DSIP

Delta sleep-inducing peptide, a naturally occurring nonapeptide first isolated from cerebral venous blood, studied for its modulating effects on sleep architecture, the stress axis and neuroendocrine signalling.

What it is

DSIP (delta sleep-inducing peptide) is a small naturally occurring nonapeptide with the sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE). It was first isolated in 1974 by the Swiss Schoenenberger-Monnier group from the cerebral venous blood of rabbits held in an electrically induced state of delta-wave sleep, which gave the peptide its name. Unlike the synthetic Russian nootropic peptides such as Semax and Selank, DSIP is an endogenous sequence rather than an engineered analogue, though the material used in research is produced by chemical synthesis.

Structurally it is unusually simple: nine residues, no disulphide bridges and no terminal modification in its native form. It is amphoteric and crosses the blood-brain barrier, which is one reason it has attracted interest as a research tool for probing sleep and stress-response biology. Supplied strictly for laboratory research use only, not for human or veterinary use.

How it works

Despite decades of study, DSIP has no single, definitively identified receptor, and its actions are best described as modulatory rather than driven by one clean pathway. Reported mechanisms in the literature include interaction with NMDA-type glutamate receptors, modulation of GABAergic signalling, and effects on voltage-gated calcium channels. Several studies describe a stress-limiting or corticotropin-releasing-inhibiting action, in which DSIP lowers basal corticotropin (ACTH) tone and blunts stress-driven glucocorticoid elevation in animal models. Its behaviour is state-dependent: the sleep-modulating effect is most apparent when sleep is disturbed and is minimal in undisturbed healthy subjects.

DSIP also touches the hypothalamic-pituitary axis more broadly. In rodent work it stimulated the release of luteinizing hormone (LH) via a hypothalamic rather than direct pituitary site of action, while leaving FSH unchanged, and it has been reported to promote release of somatoliberin and somatotropin (growth hormone), consistent with the physiological coupling of deep delta sleep to nocturnal GH secretion. The picture across the literature is genuinely mixed, and several careful human studies found no effect on ACTH or cortisol, so the neuroendocrine claims should be read as active research questions rather than settled facts.

What the research shows

The clinical literature on DSIP is small and dates largely to the 1980s. Early trials in insomnia reported improved sleep continuity and daytime mood without daytime sedation, though results across studies were inconsistent, and the peptide was described as acting more as a sleep modulator than a hypnotic. More recent work has moved into animal models, including a 2024 study using a DSIP fusion peptide in a PCPA-induced insomnia mouse model that quantified reductions in wakefulness alongside changes in monoamine neurotransmitters. The headline figures below are drawn directly from those published sources.

At a glance

Molecular formula C35H48N10O15; sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu. Values confirmed against PubChem CID 68816.

Dosing

There is no approved dose of DSIP. The figures below come from small, dated human trials run mostly in the 1980s, typically with fewer than a dozen participants each. In those studies DSIP was given by slow intravenous injection or infusion, and the dose was usually scaled to body weight at about 25 nmol/kg, which works out to roughly 21 µg/kg, or on the order of 1.5 mg for a 70 kg adult. These are historical study doses reported for laboratory and research context, not treatment instructions.

These doses come from small, old trials, most with only a handful of participants and often no modern replication. There is no established contemporary dose, and none of these studies define a standard regimen. Everything here is presented for laboratory research context only.

Preparing it

DSIP is supplied as a lyophilised powder and is reconstituted with bacteriostatic or sterile water before use in research. See the reconstitution guide for handling and mixing, and the concentration guide for working out how much diluent gives a given concentration per unit volume. Store the sealed vial cold and keep reconstituted material at 2-8 C.

Safety signals in the literature

Reported studies note an absence of daytime sedation and few acute side effects at the doses tested, which is part of why DSIP is described as a modulator rather than a sedative. That said, the trials are small and old, and the long-term safety of DSIP has not been established in controlled clinical research. Nothing here describes approved human use; the compound is a research material only.

Side Effects

The human safety record for DSIP rests on a handful of small clinical studies, most of them run in the 1980s and 1990s with only a few subjects each. Across those trials investigators generally described DSIP as well tolerated after intravenous dosing, with few or no adverse events noted. That said, the studies were tiny, short, and not designed as formal safety trials, so the absence of reported problems reflects limited observation rather than a thorough safety characterization. No modern controlled study has systematically catalogued its side effects, and DSIP is not an approved drug.

Taken together, the reassuring tolerability reports come from studies with only a few subjects, short exposures, and no modern safety monitoring, so they cannot rule out uncommon or delayed effects. The one controlled physiological study that looked closely found measurable cardiac and central effects, which underscores how thin and dated the overall evidence base remains.

Where to go next

Last updated on July 3, 2026