 Sami T (13 January 2026). "Kinoxis and Boehringer to develop oxytocin-targeting treatments for social dysfunction in $181M deal". BioWorld. Retrieved 13 January 2026.
  38. 1 2 Spotlight Showcases: Kinoxis Therapeutics Pty Ltd. 5th Annual Neruoscience Innovation Forum for Business Development, Licensing & Investment 22nd–23rd March 2022, Digital Conference. March 2022. Kinoxis' lead candidate (KNX100) is being developed for the mitigation of opioid withdrawal symptoms. KNX100 has a novel, undisclosed mechanism of action and a Phase I clinical trial has commenced under a US IND. The company is also exploring other indications for its lead compound, KNX100, as promising preclinical results have been achieved in animal models of cocaine, methamphetamine, nicotine, and alcohol use disorders, as well as models of agitation and aggression. [...] Kinoxis' second series of compounds target the oxytocin receptor, through either selective partial agonism or positive allosteric modulation. The brain oxytocin system has been identified as perhaps the most important molecular target for regulating social behaviour and is therefore a major target of interest for treating a wide range of mental disorders. The development of these compounds will be focused on treating conditions that feature social dysfunction as a core symptom, such as neurodevelopmental disorders (including autism spectrum disorder), social anxiety disorder, dementia (including Alzheimer's disease), PTSD and schizophrenia. The KNX200 series of oxytocin receptor partial agonists are undergoing candidate selection stage using several pre-clinical animal disease models (Alzheimer's, PTSD, ASD) and the KNX300/400 series of oxytocin receptor positive allosteric modulators are undergoing lead optimisation.
  39. ↑ Rahman Z, Resnick L, Rosenzweig-Lipson SJ, Ring RH,"Methods of treatment using oxytocin receptor agonists", US patent application 2007/0117794, published 2007-05-24 , assigned to Wyeth Corp
  40. ↑ Ring RH, Schechter LE, Leonard SK, Dwyer JM, Platt BJ, Graf R, et al. (January 2010). "Receptor and behavioral pharmacology of WAY-267464, a non-peptide oxytocin receptor agonist". Neuropharmacology. 58 (1): 69–77. doi:10.1016/j.neuropharm.2009.07.016. PMID 19615387. S2CID 8592340.
  41. 1 2 Borthwick AD, Liddle J (January 2013). "Retosiban and Epelsiban: Potent and Selective Orally available Oxytocin Antagonists". In Domling A (ed.). Methods and Principles in Medicinal Chemistry: Protein-Protein Interactions in Drug Discovery. Weinheim: Wiley-VCH. pp. 225–256. doi:10.1002/9783527648207.ch10. ISBN 978-3-527-33107-9.
  42. ↑ Williams PD, Anderson PS, Ball RG, Bock MG, Carroll L, Chiu SH, et al. (March 1994). "1-((7,7-Dimethyl-2(S)-(2(S)-amino-4-(methylsulfonyl)butyramido)bicyclo [2.2.1]-heptan-1(S)-yl)methyl)sulfonyl)-4-(2-methylphenyl)piperaz ine (L-368,899): an orally bioavailable, non-peptide oxytocin antagonist with potential utility for managing preterm labor". Journal of Medicinal Chemistry. 37 (5): 565–71. doi:10.1021/jm00031a004. PMID 8126695.
  43. ↑ Boccia ML, Goursaud AP, Bachevalier J, Anderson KD, Pedersen CA (September 2007). "Peripherally administered non-peptide oxytocin antagonist, L368,899, accumulates in limbic brain areas: a new pharmacological tool for the study of social motivation in non-human primates". Hormones and Behavior. 52 (3): 344–51. doi:10.1016/j.yhbeh.2007.05.009. PMC 2712625. PMID 17583705.
  44. ↑ Williams PD, Clineschmidt BV, Erb JM, Freidinger RM, Guidotti MT, Lis EV, et al. (November 1995). "1-(1-[4-[(N-acetyl-4-piperidinyl)oxy]-2-methoxybenzoyl]piperidin-4- yl)-4H-3,1-benzoxazin-2(1H)-one (L-371,257): a new, orally bioavailable, non-peptide oxytocin antagonist". Journal of Medicinal Chemistry. 38 (23): 4634–6. doi:10.1021/jm00023a002. PMID 7473590.
  45. ↑ Wyatt PG, Allen MJ, Chilcott J, Foster A, Livermore DG, Mordaunt JE, et al. (May 2002). "Identification of potent and selective oxytocin antagonists. Part 1: indole and benzofuran derivatives". Bioorganic & Medicinal Chemistry Letters. 12 (10): 1399–404. doi:10.1016/S0960-894X(02)00159-2. PMID 11992786.
  46. ↑ Ring RH, Malberg JE, Potestio L, Ping J, Boikess S, Luo B, et al. (April 2006). "Anxiolytic-like activity of oxytocin in male mice: behavioral and autonomic evidence, therapeutic implications". Psychopharmacology. 185 (2): 218–25. doi:10.1007/s00213-005-0293-z. PMID 16418825. S2CID 13647805.
  47. ↑ Kim SH, Riaposova L, Ahmed H, Kim SH, Riaposova L, Ahmed H, et al. (2019). "Oxytocin receptor antagonists, atosiban and nolasiban, inhibit prostaglandin F2α-induced contractions and inflammatory responses in human myometrium". Scientific Reports. 9 (5792): 5792. Bibcode:2019NatSR...9.5792K. doi:10.1038/s41598-019-42181-2. PMC 6453954. PMID 30962532.
  48. ↑ Klein A (31 January 2018). "A Helping Hand / The Love Drug That Could Draw People Away From Any Addiction". New Scientist. doi:10.1016/S0262-4079(18)30221-5.
  49. ↑ "KNX 100". AdisInsight. 4 August 2025. Retrieved 13 January 2026.
  50. ↑ "Delving into the Latest Updates on KNX-100 with Synapse". Synapse. 27 December 2025. Retrieved 13 January 2026.
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