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Study · Not a test of the peptide alone · 2017

1 result

Neurokinin 3 receptor antagonism decreases gonadotropin and testosterone secretion in healthy men.

Skorupskaite K, George JT, Veldhuis JD, Millar RP, Anderson RA

Clinical endocrinology5 Sept 2017Cited by 21 (Europe PMC)

Summary

ObjectivePatients with mutations of neurokinin B (NKB) and its receptor show hypogonadotrophic hypogonadism, but there is little evidence for the importance of this pathway in reproductive function in normal men, or its functional hierarchy with kisspeptin.DesignAn open label study wherein men (n = 6) were administered the NK3R antagonist MLE4901 40 mg orally twice a day for 7 days. Kisspeptin-10 (0.3 μg/kg iv bolus) was given before and on day 7 of NK3R antagonist treatment.PatientsSubjects were healthy men.MeasurementsReproductive hormones were measured before and during the NK3R antagonist administration, including frequent sampling on two occasions for analysis of pulsatile LH secretion.ResultsLH, FSH and testosterone secretion were decreased during NK3R antagonist administration. LH showed a biphasic response, being reduced after 24 hours of treatment (4.5 ± 0.6 IU/L pretreatment to 1.7 ± 0.2 IU/L, P < .05), with partial recovery thereafter, but it was again decreased on day 7 (2.5 ± 0.6 IU/L, P < .05 vs pretreatment). FSH secretion was also suppressed, with a similar temporal pattern to that of LH. Testosterone secretion was decreased from 24 hours (18.4 ± 1.6 pretreatment vs 5.6 ± 1.5 nmol/L, P < .01) and remained suppressed throughout the treatment period. Analysis of LH pulsatility showed that both basal and pulsatile LH secretion were markedly suppressed but there was no detected change in LH pulse frequency. Kisspeptin-10 stimulated LH secretion, with similar responses before and during NK3R antagonist administration.ConclusionsThese data demonstrate a central role for NKB/NK3R in the physiological regulation of reproductive function in men, and that this is functionally upstream of kisspeptin-mediated GnRH secretion.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone1

In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Kisspeptin-10.

  1. 01HumanNot a test of Kisspeptin-10 aloneNon-randomized trialEfficacy outcome

    In healthy men, kisspeptin‑10 stimulated LH secretion with similar responses before and during NK3R antagonist treatment.

    In plain wordsIn healthy men, kisspeptin‑10 raised luteinizing hormone similarly before and during treatment with an NK3R blocker.

    Outcome
    No significant changeKisspeptin-10-stimulated LH secretion during NK3R antagonist
    Study

    n = 6

    Comparator
    Before NK3R antagonist
    Outcome group
    Sex hormones and fertility · Endocrine and hormones

    Source sentences

    Summary
    Kisspeptin-10 stimulated LH secretion, with similar responses before and during NK3R antagonist administration.
    2 context sentences
    Summary · context
    An open label study wherein men (n = 6) were administered the NK3R antagonist MLE4901 40 mg orally twice a day for 7 days.
    Summary · context
    Kisspeptin-10 (0.3 μg/kg iv bolus) was given before and on day 7 of NK3R antagonist treatment.

    In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    10 Oct 2026, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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