D tier · weak
Isolated in the mid-1970s and sequenced in 1977, DSIP still has no approved indication anywhere, no identified receptor, precursor protein or gene, and the small human sleep trials that exist were weak or explicitly negative.
dsip
DSIP is a nonapeptide isolated from the cerebral venous blood of sleeping rabbits and named for an electroencephalographic delta-wave effect that later work struggled to reproduce. Nearly five decades on, no specific receptor or precursor gene has been identified and the peptide has no approved therapeutic use.
// we supply this one
available as a research reagent
≥ 99% HPLC · lyophilised powder · batch certificate published. Grade D above is our own and is not adjusted because we stock it.
the explanation
DSIP is a small peptide found in rabbit blood in the 1970s and named after a brain-wave pattern seen during deep sleep. Since then researchers have never found the receptor it is supposed to act on, and the few human sleep studies that were run showed little or no reliable benefit.
regulatory status
No approved indication in any jurisdiction
DSIP has never been approved by the FDA, EMA or any other major regulator for any indication. It exists only as a research chemical and is not an authorised medicine; it has no orphan, investigational or compassionate-use authorisation described in the reviewed literature. At the Pharmacy Compounding Advisory Committee meeting of 24 July 2026 the panel voted 6 to 7 with one abstention against adding emideltide (DSIP) to the section 503A bulks list — the only substance rejected across the two-day meeting, and by a single vote. A recommendation is non-binding, confers no approval and is not a finding of efficacy; implementation would require notice-and-comment rulemaking. FDA has not published meeting minutes and these tallies are trade-press reporting from the room.
how it works · proposed mechanism
DSIP's mechanism is genuinely unknown, and the absence of a receptor is the central unresolved problem in the field.
No identified receptor
The 2006 Journal of Neurochemistry review lists the lack of a DSIP-specific receptor and the lack of a receptor gene among the field's defining failures. Every proposed action is therefore inferred from downstream observations rather than from a characterised binding site.
No precursor protein or gene
No DSIP precursor protein has been detected and no gene encoding one has been found in any species, including the rabbit from which the peptide was originally isolated. This leaves open the question of whether endogenous DSIP occurs naturally at all.
Indirect neuromodulatory reports
Scattered preclinical reports describe interactions with NMDA and adrenergic signalling and effects on stress and thermoregulatory endpoints. These are non-specific, poorly replicated and do not constitute a defined mechanism of action.
what’s reported
evidence shape
6 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
DSIP is marketed on the strength of its name, but the delta-sleep effect that gave it that name is among the least reproducible findings attached to it. A compound with no receptor, no gene, no precursor and no approved use after five decades of investigation is better described as an unresolved research question than as a sleep agent.
key published findings
- Discovery (rabbit, in vivo): the Schoenenberger-Monnier group isolated DSIP from the cerebral venous blood of rabbits in an induced state of sleep in 1974, with amino-acid analysis, sequence and synthesis of the nonapeptide WAGGDASGE published in 1977.
- Human trial (Bes et al., Neuropsychobiology 1992, n=16 chronic insomniacs, double-blind matched-pairs parallel-group, intravenous DSIP 25 nmol/kg vs glucose placebo across three nights): modest gains in sleep efficiency and sleep latency, but the authors reported that statistically significant effects were weak and could in part be due to an incidental change in the placebo group, with no meaningful improvement in subjective sleep quality, concluding short-term DSIP treatment is not likely to be of major therapeutic benefit.
- Review (Kovalzon & Strekalova, Journal of Neurochemistry 2006;97:303-309): explicitly enumerates the lack of a detected DSIP precursor protein, precursor protein gene, specific receptor and receptor gene, and states there is still no strong evidence of the natural occurrence of DSIP.
- Replication (same review): multiple studies failed to confirm slow-wave-sleep or paradoxical-sleep promoting properties, only minor effects were found in others, and impairment of sleep has also been reported; the authors judge the sleep-factor hypothesis extremely poorly documented and still weak.
- Pharmacokinetics (in vitro/in vivo): the DSIP molecule's in vivo half-life is not more than several minutes, driven by an aminopeptidase-like enzyme that splits off the N-terminal amino-acid residue, which constrains any sustained central action from peripheral administration.
limitations of the evidence
- The controlled human sleep studies are small, decades old, and used intravenous administration under laboratory conditions that do not correspond to how the compound is currently distributed.
- Because no receptor or precursor gene exists, there is no molecular target against which purity, potency or biological activity of a given batch can be assayed.
- Much of the supporting literature is from the 1970s and 1980s, predating modern trial registration and reporting standards, so publication bias cannot be assessed.
documented safety signals
- No modern controlled safety database exists; adverse-event reporting is limited to small historical studies and is insufficient to characterise risk.
- As an unapproved research chemical there is no regulated manufacturing oversight, so identity, purity and endotoxin content of distributed material are unverified.
identity
| full name | Delta sleep-inducing peptide |
| category | Cognitive |
| modality | peptide |
| formula | C35H48N10O15 |
| molar mass | 848.82 g/mol |
| cas | 62568-57-4 |
| half-life | Not more than several minutes in vivo; degraded by an aminopeptidase-like enzyme that cleaves the N-terminal residue (Kovalzon & Strekalova, J Neurochem 2006) |
| sequence | Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE) |
laboratory handling
| storage | Lyophilised peptide is typically stored desiccated at -20 C and protected from light; reconstituted aqueous solutions are unstable given the peptide's rapid enzymatic degradation. Handling information only. |
| solubility | Water-soluble; the nonapeptide is amphiphilic with acidic Asp and Glu residues and dissolves readily in aqueous buffers. |
| co-studied with | No published controlled study has evaluated DSIP in combination with any other agent; there are no combination data to report. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
7 citedJournal of Neurochemistry · 2006 · review
Neuropsychobiology · 1992 · randomized trial
European Neurology · 1986 · clinical study
Pflugers Archiv - European Journal of Physiology · 1977 · primary research
PubMed record PMID 568769 (journal name not independently verified) · 1977 · primary research
Wikipedia · 2026 · reference
Regulatory Affairs Professionals Society · 2026 · trade press
others in Cognitive