Original delta-sleep finding in rabbits [1]
The 1977 isolation and transfer experiment that named the peptide. A genuine finding in a specific animal preparation.
PrecisePep/Peptide Library/DSIP
Neuro-Cognitive & Nootropic
DSIP
delta sleep-inducing peptide · emideltide · DSIP nonapeptide
Named for an effect it has never reliably reproduced — a nonapeptide isolated from sleeping rabbits in the 1970s, and the one compound the FDA advisory committee looked at in July 2026 and voted against.
00 Overview
DSIP is named after a finding that has proved difficult to reproduce. It was isolated in 1977 from the cerebral venous blood of rabbits in induced sleep, and infusing it into recipient rabbits increased delta-wave sleep. That result gave the peptide its name and its entire reputation.
Almost fifty years later there is still no identified receptor, no established mechanism, and a human literature that is small, old, methodologically weak and inconsistent. Several studies found no significant effect on sleep architecture at all; others reported effects on sleep latency in insomnia populations. Related work explored chronic pain, opioid withdrawal and stress resilience.[1][2]
In July 2026 it became the compound that failed. Of seven peptides the FDA's Pharmacy Compounding Advisory Committee reviewed, DSIP — as emideltide — was the only one the committee declined to recommend for the 503A Bulks List. Six others were recommended; this one was voted down.
The one that did not pass
When BPC-157, KPV, TB-500, MOTS-c, Semax and Epitalon were all recommended and DSIP was not, that tells you something about how the evidence looked to a reviewing committee. It is not a ban and it is not binding — but marketing that groups DSIP with "the peptides the FDA just approved" is describing the opposite of what happened to this one.
// Mechanism of action
No identified receptor. Nearly fifty years after isolation, no specific DSIP receptor has been characterised. This is unusual and is the central problem with the whole compound — without a target, there is no mechanistic account to reason from.
Proposed neuromodulatory effects. Reported interactions with GABAergic, opioid and somatostatin systems, and modulation of corticotropin-releasing factor. None is established as the mechanism of action.
Blood-brain barrier penetration. DSIP is reported to cross the blood-brain barrier despite being a peptide, which is part of why it remained of interest.
Very short half-life. Rapid clearance is consistently reported, which sits awkwardly with claims of effects lasting through a night.
Possible role as a modulator rather than a hypnotic. The more defensible framing from the literature is a stress-response modulator with sleep effects secondary to that, rather than a direct sleep-inducing agent. That reframing also concedes the name is misleading.
01 Reported benefits
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Inconsistent human sleep results [2]
Small human studies report mixed findings — some improvement in sleep latency or subjective quality in insomnia populations, others no significant effect on sleep architecture. The literature does not converge.
Explored in chronic pain and opioid withdrawal [2]
Older work, largely from European and Soviet-era groups, reported effects in chronic pain and withdrawal syndromes.
Stress-response and corticosteroid modulation [2]
Reported effects on stress hormone responses in animal models, supporting the modulator framing rather than the hypnotic one.
PCAC declined to recommend it, July 2026
The only one of seven peptides reviewed across the two-day meeting that the advisory committee voted against.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Improved sleep quality and depth
The reason anyone uses it, and the claim the human literature has most conspicuously failed to establish.
Circadian rhythm normalisation
Proposed, unevidenced.
Stress resilience and cortisol modulation
The better-supported framing, from the animal stress-response work.
Recovery via improved slow-wave sleep
Would follow if the sleep effect were reliable, which is exactly the open question.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Deeper sleep and easier sleep onset
The dominant community report. Sleep is unusually susceptible to expectation effects, and this is a compound whose name tells the user what to expect before they take it.
Highly inconsistent between users
Reported far more variably than most compounds here — which matches the inconsistency of the published literature rather closely.
Grogginess the next morning
Occasionally reported, more often at higher doses.
No effect at all
A very common report for this compound.
Often paired with or replaced by simpler options
Users frequently report that sleep hygiene, magnesium or established sleep medication produced a clearer result.
02 Adverse effects & risks
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Reported as well tolerated in the limited human work [2]
Small studies report few adverse effects — in the context of small samples and short exposures.
No modern safety dataset
No contemporary toxicology, pharmacokinetics or adverse-event surveillance.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Masking an undiagnosed sleep disorder
The most practically important risk. Sleep apnoea, restless legs and circadian disorders are common, treatable and diagnosable — and suppressing the symptom removes the prompt to investigate.
Unknown interactions with sedatives
Proposed GABAergic and opioid-system interactions are uncharacterised, which makes combination with sleep medication or alcohol an unquantified risk.
No mechanism means no predictable risk profile
Without an identified receptor, there is no basis for anticipating what chronic use does.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Morning grogginess
The main complaint.
Vivid dreams
Reported.
Injection-site reactions
Mild and infrequent.
03 Dosing ranges
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Historic study dosing [2]
Human studies used intravenous administration at low microgram-per-kilogram doses. The subcutaneous route common in the research market does not match this.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Evening administration
Follows from the intended effect. Practical rather than pharmacological, given the short half-life.
Investigate the cause of poor sleep first
This is the single most useful thing available on this page — sleep complaints have common, treatable, diagnosable causes.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
100–250 mcg before bed
The standard community range, subcutaneous, typically 30–60 minutes before sleep.
Used intermittently rather than nightly
Common, often because the effect is reported as inconsistent.
| Approach | Dose | Route | Timing |
|---|---|---|---|
| Standard | 100 – 250 mcg | Subcutaneous | 30–60 min before bed |
| Higher-end | 500 mcg | Subcutaneous | Before bed |
04 Synergy & interactions
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No combination studies exist
None.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
With GH secretagogues
The rationale is that deeper slow-wave sleep supports the nocturnal GH pulse. Coherent if the sleep effect is real, which is the unresolved question.
With Epitalon
Both are claimed to act on sleep and circadian rhythm by different routes. Grouped by framing rather than mechanism.
Caution with sedatives and alcohol
Proposed GABAergic interactions make additive sedation plausible and uncharacterised.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Stacked with evening GH peptides
The common context.
05 Protocols
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No established protocol
The human literature is too small and inconsistent to have produced one.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Rule out treatable sleep disorders first
Sleep apnoea in particular is common, seriously consequential and diagnosable with a home study.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
As-needed before bed
The general community pattern.
Not part of either documented protocol
Neither the Gold Standard Protocol nor the 15-Compound Matrix includes it.
05b Condition-specific interest
DSIP is named for an effect reported in rabbits in 1977, and the half-century since has not confirmed it in people. It is also the only compound in this library to have been put to a formal regulatory vote and rejected, which makes it an unusually clear case: an outside body looked at the same evidence and reached a conclusion.
No approval, no trial
DSIP was rejected by the PCAC for the 503A Bulks List, 6–7 against with one abstention. That is not a formality skipped or an application not yet made — it is the same advisory process that returned favourable votes for BPC-157, KPV, TB-500, MOTS-c, Semax and Epitalon, applied to this compound, reaching the opposite answer. Everything below should be read with that in view.
Theorized — old, small, inconsistent
Insomnia and sleep architecture — the name and the problem
Pathophysiology
Slow-wave sleep is when the largest growth hormone pulses occur and when much memory consolidation happens. Reduced slow-wave sleep is a real feature of ageing and of several disorders.
Mechanistic rationale
DSIP was isolated from rabbit cerebral venous blood during induced sleep and named for the delta-wave activity it appeared to promote. The human work that followed, mostly from the late 1970s and 1980s, was small and inconsistent, and the compound was never developed into a product. A peptide that genuinely induced slow-wave sleep would have been commercially enormous at any point in the last forty years, and its absence from the market is itself informative.
Community reports
Reports are unusually mixed for a compound in this library — some describe deeper sleep, many describe nothing, and a notable subset describe grogginess or paradoxical wakefulness. Mixed reporting in a placebo-responsive domain generally means a weak or absent effect rather than an inconsistent one.
Components carrying the argument: Mechanism never established; the receptor is unidentified
Actionable
The mechanism nobody can name
Pathophysiology
Not a condition. A gap that shapes everything else here.
Mechanistic rationale
Almost every compound in this library has an identified receptor or a defined molecular target. DSIP does not. Nearly fifty years after isolation, no receptor has been convincingly identified and no consistent mechanism described. That is unusual, and it is a reasonable part of why the regulatory vote went the way it did — it is difficult to assess safety in a compound whose mode of action is unknown.
Community reports
Community descriptions attribute mechanisms to it freely. None trace back to a primary source.
Components carrying the argument: Unidentified
Theorized — old literature, never replicated
Chronic pain
Pathophysiology
Chronic pain involves peripheral and central components, and sleep disruption both worsens pain and is worsened by it.
Mechanistic rationale
Some of the original DSIP literature reported analgesic effects, and there is a coherent indirect route — improve sleep, reduce pain amplification. Both halves of that are unestablished here: the sleep effect is not confirmed, so the pain effect downstream of it has nothing to stand on.
Community reports
Occasionally used in chronic pain and fibromyalgia contexts, generally as an adjunct to something else.
Components carrying the argument: Possible opioid-system interaction, poorly characterised
Theorized — and the same warning as Selank applies
Alcohol and opioid withdrawal
Pathophysiology
Withdrawal from alcohol can cause seizures and delirium tremens. Opioid withdrawal is rarely fatal in itself but is severe, and the period after detoxification carries a sharply elevated overdose risk because tolerance falls.
Mechanistic rationale
The older DSIP literature includes reports of use in withdrawal states, which is where the community interest originates. None of it establishes seizure protection, and substituting an unproven peptide for benzodiazepines in alcohol withdrawal removes the treatment that prevents seizures and delirium tremens. As on the Selank page: withdrawal is a supervised medical process, not something to improvise.
Community reports
Discussed in this context, which is why the warning is stated here explicitly rather than left implied.
Components carrying the argument: No anticonvulsant or cross-tolerant activity
Theorized — the softest claim here
Stress and cortisol
Pathophysiology
Chronic stress produces sustained HPA axis activation with downstream metabolic, immune and cognitive consequences.
Mechanistic rationale
Some early work reported effects on stress responses and corticosteroid levels. It is old, small, and has not been built on. Cortisol is also easy to move transiently and hard to move meaningfully, and single measurements are close to uninterpretable given its diurnal variation.
Community reports
Reported as calming by some users, which overlaps with the sleep claim and is subject to the same interpretation problem.
Components carrying the argument: HPA axis effects, poorly characterised
| Question | Position |
|---|---|
| Regulatory status | Rejected by PCAC, 6–7 against, one abstention |
| Named for | Delta-wave sleep in rabbits, 1977 |
| Human sleep evidence | Small, from the 1970s–80s, inconsistent |
| Receptor / mechanism | Never identified |
| Ever developed as a product? | No — in nearly fifty years |
| Withdrawal use | No seizure protection — do not substitute |
| Community reports | Unusually mixed, which is itself informative |
What actually has evidence for these conditions
For insomnia: cognitive behavioural therapy for insomnia is first-line, outperforms hypnotics at follow-up, and is available in digital form. Sleep restriction therapy and stimulus control are the active components. Screening for obstructive sleep apnoea and restless legs syndrome matters enormously — both are common, both are routinely missed, and both are treatable. Light exposure timing, alcohol reduction and a consistent wake time do more than most people expect.
For chronic pain: multidisciplinary management, graded activity, and condition-specific pharmacotherapy. Treating the sleep disorder is a legitimate part of this — with a treatment that works on sleep.
For withdrawal: medically supervised detoxification. Benzodiazepines for alcohol withdrawal, thiamine to prevent Wernicke encephalopathy, and opioid agonist therapy — buprenorphine or methadone — which reduces mortality substantially and is the intervention with the best evidence in opioid use disorder.
06 Handling, reconstitution & storage
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Reconstitution
Supplied lyophilised, commonly 10 mg per vial. At 200 mcg per use a 10 mg vial covers fifty doses — a long in-use period for intermittent use.
Storage
Lyophilised: refrigerated or frozen. Reconstituted: 2–8 °C.
Common vial sizes
Commonly 10 mg lyophilised vials.
Stability notes
A short nonapeptide with ordinary handling requirements.
07 Legal & regulatory status
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Not approved anywhere. DSIP has never held a marketing approval in any jurisdiction and is supplied as a research chemical.
Regulatory update — current as at August 2026
On 24 July 2026 the FDA's Pharmacy Compounding Advisory Committee declined to recommend Emideltide (DSIP) for the Section 503A Bulks List (6–7 against, one abstention). It was the only one of the seven peptides considered across the two-day meeting that the committee voted against — BPC-157, KPV, TB-500, MOTS-c, Semax and Epitalon were all recommended.
A negative advisory vote is not a ban, and it is not binding either. But it does mean this compound is the one the committee looked at and was not persuaded by, which is worth weighing against marketing that groups it with the six that passed.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: PCAC rejection 24 July 2026. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Anti-doping
Athletes subject to WADA, USADA, UKAD, NCAA or military testing should assume any peptide is prohibited unless they have verified otherwise against the current WADA Prohibited List. Several classes here (growth-hormone secretagogues, TB-4 analogues, metabolic modulators) are explicitly named. Check the current list — it is republished annually.
§ Sources & further reading
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
- PubMed: delta sleep-inducing peptide — isolation, sleep studies and mechanism (live query)Database or literature search
- PubMed: DSIP in human sleep, chronic pain and withdrawal studies (live query)Database or literature search
- FDA — Pharmacy Compounding Advisory Committee, July 23–24 2026 meeting materialsRegulatory / official document
Reminder
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.