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DSIP

Also identified as Delta sleep-inducing peptide, Emideltide

Nonapeptide

Sequence: Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu

Molecular weight
848.8
Molecular formula
C35H48N10O15
CAS
62568-57-4
Published studies reviewed
6

FOR RESEARCH USE ONLY. NOT FOR HUMAN OR VETERINARY USE. NOT FOR HUMAN CONSUMPTION.

Compounds described on this site are supplied solely for laboratory research. They are not offered for human or veterinary use or for clinical use, and they are not intended to diagnose, mitigate, cure or prevent any disease.

DSIP (delta sleep-inducing peptide) is the nine-residue peptide Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu, whose name reflects what its discoverers were investigating rather than an established property of the molecule. Six publications are reviewed: the 1977 rabbit work that characterised and named it, a laboratory study of its breakdown in blood, and four human studies published between 1981 and 1995. Three of those human studies were controlled and reported no difference their authors considered meaningful, while the fourth enrolled only six volunteers.

At a glance

Also identified as
Delta sleep-inducing peptide, Emideltide
Class
Nonapeptide
Target or mechanism
The publication that named this peptide reports electroencephalogram changes in rabbits after the peptide was given, and does not identify a receptor; no later source on this page does either.
Evidence types represented
in vitro, animal, human
Published studies reviewed
6
Last reviewed
2026-09-21

Overview

DSIP is a nine-residue peptide first described in the 1970s. Its name records what the researchers who isolated it were investigating, not an established property of the molecule.

The publications on this page are the 1977 characterisation that gave the peptide its sequence and its name, one laboratory study of how quickly it breaks down in blood, and four human studies from 1981 to 1995. Three of those four were controlled and reported no difference their authors considered meaningful: two measured sleep by polysomnography in people with chronic insomnia, and one measured ACTH and cortisol secretion in healthy men.

Those null results are the substance of the human record here, and they are printed as results. The fourth human study is the six-volunteer first-in-human crossover in healthy volunteers, which reports median total sleep time 59% higher than placebo in the 130 minutes after it was given in the morning; it is recorded with its design and its tolerance findings.

Mechanism under investigation

The publication that named this peptide reports electroencephalogram changes in rabbits after the peptide was given, and does not identify a receptor; no later source on this page does either. One laboratory study recorded here reports that the peptide is degraded in human and rat blood, which its authors give as the reason it disappears rapidly from the circulation.

Scope of the published work

Areas investigated
  • Peptide isolation and sequence
  • Electroencephalogram patterns in rabbits
  • Polysomnographic measures in chronic insomnia
  • ACTH and cortisol secretion
  • Stability in blood
Models used
  • Rabbit
  • Human and rat blood in vitro
  • Crossover studies in humans
  • Parallel-group study in humans

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Limitations

Evidence represented on this page: in vitro, animal and human. The page reviews 6 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Common questions

What is DSIP?

DSIP is a nine-residue peptide first described in the 1970s.

How does DSIP work, according to the published research?

The publication that named this peptide reports electroencephalogram changes in rabbits after the peptide was given, and does not identify a receptor; no later source on this page does either. One laboratory study recorded here reports that the peptide is degraded in human and rat blood, which its authors give as the reason it disappears rapidly from the circulation.

  • Incubation of the peptide in human or rat blood released products whose retention times on a gel filtration column matched tryptophan, with product formation depending on temperature, time and species. An iodinated N-Tyr form and a phosphorylated analogue were degraded more slowly and, unlike the peptide itself, formed complexes that an excess of unlabelled material did not displace — which the authors read as non-specific binding or aggregation. They conclude that the rapid disappearance of the peptide from blood is due to degradation. (Graf et al., 1987, PMID 3628078)

What has published research on DSIP found, and what are its limits?

This page records 6 publications, reporting laboratory (in vitro) work in 1, animal work in 1, human work in 4. Each is listed with its identifier under References.

Human studies represented: Späth-Schwalbe et al., 1995, PMID 7777652; Bes et al., 1992, PMID 1299794; Monti et al., 1987, PMID 3583493; Schneider-Helmert et al., 1981, PMID 6895513.

Evidence represented on this page: in vitro, animal and human.

The page reviews 6 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Is DSIP approved by the U.S. FDA?

This page cites no FDA approval record for DSIP; PepGenex Science states a U.S. regulatory status only where a sourced record exists.

PepGenex research materials are not FDA approved and are not for human or veterinary use.

What risks have published studies of DSIP reported?

1 published human study on this page reports adverse events or safety measurements. Each is listed with its publication in the adverse-events section of this page.

Trial events do not establish a complete safety profile.

What adverse events have been reported in published studies of DSIP?

Adverse events and safety measurements as reported by the published human studies on this page. Each entry is attributed to its publication.

Schneider-Helmert et al., 1981, PMID 6895513

Design and population
The first reported study of the synthetic peptide in humans: six healthy volunteers, four men and two women, in a double-blind crossover design with psychophysiological observation and measurement. The peptide was given in the morning.
Events reported
The authors report the compound was well tolerated and that no psychological, physiological or biochemical adverse effects were observed in the six volunteers.

Trial events do not establish a complete safety profile.

Published research

Grouped by the kind of study. Select one to narrow what is shown below.

Laboratory (in vitro)(1)

Laboratory (in vitro)

Degradation and aggregation of delta sleep-inducing peptide (DSIP) and two analogs in plasma and serum.

Graf MV, Saegesser B, Schoenenberger GA., Peptides, 1987;8(4):599-603

published

  • Incubation of the peptide in human or rat blood released products whose retention times on a gel filtration column matched tryptophan, with product formation depending on temperature, time and species. An iodinated N-Tyr form and a phosphorylated analogue were degraded more slowly and, unlike the peptide itself, formed complexes that an excess of unlabelled material did not displace — which the authors read as non-specific binding or aggregation. They conclude that the rapid disappearance of the peptide from blood is due to degradation.
Context

One laboratory finding sits underneath the human ones: in human and rat blood the peptide is broken down quickly, and the analogues that lasted longer were different molecules. Whatever reaches the circulation does not stay there long, which is the authors' own explanation for how variable the reported effects were.

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Preclinical (animal)(1)

Preclinical (animal)n = 58

Characterization of a delta-electroencephalogram (-sleep)-inducing peptide.

Schoenenberger GA, Monnier M., Proceedings of the National Academy of Sciences of the United States of America, 1977;74(3):1282-1286

published

  • Reports the isolation from rabbits of a peptide that enhanced slow-wave (delta) and spindle patterns on the electroencephalogram after the peptide was given, names it delta sleep-inducing peptide, and gives its amino acid sequence as Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu.
  • The nonapeptide, five possible metabolic fragments (residues 1-8, 2-9, 2-8, 1-4 and 5-9), two nonapeptide analogues with two residues exchanged and a related tripeptide were synthesised and given to rabbits under double-blind conditions, 58 animals including controls. Electroencephalogram leads from the neocortex and archicortex were Fourier-transformed and analysed by computer. Of the nine synthetic peptides, only the synthetic nonapeptide showed significant and specific enhancement or induction of delta and spindle patterns.
Context

The name comes from the 1977 experiment on this page: a peptide isolated from rabbits, given to rabbits, that changed one feature of the electroencephalogram. It records what that group was measuring in that species. The human studies that followed measured people, and are recorded above.

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Human study (phase not stated)(4)

Human study (phase not stated)

Delta-sleep-inducing peptide does not affect CRH and meal-induced ACTH and cortisol secretion.

Späth-Schwalbe E, Schäfer A, Uthgenannt D, Born J, Fehm HL., Psychoneuroendocrinology, 1995;20(3):231-237

published

Two experiments in healthy young men, testing a reported role for this peptide as an inhibitor of corticotropin release. In the first, five men per condition received human corticotropin-releasing hormone while the peptide, in one of two study conditions, or placebo was given. In the second, a further ten men received the peptide and midday meal-related secretion was followed.

  • Responses of ACTH and cortisol were almost identical during and after the peptide and placebo were given, and the meal-related midday surge of ACTH and cortisol was likewise not affected. The authors state their data do not support an inhibitory role for this peptide on ACTH and cortisol secretion in humans.
Limitations

Four controlled human studies are recorded here, and three of them are null or near-null: no significant difference from placebo on polysomnographic measures in one, effects the authors themselves called weak and partly attributable to the placebo group in another, and no change in ACTH or cortisol in the third. The fourth, the six-volunteer first-in-human crossover, reports median total sleep time 59% higher than placebo in the 130 minutes after it was given in the morning, with no p-value in its abstract. The studies are small — six volunteers in the first-in-human crossover, sixteen people in the parallel-groups study, five per condition and a further ten in the endocrine one, and a participant count the insomnia crossover's abstract does not give — so neither the null results nor the single favourable figure is strong evidence either way; they are the evidence that exists.

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Human study (phase not stated)n = 16

Bes et al., 1992 (title withheld on this site; see the publication record)

Bes F, Hofman W, Schuur J, Van Boxtel C., Neuropsychobiology, 1992;26(4):193-197

published

A double-blind, matched-pairs, parallel-groups study in 16 people with chronic insomnia, who slept five consecutive nights in the laboratory — night 1 for adaptation, night 2 for baseline. Before each of nights 3, 4 and 5, half received the peptide and half a glucose solution as placebo. Sleep structure was measured by polysomnography alongside self-rated sleep and tiredness assessments.

  • Polysomnography indicated higher sleep efficiency and shorter sleep latency with the peptide than with placebo, and one measure of self-rated tiredness fell within the peptide group. The authors state that the statistically significant effects were weak and could in part be due to an incidental change in the placebo group, that none of the other measures — including the self-rated sleep assessment — showed any change, and they conclude that short-term use in chronic insomnia is not likely to be of major benefit. No numeric values or p-values are given in the abstract.
Limitations

Four controlled human studies are recorded here, and three of them are null or near-null: no significant difference from placebo on polysomnographic measures in one, effects the authors themselves called weak and partly attributable to the placebo group in another, and no change in ACTH or cortisol in the third. The fourth, the six-volunteer first-in-human crossover, reports median total sleep time 59% higher than placebo in the 130 minutes after it was given in the morning, with no p-value in its abstract. The studies are small — six volunteers in the first-in-human crossover, sixteen people in the parallel-groups study, five per condition and a further ten in the endocrine one, and a participant count the insomnia crossover's abstract does not give — so neither the null results nor the single favourable figure is strong evidence either way; they are the evidence that exists.

View publication →
Human study (phase not stated)

Monti et al., 1987 (title withheld on this site; see the publication record)

Monti JM, Debellis J, Alterwain P, Pellejero T, Monti D., International Journal of Clinical Pharmacology Research, 1987;7(2):105-110

published

A double-blind crossover study in people with chronic insomnia, assessed by polysomnographic recording. The peptide or placebo was given during four nights.

  • The number of nocturnal awakenings, non-REM sleep latency, total waking time and waking time after sleep onset were all lower with the peptide, but no significant differences were found in comparison with baseline or with the double-blind placebo nights. Total sleep time and non-REM sleep time were higher, an increase the authors relate to stage 2; stage 1, slow-wave sleep and REM sleep were not modified. Where the differences from placebo did reach significance — non-REM sleep time and stage 2 — the same differences already existed in the baseline values. The authors conclude that the change in sleep is of little clinical significance.
Limitations

Four controlled human studies are recorded here, and three of them are null or near-null: no significant difference from placebo on polysomnographic measures in one, effects the authors themselves called weak and partly attributable to the placebo group in another, and no change in ACTH or cortisol in the third. The fourth, the six-volunteer first-in-human crossover, reports median total sleep time 59% higher than placebo in the 130 minutes after it was given in the morning, with no p-value in its abstract. The studies are small — six volunteers in the first-in-human crossover, sixteen people in the parallel-groups study, five per condition and a further ten in the endocrine one, and a participant count the insomnia crossover's abstract does not give — so neither the null results nor the single favourable figure is strong evidence either way; they are the evidence that exists.

View publication →
Human study (phase not stated)n = 6

Acute and delayed effects of DSIP (delta sleep-inducing peptide) on human sleep behavior.

Schneider-Helmert D, Gnirss F, Monnier M, Schenker J, Schoenenberger GA., International Journal of Clinical Pharmacology, Therapy and Toxicology, 1981;19(8):341-345

published

The first reported study of the synthetic peptide in humans: six healthy volunteers, four men and two women, in a double-blind crossover design with psychophysiological observation and measurement. The peptide was given in the morning.

  • In the 130 minutes after it was given, median total sleep time was 59% higher than after placebo in the six volunteers of the crossover. The abstract gives no p-value and no absolute sleep times for this comparison.
  • Behavioural and electroencephalogram analyses revealed no sedation of the classic pharmacological kind, which the authors set against the volunteers' immediate reports of a feeling of sleep pressure.
  • The authors report the compound was well tolerated and that no psychological, physiological or biochemical adverse effects were observed in the six volunteers.
Limitations

Four controlled human studies are recorded here, and three of them are null or near-null: no significant difference from placebo on polysomnographic measures in one, effects the authors themselves called weak and partly attributable to the placebo group in another, and no change in ACTH or cortisol in the third. The fourth, the six-volunteer first-in-human crossover, reports median total sleep time 59% higher than placebo in the 130 minutes after it was given in the morning, with no p-value in its abstract. The studies are small — six volunteers in the first-in-human crossover, sixteen people in the parallel-groups study, five per condition and a further ten in the endocrine one, and a participant count the insomnia crossover's abstract does not give — so neither the null results nor the single favourable figure is strong evidence either way; they are the evidence that exists.

View publication →

References

Published studies reviewed (6)

  1. Characterization of a delta-electroencephalogram (-sleep)-inducing peptide. — Schoenenberger GA, Monnier M., Proceedings of the National Academy of Sciences of the United States of America, 1977;74(3):1282-1286
    DOI 10.1073/pnas.74.3.1282 · PMID 265572 · PMC430668
  2. Acute and delayed effects of DSIP (delta sleep-inducing peptide) on human sleep behavior. — Schneider-Helmert D, Gnirss F, Monnier M, Schenker J, Schoenenberger GA., International Journal of Clinical Pharmacology, Therapy and Toxicology, 1981;19(8):341-345
    PMID 6895513
  3. Monti et al., 1987 (title withheld on this site; see the publication record) — Monti JM, Debellis J, Alterwain P, Pellejero T, Monti D., International Journal of Clinical Pharmacology Research, 1987;7(2):105-110
    PMID 3583493
  4. Bes et al., 1992 (title withheld on this site; see the publication record) — Bes F, Hofman W, Schuur J, Van Boxtel C., Neuropsychobiology, 1992;26(4):193-197
    DOI 10.1159/000118919 · PMID 1299794
  5. Delta-sleep-inducing peptide does not affect CRH and meal-induced ACTH and cortisol secretion. — Späth-Schwalbe E, Schäfer A, Uthgenannt D, Born J, Fehm HL., Psychoneuroendocrinology, 1995;20(3):231-237
    DOI 10.1016/0306-4530(94)00050-k · PMID 7777652
  6. Degradation and aggregation of delta sleep-inducing peptide (DSIP) and two analogs in plasma and serum. — Graf MV, Saegesser B, Schoenenberger GA., Peptides, 1987;8(4):599-603
    DOI 10.1016/0196-9781(87)90031-3 · PMID 3628078

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