Peptide Health Lab

Goal

Sexual health

Also known as: Libido, Sexual function

A research reference for the compounds mapped to sexual desire and sexual function, one of them FDA-approved with a labeled contraindication, one carrying the largest randomized literature in this library, and one whose approved use is local rather than systemic.

Last reviewed August 3, 2026

What "sexual health" actually means in the research

Sexual health is a phrase people bring to a search engine. The studies underneath these compounds do not use it. They use a desire-domain score on a validated questionnaire, a single distress item, a count of satisfying sexual events, a percentage of parabasal cells on a vaginal smear, and a daily questionnaire about sexual activity. Knowing which of those a given result came from is most of what this page can do for a reader.

The trials measured four different things. One programme measured desire and desire-related distress in premenopausal women who met diagnostic criteria for acquired, generalized hypoactive sexual desire disorder.[5] One measured sexual activity, desire, and erectile function in men aged 65 and over selected on a laboratory testosterone value.[3] One pooled 36 randomized trials of testosterone in women, mostly postmenopausal, across a battery of sexual function domains.[4] One measured pain at sexual activity, alongside vaginal cytology and pH, in postmenopausal women with vulvovaginal atrophy.[2]

Four populations, four endpoints. A result in one of them says nothing automatically about any of the others, and this is the goal page where that mistake is easiest to make, because the words people use for it, libido and drive and performance, flatten all four into one.

What the evidence supports

Bremelanotide, in the population it was approved for. Two identical phase 3 randomized, double-blind, placebo-controlled trials randomized 1,267 premenopausal women to as-needed subcutaneous bremelanotide or placebo for 24 weeks. Both coprimary endpoints separated from placebo: desire rose and desire-related distress fell, with integrated changes of 0.35 and −0.33 respectively, each at P<.001.[5] This is the strongest evidence on the page in the sense that matters most. It is randomized, it is placebo-controlled, and it was generated in exactly the population the product is approved for. It is also modest in size, and the trials were funded by the companies that developed the drug.

Testosterone in men, where the deficiency was measured first. 790 men aged 65 and over with a serum testosterone below 275 ng per deciliter and symptoms suggesting hypoandrogenism received testosterone gel or placebo gel for a year. Sexual activity increased significantly, as did sexual desire and erectile function.[3] The selection criterion is the load-bearing detail: this is evidence about correcting a measured deficiency, not evidence about raising testosterone in someone whose concentration is already normal.

Testosterone in women, from a large pooled analysis. Thirty-six blinded randomized controlled trials comprising 8,480 participants were pooled; testosterone significantly increased satisfactory sexual event frequency, desire, arousal, orgasm, pleasure, responsiveness, and self-image, and reduced sexual concerns and distress. The route mattered. Oral administration raised LDL cholesterol and lowered HDL while non-oral routes did not.[4]

Prasterone, locally. In postmenopausal women with vulvovaginal atrophy, daily intravaginal prasterone met all four co-primary objectives at 12 weeks: parabasal cells fell, superficial cells rose, vaginal pH fell, and moderate to severe dyspareunia improved over placebo, with serum steroids remaining within postmenopausal reference ranges.[2] That last clause is what makes this a local result rather than a systemic one.

Where the evidence is weak

The approved product's label carries limits that the peptide framing erases. Bremelanotide's labeling states a contraindication in patients who have uncontrolled hypertension or known cardiovascular disease. It also states the product is not indicated for hypoactive sexual desire disorder in postmenopausal women or in men, and not indicated to enhance sexual performance; it caps frequency at one dose in 24 hours and no more than 8 doses per month, and directs discontinuation after 8 weeks without symptom improvement. Those are descriptions of a regulated document rather than instructions from this page, and they are read from the label itself rather than from any published review. The published programme-wide safety review, written by an author group including employees of the developing companies, uses the softer formulation that the drug "should be used with caution" in patients at cardiovascular risk. Where a sponsor-authored review and a label diverge, the label is the regulated statement.[6]

Tolerability is the real cost, and it is common rather than rare. Nausea occurred in 40.0% of bremelanotide recipients versus 1.3% on placebo and was the most common reason for stopping; flushing and headache followed. Focal hyperpigmentation was rare at labeled frequency but occurred in more than a third of subjects after up to 16 consecutive daily doses, and 70% of the bremelanotide group continued into the open-label phase against 87% of the placebo group.[6]

Most of the male sexual-health conversation happens outside the evidence. The randomized testosterone result belongs to men selected on a measured laboratory value. There is no equivalent trial in men whose testosterone is normal, and the trial that exists was explicit that its participant count was too small to draw conclusions about the risks of treatment.[3] Meanwhile bremelanotide, the compound most often discussed as a male option, is not indicated in men at all, and the trials that support it did not enrol any.[5]

Systemic DHEA has been tested for the claims attached to it and did not deliver. Two years of DHEA in elderly men and women with low DHEA sulfate raised the hormone substantially and produced no significant effect on body composition, peak oxygen consumption, muscle strength, insulin sensitivity, or quality of life.[1] The positive DHEA result on this page is a local one, at a different site, in a different formulation.

Androgenic effects are part of the deal. In the pooled female testosterone data, acne and hair growth were significantly more likely with treatment, and the effects on musculoskeletal health, cognition, and long-term safety were left explicitly unresolved.[4]

How to decide between these

The framework above the citations is the short version. The principle underneath it is that on this goal, unusually, the right comparison sometimes is between two things on this page, because one of them is approved, was tested in a defined population, and comes with a label.[5]

Three filters do most of the work. First, name the specific complaint, because desire, pain, and erectile function have separate trial literatures and separate approved products.[2] Second, check whether you are inside or outside the studied population. The strongest result on this page was generated in premenopausal women with a specific diagnosis, and the strongest male result in men below a specific laboratory threshold.[3] Third, weigh the tolerability profile before the efficacy number rather than after it; a 40% nausea rate[6] is not a footnote to a 0.35-point desire change.[5]

The stack assessment on this site is built to structure that conversation rather than to answer it, and its output is a starting point for a provider visit.

Questions to bring to a provider

The productive version of this conversation is not "should I try PT-141." It is "here is what changed, here is when, and here is what else was going on."

  • What is the working diagnosis, and does it match the population the evidence was generated in?[5]
  • Is there a blood pressure or cardiovascular history that makes the labeled contraindication relevant, and how is that assessed before anything is considered?[6]
  • If testosterone is on the table, what was the measured concentration, on what kind of assay, and how many times?[3]
  • For a woman considering testosterone, how does the route change the lipid picture, and what is the plan for monitoring acne and hair growth?[4]
  • If the complaint is pain rather than desire, does a local treatment answer it more directly than a systemic one?[2]
  • If an over-the-counter systemic supplement is proposed instead, what would be measured to test it? The two-year trial of oral DHEA used body composition, peak oxygen consumption, strength, insulin sensitivity, and quality of life, and none of them moved.[1]

Anti-doping status

Two of the three compounds mapped on this page are named in the World Anti-Doping Agency Prohibited List in force for 2026, both in the same section:

  • Testosterone: section S1.1, anabolic androgenic steroids. Listed by name.
  • DHEA: section S1.1, listed by its approved name, prasterone, with dehydroepiandrosterone given as a synonym in the same entry.

Substances in S1 are prohibited at all times, in and out of competition, and are non-Specified Substances. That classification carries different sanctioning consequences from a Specified Substance, and it is worth raising with a national anti-doping organization rather than settling from a web page. The over-the-counter availability of DHEA as a dietary supplement in the United States has no bearing on its status under anti-doping rules; the List is indifferent to how a substance is sold.

Bremelanotide is not named anywhere on the 2026 List. That is not the same as a clearance: section S0 covers any pharmacological substance not addressed elsewhere on the List and with no current approval by any governmental regulatory health authority for human therapeutic use, which is a category defined by regulatory status rather than by name, and it is worth confirming with a national anti-doping organization rather than inferring from an absence.

The status above is read from the published Prohibited List itself rather than from any research paper, because a citation can be real, correctly quoted, and still carry a false statement of regulatory fact. What the literature contributes is the clinical claim beside it: the androgenic effects that make testosterone detectable in sport, acne and increased hair growth, are the same ones the pooled trial data report as more frequent with treatment.[4] The List is reissued every year and sections renumber, so a competing athlete should confirm the current year's edition rather than this page.

What the evidence supports for this goal

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Bremelanotide for hypoactive sexual desire disorder in premenopausal women
Human RCT evidence human RCT

Two identical phase 3, randomized, double-blind, placebo-controlled multicentre trials randomized 1,267 premenopausal women 1:1 to 24 weeks of as-needed subcutaneous bremelanotide or placebo. Both coprimary endpoints moved: sexual desire rose (integrated change 0.35, P<.001) and desire-related distress fell (integrated change −0.33, P<.001) versus placebo. The effects are statistically clear and numerically modest, and the trials were funded by the drug's developers.

[5]

Bremelanotide tolerability and blood pressure
Human RCT evidence human RCT

Across a development programme of 3,500 subjects in 43 completed studies, the most common adverse events in the integrated double-blind phase 3 data were nausea (40.0% versus 1.3% on placebo), flushing (20.3% versus 1.3%), and headache (11.3% versus 1.9%); nausea was the most common reason for discontinuation. Focal hyperpigmentation was rare at labeled frequency but occurred in more than a third of subjects after up to 16 consecutive daily doses, and ambulatory monitoring showed small, transient, statistically significant blood-pressure increases. 70% of the bremelanotide group continued into the open-label phase versus 87% of the placebo group.

[6]

Testosterone and sexual function in older men with measured low testosterone
Human RCT evidence human RCT

790 men aged 65 or older with a serum testosterone below 275 ng per deciliter and symptoms suggesting hypoandrogenism were randomized to testosterone gel or placebo gel for one year. Sexual activity increased significantly, as did sexual desire and erectile function. In the same programme there was no significant benefit for vitality, and the six-minute walking distance endpoint was not met in the Physical Function Trial itself. The investigators stated the sample was too small to draw conclusions about the risks of treatment.

[3]

Testosterone for women with low sexual desire
Human RCT evidence review

A systematic review and meta-analysis of 36 blinded randomized controlled trials comprising 8,480 participants found that testosterone significantly increased satisfactory sexual event frequency (mean difference 0.85), desire, arousal, orgasm, pleasure, and self-image, and reduced sexual concerns and distress, in postmenopausal women. Oral administration raised LDL cholesterol and lowered HDL and triglycerides while non-oral routes did not; acne and hair growth were significantly more likely; no serious adverse events were recorded, and effects on musculoskeletal and cognitive health and long-term safety were left open.

[4]

Systemic oral DHEA for the claims it is best known for
Human RCT evidence human RCT

In a two-year, placebo-controlled, double-blind trial in 87 elderly men and 57 elderly women with low DHEA sulfate, DHEA raised the hormone substantially and produced no significant effect on body composition, peak oxygen consumption, muscle strength, insulin sensitivity, or quality of life. The authors concluded that neither DHEA nor low-dose testosterone replacement had physiologically relevant beneficial effects in this population.

[1]

Intravaginal prasterone for pain at sexual activity
Human RCT evidence human RCT

A prospective, randomized, double-blind, placebo-controlled phase 3 trial in postmenopausal women with vulvovaginal atrophy met all four co-primary objectives after 12 weeks of daily intravaginal prasterone: parabasal cells fell, superficial cells rose, vaginal pH fell, and moderate to severe dyspareunia improved over placebo. Serum steroid concentrations remained within postmenopausal reference ranges, consistent with a local rather than systemic action, and all endometrial biopsies at 12 weeks showed atrophy.

[2]

Compounds people map to this goal

Each card carries the compound's FDA status and its overall evidence grade, plus why it shows up on this goal in particular. Follow the card to the full library page for the claim-by-claim evidence review and what published research reported. Dosing and protocol ranges are never on this page.

PT-141

Also known as: Bremelanotide, Vyleesi

FDA approved Human RCT evidence

A research reference for PT-141, an FDA-approved melanocortin agonist for hypoactive sexual desire disorder in premenopausal women, with statistically significant but small trial effects and a heavy tolerability burden.

Why it's on this page

The one compound on this page approved by the FDA for a sexual-desire indication, and the only one whose evidence was generated in the exact population it is approved for: premenopausal women with acquired, generalized hypoactive sexual desire disorder. Its labeling carries a contraindication in uncontrolled hypertension or known cardiovascular disease, which is the single most consequential fact a reader of "PT-141 the peptide" is likely never to encounter. Not named on the WADA Prohibited List.

Last reviewed August 2, 2026

Testosterone

Also known as: Testosterone replacement therapy, TRT

FDA approved Human RCT evidence

A research reference for testosterone therapy, the one compound in this library with a large randomized trial literature, and a prescription hormone that requires a diagnosis, a prescriber, and ongoing lab monitoring.

Why it's on this page

Mapped here because it carries the largest randomized human literature of anything in this library for sexual function. That literature spans two populations with two different effect sizes: symptomatic older men with measured low testosterone, and postmenopausal women with distressing low desire. Prohibited in tested sport at all times under WADA section S1.1.

Last reviewed August 2, 2026

DHEA

Also known as: Dehydroepiandrosterone, Prasterone

Rx via compounding Human RCT evidence

A research reference for DHEA, an adrenal steroid precursor sold over the counter as a dietary supplement in the US, dispensed as an approved prescription product only in a local vaginal form and through compounding pharmacies, with randomized evidence that is positive in adrenal insufficiency and largely negative for the anti-aging claims it is best known for.

Why it's on this page

On this page because its approved prescription use is genuinely local rather than systemic: an intravaginal insert for moderate to severe dyspareunia. The oral supplement most people mean by "DHEA" was tested over two years against placebo for the systemic anti-aging claims and did not deliver them. Named as prasterone in WADA section S1.1.

Last reviewed August 2, 2026

How to decide between them

These are the questions that actually change the answer. Work through them with a licensed provider. None of them can be answered by a page that does not know your labs, your history, or your medications.

  1. Is the problem desire, arousal, pain during sex, or erectile function?

    These are separate literatures with separate endpoints and separate approved products, and picking the wrong one is how a reader ends up weighing a compound that was never studied for what they have. Desire in premenopausal women is what the bremelanotide trials measured, using a desire-domain score and a distress item. Pain at sexual activity is what the intravaginal prasterone trials measured, alongside vaginal cytology and pH. Neither trial programme measured the other's endpoint.

    Human RCT evidence [5] [2]

  2. Are you the population the approval actually covers?

    This is the question that decides whether the strongest evidence on the page applies to you at all. Bremelanotide's approval covers premenopausal women with acquired, generalized hypoactive sexual desire disorder. Acquired means desire that was previously present and declined; generalized means not specific to a partner or situation. The labeling states it is not indicated for hypoactive sexual desire disorder in postmenopausal women or in men, and not indicated to enhance sexual performance. Outside that population the trial results are not evidence about you; they are evidence about someone else.

    Human RCT evidence [5]

  3. How large an effect would be worth the tolerability cost?

    Ask this before reading any result, because the answer changes what counts as a win. In the two phase 3 trials the improvements in desire and in desire-related distress were statistically significant and small: a change of 0.35 on the desire domain and −0.33 on the distress item in the integrated analysis. Across the development programme nausea occurred in 40.0% versus 1.3% on placebo and was the most common reason for stopping. A small mean benefit and a common, unpleasant, self-limiting side effect is a trade-off a person can only weigh for themselves.

    Human RCT evidence [5] [6]

  4. Has low testosterone been measured, or assumed?

    The randomized evidence for testosterone and sexual function comes from men who were selected on a laboratory value and on symptoms, not on how they felt about their libido. Entry required a serum testosterone below 275 ng per deciliter. Within that group, raising concentrations to the mid-normal range for men aged 19 to 40 for a year produced a moderate benefit for sexual activity, desire, and erectile function, and no benefit for vitality or walking distance. Outside that group there is no equivalent trial, and the trial's own authors noted the participant count was too small to draw conclusions about risk.

    Human RCT evidence [3]

  5. Are you expecting DHEA to do systemically what it does locally?

    It is the same molecule and two different questions. Given daily as an intravaginal insert to postmenopausal women with vulvovaginal atrophy, it changed vaginal cytology and pH and reduced moderate to severe dyspareunia against placebo, with serum steroid concentrations staying within postmenopausal reference ranges. Given orally for two years to elderly men and women with low DHEA sulfate, it produced no significant effect on body composition, physical performance, insulin sensitivity, or quality of life. A local effect does not generalize into a systemic one.

    Human RCT evidence [2] [1]

  6. Do you compete in a tested sport, at any level?

    Then two of the three compounds mapped here are settled before any evidence question. Testosterone and prasterone, the approved name for DHEA, are both named in section S1.1 of the WADA Prohibited List in force for 2026 as anabolic androgenic steroids, prohibited at all times, in and out of competition. Bremelanotide is not named. That is read from the published list itself rather than from the literature; what the literature contributes is the separate finding that testosterone's measured benefit in women came with more reported acne and hair growth, which is the same androgenic signal anti-doping rules exist to detect.

    [4]

Questions for your provider

Bring this goal page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here applies to your situation. This goal page cannot. Peptide Health Lab does not prescribe and does not sell peptides.

A goal is not a diagnosis. The most useful version of this conversation usually starts with what is actually driving the symptom, not with which compound to try.

Citations

6 sources · every identifier checked against PubMed

Before you act on any of this

This page is educational only and is not medical advice. It does not diagnose, treat, or prescribe. Review it with a licensed provider before making any health decision. Peptide Health Lab does not sell peptides.

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