Does Kisspeptin Work for IVF? What the Trials Measured

Three human trials, 175 women, babies born.¹²³ That is more evidence than almost anything else sold as a peptide. All of it belongs to kisspeptin-54.

You cannot buy kisspeptin-54 from a peptide seller. What sells is kisspeptin-10. The FDA named that form when it listed kisspeptin among bulk drugs that raise safety risks.⁴

The trials asked whether eggs matured. None asked whether kisspeptin makes more babies than the standard trigger. None had a control group.¹²³ Each dose went in 36 hours before a booked egg retrieval. Women were already on fertility drugs and watched by scan. The drug timed one step in a procedure.

How many human trials of kisspeptin in IVF are there?

Three, and the same group in London ran all of them.

Trial	Year	Women	Design
Jayasena, Journal of Clinical Investigation	2014	53 treated	single-center proof of concept, dose escalation
Abbara, JCEM	2015	60	Phase 2, four doses, all received kisspeptin
Abbara, Human Reproduction	2017	62 randomized	Phase 2, second dose against saline

Everything published on kisspeptin and IVF comes from one place. All three trials came from Waljit Dhillo's team at Imperial College London and Hammersmith Hospital, between 2014 and 2017. Sourcing tier per trial in the footnotes.

Three trials from one group is a real evidence base for a peptide and a thin one for a fertility treatment. Nothing has followed: no Phase 3, and no new trial since 2017.

One detail complicates calling them three separate registered trials. All three papers cite the same registration number.¹²³ Whether that covers one protocol in three parts or is loose citation in some of them could not be established, because the trials registry refused every available route.

What did the kisspeptin IVF trials measure?

Eggs maturing. That was the endpoint in all three.

Jayasena 2014 states it plainly: "The primary outcome was egg maturation during a single treatment cycle."¹ Abbara 2015 says "The primary outcome was oocyte maturation."² In 2017 the primary outcome was the proportion of patients reaching an oocyte yield "of at least 60%."³

Maturation results were good. In the 2015 Phase 2, "Oocyte maturation (≥ 1 mature oocyte) was observed in 95% (57/60) of women who received kisspeptin-54."² Jayasena 2014 found "similar rates of egg maturation (proportion of recovered eggs that were mature), between 75% and 85%, were observed following all doses."¹

Nobody measured whether more babies result. Live birth appears in all three papers, but as a descriptive outcome, not the thing the trial was built to test. A trigger that matures eggs and a treatment that produces a baby are different claims, and only the first was tested.

Did anyone compare kisspeptin against the standard trigger?

No randomized trial has ever done it. The researchers say so themselves.

None of the three trials had an hCG arm. Nor did any have a GnRH agonist arm. In 2014 and 2015 the studies compared kisspeptin doses against each other, with every participant receiving kisspeptin. The 2017 trial randomized 62 women, and what it randomized was whether they got a second kisspeptin dose or a saline injection ten hours after the first.³

So the one placebo-controlled randomization in the whole program tested adding a dose, not kisspeptin against anything else.

Their own 2022 review is explicit: "Pregnancy rates following kisspeptin have yet to be directly prospectively compared to other triggers," and "Direct prospective randomised comparison between kisspeptin and currently available clinical triggers is needed."⁵

Two retrospective comparisons exist, which is a different thing from a trial.⁵⁶ Retrospective means looking back at records of people who were given different triggers for reasons nobody randomized.

What about the claim that kisspeptin avoids ovarian hyperstimulation?

The argument has three supports. Not one of them is a randomized comparison.

Ovarian hyperstimulation syndrome is the complication the standard hCG trigger can cause, and avoiding it is the clinical argument for kisspeptin. How kisspeptin sits beside hCG and the other options is covered in our four-way comparison. Its support comes from three places.

What it is	What it shows	What it is not
The 2015 Phase 2 in 60 high-risk women	three mild early cases, one mild late, "no woman had moderate, severe, or critical OHSS"	a comparison, since nobody got hCG
A historical expectation	the authors say "we might have expected 27% of the patients in our study (16/60) to have developed moderate to severe OHSS"	measured, since it comes from other groups' published criteria
A 2018 retrospective cohort	odds of OHSS "significantly higher following hCG (OR 33.6, 95% confidence interval (CI) 12.6-89.5)" than kisspeptin	randomized, and this page could not read it in the original

Figures quoted from the sources named in the footnotes. The odds ratios come through the group's own later review, not the 2018 paper, whose publisher could not be reached.

The signal points one way and it may well be real. What does not exist is the study that would establish it. The researchers end their own review asking for "a prospective study directly and objectively characterising signs and symptoms of OHSS."⁵

Were there live births?

Yes, in all three trials. The numbers need their denominators.

Trial	Live births	Of what
2014	ten women gave birth	53 treated
2015	23	51 embryo transfers, a 45% rate per transfer
2017	6 single dose, 12 double dose	31 and 31

Figures as each paper reports them. The denominators differ between trials, so the rates are not directly comparable.

Those are real babies. What they cannot tell you is whether kisspeptin did better than the alternative, because nobody in these trials received the alternative. The 2017 trial's difference in clinical pregnancy between one dose and two was not statistically significant at P = 0.199, even though the live birth numbers look far apart.³

One discrepancy to know about if you check the sources. The 2022 review's table gives a 30.0% live birth rate per transfer for the 2017 trial while its own text gives 39% per protocol.⁵ Different denominators, not interchangeable, and the kind of gap that produces confident wrong numbers in secondhand coverage.

Which kisspeptin did the trials use?

Kisspeptin-54, every time.

All three trigger trials used kisspeptin-54 by subcutaneous injection.¹²³ The 2014 paper names the manufacturer in its methods: "Kisspeptin-54 was synthesized and purified by Bachem."¹

Kisspeptin comes in several lengths cut from the same precursor protein, a 145 amino acid chain.⁷ The fertility trials used the 54-residue form. Kisspeptin-10 is the last ten amino acids of it. Both go by competing numbering systems that make catalog listings hard to read. One system counts from the start of the precursor, so the short fragment becomes residues 112 to 121. The other counts from the start of the 54-residue peptide, so the same fragment becomes 45 to 54. Nothing in the literature reconciles them, which is why the same molecule appears under two sets of numbers.

	Kisspeptin-54	Kisspeptin-10
Length	54 amino acids	10 amino acids
Position in the precursor	residues 68 to 121	residues 112 to 121
Also written as	metastin 1-54	metastin 45-54
Approximate mass	5,858 daltons	1,302 daltons
Half-life	roughly 28 minutes	roughly 4 minutes
IVF trigger trials	three	none

Positions and masses from supplier catalog records; half-lives from the published reviews. Both numbering conventions appear in the literature without explanation.

Which kisspeptin is actually sold?

Kisspeptin-10. The FDA named that one specifically.

On September 29, 2023 the FDA placed "Kisspeptin-10" in category 2 of its compounding list, meaning bulk drug substances that raise significant safety risks. Its stated concerns are that compounded drugs containing it "may pose risk for immunogenicity for certain routes of administration" and "may have complexities with regard to peptide-related impurities and API characterization," and that the agency "lacks sufficient information to know whether the drug would cause harm when administered to humans."⁴

Kisspeptin-54 appears nowhere on that list, or on any FDA compounding list.⁴

The regulator wrote down the form people buy. The form that was trialled is not sold to consumers at all; it is stocked by laboratory reagent houses, including the firm named in the 2014 trial's own methods.

Can you buy the kisspeptin that was trialled?

Not from a consumer seller, and the price index gives the count.

Across 91 kisspeptin listings from 70 distinct sellers, captured between September 27 and October 4, 2026, 66 name the 10-residue form explicitly. None names the 54-residue form. No listing in that capture uses kisspeptin-54, KP-54 or metastin, and neither does any listing for the other 159 compounds tracked alongside it.

Another 25 listings name no form at all. Twenty-one of those give only a milligram size, which is a quantity and not an identity. A vial sold as "Kisspeptin 10mg" states how much is inside, not which fragment it is.

Kisspeptin-54 is stocked instead by laboratory reagent suppliers, who sell milligram quantities against institutional purchase orders. That is where the 2014 trial got its material, as its methods section records.¹

The two forms point in opposite directions. The form carrying three trials, and the 51 live births those papers add up to, is not on the consumer market at all. The form that is on the consumer market, in 91 listings, has never been given to a human as an IVF trigger.

Is kisspeptin-10 a weaker version or a different drug?

Neither, and getting this right matters.

One tempting argument says the market sells the wrong molecule and it therefore does nothing. That overstates it. A 2025 review states that the kisspeptin fragments "exhibit the same affinity and efficacy at the kisspeptin receptor despite their different lengths," and that all of them "act as agonists of KISS1R."⁸

So kisspeptin-10 hits the same receptor just as hard. The difference is how long it lasts: roughly four minutes against roughly 28, a gap of about tenfold.⁷

For a compound whose entire tested use is a single timed injection meant to drive a hormone surge over several hours before a scheduled surgery, that gap is not a technicality. It is the variable the whole protocol depends on. But the accurate statement is that kisspeptin-10 has the same receptor activity with a far shorter duration and has never been given to a human being as an IVF trigger, not that it is inert.

The kisspeptin half-life figures do not agree with each other either. The same group's 2020 study measured kisspeptin-54 at 1.7 hours and called that "longer than that previously reported (~0.5 hours)," while that paper's own introduction still prints the 27.6 minute figure.⁹ The published number for the trialled molecule is not settled.

What was the trial actually doing?

Timing one injection at a fixed point inside a medical procedure.

Almost every element of that design is missing from a person injecting at home.

Participants had diagnosed infertility and were mid-way through IVF.¹² Each woman had already completed controlled ovarian stimulation, described in the 2015 trial as "a recombinant FSH/GnRH antagonist protocol," with "pelvic ultrasound scan was performed 5 days after commencing injections to determine ovarian follicular development."² Eligibility was narrow: ages 18 to 34, body mass index 18 to 29, regular cycles.¹ Later trials additionally required high ovarian reserve on blood and ultrasound measures.² Then came one injection, given by a study investigator, "36 hours prior to oocyte retrieval."² Thirty-six hours later a surgeon removed the eggs.

Strip any part of that away and the trial stops describing what is happening. Without stimulation there are no follicles to mature. Without monitoring nobody knows whether the follicles are ready. Without the retrieval the matured eggs stay where they are. In these studies it did one job, timing a step that only exists inside the procedure.

Does kisspeptin help fertility if you are not doing IVF?

Nothing in the human literature tests that.

The kisspeptin fertility claim rests on nothing tested. No trial has given kisspeptin to people with normal fertility to see whether they conceive more easily, which is the usual situation for compounds sold this way. The participants in all three trigger trials had diagnosed infertility and were mid-cycle in an IVF protocol.¹²³

Two research lines come nearest, and neither answers the question. A newer analogue derived from kisspeptin-10 has been given to healthy premenopausal women, measuring hormone levels and ovulation timing by ultrasound, with no oocyte, retrieval or pregnancy outcome recorded at all.⁹¹⁰ And two randomized crossover trials gave kisspeptin-54 by intravenous infusion to men and women with low sexual desire, measuring brain activity.¹¹¹² Those are brain studies, not fertility studies.

What happens if you use kisspeptin repeatedly?

The response fades. Somebody measured that rather than theorizing it.

A 2009 study gave kisspeptin-54 twice daily to women with absent periods. Its title says the finding: acute stimulation, then tachyphylaxis with chronic administration.¹³ Our PT-141 and kisspeptin comparison records the figures, with the luteinizing hormone response falling from 24.0 on day one to 2.5 by day fourteen on the same dose.

Every trigger trial used one or two doses inside a single cycle. Repeat-dose and long-term safety data do not exist in the IVF program at all, and the one published chronic-dosing signal points at the response collapsing.

What would settle the kisspeptin IVF question?

Three studies. One of them is what the researchers have been asking for in print since 2022.

What is missing	Why it would settle something
A randomized trial against hCG	no trial has ever compared kisspeptin to the standard trigger
An ovarian hyperstimulation comparison	the safety advantage rests on single-arm data and one retrospective cohort
Any human study of kisspeptin-10 as a trigger	the trialled form is not the sold form, and the sold form has never been tested this way

Those first two sit on the group's own published wish list. The third is nobody's research priority, because the clinical program has no reason to test the shorter fragment when it already uses the longer one.

Which sources could not be checked?

Six sources or records could not be opened.

• The trials registry. Every available route was refused, so the registration covering all three trials could not be examined, no kisspeptin trial could be enumerated independently, and a Phase 3 could not be ruled out by registry search.
• The 2018 retrospective cohort in the original. Its publisher could not be reached, so its odds ratios come through the group's own 2022 review instead of the paper.
• The 2014 trial's per-dose results table, which did not render across two reads of the full text. Only the 75 to 85% range and one confidence interval were obtainable.
• Drugs@FDA by direct query, which requires a form submission. The absence of an approved kisspeptin product in the United States rests on an openFDA search returning nothing where a control search returned a result.
• Regulators outside the United States, none of which were checked.
• The supplementary safety tables of the 2023 men's brain-imaging trial.

Common questions

Does kisspeptin work for IVF?

Has kisspeptin produced live births?

Is kisspeptin approved for fertility treatment?

Which kisspeptin did the IVF trials use?

Is kisspeptin-10 the same thing?

Why does the half-life difference matter so much here?

Does kisspeptin prevent ovarian hyperstimulation?

Can kisspeptin improve fertility if I am not doing IVF?

What dose did the trials use?

Does kisspeptin keep working if you use it regularly?

What are the side effects of kisspeptin?

Is kisspeptin safe?

What is kisspeptin?

Is kisspeptin the same as metastin?

How many babies have been born after a kisspeptin trigger?

Can you buy kisspeptin-54?

Can a doctor prescribe kisspeptin in the United States?

Why is there no kisspeptin IVF research newer than 2017?

Sources

1. Jayasena CN, Abbara A, Comninos AN, Nijher GMK, Christopoulos G, Narayanaswamy S, Izzi-Engbeaya C, Sridharan M, Mason AJ, Warwick J, Ashby D, Ghatei MA, Bloom SR, Carby A, Trew GH, Dhillo WS. Kisspeptin-54 triggers egg maturation in women undergoing in vitro fertilization. Journal of Clinical Investigation 2014;124(8):3667-3677. DOI 10.1172/JCI75730. Read at source across two passes; the per-dose results table did not render in either. Described by the authors as a "single-center, proof-of-concept study." Sixty patients screened, 53 treated, with 1:1 randomization only between the two highest doses (n=24 each). Single subcutaneous kisspeptin-54 at 1.6, 3.2, 6.4 or 12.8 nmol/kg, with the manufacturer named in the methods and quoted in the body. No hCG, agonist or placebo arm. Primary outcome was egg maturation in a single cycle, quoted in the body. Maturation "between 75% and 85%" across doses; the only inferential statistic reported for efficacy is a difference of 1.2 mature eggs between the top two doses (95% CI, -1.0 to 3.5). No p-value is given for any efficacy comparison. Pregnancy rates 40% biochemical and 23% clinical; ten women gave birth. "Kisspeptin-54 administration was well tolerated in all 53 subfertile patients in this study." Registration cited as NCT01667406. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11
2. Abbara A, Jayasena CN, Christopoulos G, Narayanaswamy S, Izzi-Engbeaya C, Nijher GMK, Comninos AN, Peters D, Buckley A, Ratnasabapathy R, Prague JK, Salim R, Lavery SA, Bloom SR, Szigeti M, Ashby DA, Trew GH, Dhillo WS. Efficacy of kisspeptin-54 to trigger oocyte maturation in women at high risk of ovarian hyperstimulation syndrome during in vitro fertilization therapy. Journal of Clinical Endocrinology and Metabolism 2015;100(9):3322-3331. DOI 10.1210/jc.2015-2332. Read at source across two passes. Sixty women at high risk of OHSS, all receiving kisspeptin-54 at 3.2, 6.4, 9.6 or 12.8 nmol/kg; no concurrent comparator. "Kisspeptin-54 was administered 36 hours prior to oocyte retrieval (between 2030 and 2300 h)." Stimulation was "a recombinant FSH/GnRH antagonist protocol." Primary outcome was oocyte maturation, and the 95% (57/60) maturation result is quoted in the body. Live birth 45% per transfer, 23 births from 51 transfers. OHSS: "only three (5%) were diagnosed with mild early OHSS and one with mild late OHSS (2%)," and "no woman had moderate, severe, or critical OHSS and no woman required medical intervention for OHSS." The 27% counterfactual is the authors' own expectation drawn from another group's published criteria, not a measured comparison. Note an internal inconsistency: the abstract calls the trial "open-label" while the methods state that participants, embryologists and retrieval clinicians "were all blinded to the dose allocation." Registration cited as NCT01667406. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11
3. Abbara A, Clarke S, Islam R, Prague JK, Comninos AN, Narayanaswamy S, Papadopoulou D, Roberts R, Izzi-Engbeaya C, Ratnasabapathy R, Nesbitt A, Vimalesvaran S, Salim R, Lavery SA, Bloom SR, Huson L, Trew GH, Dhillo WS. A second dose of kisspeptin-54 improves oocyte maturation in women at high risk of ovarian hyperstimulation syndrome: a Phase 2 randomized controlled trial. Human Reproduction 2017;32(9):1915-1924. DOI 10.1093/humrep/dex253. Read at source. Sixty-two women randomized 1:1; all received kisspeptin-54 at 9.6 nmol/kg 36 hours before retrieval, then either a second dose or saline ten hours later. The randomized comparison is therefore second dose against saline, not kisspeptin against another trigger. Primary outcome was the proportion reaching an oocyte yield "of at least 60%": 45% single against 71% double, difference +26%, CI 2-50%, P = 0.042. Live birth 19.4% (6/31) single and 39% (12/31) double; clinical pregnancy difference P = 0.199, not significant. "There was no difference in the occurrence of OHSS between those who received a single or double dose." Note two internal discrepancies: the abstract gives the double group as 21/31 while the results table gives 22 (71.0%), and OHSS percentages are reported against inconsistent denominators. Registration cited as NCT01667406. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8
4. US Food and Drug Administration. "Kisspeptin-10" appears under 503A category 2, bulk drug substances that raise significant safety risks, in the agency's nomination list (Bulk Drug Substances Nominated for Use in Compounding Under Section 503A, updated May 14, 2026) and in the category 2 table on the agency's significant-safety-risks page (content current as of April 22, 2026), with a date added of September 29, 2023. Both read at source. The agency's three stated concerns are quoted in full in the body of this page. Kisspeptin-54, KP-54, KP-10 and metastin do not appear on that list or on the 503B list in any form. Absence of an approved US product rests on an openFDA drug application search returning no match where a control query on another compound returned one, not on a published statement; Drugs@FDA could not be queried directly because its search requires a form submission unavailable to this page. ↩1 ↩2 ↩3
5. Sharma B, Koysombat K, Comninos AN, Dhillo WS, Abbara A. Use of kisspeptin to trigger oocyte maturation during in vitro fertilisation (IVF) treatment. Frontiers in Endocrinology 2022;13:972137. DOI 10.3389/fendo.2022.972137. Read at source. Source for "Pregnancy rates following kisspeptin have yet to be directly prospectively compared to other triggers," "Direct prospective randomised comparison between kisspeptin and currently available clinical triggers is needed," and "a prospective study directly and objectively characterising signs and symptoms of OHSS is needed." Also the route by which the 2018 odds ratios reach this page. Note that this review's table gives 30.0% live birth per transfer for the 2017 trial while its text gives 39% per protocol, and that it describes the 2014 study as a phase 2 randomized trial where the paper itself calls it a proof-of-concept study. ↩1 ↩2 ↩3 ↩4
6. Abbara A, Islam R, Clarke SA, Jeffers L, Christopoulos G, Comninos AN, Salim R, Lavery SA, Vuong TNL, Humaidan P, Kelsey TW, Trew GH, Dhillo WS. Clinical parameters of ovarian hyperstimulation syndrome following different hormonal triggers of oocyte maturation in IVF treatment. Clinical Endocrinology 2018;88(6):920-927. DOI 10.1111/cen.13569. Retrospective single-center cohort, hCG n=40, GnRH agonist n=99, kisspeptin n=122. Not read in the original: the publisher is unreachable from this site. The odds ratios quoted on this page, 33.6 (95% CI 12.6-89.5) for hCG and 3.6 (95% CI 1.8-7.1) for GnRH agonist against kisspeptin, are quoted from the 2022 review at footnote 5, so they are reported here at one remove. Author list verified through a bibliographic record. ↩1
7. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH pathway in human reproductive health and disease. Human Reproduction Update 2014;20(4):485-500. DOI 10.1093/humupd/dmu009. Read at source. Source for the kisspeptin-54 half-life of "27.6 ± 1.1 min" against "about 4 min for kisspeptin-10," for the 145 amino acid precursor, for the naming of the 54-residue transcript as metastin, and for the precursor being cleaved to 14, 13 and 10 amino acid peptides. Residue positions and molecular masses in the comparison table come from supplier catalog records, which use two numbering conventions for the same molecules without reconciling them. ↩1 ↩2
8. Chen X, Yang S, Shaw ND, Xia M. Kisspeptin receptor agonists and antagonists: strategies for discovery and implications for human health and disease. International Journal of Molecular Sciences 2025;26(10):4890. DOI 10.3390/ijms26104890. Read at source. Source for the two statements quoted in the body: that the fragments share affinity and efficacy at the receptor despite differing in length, and that all of them agonize KISS1R. The review describes human administration only for kisspeptin-54 and kisspeptin-10; no human administration data for the 13 or 14 residue fragments was located for this page. ↩1
9. Abbara A, Eng PC, Phylactou M, et al. (corresponding author Dhillo WS). Kisspeptin receptor agonist has therapeutic potential for female reproductive disorders. Journal of Clinical Investigation 2020;130(12):6739-6753. DOI 10.1172/JCI139681. Read at source. Source for the half-life inconsistency: this study measured kisspeptin-54 at 1.7 hours and said so in the words quoted in the body, while its own introduction states 27.6 minutes. Also the first-in-women study of MVT-602, described as "a nanopeptide KISS1R agonist" developed from kisspeptin-10, in healthy women, women with polycystic ovary syndrome and women with hypothalamic amenorrhoea, with no oocyte, retrieval or pregnancy outcome measured. "No serious adverse effects were identified after injection of either MVT-602 or KP54." The authors note that whether its profile "translates to improved clinical outcomes during IVF treatment would be of great interest," which is a statement that it has not been tested there. ↩1 ↩2
10. Endocrine profile of the kisspeptin receptor agonist MVT-602 in healthy premenopausal women with and without ovarian stimulation: results from 2 randomized, placebo-controlled clinical trials. Fertility and Sterility 2024;121(1):95-106. DOI 10.1016/j.fertnstert.2023.10.031. Abstract only, read through a bibliographic record; the publisher is unreachable from this site. Phase 1 without stimulation n=24 and Phase 2a with ovarian stimulation n=75, doses 0.1 to 3.0 µg subcutaneously, with triptorelin and placebo comparators. Oocyte maturation, retrieval and pregnancy were not measured. ↩1
11. Thurston L, Hunjan T, Ertl N, et al. Effects of kisspeptin administration in women with hypoactive sexual desire disorder: a randomized clinical trial. JAMA Network Open 2022;5(10):e2236131. DOI 10.1001/jamanetworkopen.2022.36131. Read at source. Double-masked placebo-controlled two-way crossover; 40 randomized, 32 completed both visits. Kisspeptin-54 at 1 nmol/kg/h intravenously for 75 minutes. The primary outcome was brain activity on functional imaging, not any fertility measure. "Kisspeptin was well-tolerated with no reported adverse effects." ↩1
12. Mills EG, Ertl N, Wall MB, et al. Effects of kisspeptin on sexual brain processing and penile tumescence in men with hypoactive sexual desire disorder: a randomized clinical trial. JAMA Network Open 2023;6(2):e2254313. DOI 10.1001/jamanetworkopen.2022.54313. Read at source. Double-blind two-way crossover; 37 randomized, 32 completed. Kisspeptin-54 at 1 nmol/kg/h intravenously for 75 minutes. "The primary outcome was change in brain activity on whole-brain analysis." The supplementary safety tables were not retrieved for this page. ↩1
13. Jayasena CN, et al. Subcutaneous injection of kisspeptin-54 acutely stimulates gonadotropin secretion in women with hypothalamic amenorrhea, but chronic administration causes tachyphylaxis. Journal of Clinical Endocrinology and Metabolism 2009;94(11):4315-4323. DOI 10.1210/jc.2009-0406. Title and bibliographic record only; the full text was not read for this page. The finding named in the title is the basis for the statement here that the response fades with repeated dosing; the day one and day fourteen figures appear on this site's PT-141 and kisspeptin comparison page, which cites this study. ↩1