Compounds
DSIP (Delta Sleep-Inducing Peptide): Does It Work? Dosage, Timing, Safety
What DSIP (delta sleep-inducing peptide, emideltide) is, what the small 1981 to 1992 human trials in insomnia and withdrawal found, studied intravenous doses versus the charts sold online, the safety unknowns, the July 2026 FDA committee vote against it, and what has real evidence for sleep.
Published October 12, 2026 · 15 min read
Key takeaways
- DSIP (delta sleep-inducing peptide, international name emideltide) is a nine-amino-acid peptide isolated from rabbit brain in 1977. Nearly fifty years later nobody has found its gene, its precursor or its receptor, and the researchers who studied it longest call the sleep-factor hypothesis "extremely poorly documented."
- The human evidence is a handful of studies from 1981 to 1992, all intravenous, none larger than 18 patients in the sleep trials: one Swiss group reported normalized sleep in chronic insomniacs, and two independent double-blind studies found no meaningful benefit. Nothing on sleep has been published since.
- The studied dose was about 1.5 to 1.8 mg given slowly into a vein; the charts sold online list 100 to 300 mcg under the skin, a route and dose no human study has ever used.
- Safety is a blank. The old trials reported good tolerance and a few headaches; there is no modern safety data, and FDA's concerns include immunogenicity and the fact that products sold under the DSIP name are not all the same molecule.
- Legally, DSIP has no path. FDA listed it as a safety risk in 2023, took it off that list in April 2026 only because the nomination was withdrawn, and on July 24, 2026 its advisory committee voted 6 to 7 against allowing it to be compounded for insomnia, narcolepsy or opioid withdrawal. No US pharmacy may make it, so there is no legal version to buy, and this page contains no purchase guidance.
DSIP (emideltide) at a glance
- Also called
- delta sleep-inducing peptide, emideltide, DSIP acetate, Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu nonapeptide
- Class
- Nine-amino-acid peptide isolated from rabbit brain in 1977 and proposed as a sleep-modulating neuropeptide; no gene, precursor or receptor has ever been identified
- Route
- Studied as slow intravenous injection or infusion; sold online for subcutaneous or intranasal use, routes with no human data
- FDA status
- Never approved as a drug anywhere. Placed in FDA's Category 2 on September 29, 2023, removed on April 15, 2026 after its nomination was withdrawn, then voted down 6 to 7 (with 1 abstention) by FDA's advisory committee on July 24, 2026 for chronic insomnia, narcolepsy and opioid withdrawal. Not legally compoundable; no legal version exists.
- FDA Category 2 (compounding restricted)
- No
- Available by prescription (US)
- Not as a prescription product
- Best-studied use
- Chronic insomnia and alcohol or opioid withdrawal in small trials from 1981 to 1992; no sleep trial has been published since
What DSIP is and how it was discovered
In 1977 Guido Schoenenberger and Marcel Monnier in Basel reported isolating a peptide from the blood of rabbits whose brains had been electrically stimulated into sleep. Infused into the brain ventricles of other rabbits, the synthetic version increased delta (slow-wave) and spindle activity on the EEG, which is where the name came from. The sequence is nine amino acids, Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu, and in the original double-blind experiment on 58 rabbits only the full nonapeptide, not its fragments or analogues, produced the effect (Schoenenberger 1977).
That was the high point. A peptide that regulates sleep should have a gene that encodes it, a larger precursor protein it is cut from, and a receptor it binds. None of the three has ever been found. A 2006 review by Russian sleep researchers who had spent decades on the question concluded that the link between DSIP and sleep "has never been further characterized," that the hypothesis is "extremely poorly documented and still weak," and that in their own animal work certain synthetic analogues promoted slow-wave sleep while DSIP itself did not. Their best guess was that an unidentified DSIP-like peptide, not DSIP, accounts for the immunoreactivity found in brain tissue (Kovalzon 2006). In plain terms: the molecule sold as a sleep hormone may not be a hormone at all.
The international nonproprietary name is emideltide, which is what FDA calls it. The distinction matters, because over the years several different active peptides and analogues have been sold or studied under the DSIP label, a point FDA raised when the compound came up for review in 2026.
What the human trials actually found
Every human study of DSIP for sleep was done between 1981 and 1992, all with intravenous dosing, most by one group. Here is the record, graded.
| Claim | Grade | What the evidence shows | Sources |
|---|---|---|---|
| DSIP is a natural sleep hormone | D | Isolated from rabbit blood in 1977; intraventricular infusion increased delta and spindle EEG activity in rabbits. No gene, precursor or receptor has been identified in any species since, and DSIP itself did not promote slow-wave sleep in later rabbit and rat work by an independent group. | Schoenenberger 1977; Kovalzon 2006 |
| Promotes sleep in healthy people | B | First human study: 6 volunteers, double-blind crossover, 25 nmol/kg by slow intravenous infusion in the morning. Median sleep in the next 130 minutes rose 59% versus placebo; the following night showed shorter sleep onset and better efficiency; no classic sedation. Well tolerated. | Schneider-Helmert 1981 |
| Normalizes sleep in chronic insomnia | B | 18 chronic insomniacs (aged 29 to 83) given 30 nmol/kg intravenously six times over a week in a sleep laboratory: sleep improved to normal values and was maintained a week later; the abstract describes no placebo group. A separate study of 14 middle-aged chronic insomniacs, placebo-controlled and double-blind over 7 nights, reported substantially improved night sleep, daytime alertness and performance. Both from the same investigator. | Schneider-Helmert 1986; Schneider-Helmert 1987 |
| The insomnia effect replicates in other hands | B | No. In a double-blind crossover in chronic insomniacs (25 nmol/kg intravenously on four nights), awakenings and wake time fell but not significantly versus placebo, and the authors called the improvement of little clinical significance. In 16 chronic insomniacs in a double-blind parallel study (25 nmol/kg on three afternoons), sleep efficiency and latency improved slightly, but the authors judged the effects weak, possibly due to a chance change in the placebo group, and concluded short-term DSIP was unlikely to be of major benefit. | Monti 1987; Bes 1992 |
| Treats alcohol and opioid withdrawal | B | Uncontrolled: 107 inpatients (47 alcohol, 60 opiate) given intravenous DSIP; by physician and nursing assessment, symptoms resolved or improved markedly in 87% of alcohol and 97% of opiate patients, with headaches in a few. A 1998 open trial in opioid detoxification is the last human report. No placebo-controlled withdrawal trial exists. | Dick 1984; Backmund 1998 |
| Lowers cortisol and stress hormones | B | Tested and negative: intravenous infusions of 3 to 4 mg in healthy young men did not change ACTH or cortisol responses to CRH injection or to a midday meal. | Späth-Schwalbe 1995 |
| A sedative that deepens sleep or anesthesia | B | In 24 women under isoflurane anesthesia, bolus doses of 25 to 100 nmol/kg raised heart rate, reduced heart-rate variability and, paradoxically, reduced EEG delta activity and lightened anesthetic depth. The most recent human study of DSIP (2009) found the opposite of a sedative effect. | Pomfrett 2009 |
| Deep sleep for recovery, longevity, anti-aging | D | No human study has measured recovery, aging or any long-term outcome. No sleep study of any kind has been published since 1992, and no study has used the subcutaneous or intranasal routes sold online. | Kovalzon 2006 |
Three things stand out.
One group, small numbers, old methods. The positive sleep findings come from a single Swiss investigator working with the peptide's discoverers, in studies of 6, 14 and 18 people, more than 35 years ago. That is not an accusation; it is the shape of the evidence, and it is why the two independent attempts to replicate it matter so much.
The replications failed. Monti's crossover and Bes's parallel-group study were both double-blind and both used the same intravenous dose, and both concluded the benefit was too small to matter (Monti 1987) (Bes 1992). When FDA's committee member said in July 2026 that "the sole supporting study is over 30 years old," this is the file he was describing.
The trail goes cold in 1992. After the Bes study, no one published another sleep trial. The last human studies were a cortisol experiment that found nothing (Späth-Schwalbe 1995), an open detoxification trial, and an anesthesia study in which the peptide lightened rather than deepened anesthesia (Pomfrett 2009). A compound with a real effect on sleep would have attracted a modern polysomnography trial in the 34 years since. None came.
What you are promised versus what is documented
Sellers describe DSIP as a natural deep-sleep peptide that lowers cortisol, blunts stress, relieves pain, improves recovery and, in the longevity framing, "restores" the sleep architecture of youth. The evidence sorts those claims into three bins.
- Documented in humans: a short-term increase in sleep after intravenous infusion in 6 volunteers; improved sleep in small 1980s insomnia studies from one group; symptom relief in uncontrolled withdrawal reports.
- Tested and not found: any effect on ACTH or cortisol; a consistent benefit in chronic insomnia under independent double-blind conditions; a sedative or anesthesia-deepening effect.
- Never tested: deep-sleep architecture in modern polysomnography, recovery, pain in a controlled study, longevity, and anything at all by the subcutaneous or intranasal routes people actually use.
A fourth bin is specific to DSIP: claims that may be about a different molecule. Because the name has covered more than one active peptide, a benefit reported for "DSIP" in one decade and a vial labeled DSIP in another are not guaranteed to share a sequence.
DSIP vs sermorelin, MK-677 and CBT-I
| DSIP (emideltide) | Sermorelin | MK-677 (ibutamoren) | CBT-I | |
|---|---|---|---|---|
| What it is | Nonapeptide of unknown function | GHRH(1-29) analog; raises growth hormone | Oral non-peptide ghrelin-receptor agonist | Structured behavioral treatment for insomnia |
| Evidence for sleep | Small intravenous trials 1981 to 1992, conflicting; nothing since | GHRH raised slow-wave sleep in small studies of healthy men; no sermorelin trial with objective sleep outcomes in the marketed population | Stage IV sleep up about 50% and REM up about 20% in 8 young adults; REM up about 50% in 6 older adults (1997) | Strong recommendation as first-line treatment for chronic insomnia (AASM 2021) |
| Route | Intravenous in studies; subcutaneous or nasal as sold | Subcutaneous, nightly | Oral | Sessions with a trained clinician or validated digital program |
| Legal status (October 2026) | Never approved; committee voted against, July 2026; not compoundable | Formerly approved; compoundable on prescription | Category 2 since 2023; committee voted against, October 2024; not compoundable | Standard of care |
| Typical cost | No legitimate price | $150 to $400 a month | No legitimate price | Varies; often covered by insurance |
The honest reading of that table is that the row with the most evidence is not a peptide, and the peptide row with a legal path is sermorelin, whose sleep claim rests on GHRH physiology rather than on a sermorelin trial. DSIP has neither evidence nor a path.
Dosage: what was studied versus the charts sold online
| Setting | Dose and route | Population | Result |
|---|---|---|---|
| Schneider-Helmert 1981 | 25 nmol/kg by slow intravenous infusion, once, in the morning | 6 healthy volunteers | Sleep increased 59% over the next 130 minutes; better night sleep |
| Schneider-Helmert 1986 | 30 nmol/kg intravenously, six doses over one week | 18 chronic insomniacs | Sleep reported normalized; no placebo group described |
| Schneider-Helmert 1987 | Nightly intravenous DSIP for 7 nights (placebo-controlled) | 14 chronic insomniacs | Improved night sleep and daytime performance |
| Monti 1987; Bes 1992 | 25 nmol/kg intravenously on 3 or 4 occasions | Chronic insomniacs (16 in the 1992 study) | No significant or clinically meaningful benefit |
| Dick 1984 | Intravenous injections, repeated as needed | 107 inpatients in withdrawal | Uncontrolled symptom improvement; headaches in a few |
| Späth-Schwalbe 1995 | 3 to 4 mg by intravenous infusion over two hours | Healthy young men | No effect on ACTH or cortisol |
| Pomfrett 2009 | 25, 50 or 100 nmol/kg intravenous bolus | 24 women under anesthesia | Faster heart rate; lighter anesthesia |
| Charts sold online (2026) | 100 to 300 mcg subcutaneously 30 to 60 minutes before bed, several nights a week; nasal sprays also sold | Adults, wellness use | No human data at this dose or by this route |
The conversion matters. DSIP weighs about 849 daltons, so 25 nmol/kg is about 21 mcg/kg, and 30 nmol/kg about 25 mcg/kg: roughly 1.5 to 1.8 mg for a 70 kg adult, delivered into a vein, slowly. The investigators reported that slow injection was essential to the effect. The online chart dose of 100 to 300 mcg under the skin is five to fifteen times smaller, by a route that was never studied, with no published human pharmacokinetics to say how much of a subcutaneous dose reaches the blood or the brain. Nasal "DSIP sprays" have no human data of any kind.
We do not include a reconstitution example for DSIP because there is no legal product to reconstitute. Our reconstitution calculator exists for prescribed vials with a pharmacy label, and a label is exactly what a DSIP vial lacks.
Safety: what is known and what is not
What the old trials recorded. Good tolerance in the sleep studies, "no psychologic, physiologic, or biochemical side effects" in the first six volunteers (Schneider-Helmert 1981), and headaches in a few of the withdrawal patients (Dick 1984). Those observations come from intravenous use, in supervised settings, decades ago, in fewer than 200 people in total.
What was found later. Under anesthesia, DSIP raised heart rate and reduced heart-rate variability, which the authors read as reduced parasympathetic tone (Pomfrett 2009). It is a small signal in an artificial setting, but it is the only cardiovascular data that exists.
What nobody knows. Whether repeated subcutaneous injection of a nine-amino-acid peptide provokes antibodies (immunogenicity) has never been studied, and FDA's reviewers raised it as a concern tied to incomplete data on impurities. Whether the product in a given vial is emideltide, an analogue or something else is unknowable without testing, and FDA's position in 2026 was that the common name has covered different active molecules (Hyman Phelps 2026). Long-term effects, drug interactions, use in pregnancy, use with sedatives or alcohol: none has data.
Who should not use it. Given the absence of a legal product, the honest answer is everyone. If the question is who would be at greatest risk from an unregulated injectable of unknown content, the list is the usual one: pregnant or breastfeeding women, anyone on sedatives or opioids, anyone with heart rhythm problems, and anyone whose insomnia has not yet been evaluated for the common causes (sleep apnea, depression, medications, pain) that a peptide would mask.
Legal status in the United States
DSIP's regulatory history is short, recent and unambiguous. For the general framework, read are peptides legal?.
- Never approved. Emideltide has never been an approved drug in the United States or, as far as we can find, anywhere else. It has no USP monograph and is not a component of any approved product, so it fails all three tests that would let a 503A pharmacy compound it.
- Category 2, September 29, 2023. FDA added "Emideltide (DSIP)" to Category 2 of its compounding categories, the list of nominated substances that raise significant safety risks, alongside BPC-157, CJC-1295, ipamorelin, TB-500, epitalon and others (FDA categories update 2023). Category 2 substances are not compounded.
- Removed from Category 2, April 15, 2026. FDA took twelve peptides, DSIP among them, off the Category 2 list after their nominations were withdrawn, and scheduled seven of them for advisory review. Removal ended the safety flag; it did not permit compounding.
- Voted down, July 24, 2026. On the second day of its July meeting, FDA's Pharmacy Compounding Advisory Committee considered emideltide (free base and acetate) for chronic insomnia, narcolepsy and opioid withdrawal (Kelley Drye 2026). FDA's reviewers had recommended against all seven peptides on the agenda, citing insufficient evidence of safety and effectiveness, insufficient or nonexistent human trial data, inadequate characterization and quality information, uncertainty about identity and composition, and immunogenicity risk. For emideltide specifically, testimony supporting FDA's position argued that the common name covers different active molecules, that immunogenicity could not be assessed with incomplete impurity data, and that the efficacy data are flawed, small trials with nothing more recent than 1992. The vote failed, 6 in favor, 7 against, 1 abstaining, with dissenting members citing low-quality efficacy evidence, poor characterization, the existence of approved therapies and an uncertain dosing regimen. It was the only one of the seven peptides rejected that month (Hyman Phelps 2026).
- Not compoundable as of October 2026. No state-licensed 503A pharmacy and no 503B outsourcing facility may legally prepare DSIP, and because the committee voted against it, there is no pending rulemaking that would change that. A prescription cannot create a legal source.
What that means in practice: every DSIP vial or nasal spray sold in the United States in 2026 is an unapproved drug sold as a research chemical. FDA's 2026 warning letters to peptide vendors treated dosing guides, reconstitution instructions and bundled bacteriostatic water as evidence of intended human use, and rejected the research-use label as a defense. Nothing on this page should be read as guidance on buying one.
What actually has evidence for sleep
The useful question is not whether DSIP works but what to do instead, and here the evidence is good.
Cognitive behavioral therapy for insomnia (CBT-I). The American Academy of Sleep Medicine's 2021 guideline makes multicomponent CBT-I its single strong recommendation for chronic insomnia in adults, with brief therapies, stimulus control, sleep restriction and relaxation as conditional options, and recommends against sleep hygiene alone (Edinger 2021). It works without a drug, the benefit lasts after treatment ends, and it is increasingly available through validated digital programs. When CBT-I alone is not enough, FDA-approved insomnia medications have labeled doses, known risks and a clinician to adjust them.
GHRH and slow-wave sleep. The one peptide signal with real physiology behind it is growth hormone-releasing hormone. In seven healthy men, four intravenous boluses of 50 mcg GHRH given at 10 p.m., 11 p.m., midnight and 1 a.m. raised the share of the night spent in slow-wave sleep from 14.0% to 20.2% and blunted overnight cortisol (Steiger 1992). A later study in healthy volunteers found the effect depends on delivery: four 50 mcg pulses increased slow-wave sleep versus placebo, while the same 200 mcg as a continuous infusion did not (Marshall 1996). That is why sermorelin, a short-acting GHRH analog injected at bedtime, is the peptide clinicians reach for when a patient asks about sleep, and it is a peptide a licensed pharmacy can dispense. The caveat is in the sermorelin profile: no sermorelin trial has measured sleep objectively in the adults it is marketed to, so "may deepen slow-wave sleep" is a physiological inference, not a demonstrated outcome.
MK-677, for completeness. The oral secretagogue ibutamoren increased stage IV sleep by about 50% and REM sleep by more than 20% in eight young adults, and REM by nearly 50% in six older adults, in a small 1997 crossover study (Copinschi 1997). It is not a peptide, it raises blood sugar, and FDA's committee voted against compounding it in October 2024, so it is not an option either.
What that leaves. For most people with chronic insomnia the sequence is evaluation (apnea, depression, pain, medications, alcohol), CBT-I, and medication only if needed. For a patient with documented low IGF-1 who also sleeps poorly, a prescribed GHRH analog with IGF-1 monitoring is a defensible experiment. An intravenous rabbit peptide reconstituted from an unlabeled vial is not on the list.
Bottom line
DSIP is a 1977 discovery that never became a drug because the science never caught up with the name: no gene, no receptor, a few small intravenous trials in the 1980s that independent groups could not replicate, and nothing on sleep since 1992. The doses sold online are a fraction of the studied doses by a route that was never studied, the safety record is forty years old and thin, and FDA's advisory committee looked at the whole file in July 2026 and voted no. There is no legal version, and there is no honest version of the sleep claim.
If sleep is the problem, the treatments with evidence are CBT-I and, where needed, approved medication; if a peptide conversation is unavoidable, sermorelin is the one with a prescription path, and even its sleep claim should be held loosely.
Frequently asked questions
+What is the DSIP peptide dosage?
There is no established dose, because DSIP has never been approved or dosed in a modern trial. The 1980s and 1990s studies gave 25 to 30 nmol per kilogram, about 1.5 to 1.8 mg for a 70 kg adult, as a slow intravenous injection or infusion, sometimes repeated nightly for a week; a 1995 study infused 3 to 4 mg intravenously. The 100 to 300 mcg subcutaneous doses on charts sold online are a fraction of the studied dose by a route that has never been studied in a human. We report studied doses so you can judge a claim, not as a recommendation.
+Does DSIP work for sleep?
The evidence is small, old and split. One research group reported that intravenous DSIP normalized sleep in chronic insomniacs in studies of 14 to 18 people in the 1980s. Two independent double-blind studies, in 1987 and 1992, found no significant difference from placebo or effects too weak to matter. No sleep study has been published since 1992, and FDA's advisory committee voted against the peptide in July 2026 on the strength of exactly that record.
+What are the benefits of DSIP?
The documented effects in humans are limited to short-term sleep changes in a few dozen insomniacs in the 1980s, with conflicting results, and symptom relief in uncontrolled reports of alcohol and opioid withdrawal. The benefits marketed online, deeper sleep, lower cortisol, less pain, longevity, better recovery, have no modern trial behind them, and the one controlled study of cortisol found DSIP did nothing to ACTH or cortisol in healthy men.
+Is there a DSIP dosing chart?
Charts circulate, usually listing 100 to 300 mcg under the skin 30 to 60 minutes before bed, several nights a week. They are not derived from any human study. The studied route was intravenous, the studied dose was roughly five to fifteen times larger, and the researchers who ran the original studies reported that slow injection was essential. A chart is a seller's claim, and the seller is not accountable for what is in the vial.
+Is DSIP legal or FDA approved?
DSIP has never been FDA-approved. In September 2023 FDA placed it in Category 2 of its compounding list as a significant safety risk; in April 2026 it was removed after the nomination was withdrawn; and on July 24, 2026 FDA's Pharmacy Compounding Advisory Committee voted 6 to 7 against recommending it for the permitted list, the only one of seven peptides reviewed that month to be rejected. No US pharmacy may compound it. Possessing it is not a crime, but selling it for human use is, whatever the label says.
+Is DSIP the same as emideltide?
Yes. Emideltide is the international nonproprietary name for the nine-amino-acid DSIP sequence, and it is the name FDA used in its 2023 Category 2 listing and the July 2026 committee review. One of FDA's concerns was that products sold as DSIP are not necessarily the same molecule: the common name has been applied to different active peptides and analogues over the years, so a vial labeled DSIP may not contain emideltide.
+What are the side effects of DSIP?
The 1980s trials reported good tolerance, with headaches in a few patients during withdrawal treatment, and one anesthesia study found it raised heart rate and lightened anesthetic depth. That is nearly the entire human safety record, gathered from intravenous use decades ago. For the subcutaneous vials sold now there is no safety data at all, and FDA's reviewers flagged immunogenicity, meaning an immune reaction to the peptide or its impurities, as an unresolved concern. The practical risks are those of any unregulated injectable: unknown content, unknown sterility and nobody to call.
+What is the best peptide for sleep?
No peptide is a proven sleep treatment. The best-supported first-line treatment for chronic insomnia is cognitive behavioral therapy for insomnia, which the American Academy of Sleep Medicine recommends strongly. Among peptides, the closest thing to evidence is for GHRH, which increased slow-wave sleep in small studies of healthy men when given in pulses; sermorelin is the prescribable GHRH analog, though no sermorelin trial has measured sleep objectively in the people it is marketed to. The oral secretagogue MK-677 improved deep and REM sleep in a small 1997 study, but it is not a peptide and cannot be legally compounded.
+Can you take DSIP with melatonin or sleep medication?
There is no interaction data, because there is no modern DSIP study of any kind. Combining an unregulated injectable of unknown content with a prescription hypnotic or an over-the-counter sleep aid stacks an unknown on top of a known sedative, which is the wrong direction for safety. If sleep is bad enough to consider injections, it is bad enough to see a clinician about CBT-I and, where needed, an approved medication.
Sources
- StudySchoenenberger GA, Monnier M. Characterization of a delta-electroencephalogram (-sleep)-inducing peptide. Proc Natl Acad Sci USA 1977;74:1282-6. (1977)
- StudySchneider-Helmert D et al. Acute and delayed effects of DSIP (delta sleep-inducing peptide) on human sleep behavior. Int J Clin Pharmacol Ther Toxicol 1981;19:341-5. (1981)
- StudySchneider-Helmert D. Efficacy of DSIP to normalize sleep in middle-aged and elderly chronic insomniacs. Eur Neurol 1986;25:448-53. (1986)
- StudySchneider-Helmert D. Effects of delta-sleep-inducing peptide on 24-hour sleep-wake behaviour in severe chronic insomnia. Eur Neurol 1987;27:120-9. (1987)
- StudyMonti JM et al. Study of delta sleep-inducing peptide efficacy in improving sleep on short-term administration to chronic insomniacs. Int J Clin Pharmacol Res 1987;7:105-10. (1987)
- StudyBes F et al. Effects of delta sleep-inducing peptide on sleep of chronic insomniac patients. A double-blind study. Neuropsychobiology 1992;26:193-7. (1992)
- StudyDick P et al. DSIP in the treatment of withdrawal syndromes from alcohol and opiates. Eur Neurol 1984;23:364-71. (1984)
- StudyBackmund M et al. Opioid detoxification with delta sleep-inducing peptide: results of an open clinical trial. J Clin Psychopharmacol 1998;18:257-8. (1998)
- StudySpäth-Schwalbe E et al. Delta-sleep-inducing peptide does not affect CRH and meal-induced ACTH and cortisol secretion. Psychoneuroendocrinology 1995;20:231-7. (1995)
- StudyPomfrett CJ et al. Delta sleep-inducing peptide alters bispectral index, the electroencephalogram and heart rate variability when used as an adjunct to isoflurane anaesthesia. Eur J Anaesthesiol 2009;26:128-34. (2009)
- ReviewKovalzon VM, Strekalova TV. Delta sleep-inducing peptide (DSIP): a still unresolved riddle. J Neurochem 2006;97:303-9. (2006)
- StudySteiger A et al. Effects of growth hormone-releasing hormone and somatostatin on sleep EEG and nocturnal hormone secretion in male controls. Neuroendocrinology 1992;56:566-73. (1992)
- StudyMarshall L et al. Greater efficacy of episodic than continuous growth hormone-releasing hormone (GHRH) administration in promoting slow-wave sleep (SWS). J Clin Endocrinol Metab 1996;81:1009-13. (1996)
- StudyCopinschi G et al. Prolonged oral treatment with MK-677, a novel growth hormone secretagogue, improves sleep quality in man. Neuroendocrinology 1997;66:278-86. (1997)
- GuidelineEdinger JD et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med 2021;17:255-62. (2021)
- RegulatoryFDA. Bulk drug substances nominated for use in compounding under section 503A: notice of updates to categories, September 29, 2023 (emideltide (DSIP) and others added to Category 2 for significant safety risks). Copy hosted by the Alliance for Pharmacy Compounding. (2023)
- NewsSnow CD, Palmer KL, Bass M. PCAC adds two more bulk drug substances for the 503A list (epitalon, semax; emideltide rejected 6 to 7 with 1 abstention). FDA Law Blog, Hyman Phelps & McNamara, July 28, 2026. (2026)
- NewsKelley Drye. FDA advisory committee recommends several peptides for compounding despite staff opposition: what stakeholders need to know (emideltide proposed for opioid withdrawal, chronic insomnia and narcolepsy; FDA staff concerns). July 30, 2026. (2026)
Written by
The Peptide Doctrine Editorial Team
Our editors write from primary sources — peer-reviewed studies, FDA documents and pharmacy records — and grade every claim by the strength of its evidence. See our editorial policy for how articles are researched, reviewed and updated.
Disclosure. The Peptide Doctrine is an independent editorial project. It currently has no sponsor and runs no advertising: we accept no payment for reviews, rankings or placements, we run no affiliate links, and we do not sell or link to "research-use" peptide vendors. Content is educational and is not medical advice.
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