Cagrilintide, 5-Amino-1MQ and kisspeptin-10: three thinly documented compounds

Last reviewed 9 August 2026

Three compounds sit beside each other in most research-market catalogues, and a reader moving between them would reasonably assume the published record behind each runs to about the same depth. It does not. One has been through phase 3 trials randomising thousands of participants. One has never appeared in a registered clinical trial of any kind. One has a real academic literature going back to 2001 with a specific, narrow hole in the middle of it.

This page sets out what has been published on cagrilintide, 5-Amino-1MQ and kisspeptin-10, and where each record stops. Counts were taken on 9 August 2026 and the queries behind them are stated, so they can be repeated. Nothing here states what these substances do; it states what has been studied, in what model, and by whom.

Three records, counted the same way

A count is a starting point, not an answer, and two figures above prove it. The five kisspeptin-10 records typed as randomised controlled trials are not five randomised trials of kisspeptin-10: one is a non-human primate study, in which kisspeptin-54 release was measured in female rhesus monkeys and kisspeptin-10 was infused through a microdialysis probe rather than administered to a human participant (Keen et al., 2008), and another administered kisspeptin-54 to humans (Dhillo et al., 2005). The figure of 4 undercounts in the other direction, because most papers on 5-Amino-1MQ name the enzyme target in the title rather than the molecule. So every record below was opened.

Method. PubMed counts are [Title/Abstract] searches, with AND randomized controlled trial[Publication Type] for the second column. 5-Amino-1MQ is searched as the union of its three published designations — "5-amino-1-methylquinolinium", "5A1MQ" and "5-amino-1MQ" — because no single one of them retrieves the whole set, and the bare abbreviation retrieves none of it. Registry counts are ClinicalTrials.gov intervention-field queries, one name each. Identity is from PubChem by CID rather than by name, and anti-doping status from the 2026 WADA Prohibited List read in full rather than any summary of it; the glossary holds the definitions its terms carry.

What the bands turn on

The letters follow the published band method, in which one qualifying citation sets the band and volume of literature moves nothing. Each turns on a single identifiable record:

• Cagrilintide, band A — a published randomised controlled trial of confirmatory design and scale. REDEFINE 1 randomised 3,417 participants across four arms, one of them cagrilintide alone (n = 302), with pre-specified co-primary endpoints and a registered protocol.
• Kisspeptin-10, band B — randomised controlled studies of the decapeptide exist, none confirmatory in design or scale, and no approval anywhere.
• 5-Amino-1MQ, band D — published work in live vertebrate models, no human study of the molecule as administered.

None of the three letters says anything about direction of result, safety, or the material in any particular vial.

Cagrilintide

Identity

Cagrilintide is a lipidated synthetic analogue of human amylin. The parent hormone, islet amyloid polypeptide, is a 37-residue peptide with an intramolecular disulphide bridge and a C-terminal amide (UniProt P10997: mature chain 34–70, disulphide 35–40, amidated tyrosine at 70). PubChem CID 171397054 gives C₁₉₄H₃₁₂N₅₄O₅₉S₂, average mass 4409 g/mol, monoisotopic mass 4406.2515, CAS 1415456-99-3, UNII AO43BIF1U8; the two sulphur atoms are the retained disulphide. It appears in the development literature as AM833 and NNC0174-0833.

In vitro and structural work

Kruse and colleagues (2021) reported the medicinal-chemistry programme behind the candidate, including the substitutions and the fatty-diacid acylation. Fletcher and colleagues (2021) profiled AM833 across calcitonin-family receptors in HEK293 cells against six comparator agonists and reported a distinct profile across binding, activation and regulation. Cao and colleagues (2025) resolved cryo-EM structures at the calcitonin receptor and three amylin receptors. Alhalabi and colleagues (2026) characterised its metabolic profile in human S9 fractions as preventive doping research.

Rodent models

Carvas and colleagues (2025) reported body-weight loss in wild-type high-fat-diet mice and that the absence of RAMP1 and RAMP3 impeded cagrilintide’s potency. Ludwig and colleagues (2026) assembled a cross-species atlas of the dorsal vagal complex across rat, mouse, macaque and human tissue and reported conserved neuronal populations associated with the energy-balance effects seen in those models; the human component was gene expression, not administration.

Human trials

REDEFINE 1’s co-primary endpoints were set for the combination: Garvey and colleagues (2025) reported a mean body-weight change of −20.4% against −3.0% for placebo at week 68, with gastrointestinal adverse events in 79.6% against 39.9%, which the authors describe as mainly transient and mild to moderate.

Where this record stops

Three limits sit inside an unusually deep file. First, most of it is about a combination. Only four of the ten reports randomised anyone to cagrilintide alone: the whole of Lau 2021, an arm in Friás 2023, one of 302 in REDEFINE 1 and one of 152 in REIMAGINE 2. Every phase 3 confirmatory endpoint was set for the fixed combination with semaglutide. Second, the programme is sponsor-run and no regulator has completed a benefit–risk assessment: a new drug application for the combination went to the US Food and Drug Administration on 18 December 2025 and remains under review, with no marketing authorisation anywhere. Third, no published stability dataset for reconstituted cagrilintide outside the sponsor’s investigational presentation was located, so any assumption about a solution’s in-use life is extrapolation from general peptide practice.

5-Amino-1MQ

Identity

It is not a peptide. 5-Amino-1MQ is a low-molecular-weight quaternary quinolinium salt with no amino-acid sequence. It is catalogued alongside the metabolic compounds because that is where its literature sits, not because it is a peptide. PubChem CID 66522933 gives the iodide as C₁₀H₁₁IN₂, 286.11 g/mol, monoisotopic mass 285.9967, CAS 42464-96-0. The ring nitrogen carries a permanent positive charge, so the substance exists as a salt and requires a counter-ion.

That matters before any arithmetic. A stated mass may refer to the salt as weighed or to the cation alone: 159.21 against 286.11 for the iodide, a ratio of 0.556. Where a specification does not say which basis it uses, the two figures differ by nearly a factor of two.

In vitro work

Neelakantan and colleagues (2017a) reported a fluorescent assay for monitoring nicotinamide N-methyltransferase activity, built for inhibitor screening; the same group (2017b) reported a structure–activity study across a series spanning a greater than 1000-fold range of activity, in which quinolinium scaffolds reached micromolar inhibition. Akar and colleagues (2021) — the one independent group in the file — reported concentration- and time-dependent anti-proliferative activity in HeLa cells over 0.1–500 µM, without a comparable effect in HEK-293 cells.

Rodent models

Neelakantan and colleagues (2018) reported the first detailed characterisation: selectivity screening, membrane permeability by PAMPA and Caco-2, and an 11-day in vivo phase in high-fat-diet C57BL/6 mice measuring body weight, fat-pad mass and adipocyte size. The same group (2019) reported muscle stem cell activity, myofibre cross-sectional area and contractile torque in 24-month-old mice after acute muscle injury. Sampson and colleagues (2021) combined the inhibitor with a reduced-calorie diet in diet-induced obese mice; Dimet-Wiley and colleagues (2022) reported gut microbiome composition in the same model, and (2024) grip strength, torque, fibre type and muscle proteome and metabolome in mice treated from 22 to 24 months of age. Babula and colleagues (2024) reported a 28-day treatment period in diet-induced obese mice.

Where this record stops

ClinicalTrials.gov returns zero studies naming 5-Amino-1MQ as an intervention. There is no published phase 1, no human pharmacokinetic dataset and no human safety dataset. The in vivo literature also traces to one laboratory: Watowich is an author on every enzymology and rodent paper above, and the 2024 papers declare that he founded, and that co-authors are employed or formerly employed by, the company developing the series. A declared interest is a disclosure, not a defect — but nothing in that file has been independently reproduced in vivo, and the one independent report is a cell-culture study. Its relationship to NAD⁺ metabolism sits alongside the mitochondrial compounds and is a separate literature.

Kisspeptin-10

Identity

Kisspeptin-10 is a C-terminally amidated decapeptide corresponding to residues 45–54 of metastin, the KISS1 gene product. PubChem CID 25240297: sequence YNWNSFGLRF in one-letter notation, formula C₆₃H₈₃N₁₇O₁₄, average mass 1302.4 g/mol, monoisotopic mass 1301.6305, CAS 374675-21-5, UNII FS1N52VS3S. It is catalogued among the reproductive compounds.

In vitro work

Three groups reported in 2001 that the KiSS-1 gene product is the ligand of the orphan receptor GPR54 (Kotani et al.; Ohtaki et al.; Muir et al.), and that the C-terminal decapeptide retains the parent’s activity. Takino and colleagues (2003) reported that matrix metalloproteinases cleave the Gly–Leu bond of the decapeptide and that digestion abolished ligand activity, which identifies the most labile position in the sequence.

Rodent models

Thompson and colleagues (2004) reported dose-related rises in LH, FSH and testosterone in male rats, and Messager and colleagues (2005) direct stimulation of GnRH release via GPR54. Two chronic-exposure reports matter more than their citation counts suggest. Thompson and colleagues (2006) administered kisspeptin-54 to adult male Wistar rats over 13 days and reported decreased testicular weight and degeneration of the seminiferous tubules with a fall in circulating inhibin B. Ramzan and Qureshi (2011) administered kisspeptin-10 to five-week-old male rats over 12 days and reported dose-dependent falls in plasma LH and testosterone, reduced Sertoli cell efficiency across the range examined, and tubular necrosis on histology.

Human studies

The human file is better developed than the compound’s market profile suggests, and it is small and mechanistic throughout. George and colleagues (2011) reported dose-related LH rises and increased pulse frequency in men; Chan and colleagues (2011) that a single administration in 13 men induced an LH pulse irrespective of the timing of the preceding one; Jayasena and colleagues (2011) a sexually dimorphic response. Jayasena and colleagues (2015) compared kisspeptin-10, kisspeptin-54 and GnRH in 15 healthy men, five per group, and reported serum LH and FSH about three-fold higher on GnRH. Skorupskaite and colleagues (2016, 2020) reported randomised crossover studies in healthy women and in women with polycystic ovary syndrome. Yeung and colleagues (2026) reported a randomised, single-blinded, placebo-controlled study in 15 healthy men with 12 controls, in which repeated administration over 12 days sustained gonadotrophin increases.

Where this record stops

Twelve days is the longest published human exposure. Everything before it is single-administration or short-exposure physiology in single-figure to low-double-figure groups, run by roughly three collaborating academic centres. There is no completed randomised controlled trial with a clinical endpoint and no licensed indication anywhere, so no published human dataset covers repeated exposure beyond that window. The two rodent reports above are the only chronic-exposure findings in the file, and one used kisspeptin-54 rather than the decapeptide — the same kind of distinction that separates a parent protein from a fragment, and one to check rather than assume.

The rules in force, and the one that is routinely misread

No marketing authorisation was identified for any of the three in the United Kingdom, the European Union or the United States. When supply of an unlicensed substance becomes unlawful is set out in the MHRA position: the claim attached to a substance, not the identity of the molecule, is what changes its status.

On the 2026 WADA Prohibited List, in force from 1 January 2026, kisspeptin is named. S2.2.1, “Testosterone-stimulating peptides in males”, lists “kisspeptin and its agonist analogues” alongside chorionic gonadotrophin, luteinising hormone and the GnRH agonists. All S2 substances are non-Specified, and the section is expressly limited to males.

Neither cagrilintide nor 5-Amino-1MQ is named on that List, and no amylin analogue and no NNMT inhibitor appears as a class. That absence is regularly read as permission, and on the text of the List it is not. S0 reads: Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development or discontinued, designer drugs, substances approved only for veterinary use) is prohibited at all times. Both are unapproved everywhere and neither is addressed by a later section, so S0 applies on its face; all S0 substances are Specified. The contrast is the point: semaglutide holds approvals, so S0 cannot reach it, while its investigational partner molecule has none. The List is reissued annually, so every line here needs re-reading against the current edition.

Handling, and what the arithmetic gives

Concentration after reconstitution is the mass in the vial divided by the volume of diluent added, and nothing else: 10 mg into 2 ml gives 5 mg/ml, the same 10 mg into 1 ml gives 10 mg/ml. That relation is identical for all three, and the calculator resolves it from vial strength and diluent volume. Its boundary is this page’s boundary: the volume is arithmetic and is ours to calculate, a target amount is not, and none appears anywhere here. The only compound-specific trap is the salt basis on 5-Amino-1MQ, which changes the number rather than the method.

A band is a statement about a published literature. It says nothing about the identity or purity of material in a particular vial, which are batch properties established by analysis and read off a certificate. NovoVita’s published position is one sentence: Third-party tested at greater than 99% purity. Neither question answers the other.

References

1. World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. In force 1 January 2026. Sections S0 and S2.2.1. (regulatory)
2. UniProt Consortium. UniProtKB entry P10997, Islet amyloid polypeptide (human). Mature peptide 34–70; disulphide 35–40; C-terminal tyrosine amide. (reference database)
3. National Center for Biotechnology Information. PubChem Compound Summary for CID 171397054 (cagrilintide), CID 66522933 (5-amino-1-methylquinolinium iodide) and CID 25240297 (kisspeptin-10). (reference database)
4. Kruse T, et al. Development of Cagrilintide, a Long-Acting Amylin Analogue. J Med Chem. 2021;64(15):11183–11194. PMID 34288673. DOI 10.1021/acs.jmedchem.1c00565. (in vitro / medicinal chemistry)
5. Fletcher MM, et al. AM833 Is a Novel Agonist of Calcitonin Family G Protein-Coupled Receptors: Pharmacological Comparison with Six Selective and Nonselective Agonists. J Pharmacol Exp Ther. 2021;377(3):417–440. PMID 33727283. DOI 10.1124/jpet.121.000567. (in vitro)
6. Cao J, et al. Structural and dynamic features of cagrilintide binding to calcitonin and amylin receptors. Nat Commun. 2025;16(1):3389. PMID 40204768. DOI 10.1038/s41467-025-58680-y. (in vitro / structural)
7. Alhalabi H, et al. In vitro metabolic profiling of weight-loss-inducing amylin receptor agonists in the context of preventive doping research. J Pharm Biomed Anal. 2026;273:117418. PMID 41702251. DOI 10.1016/j.jpba.2026.117418. (in vitro)
8. Carvas AO, et al. Cagrilintide lowers bodyweight through brain amylin receptors 1 and 3. EBioMedicine. 2025;118:105836. PMID 40609154. DOI 10.1016/j.ebiom.2025.105836. (rodent)
9. Ludwig MQ, et al. A cross-species atlas of the dorsal vagal complex reveals neural mediators of the effects of cagrilintide on energy balance. Nat Metab. 2026;8(6):1350–1367. PMID 42260119. DOI 10.1038/s42255-026-01539-3. (rodent and comparative)
10. Enebo LB, et al. Safety, tolerability, pharmacokinetics, and pharmacodynamics of concomitant administration of multiple doses of cagrilintide with semaglutide 2·4 mg for weight management: a randomised, controlled, phase 1b trial. Lancet. 2021;397(10286):1736–1748. PMID 33894838. DOI 10.1016/S0140-6736(21)00845-X. (human trial)
11. Lau DCW, et al. Once-weekly cagrilintide for weight management in people with overweight and obesity: a multicentre, randomised, double-blind, placebo-controlled and active-controlled, dose-finding phase 2 trial. Lancet. 2021;398(10317):2160–2172. PMID 34798060. DOI 10.1016/S0140-6736(21)01751-7. (human trial)
12. Frías JP, et al. Efficacy and safety of co-administered once-weekly cagrilintide 2·4 mg with once-weekly semaglutide 2·4 mg in type 2 diabetes: a multicentre, randomised, double-blind, active-controlled, phase 2 trial. Lancet. 2023;402(10403):720–730. PMID 37364590. DOI 10.1016/S0140-6736(23)01163-7. (human trial)
13. Garvey WT, et al. Coadministered Cagrilintide and Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2025;393(7):635–647. PMID 40544433. DOI 10.1056/NEJMoa2502081. (human trial)
14. Davies MJ, et al. Cagrilintide-Semaglutide in Adults with Overweight or Obesity and Type 2 Diabetes. N Engl J Med. 2025;393(7):648–659. PMID 40544432. DOI 10.1056/NEJMoa2502082. (human trial)
15. Yamauchi T, et al. Efficacy and safety of co-administered cagrilintide and semaglutide versus semaglutide alone in adults with overweight or obesity with or without type 2 diabetes in Japan and Taiwan (REDEFINE 5). Lancet Diabetes Endocrinol. 2026;14(6):450–462. PMID 42009015. DOI 10.1016/S2213-8587(25)00402-4. (human trial)
16. Aroda VR, et al. Efficacy and safety of once-weekly cagrilintide-semaglutide (CagriSema) in adults with type 2 diabetes inadequately controlled on diet and exercise (REIMAGINE 1). Lancet Diabetes Endocrinol. 2026;14(8):649–661. PMID 42251860. DOI 10.1016/S2213-8587(26)00126-9. (human trial)
17. Buse JB, et al. Cagrilintide-semaglutide (CagriSema) versus semaglutide or cagrilintide in people with type 2 diabetes (REIMAGINE 2): a double-blind, randomised, controlled, phase 3 study. Lancet Diabetes Endocrinol. 2026;14(8):662–677. PMID 42251859. DOI 10.1016/S2213-8587(26)00125-7. (human trial)
18. Rosenstock J, et al. Cagrilintide-semaglutide (CagriSema) as an add-on to basal insulin in adults with type 2 diabetes (REIMAGINE 3). Lancet. 2026;408(10549):38–51. PMID 42251856. DOI 10.1016/S0140-6736(26)01022-6. (human trial)
19. Nielsen MJF, et al. Renal or Hepatic Impairment Does Not Affect Pharmacokinetics, Safety, or Tolerability of Subcutaneous Cagrilintide. Clin Pharmacokinet. 2026;65(7):1087–1099. PMID 42228334. DOI 10.1007/s40262-026-01654-0. (human trial)
20. Novo Nordisk. Company announcement, 18 December 2025: new drug application for the cagrilintide–semaglutide fixed-dose combination submitted to the US Food and Drug Administration. (regulatory / company disclosure)
21. Neelakantan H, et al. Noncoupled Fluorescent Assay for Direct Real-Time Monitoring of Nicotinamide N-Methyltransferase Activity. Biochemistry. 2017;56(6):824–832. PMID 28121423. DOI 10.1021/acs.biochem.6b01215. (in vitro)
22. Neelakantan H, et al. Structure-Activity Relationship for Small Molecule Inhibitors of Nicotinamide N-Methyltransferase. J Med Chem. 2017;60(12):5015–5028. PMID 28548833. DOI 10.1021/acs.jmedchem.7b00389. (in vitro)
23. Neelakantan H, et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018;147:141–152. PMID 29155147. DOI 10.1016/j.bcp.2017.11.007. (rodent)
24. Neelakantan H, et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2019;163:481–492. PMID 30753815. DOI 10.1016/j.bcp.2019.02.008. (rodent)
25. Akar S, et al. Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells. J Obstet Gynaecol. 2021;41(8):1240–1245. PMID 33645410. DOI 10.1080/01443615.2020.1854696. (in vitro)
26. Sampson CM, et al. Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice. Sci Rep. 2021;11(1):5637. PMID 33707534. DOI 10.1038/s41598-021-85051-6. (rodent)
27. Dimet-Wiley A, et al. Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice. Sci Rep. 2022;12(1):484. PMID 35013352. DOI 10.1038/s41598-021-03670-5. (rodent)
28. Dimet-Wiley AL, et al. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Sci Rep. 2024;14(1):15554. PMID 38969654. DOI 10.1038/s41598-024-66034-9. (rodent)
29. Babula JJ, et al. Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes Obes Metab. 2024;26(11):5272–5282. PMID 39161060. DOI 10.1111/dom.15879. (rodent)
30. Kotani M, et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J Biol Chem. 2001;276(37):34631–34636. PMID 11457843. DOI 10.1074/jbc.M104847200. (in vitro)
31. Ohtaki T, et al. Metastasis suppressor gene KiSS-1 encodes peptide ligand of a G-protein-coupled receptor. Nature. 2001;411(6837):613–617. PMID 11385580. DOI 10.1038/35079135. (in vitro)
32. Muir AI, et al. AXOR12, a novel human G protein-coupled receptor, activated by the peptide KiSS-1. J Biol Chem. 2001;276(31):28969–28975. PMID 11387329. DOI 10.1074/jbc.M102743200. (in vitro)
33. Takino T, et al. Cleavage of metastasis suppressor gene product KiSS-1 protein/metastin by matrix metalloproteinases. Oncogene. 2003;22(30):4617–4626. PMID 12879005. DOI 10.1038/sj.onc.1206542. (in vitro)
34. Thompson EL, et al. Central and peripheral administration of kisspeptin-10 stimulates the hypothalamic-pituitary-gonadal axis. J Neuroendocrinol. 2004;16(10):850–858. PMID 15500545. DOI 10.1111/j.1365-2826.2004.01240.x. (rodent)
35. Messager S, et al. Kisspeptin directly stimulates gonadotropin-releasing hormone release via G protein-coupled receptor 54. Proc Natl Acad Sci U S A. 2005;102(5):1761–1766. PMID 15665093. DOI 10.1073/pnas.0409330102. (rodent)
36. Thompson EL, et al. Chronic subcutaneous administration of kisspeptin-54 causes testicular degeneration in adult male rats. Am J Physiol Endocrinol Metab. 2006;291(5):E1074–E1082. PMID 16787965. DOI 10.1152/ajpendo.00040.2006. (rodent; kisspeptin-54, not the decapeptide)
37. Ramzan F, Qureshi IZ. Intraperitoneal kisspeptin-10 administration induces dose-dependent degenerative changes in maturing rat testes. Life Sci. 2011;88(5–6):246–256. PMID 21112339. DOI 10.1016/j.lfs.2010.11.019. (rodent)
38. Dhillo WS, et al. Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. J Clin Endocrinol Metab. 2005;90(12):6609–6615. PMID 16174713. DOI 10.1210/jc.2005-1468. (human trial; kisspeptin-54)
39. Keen KL, et al. An increase in kisspeptin-54 release occurs with the pubertal increase in luteinizing hormone-releasing hormone-1 release in the stalk-median eminence of female rhesus monkeys in vivo. Endocrinology. 2008;149(8):4151–4157. PMID 18450954. DOI 10.1210/en.2008-0231. (non-rodent animal)
40. George JT, et al. Kisspeptin-10 is a potent stimulator of LH and increases pulse frequency in men. J Clin Endocrinol Metab. 2011;96(8):E1228–E1236. PMID 21632807. DOI 10.1210/jc.2011-0089. (human trial)
41. Chan YM, et al. Kisspeptin resets the hypothalamic GnRH clock in men. J Clin Endocrinol Metab. 2011;96(6):E908–E915. PMID 21470997. DOI 10.1210/jc.2010-3046. (human trial)
42. Jayasena CN, et al. The effects of kisspeptin-10 on reproductive hormone release show sexual dimorphism in humans. J Clin Endocrinol Metab. 2011;96(12):E1963–E1972. PMID 21976724. DOI 10.1210/jc.2011-1408. (human trial)
43. Jayasena CN, et al. Direct comparison of the effects of intravenous kisspeptin-10, kisspeptin-54 and GnRH on gonadotrophin secretion in healthy men. Hum Reprod. 2015;30(8):1934–1941. PMID 26089302. DOI 10.1093/humrep/dev143. (human trial)
44. Skorupskaite K, et al. Interactions Between Neurokinin B and Kisspeptin in Mediating Estrogen Feedback in Healthy Women. J Clin Endocrinol Metab. 2016;101(12):4628–4636. PMID 27636018. DOI 10.1210/jc.2016-2132. (human trial)
45. Skorupskaite K, et al. Kisspeptin and neurokinin B interactions in modulating gonadotropin secretion in women with polycystic ovary syndrome. Hum Reprod. 2020;35(6):1421–1431. PMID 32510130. DOI 10.1093/humrep/deaa104. (human trial)
46. Yeung AC, et al. Chronic subcutaneous kisspeptin-10 stimulates gonadotropin secretion for 12 days in healthy men. Eur J Endocrinol. 2026;195(2):206–216. PMID 42549827. DOI 10.1093/ejendo/lvag134. (human trial)
47. ClinicalTrials.gov. Intervention-field queries for “cagrilintide”, “kisspeptin” and “5-amino-1MQ”, run 9 August 2026. (registry)