The Sleep Reset
DSIP
Also known as Delta Sleep-Inducing Peptide
At a glance
- What it is
- A neuropeptide studied for deep, delta-wave sleep: depth, not sedation.
- Evidence
- Small human studiesHow the tiers workThree small human trials from the 1980s–90s (6–25 participants); one double-blind trial showed statistically significant improvements in sleep efficiency and latency, and research largely paused after the 1990s. Why this tier
- Half-life
- Not established in available literature
- Routes
- Subcutaneous, Intranasal
- Category
- Sleep
- WADA
- We do not state a status
- Amino acids
- 9
Putting DSIP on a schedule, with the vial it comes from and a log of each dose, happens in the app: Claritide for iPhone.
Why this tier
Three small human trials from the 1980s–90s (6–25 participants); one double-blind trial showed statistically significant improvements in sleep efficiency and latency, and research largely paused after the 1990s. FDA’s search of its adverse-event database (FAERS) through 3 March 2024 found zero reports, which is not evidence of safety. In July 2026 an FDA advisory committee voted 6–7–1 against recommending it for compounding, the only rejection in that batch.
What it is
DSIP is a naturally occurring 9-amino-acid neuropeptide first isolated in 1977 from the cerebral venous blood of rabbits during electrically induced sleep. It promotes delta-wave activity, the brainwave pattern that defines the deepest stage of sleep, and modulates cortisol rather than sedating you. Clinical studies are small and mostly from the 1980s and 90s, but they consistently describe improved sleep efficiency in people whose sleep is already disrupted.
How it works
DSIP works on sleep architecture rather than sleep timing. It increases delta-wave (0.5–4 Hz) brain activity, which defines Stage 3 NREM sleep, the phase where growth hormone secretion peaks, cellular repair happens and the brain clears waste. It does not simply add sleep hours; it reorganises the proportion of the night spent in deep sleep. It also modulates the HPA axis, the hormonal chain that produces cortisol and ACTH, which helps normalise the elevated evening cortisol that drives both sleep-onset insomnia and early waking. Its effect on GABA, the brain's main calming neurotransmitter, is indirect: it appears to make GABA-A receptors more sensitive rather than binding them directly the way a benzodiazepine does, which is the standard explanation for why no tolerance or dependency has been observed. A recurring finding is that DSIP is context-sensitive: strong effects when sleep is already broken, minimal effect in healthy sleepers.
Commonly researched ranges
- Starting100 mcg
The entry point in community protocols, held for 3–5 days before any increase is considered.
- Maintenance200–300 mcg
Community protocols stop here. The widely repeated line that more than 300 mcg worsens sleep is not a human finding: no human dose-ranging study of DSIP has ever been run, and the claim traces to animal and in-vitro pituitary work. The only dose any controlled human sleep study used was 25 nmol/kg intravenously, roughly 1.5 mg in a 70 kg adult, which is a different route and roughly five times this range.
| Phase | Amount | Frequency | Timing | Note |
|---|---|---|---|---|
| Starting | 100 mcg | Once daily | Afternoon or early evening, 4–6 PM | The entry point in community protocols, held for 3–5 days before any increase is considered. |
| Maintenance | 200–300 mcg | Once daily, or 5 days on / 2 days off | Afternoon or early evening, 4–6 PM, not at bedtime | Community protocols stop here. The widely repeated line that more than 300 mcg worsens sleep is not a human finding: no human dose-ranging study of DSIP has ever been run, and the claim traces to animal and in-vitro pituitary work. The only dose any controlled human sleep study used was 25 nmol/kg intravenously, roughly 1.5 mg in a 70 kg adult, which is a different route and roughly five times this range. |
- Cycle guidance
- 2–4 weeks is the standard cycle; some clinical studies ran to 6 weeks. Benefits often persist for days to weeks after stopping. Long-term safety beyond 6 weeks is not characterised. Cycle off and reassess.
- Goals
- Sleep, Recovery
Where this sits with the FDA
FDA 503A bulks list · nomination considered and voted down
DSIP is the only compound in the July 2026 batch the advisory committee voted down. It came off Category 2 in April 2026, which removed a warning rather than granting permission.
Last change · 24 July 2026 · PCAC voted 6–7–1 against adding DSIP (emideltide) to the 503A bulks list.
Primary sourceHow it got here
- 22 April 2026
FDA removed 12 peptide bulk substances from Category 2 after the nominators withdrew their nominations. Announced 15 April 2026, effective 22 April 2026. Removal from Category 2 is not permission to compound.
- 24 July 2026
PCAC voted against recommending DSIP (emideltide) for the 503A bulks list, the only rejection across the two-day meeting.
Vote 6–7–1
An advisory vote is not law. In July 2026 an FDA advisory committee voted in favour of adding several peptides to the 503A bulks list, over the explicit recommendation of FDA’s own scientific reviewers, who recommended against all seven. FDA would still have to write a rule, and it has not proposed one or given a date. None of these compounds is lawfully compoundable today.Note what FDA actually assessed: BPC-157 for ulcerative colitis, TB-500 for wound healing, KPV for wound healing and inflammatory conditions, MOTS-c for obesity and osteoporosis, Epitalon for insomnia, Semax for cerebral ischaemia, migraine and trigeminal neuralgia. Whatever emerges from rulemaking will be scoped to those indications.
WADA status
Not named on WADA’s 2026 Prohibited List. Its S0 section also bans drugs it does not name, when no government health authority currently approves them for human treatment. DSIP has been registered in Russia since 2016 as Deltaran, a nasal medicine for stress and alcohol withdrawal. So S0 may not cover it, and we do not state a status.
We looked and could not resolve it. This is not the same as "not prohibited". Treat it as unresolved and check with your federation before competing.
The FDA reclassification has no effect whatsoever on WADA status.
Mixing recipes our sources document
- 10 units100 mcg
- 20 units200 mcg
- 30 units300 mcg
Week by week
- 1Nights 1–3
Subtle or nothing. Some notice slightly easier sleep onset or better morning alertness; many notice nothing. Do not increase the dose yet.
- 2Days 4–7
Deeper sleep, fewer middle-of-the-night awakenings, more vivid dreaming, described in our sources as a positive sign of normalising sleep architecture. Morning energy improves.
- 3Week 2–3
Full benefits. Noticeably more restorative sleep, better daytime energy and mood, improved stress resilience. Some report reduced caffeine dependence.
- 4Week 4+
Benefits plateau. Consider cycling off. Many find improvements persist for days to weeks after stopping.
- 5After stopping
No rebound insomnia and no withdrawal reported, the key difference from pharmaceutical sleep aids. Sleep may gradually return to baseline in people with chronic underlying issues.
Side effects
Common
- Morning drowsiness
- Vivid dreams
Uncommon
- Mild headache
- Injection site irritation
Contraindications and interactions
Do not use if
- Concurrent ACE inhibitors: interactions have been noted
- Concurrent benzodiazepines or other CNS depressants: additive GABA effects
- Pregnancy or nursing: no safety data exists
- Alcohol or sedatives, particularly when starting
Interactions
- Benzodiazepines and CNS depressantsavoid
Overlapping GABA pathway activity: additive effects.
- ACE inhibitors (e.g. captopril)caution
Interactions have been noted in the DSIP literature.
- Alcoholcaution
Additive sedation, particularly in the first days.
Absence from this list does NOT mean safety. It means lack of research.
Storage and cost
- Storage
- Lyophilized powder: refrigerator 2–8°C for several months, freezer −20°C for 1–2+ years. Reconstituted with bacteriostatic water: refrigerate 2–8°C and discard after 28 days. Never freeze reconstituted solution.
- Cost
- $30–$50 per 2–4 week cycle (one 2 mg vial)
Stacks with
DSIP in full
What it actually is
DSIP is nine amino acids long and it was found by accident. In 1977, Schoenenberger and Monnier drew cerebral venous blood from rabbits during electrically induced sleep, isolated a fraction from it, and injected that fraction into other rabbits. The recipients showed increased delta-wave EEG activity. The peptide is named for exactly that: delta sleep induction.
It occurs naturally in the human brain, circulates in the bloodstream, and crosses the blood-brain barrier freely. Our sources describe it as having a relatively long half-life for a peptide but do not give a figure, so we do not publish one.
Depth, not timing
The most useful thing to understand about DSIP is the contrast with melatonin, because people arrive expecting the same product.
Melatonin is a timing signal. It tells your brain what time of night it is. It helps you fall asleep and it fixes jet lag. It does not change what happens once you are asleep.
DSIP works on architecture, the structure of the night. It increases the proportion of time spent in Stage 3 NREM, the delta-wave phase where growth hormone peaks, tissue repairs, and the glymphatic system clears metabolic waste. It is the phase melatonin does not touch, and the phase most degraded by insomnia, ageing, stress and bad habits.
This is why the timing instruction is counterintuitive. Practitioners commonly dose DSIP at 4–6 PM, not at bedtime. The effect builds over hours, and earlier dosing is described as improving that night's sleep quality rather than that evening's drowsiness.
The second mechanism people miss
DSIP modulates the HPA axis, the hypothalamic-pituitary-adrenal chain that produces cortisol and ACTH. Elevated evening cortisol is one of the most common reasons people lie awake with a busy head at 11 PM, or snap awake at 3 AM. DSIP's effect there operates independently of its direct sleep-promoting action.
Its relationship with GABA is worth being precise about. It does not bind GABA receptors the way a benzodiazepine does. It appears to enhance GABA-A receptor sensitivity and possibly increase endogenous GABA release. That indirect route is the standard explanation for the most striking clinical observation about DSIP: across weeks of use in multiple studies, no tolerance, no dependency, no rebound insomnia, and no next-day psychomotor deficit.
What the evidence actually supports
Three small human trials, 6 to 25 participants, published in the 1980s and early 90s. One double-blind trial in chronic insomnia patients showed statistically significant improvements in sleep efficiency and sleep latency. Research effectively paused after the 1990s. There are no large modern RCTs.
A repeated finding is that DSIP is context-sensitive: effects are strongest when sleep is already disturbed and minimal in healthy sleepers. It behaves more like a normaliser than a sedative. If you already sleep well, the literature predicts you will notice very little.
Running it
Start at 100 mcg subcutaneously and hold there for three to five days. Maintenance is 200–300 mcg. Timing is 4–6 PM. Frequency is daily or five days on, two off. Cycles run 2–4 weeks.
The ceiling everyone quotes, that above 300 mcg sleep gets worse, is worth reading carefully. It is not a human finding. No dose-ranging study of DSIP has ever been run in people; the claim traces back to animal and in-vitro pituitary work, and the community range above was built on top of it. The only dose used in the controlled human sleep studies was 25 nmol/kg intravenously, about 1.5 mg in a 70 kg adult, by a route nobody self-administers. So there is no published human ceiling, which is a different statement from "there is no ceiling".
Reconstitution is clean. A 2 mg vial with 2 mL of bacteriostatic water gives 1 mg/mL, which puts 100 mcg at exactly 10 units on a U-100 syringe and 200 mcg at 20.
The honest cautions
DSIP touches the GABA system, which is the same system benzodiazepines act on. Combining it with benzodiazepines, other CNS depressants, or alcohol is the interaction that matters most. ACE inhibitors are the other flag our sources raise specifically.
Long-term safety beyond about six weeks is not characterised. The cycling advice is not ritual. It reflects the edge of the data.
Sources
- 1Bes et al., 1992 · Effects of DSIP on sleep of chronic insomniac patients, a double-blind study, Neuropsychobiology 26(4)
- 2Schneider-Helmert et al., 1981 · Acute and delayed effects of DSIP on human sleep behavior
- 3Schoenenberger & Monnier, 1977 · Characterization of a delta-EEG (sleep)-inducing peptide, PNAS 74(3)
- 4Graf & Kastin, 1986 · Delta-sleep-inducing peptide (DSIP): an update, Peptides 7(6)
- 5Kovalzon & Strekalova, 2006 · DSIP: a still unresolved riddle, J Neurochem 97(2)
- 6Schneider-Helmert, 1981 · DSIP in chronic insomnia, the 25 nmol/kg intravenous dose every controlled human sleep study used (dose review, 2026-08-17)
- 7Schneider-Helmert, 1987 · DSIP in insomniacs and normal sleepers, same intravenous dose (dose review, 2026-08-17)
- 8FDA · emideltide (DSIP) briefing document for the Pharmacy Compounding Advisory Committee, 11 May 2026: FAERS searched through 3 March 2024, zero reports
Every record in this library is free to read, and it stays free. Your own schedule, vials and log live in the app: Claritide for iPhone.