DSIP.
DSIP (Delta Sleep-Inducing Peptide) is a small endogenous nonapeptide with the amino acid sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE), molecular weight roughly 850 Da.
DSIP (Delta Sleep-Inducing Peptide) is a small endogenous nonapeptide with the amino acid sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE), molecular weight roughly 850 Da. DSIP is research / preclinical, and PepCue grades its published evidence F tier (22/100). Also known as delta sleep-inducing peptide. This is a research reference, not medical or dosing advice.
What it is
DSIP (Delta Sleep-Inducing Peptide) is a small endogenous nonapeptide with the amino acid sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE), molecular weight roughly 850 Da. It was first isolated in 1974 by Schoenenberger, Monnier and colleagues in Switzerland from the cerebral venous blood of rabbits placed in an electrically induced state of slow-wave (delta) sleep, and named for that apparent sleep-promoting property. DSIP-like immunoreactive material has since been detected in various mammalian tissues and human fluids (including breast milk), but it remains a biochemical "riddle": no gene, precursor protein, or specific receptor for it has been definitively identified.
How it works
DSIP has no single confirmed receptor or signaling pathway; its mechanism remains genuinely unresolved despite decades of study. Reported preclinical interactions are diffuse and concentration-dependent, including modulation of NMDA-receptor activity, effects on glucocorticoid/stress-axis regulation, and engagement of MAPK signaling cascades, along with proposed influences on GABAergic, opioid/enkephalin, and somatostatin systems. It does not behave like a classical hypnotic acting at a defined target; instead it has been framed as a neuromodulator or "homeostatic" regulator with dose- and timing-dependent, sometimes bidirectional, effects on arousal. Its very short circulating half-life (on the order of minutes) further complicates any straightforward receptor-occupancy mechanism.
Mechanism pathways
Peptides that tune monoamine, GABA, opioid, ion-channel, and social-behaviour circuits.
Neuromodulation differs from neurotransmission. A neurotransmitter carries a discrete signal across a synapse; a neuromodulator adjusts how strongly and for how long many synapses respond, acting over a broader area and a longer timescale. Most of the compounds grouped here are neuromodulators, which is why their reported effects are described as shifts in tone rather than as switching a function on or off, and why their effects are often bidirectional depending on the starting state. Several routes are represented. One compound is a selective blocker of TREK-1, a two-pore-domain potassium channel. These channels set the resting membrane potential and therefore how easily a neuron fires. TREK-1 is expressed in mood-relevant regions and has been implicated in resistance to conventional antidepressants, and blocking it is proposed to increase serotonergic neurotransmission and support hippocampal neurogenesis. This is a well-defined molecular target, which distinguishes it from most of the group. Another is derived from an immune-active parent peptide and retains immunomodulatory activity while shifting toward central effects. Its proposed actions include modulation of serotonin, dopamine, and noradrenaline systems, interaction with GABAergic signalling, and inhibition of enkephalin-degrading enzymes, which prolongs the action of the body's own opioid peptides rather than adding an exogenous one. A third acts on the oxytocin receptor, a G-protein-coupled receptor. Peripherally this drives uterine contraction and the milk ejection reflex, which is the basis of its approved obstetric use. Centrally, oxytocin signalling in the amygdala, nucleus accumbens, and hypothalamus is associated with social salience, threat processing, and reward related to social interaction. Effects here are strongly context-dependent and are not reliably prosocial. A fourth has no confirmed receptor at all despite decades of study. Reported interactions are diffuse and concentration-dependent, spanning NMDA receptor modulation, stress-axis regulation, and several neuropeptide systems, and it has been framed as a homeostatic regulator with dose- and timing-dependent effects rather than as a sedative acting at a defined site. Honest assessment: one member is an approved medicine for a narrow peripheral indication, and its central effects remain an active research question rather than an established therapy. The others are unapproved research compounds whose mechanisms rest largely on rodent and in vitro work, with limited independent human evidence. Compounds affecting mood and arousal circuits also interact unpredictably with psychiatric medication.
The evidence
Human data exist but are old, small, and mixed. Small studies from the early 1980s (e.g., Schneider-Helmert and colleagues, Experientia 1981; Int J Clin Pharmacol Ther Toxicol 1981) reported acute and delayed improvements in sleep efficiency, latency and continuity in insomniac and normal subjects after intravenous DSIP, with good tolerability. However, a later double-blind matched-pairs study in 16 chronic insomniacs (Neuropsychobiology, 1992) found higher sleep efficiency and shorter latency yet concluded short-term DSIP is "not likely to be of major therapeutic benefit." A 1984 clinical trial (European Neurology) and a pilot study in chronic pain also reported effects, and a 2009 anaesthesia study (European Journal of Anaesthesiology) found DSIP altered bispectral index/EEG as an isoflurane adjunct. A 2006 Journal of Neurochemistry review explicitly calls DSIP "a still unresolved riddle," underscoring that no modern, adequately powered, registration-quality trial has confirmed a clinical sleep benefit.
The evidence, in brief
Delta sleep-inducing peptide, a nonapeptide proposed to promote slow-wave sleep. Across the literature, human sleep results have been inconsistent; it never reached established clinical use and its physiological role remains unresolved.
- Acute and delayed effects of DSIP on human sleep behavior (double-blind study)Int J Clin Pharmacol Ther Toxicol, 1981 (PMID 6895513)
Evidence maturity
An evidence-only reading: approval status, human vs preclinical data, mechanism and safety. Popularity never raises it. Research file #017
Mostly preclinical or mechanistic; little human data.
Mostly online reports, no real study base yet.
Claim receipts
Popular claims about DSIP, checked against the state of the evidence. The verdict describes evidence maturity, never an invented study result.
The name has been tested against data: a later double-blind study in chronic insomniacs concluded that short-term use is not likely to be of major therapeutic benefit, and a subsequent review described the peptide as an unresolved riddle.
The name comes from the circumstances of its discovery and does far more work for its reputation than the evidence does; no modern, adequately powered, registration-quality trial has confirmed a clinical sleep benefit.
The human studies are small and date mainly from the 1980s and early 1990s, with mixed conclusions, and nothing of registration quality has been run since.
These uses trace to a pilot study and scattered small reports rather than controlled trials designed to test those outcomes.
Those trials were tiny, short and decades old, so the safety database is thin, with essentially no modern controlled long-term, immunogenicity or chronic-exposure data.
Safety profile
In the small historical human studies DSIP was generally described as well tolerated with few reported acute side effects, including reports of no daytime sedation hangover. However, these trials were tiny, short-term, and decades old, so the safety database is thin and there is essentially no modern controlled long-term safety, immunogenicity, or chronic-exposure data. Material sold for "research" is unregulated, of unverified purity and identity, and not produced to pharmaceutical standards, which introduces contamination and mislabeling risks independent of the peptide itself. Long-term effects, drug interactions, and effects in any specific population remain unknown.
Compound notes
- DSIP (Delta Sleep-Inducing Peptide) is an endogenous neuropeptide named for its association with delta-wave sleep.
- It is studied for sleep and stress modulation, but the evidence is old and inconsistent.
- Not FDA-approved; research-only.
- It is not an established sleep treatment.
Regulatory status
DSIP is not approved by the FDA (or, to public knowledge, any major regulator) as a drug for sleep or any other indication; it has only ever been an investigational/experimental compound and is currently sold as a research-use-only chemical. It is not a WADA-prohibited substance by name, but it is not a legitimate, quality-controlled medicine.
Sold research-use-only; human evidence is limited or preclinical.
By the numbers
- 01Nonapeptide, sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE), ~850 Da
- 02First isolated 1974 from cerebral venous blood of sleep-induced rabbits (Schoenenberger/Monnier, Switzerland)
- 03No gene, precursor, or specific receptor has been definitively identified for DSIP
- 04Very short reported half-life (on the order of minutes)
- 05Best human evidence is small early-1980s sleep studies with mixed/conflicting results
- 06A 2006 review labels it a 'still unresolved riddle'; not an approved drug
DSIP: research formats
Choose the format you are researching to see route-specific notes.
Short-acting neuropeptide; SC injection is the standard research format.
DSIP (delta sleep-inducing peptide) contains a tryptophan residue and is light-sensitive. Store in amber glass. Sold as a 5 mg vial; reconstituted with BAC water.
Tryptophan-containing peptide: photosensitive. Use amber vials; minimise light exposure during preparation. Trp can degrade 25–40% within 24 hours in clear glass under fluorescent light.
Sources
Every factual claim above resolves to a real, published source.
- Delta-sleep-inducing peptide (DSIP): a reviewNeuroscience and Biobehavioral Reviews, 1984, PMID 6145137
- Delta sleep-inducing peptide (DSIP): a still unresolved riddleJournal of Neurochemistry, 2006, PMID 16539679
- Effects of delta sleep-inducing peptide on sleep of chronic insomniac patients. A double-blind studyNeuropsychobiology, 1992, PMID 1299794
- Delta sleep-inducing peptide alters bispectral index, the EEG and heart rate variability as an adjunct to isoflurane anaesthesiaEuropean Journal of Anaesthesiology, 2009, PMID 19142086
Cite this page
PepCue. “DSIP: the evidence.” PepCue, reviewed June 1, 2026. https://www.pepcue.app/p/dsip.
Log your doses, run the vial math, and keep a provider-ready record in PepCue.