Reference

Last reviewed: 28 Apr 2026
Sources cited: 9
Residues: 9

Primary structure9 residues · 848.8 Da

01TrpTryptophan

02AlaAlanine

03GlyGlycine

04GlyGlycine

05AspAspartate

06AlaAlanine

07SerSerine

08GlyGlycine

09GluGlutamate

Nonpolar Polar Acidic Basic Aromatic Gly/Pro

DSIP

Last verified: 2026-04-24

At a glance


Also known as	Delta Sleep-Inducing Peptide, DSIP (nonapeptide)
Class	Endogenous nonapeptide neuropeptide
Typical route	Subcutaneous injection, intranasal (less common: IV in clinical research)
Plasma half-life	~7–8 min (human); ~15 min in vitro; 4–5 min in animal studies
Duration of effect	Short plasma presence; behavioural/sleep effects reported over hours to days; mechanism of persistence not well understood
Molecular weight	848.8 Da
Sequence	Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (9 amino acids)

What it is

DSIP is an endogenous neuropeptide — meaning your body already produces it. It was discovered in 1974 by the Swiss Schoenenberger-Monnier group, isolated from the cerebral venous blood of rabbits that had been placed in an induced sleep state by electrical stimulation. Hence the name: delta-wave (slow-wave) sleep-inducing peptide.

It has been studied for over fifty years, primarily in Europe and Russia. Despite that long history, its mechanism remains poorly characterised, and the clinical evidence base is genuinely thin — the most-cited controlled trial (Schneider-Helmert 1992) concluded DSIP was “not likely to be of major therapeutic benefit” for chronic insomnia.1 Community use is driven more by the concept and historical interest than by robust clinical data.

DSIP occupies an unusual niche: widely discussed, widely sold, long-studied — and genuinely unresolved.

Mechanism

DSIP’s proposed mechanisms are plural and largely speculative. No single pathway has been firmly established.

Delta-wave (slow-wave) sleep modulation. Original rabbit studies showed DSIP increases EEG delta and spindle activity. Animal studies have broadly replicated this, with most suggesting DSIP enhances slow-wave sleep architecture rather than simply sedating — a distinction that matters because sedation and genuine SWS are pharmacologically different.
GABA-A and NMDA receptor modulation. Some evidence DSIP interacts with both systems. The GABA-A interaction is relevant to sleep, the NMDA interaction to its reported anti-stress and analgesic properties. Both mechanisms are proposed, neither firmly established.
Cortisol and ACTH suppression. DSIP has been reported to modulate HPA-axis output, particularly suppressing corticotropin (ACTH) and cortisol. This is the basis for its “anti-stress” framing.
Growth hormone (GH) release during sleep. Some evidence DSIP enhances GH secretion, though the effect is modest and inconsistent across studies.
Opioid receptor interaction (possible). The withdrawal-syndrome studies from the 1980s proposed agonistic activity on opioid receptors, though this has not been rigorously confirmed.

The honest summary: DSIP probably does something to sleep architecture, stress-axis output, and possibly pain signalling — but exactly what, through which receptors, at what doses, is not resolved after five decades of research. A 2006 review titled “Delta sleep-inducing peptide: a still unresolved riddle” remains a fair description.2

Routes of administration

Subcutaneous injection


Bioavailability	Not formally quantified in humans; assumed high (standard subQ peptide delivery)
Onset	10–30 minutes subjective effect
Duration	Effects reported overnight despite short plasma presence
Typical dose (this route)	100–500 mcg before bed
Equipment	Insulin syringe, BAC water, alcohol wipes
When this route makes sense	Highest-confidence dosing, clinical-research-aligned route, systemic delivery

The community default. Most clinical studies used injection (intravenous or subcutaneous). Dosed 30–60 minutes before bed to align with the natural sleep onset window.

Intranasal


Bioavailability to CNS	Plausibly high via nose-to-brain transport, but less well-characterised than for Semax/Selank
Onset	15–45 minutes
Duration	Similar overnight window
Typical dose (this route)	100–300 mcg before bed
Equipment	0.1% solution, calibrated nasal spray
When this route makes sense	Needle-averse users, convenience, potentially faster CNS delivery

Increasingly common in the biohacker community. The pharmacological logic is similar to Semax/Selank — direct CNS access via olfactory/trigeminal pathways — though DSIP has been less rigorously studied via this route than its Russian-developed cousins. Commercial DSIP nasal sprays are available and convenient, but the underlying evidence base uses injection.

Intravenous (clinical research only)


Bioavailability	100% (direct bloodstream)
Dose used	25 nmol/kg body weight in the Schneider-Helmert 1992 trial (~30 mcg/kg for reference)1
When this route makes sense	Clinical research only. Not a community route.

Most of the rigorous clinical evidence used IV DSIP. Not relevant for community use.

Oral / sublingual


Bioavailability	Likely negligible. No formal characterisation exists in humans.
Typical dose (this route)	Not recommended
When this route makes sense	Rarely. Some sublingual preparations are sold but evidence for meaningful absorption is essentially absent.

Cross-route comparison

SubQ injection is the most evidence-aligned route — most clinical studies used injection (IV or SC), and community consensus has settled on subQ as the practical default. Intranasal is a reasonable alternative for needle-averse users, with the caveat that it’s less formally studied than for Semax/Selank. Timing matters more than route for DSIP — dose 30–60 minutes before intended sleep onset regardless of route.

What the evidence says

Honest summary: long research history, thin rigorous evidence, the most-cited controlled trial was negative.

Clinical trials:

Schneider-Helmert (1992) — the canonical clinical reference. Double-blind, matched-pairs parallel-groups design, 16 chronic insomnia patients, IV DSIP at 25 nmol/kg over 5 nights vs glucose placebo. Found modest increases in sleep efficiency and shorter sleep latency, but the authors themselves concluded effects were “weak and in part could be due to an incidental change in the placebo group.” Subjective sleep quality did not improve. The study’s own conclusion: “short-term treatment of chronic insomnia with DSIP is not likely to be of major therapeutic benefit.”1 This is the most important source on DSIP and is widely misquoted as positive by secondary biohacker summaries.
Withdrawal syndrome studies (1980s) — reports in opiate-dependent (97%) and alcohol-dependent (87%) patients showing symptom alleviation after DSIP administration.3 Methodological rigour of these studies is limited by modern standards; sample sizes small; no Western replication.
Chronic pain pilot study (1980s) — DSIP reported to reduce chronic pain intensity in a small clinical pilot. Not replicated.4

Preclinical / mechanism:

Numerous animal studies support SWS enhancement, anti-stress effects (cortisol suppression), modulation of pain responses, and possible GH-release modulation.
A 2024 study on a DSIP-fusion peptide crossing the blood-brain barrier in an insomnia mouse model represents one of the more recent meaningful publications.5
A 2021 stroke-recovery study in rats showed motor function improvement post-focal stroke.6

Community evidence:

DSIP is moderately popular as a sleep peptide. Reports are genuinely mixed: some users describe deeper, more restorative sleep with faster sleep onset; others report no effect, or paradoxical next-day grogginess.
It is often stacked with other sleep-focused interventions (magnesium glycinate, apigenin, melatonin) rather than used in isolation.
Compared to compounds with strong clinical signal (e.g. benzodiazepines for acute insomnia), DSIP’s effect is reported as subtle or inconsistent.

Typical use patterns

Observations, not recommendations.

Dose:

Community standard: 100–500 mcg per dose, taken 30–60 minutes before bed
Clinical IV dose: 25 nmol/kg ≈ ~30 mcg/kg for a 70 kg adult that’s ~2,100 mcg IV — much higher than community subQ doses, but IV is the least bioavailable-lossy route
Starting point most commonly cited: 100–200 mcg subQ for a first protocol

Timing:

30–60 minutes before intended sleep onset
Not effective as an as-needed sleep aid during the night — onset is too slow
Not dosed during the day (unlike Semax/Selank) — the compound is specifically for sleep

Cycle:

Commonly dosed nightly for 2–4 week cycles, then breaks
Some users dose only 3–4 nights per week, preserving response
Long-term continuous nightly dosing (>30 days) is not characterised in published literature — community practice varies

Stacking:

Magnesium glycinate, apigenin, glycine for complementary sleep effects
Occasionally stacked with MOTS-c or Epithalon for broader “night-time recovery” protocols
Not advisable to stack with benzodiazepines, z-drugs, or significant alcohol — shared GABA-A/NMDA mechanisms create additive sedation risk

For sensitive systems

DSIP is worth considering for sensitive populations because sleep disruption is a near-universal feature of MCAS, UARS, POTS, long COVID, ME/CFS, and PMDD — and many of the mainstream sleep medications (benzos, z-drugs, trazodone) are poorly tolerated in these groups due to excipient reactions, morning grogginess, or paradoxical effects.

Start dose. 50–100 mcg subQ or intranasal before bed. Hold 3–5 nights before adjusting.

Ramp. Unlike peptides where you’re ramping up for more effect, DSIP response is typically non-linear — many users find 100–200 mcg produces the same effect as 400–500 mcg. Don’t chase dose escalation; if the starting dose doesn’t help after 7–10 nights, it likely won’t at higher doses either.

Expected adjustment profile:

Morning grogginess — the most common reported side effect; usually transient but worth watching for
Mild headache (reported in a few patients in clinical trials)1
Vivid dreams or increased dream recall — not unwelcome for some users but can be disruptive
Occasional vertigo or lightheadedness on first use
No documented histamine/mast-cell provocation mechanism — unlike BPC-157, DSIP is not a known mast cell trigger

What’s not normal and warrants stopping: significant next-day fatigue that doesn’t resolve, worsening of baseline sleep, paradoxical insomnia, mood changes.

Why DSIP may be useful for sensitive systems:

HPA-axis modulation (cortisol/ACTH suppression) is directly relevant to populations with cortisol dysregulation (adrenal-fatigue-adjacent presentations, chronic stress state, PMDD luteal-phase cortisol peaks)
Works via different mechanisms than benzos and z-drugs, so users who’ve failed those medications still have a reasonable chance with DSIP
Low histamine-provocation risk relative to most peptides

What to have on hand:

Saline rinse if using intranasal
Sleep-hygiene basics (consistent wake time, reduced evening light) — DSIP works better when sleep pressure is properly accumulated

Interactions worth considering:

Benzodiazepines, z-drugs (zolpidem, zopiclone), barbiturates: shared sedative mechanism. Additive risk. Not advisable to stack.
Alcohol: additive GABA-A and CNS depressant effect. Do not combine.
Trazodone, mirtazapine, quetiapine (low-dose for sleep): mechanistic overlap. Layering is not well studied and potentially additive.
Melatonin: no specific interaction. Commonly stacked, generally well-tolerated.
Cortisol-modulating treatments (hydrocortisone replacement, adrenal support supplements): DSIP’s ACTH suppression is theoretically relevant; not a contraindication but worth tracking your cortisol if you monitor it.
LDN (Low Dose Naltrexone): no documented interaction; some mechanistic overlap via possible opioid-receptor interaction, but community reports suggest they coexist fine.

PMDD note: the HPA-axis suppression angle is particularly interesting for PMDD luteal-phase cortisol and sleep issues. Mechanism-guided speculation, with no specific research yet.

Reasonable expectations

Onset. Subjective sleep effect typically reported within 30–60 minutes of dosing. Changes in sleep architecture (deeper slow-wave sleep, fewer awakenings) may emerge across 3–7 nights of consistent dosing.

Response rate. Genuinely polarised. Community surveys suggest roughly half of users report a clear benefit; the remaining half report nothing obvious or mild morning grogginess. The polarisation is consistent with the Schneider-Helmert finding that objective sleep metrics improved modestly while subjective sleep quality did not.

What the literature actually supports.

Modest objective sleep improvements in one small controlled trial (n=16), with the authors explicitly concluding the effect was weak and possibly artefactual1
Cortisol/ACTH suppression and HPA-axis modulation in animal models: reasonable preclinical signal
SWS-enhancing EEG effects in animal models: well-replicated
Withdrawal-syndrome alleviation: interesting 1980s reports, no replication to modern standards

What not to expect.

A pharmaceutical-grade sleep aid. DSIP is not zolpidem, diazepam, or trazodone in potency — at any dose.
Reliable sleep induction on a bad night. It’s too subtle and slow-acting for rescue use.
A replacement for sleep hygiene. Users who dose DSIP onto a caffeine + screen-time + inconsistent-bedtime foundation will likely see little.
Dramatic, obvious effects. If Semax’s effect is subtle, DSIP’s is even more so. Many users need 2–3 weeks of consistent dosing to judge whether it’s doing anything.

Cost

Approximate as of April 2026, research-chemical market, UK-focused. Vendor-neutral.


5 mg lyophilised vial (injectable)	£30–60
0.1% nasal spray (3 mL)	£35–65
Cost per month, community-standard (200 mcg/night subQ)	~£15–25
Cost per month, sensitive-start (100 mcg/night)	~£8–15
Cost per 14-night protocol (300 mcg/night subQ)	~£25–35

DSIP is in the cheaper tier of peptides to run. A 5 mg vial reconstituted to 2 mL provides 25 doses at 200 mcg — typically enough for a month of use.

Reconstitution

5 mg lyophilised DSIP:

Reconstitute in 2 mL bacteriostatic water → 2.5 mg/mL
100 mcg dose = 0.04 mL = 4 IU on a U-100 insulin syringe
200 mcg dose = 0.08 mL = 8 IU
300 mcg dose = 0.12 mL = 12 IU

Nasal spray (0.1%):

A 100 µL spray delivers ~100 mcg
For 200 mcg: 2 sprays (1 per nostril)

Open the Vial Plan calculator

Reconstituted DSIP is stable in BAC water, refrigerated, for ~30 days. Nasal preparations should also be refrigerated between uses. Do not freeze reconstituted solution.

Areas of concern ⚠

Safety signals

No rigorous modern safety data. Most available safety information comes from small studies conducted in the 1980s–90s under different regulatory standards.
DSIP is described as “incredibly safe” in some reviews — no lethal dose identified in animal studies, limited reported human adverse events — but this is an artefact of how little it’s been studied, not a clean bill of health.
Transient adverse effects documented: headache, nausea, vertigo, reported in a small number of clinical trial participants.1

The evidence base is genuinely weaker than most biohacker content suggests

The most-cited clinical trial (Schneider-Helmert 1992) concluded DSIP was unlikely to be of major therapeutic benefit — a finding almost universally omitted or misquoted by secondary sources
The most enthusiastic 1980s withdrawal-syndrome studies have not been replicated by any independent research group in 40 years
Be wary of sources claiming “studies show DSIP” without specific citations — the underlying evidence is often one small, old, unreplicated trial

Interaction risks

Shared GABA-A / NMDA / opioid-receptor mechanisms mean stacking with benzos, z-drugs, alcohol, or sedating medications has additive risk
DSIP’s mechanism overlap with multiple sedative pathways is one reason it was historically considered for addiction-withdrawal contexts — the same mechanism means careful attention to polypharmacy

HPA-axis modulation

DSIP’s cortisol/ACTH-suppressing effect is typically framed as beneficial for stress-related sleep disruption, but in individuals with cortisol insufficiency (e.g. on hydrocortisone replacement, Addisonian, steroid-withdrawing), additional HPA suppression is not desirable
Users with known HPA-axis dysfunction should treat this as a reason for extra caution rather than reassurance

Morning grogginess

The most commonly reported negative effect. Dosing too late (within 30 min of sleep) or too high a dose increases risk
Typically resolves after 3–5 consecutive nights as the dosing window is optimised

Quality and sourcing

DSIP is supplied by research-chemical vendors. Purity testing is rare.
Commercial nasal sprays vary in preservative content — benzalkonium chloride reactions worth watching for
Note on suppliers: DSIP is one of the older peptides in the biohacker market, which means vendor lineages are longer — some established suppliers exist, though independent purity verification remains rare
Storage: lyophilised is stable at room temperature; reconstituted solution should be refrigerated, used within 30 days

Populations where caution is warranted

Pregnancy and breastfeeding — no data, default contraindication
Active HPA-axis suppression or cortisol insufficiency — theoretical but relevant given DSIP’s mechanism
Concurrent sedative medication use — benzos, z-drugs, heavy alcohol consumption
History of paradoxical reactions to sedatives — GABAergic mechanism overlap
Severe sleep disorders (sleep apnoea, central hypoventilation) — any sedating agent is relatively contraindicated pending proper diagnosis and treatment; DSIP is not enough of a sleep aid to justify the risk
Under 18 — no data

FDA / regulatory status

Jurisdiction	Status	Last verified
US (FDA)	Not approved. Currently not on 503A Category 1 or Category 2 in 2026. Expected to be among the peptides considered for Category 1 reclassification per the February 2026 HHS announcement, but no formal rule has been published.	2026-04-24
UK (MHRA)	Not licensed. Not a controlled substance. Sold as research chemical with “not for human consumption” labelling.	2026-04-24
EU (EMA)	Not approved. Similar posture to UK.	2026-04-24
WADA (sport)	Not explicitly listed. Treat as prohibited for tested athletes under general peptide/hormone category.	2026-04-24

Narrative. DSIP has one of the longest research histories of any biohacker peptide (since 1974) and has never achieved regulatory approval anywhere, including Russia. It sits in the “legally ambiguous but not controlled” category across most Western jurisdictions. The February 2026 HHS announcement about peptide reclassification mentioned DSIP as a candidate for potential Category 1 consideration, but no FDA action has been taken as of April 2026.

For UK readers: DSIP is legally available as a research chemical from UK-based suppliers. Not a controlled substance. Personal possession is not an offence. Sale for human consumption is not permitted.

What to track in Peptrax

DSIP is a sleep compound with a famously erratic responder pattern — some users find it transformative, others get nothing. The honest test is sleep architecture, not total time in bed. Track time-to-fall-asleep, number of night wakings, time of first awakening, and morning grogginess on a 0–5 scale. A wearable’s sleep stages (deep, REM) is a useful supplement; without one, the subjective rating fields are still meaningful as long as they’re consistent.

The on/off contrast carries more signal than any single night. Two weeks of DSIP nights against two weeks of clean nights, same bedtime, same wind-down routine, is the readout that actually answers the question. Logging cycle dates, route (subQ is dominant; intranasal is sometimes used), and time of dose relative to bed makes that comparison possible — DSIP is genuinely sensitive to timing in a way most peptides aren’t.

For users with diagnosed sleep disorders (UARS, sleep apnoea, insomnia), DSIP is not a substitute for treatment of the underlying condition, and the tracking question becomes whether it adds anything on top of CPAP, therapy, or other interventions. Logging concurrent treatment alongside DSIP cycles is the only way that comparison stays honest.

For personal tracking and informational purposes only — not medical advice.