Goal
Best-studied peptides for sleep
Ranked by the strongest evidence rung each compound holds, with what the study measured beside it. 30 were checked; 9 produced a graded row.
Last updated
30 compounds were read against these 2 conditions; 9 produced a graded row. The other 21 are named further down.
The ranking, and the key it uses
Ordered by the best rung the compound holds anywhere in this goal; then by what that study measured; then by how many graded rows it holds here, as a tie-break only; then by name. There is no blended score — one number mixing the rung and what was measured would invent a third scale nothing was graded against. Every rung links to the rubric that assigned it.
Reading the strip
1 human RCT2 human observational3 human case series4 animal in vivo5 in vitro6 theoretical7 computational
A filled cell means at least one graded row at that rung. Its colour is what the strongest such study measured: direct outcome · surrogate marker · mechanistic only. An outlined cell means no row at that rung.
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hGH
human RCT · direct outcome · 2 graded rows across 2 of 2 conditions
2 graded rows, 2 sources
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Obstructive sleep apnoea
human RCT Direct outcome Not approved for this condition
- Who was studied
- adults with Prader-Willi syndrome, 15 men and 22 women, n=37 randomised to 1 year of growth hormone (n=19) or placebo (n=18) followed by 2 years of growth hormone for all; median age 29.5, median baseline apnoea-hypopnoea index 1.4 events/h, so the group did not have obstructive sleep apnoea at entry
Polysomnography every six months found no difference in any sleep or respiratory parameter between the growth hormone and placebo groups; sleep efficiency improved across the study in both arms, and the apnoea-hypopnoea index rose inconsistently while staying inside the normal range. The question this trial was built to answer is whether growth hormone worsens breathing during sleep in Prader-Willi syndrome, not whether it treats obstructive sleep apnoea, and the participants did not have the condition at baseline. No trial of growth hormone in people who have obstructive sleep apnoea is on file.
Source PubMed Central 1 primary source read for this row
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Insomnia
human RCT Surrogate marker Not approved for this condition
- Who was studied
- Two crossover sleep-laboratory studies in healthy men, neither in an insomnia population. Kern 1993: double-blind within-subject crossover, 12 men then 3 men then 10 men, 5 IU intramuscularly and 5 and 48 IU intravenously, sleep stages scored across the night. Mendelson 1980: crossover against saline in normal volunteers, 2 units and 5 units intramuscularly 15 minutes before bed.
Exogenous growth hormone has been given to healthy men in a sleep laboratory twice, and neither result supports it as a sleep aid. In a double-blind crossover, 5 IU intramuscularly and 5 and 48 IU intravenously changed neither total sleep time nor time in any sleep stage. In an earlier crossover, 2 units had no effect on the sleep EEG and 5 units cut slow-wave sleep by 19 per cent and raised REM sleep by 13 per cent. The direction of the larger dose is the opposite of the effect attributed to the GH axis in marketing copy, which rests on GHRH studies rather than on hGH studies. Both studies scored sleep architecture in healthy men; nobody with insomnia was studied, and no trial of hGH with an insomnia outcome is on file.
Source PubMed 2 primary sources read for this row
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1 graded row, 1 source
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Insomnia
human RCT Direct outcome Not approved for this condition
- Who was studied
- patients with chronic insomnia, n=16 in a matched-pairs parallel-groups design (8 DSIP, 8 placebo), 5 consecutive laboratory nights; sex and age not reported in the source
A double-blind trial gave 25 nmol/kg intravenously in the afternoon before each of three consecutive nights and measured polysomnographic sleep structure, subjective sleep quality and subjective tiredness; sleep efficiency and sleep latency favoured DSIP, but the authors judged the significant effects weak and partly attributable to an incidental change in the placebo group, and concluded that short-term treatment of chronic insomnia with DSIP is unlikely to be of major therapeutic benefit. A separate double-blind crossover study at the same 25 nmol/kg intravenous dose found the same differences already present at baseline and described the sleep improvement as of little clinical significance, while a 1987 seven-night study in 14 middle-aged insomniacs reported a substantial improvement. Every controlled human trial on file is intravenous and dates from 1984 to 1992; no controlled trial has been published since, and no human trial of subcutaneous DSIP, the route it is sold in, exists on file.
Source PubMed 4 primary sources read for this row
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1 graded row, 1 source
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Insomnia
human RCT Direct outcome Not approved for this condition
- Who was studied
- n=388 pooled across 9 randomised controlled trials, 8 of which enrolled postmenopausal women; oral micronised progesterone; participants were not required to carry an insomnia diagnosis
A systematic review and meta-analysis of nine randomised controlled trials measured sleep by polysomnography and by self-report; pooling four of them favoured oral micronised progesterone for sleep onset latency (effect size 7.10, CI 1.30 to 12.91) but showed no difference in total sleep time or sleep efficiency, and the reviewers noted that concomitant oestradiol and improvement in vasomotor symptoms limit what several trials can be read to show. In the most detailed single trial, eight postmenopausal women aged 48 to 74 without sleep complaints had 300 mg nightly for three weeks: sleep was the same as placebo on an undisturbed night, and differed only on a night deliberately fragmented by 15-minute blood sampling. No trial in a population with diagnosed chronic insomnia is on file, and medroxyprogesterone acetate, a different molecule, must not be read across to this record.
Source PubMed 2 primary sources read for this row
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1 graded row, 1 source
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Insomnia
human RCT Direct outcome Not approved for this condition
- Who was studied
- 19 healthy older adults (10 women, 9 men), aged 55 to 71, no sleep disorder reported. Single-blind randomised placebo-controlled trial of five months: four weeks placebo followed by 16 weeks of [Nle27]GHRH(1-29)NH2, 10 mcg/kg, self-administered subcutaneously each night. Sleep quality was a secondary self-reported measure; no polysomnography.
The only trial on file that administered a named GHRH(1-29) molecule and recorded a sleep endpoint reported that sleep quality was unaffected in both sexes after 16 weeks of nightly subcutaneous dosing at 10 mcg/kg. The molecule was [Nle27]GHRH(1-29)NH2, an analogue of sermorelin rather than sermorelin itself, and the endpoint was self-report rather than polysomnography. The acute sleep-EEG literature people cite here is a different body of work: repeated intravenous boluses, typically 4 x 50 mcg between 22.00 and 01.00, raised slow-wave and non-REM sleep in healthy men, and intranasal 300 mcg raised slow-wave and REM sleep in young and aged men. Those reports name only "GHRH" and do not state which fragment was given, so whether they were sermorelin cannot be established from the published abstracts, and an intravenous bolus is not the nightly subcutaneous route people use. The direction is also not uniform by sex: with 4 x 50 mcg intravenously, non-REM sleep rose in men and fell in women, in both depressed patients and controls. No trial in an insomnia population is on file for any GHRH preparation.
Source PubMed 1 primary source read for this row
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Tirzepatide
human RCT · direct outcome · 1 graded row across 1 of 2 conditions
1 graded row, 1 source
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Obstructive sleep apnoea
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with moderate-to-severe obstructive sleep apnoea and obesity; trial 1 n=234 not on positive airway pressure (67.1% male, mean age 47.9, mean BMI 39.1), trial 2 n=235 on positive airway pressure (72.3% male, mean age 51.7, mean BMI 38.7); 52 weeks
Two phase 3 double-blind placebo-controlled trials measured the apnoea-hypopnoea index directly at 52 weeks, at the maximum tolerated dose of 10 mg or 15 mg weekly. Against baseline means of 51.5 and 49.5 events per hour, the treatment difference from placebo was -20.0 events per hour in trial 1 and -23.8 in trial 2, and hypoxic burden, body weight, high-sensitivity C-reactive protein, systolic blood pressure and patient-reported sleep measures all moved with it. The FDA has approved tirzepatide, as Zepbound, to treat moderate to severe obstructive sleep apnoea in adults with obesity alongside a reduced-calorie diet and increased physical activity; both trials were funded by the manufacturer, and no trial in people who have obstructive sleep apnoea without obesity is on file.
Source PubMed Central 2 primary sources read for this row
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GHRH (Growth Hormone-Releasing Hormone)
human RCT · surrogate marker · 1 graded row across 1 of 2 conditions
1 graded row, 1 source
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Insomnia
human RCT Surrogate marker Not approved for this condition
- Who was studied
- 48 normal women and men aged 19 to 67 years, studied across a baseline night and a recovery night after 40 hours of sleep deprivation; GHRH, corticotropin-releasing hormone or placebo injected repetitively during the recovery night
Sleep was measured directly by electroencephalography. After GHRH the rise in non-rapid-eye-movement sleep and the fall in wakefulness were larger than after placebo, and growth hormone rose while cortisol fell. Two things stop this being a result about insomnia. The participants were normal sleepers deprived of sleep for 40 hours, not patients with a sleep disorder, and recovery sleep is described by the authors as differing markedly from spontaneous sleep. The direction is also not the same in both sexes: earlier work in this line reports that GHRH promotes sleep in men and impairs it in women, though no sex difference appeared in this particular study. The abstract does not state which GHRH preparation was used. A separate experiment cuts the other way — blocking endogenous GHRH receptors overnight in healthy men suppressed the growth hormone response by 93 per cent yet left the percentage of slow-wave sleep unchanged, from which those authors concluded that endogenous GHRH is unlikely to generate slow-wave sleep. No trial has given GHRH to people with insomnia and measured whether their insomnia improved. Rung set from the study's own design wording, "Randomized Controlled".
Source PubMed 2 primary sources read for this row
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1 graded row, 1 source
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Insomnia
human RCT Mechanistic only Not approved for this condition
- Who was studied
- patients with depression on a stable dose of trimipramine, n=10, sex not reported; four hourly intravenous boluses of 50 mcg between 09:00 and 12:00 on each of two days, crossed over with placebo on two further days
Recorded, and not evidence for this condition
The primary measure was the change in the Hamilton depression rating scale, not sleep; the sleep electroencephalogram was recorded once after placebo and once after galanin, and the overall change was driven mainly by a longer rapid-eye-movement latency that did not itself reach significance. An earlier study in healthy young men, at the same dose and at three times it, found changes resembling rapid-eye-movement sleep deprivation rather than sedation. No study measured insomnia in any population, so the reviews that list galanin among the sleep-promoting peptides are summarising these electroencephalogram changes and animal work, not an insomnia result.
Source PubMed 2 primary sources read for this row
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Urotensin II
human observational · mechanistic only · 1 graded row across 1 of 2 conditions
1 graded row, 1 source
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Obstructive sleep apnoea
human observational Mechanistic only Not approved for this condition
- Who was studied
- 89 people with obstructive sleep apnoea (66 men, mean age 52.5, median apnoea-hypopnoea index 39.0 events/h) and 89 matched controls (64 men, mean age 50.1); cross-sectional, enrolled April 2018 to April 2020
Recorded, and not evidence for this condition
Serum urotensin-II was measured, never administered: it was higher in the obstructive sleep apnoea group than in matched controls (3.41 against 2.18 ng/mL) and was associated with the apnoea-hypopnoea index, systolic blood pressure and high-sensitivity C-reactive protein. That is an association between a circulating peptide and disease severity in one cross-sectional sample. No study has given urotensin-II to a person with obstructive sleep apnoea, and nothing here measures what happens to sleep-disordered breathing when it is given.
Source PubMed Central 1 primary source read for this row
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Neuropeptide Y
human case series · surrogate marker · 1 graded row across 1 of 2 conditions
1 graded row, 1 source
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Insomnia
human case series Surrogate marker Not approved for this condition
- Who was studied
- healthy young men, n=9 given 4 x 50 mcg and n=11 given 4 x 100 mcg as hourly intravenous boluses from 22:00 to 01:00 on a single night, against saline; no participant had insomnia
Overnight sleep electroencephalography showed longer sleep period time and stage 2 sleep and shorter sleep latency and time awake after the peptide, alongside lower overnight ACTH and cortisol. The report does not describe randomisation or blinding, which is why this sits on the lowest human rung: the same laboratory's later study — a fixed adaptation night, then a placebo night, then a peptide night, in patients with depression and in controls — reproduced the shorter sleep onset latency but attributed part of it to an adaptation effect. Neither study enrolled anyone with insomnia, and no trial of neuropeptide Y in an insomnia population is on file.
Source PubMed 2 primary sources read for this row
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Checked, and nothing on file
21 compounds were read against these conditions and produced no gradeable row. They are named here rather than left off, because a list of 9 reads identically whether 9 survived 30 or 9 were all anyone thought of.
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Agouti-Related Protein (AgRP)
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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ARA-290
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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C-Max
No rung — nothing on file to grade
Checked against insomnia. No study meeting the rubric was found for any of them.
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CART (Cocaine- and Amphetamine-Regulated Transcript)
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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CJC-1295 DAC on insomnia
No rung — nothing on file to grade Not approved for this condition
No sleep measure of any kind has been recorded in a human given CJC-1295 with DAC. The published human trials measured growth hormone and IGF-I concentrations only. The sleep-EEG work sometimes cited alongside this compound used repeated short intravenous pulses of GHRH, and the one determinant that work identified was pulsatility: episodic dosing raised slow-wave sleep where a continuous infusion of the same 200 mcg did not. CJC-1295 with DAC is built to do the opposite of pulsing, binding albumin to hold the growth hormone axis stimulated for days, so the acute pulse findings are not evidence for it. Nobody with insomnia has been given it in a published study.
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CJC-1295 no-DAC on insomnia
No rung — nothing on file to grade Not approved for this condition
Nothing is recorded for CJC-1295 without DAC in humans against any endpoint, sleep included. Searches of the published literature return the DAC form only, plus doping-control assay development. The two forms are different molecules with different durations of action, and a result for one is not a result for the other. Where a source cites GHRH sleep-EEG studies here, note that those reports name only "GHRH" and do not state the fragment given, so they cannot be attributed to this compound either.
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CRH (Corticotropin-Releasing Hormone) on insomnia
No rung — nothing on file to grade Not approved for this condition
CRH infusion is used experimentally to disrupt sleep architecture as a model of depressive sleep. It is a provocation, and a harmful one; no trial gives it to improve sleep.
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Epitalon
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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GHRP-1 on insomnia
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no polysomnographic study of GHRP-1 was retrieved.
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GHRP-2 on insomnia
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no polysomnographic study of GHRP-2 was retrieved. The sleep work in this family used ghrelin and growth hormone-releasing hormone.
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GHRP-6 on insomnia
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no polysomnographic study of GHRP-6 was retrieved.
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Hexarelin on insomnia
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no polysomnographic study of hexarelin was retrieved.
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Ipamorelin on insomnia
No rung — nothing on file to grade Not approved for this condition
No sleep measure has been recorded in a human given ipamorelin. The one published human trial studied postoperative ileus and did not record sleep. Ipamorelin is a ghrelin-receptor agonist rather than a GHRH analogue, so GHRH sleep findings do not carry across, and within its own class the results run in both directions: ghrelin raised slow-wave sleep in healthy men, while hexarelin, another ghrelin-receptor agonist, decreased it. Which of those ipamorelin would resemble is not on file, and nobody with insomnia has been given it in a published study.
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Melanotan II
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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Orexin-A on insomnia
No rung — nothing on file to grade Not approved for this condition
Orexin-A is an agonist at the orexin receptors and promotes wakefulness. The licensed insomnia medicines that act on this system are orexin receptor antagonists — different molecules with the opposite action — and no result about them transfers to this peptide. The only controlled human study of administered orexin-A on sleep that could be located enrolled eight people with narcolepsy with cataplexy, the opposite complaint, and gave a single 435 nmol intranasal dose before one night of polysomnography; it found no significant change in nocturnal wakefulness and reduced rapid-eye-movement sleep. No trial of orexin-A in insomnia exists on file.
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Orexin-B
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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Sauvagine
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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Selank
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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Semax
No rung — nothing on file to grade
Checked against insomnia, obstructive sleep apnoea. No study meeting the rubric was found for any of them.
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Simonson Alpha 1
No rung — nothing on file to grade
Checked against insomnia. No study meeting the rubric was found for any of them.
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Vasopressin on insomnia
No rung — nothing on file to grade Not approved for this condition
Endogenous vasopressin varies with the sleep-wake cycle; no study administers it as a sleep intervention.
What this page does not say
It reports what was measured, in whom, and how directly. It does not say what to take or at what dose, and a position here is a record of study depth rather than a reason to use anything. A compound at the top of this list is the most studied against these conditions; that is not the same claim as the most effective, and nothing on this page makes the second one.
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