Evidence reviewed on: August 27, 2026
Evidence state: Low certainty for human outcomes. The literature consists of laboratory and animal experiments, very small human studies, and uncontrolled historical reports. The largest controlled insomnia study in this source set enrolled 16 people and concluded that the observed effects were weak and unlikely to provide major therapeutic benefit.
This page summarizes published research and regulatory records. It does not provide medical advice or instructions for administering any substance. A study of DSIP does not establish that a catalog material has the same identity, form, purity, stability, or biological behavior as the material used by the investigators.
What is DSIP?
DSIP is short for delta sleep-inducing peptide, also called delta EEG sleep-inducing peptide. FDA’s preferred substance name is emideltide. The free-base peptide contains nine amino acids and has the one-letter sequence WAGGDASGE, corresponding to H-Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu-OH. PubChem lists molecular formula C35H48N10O15, molecular weight 848.8 g/mol, CID 68816, and CAS 62568-57-4. FDA assigns the free base UNII YN28Z5YZ73.
Identity needs more than the name “DSIP.” FDA reviewed emideltide free base and emideltide acetate as distinct bulk drug substances. A material description should therefore identify the form, counterion, sequence, and analytical record. Older papers also use the phrase “DSIP-like immunoreactivity.” That phrase describes an assay signal; it does not necessarily prove that intact endogenous emideltide was chemically identified.
Evidence by tier
In-vitro and ex-vivo evidence
In rat lower-brainstem slices, investigators reported that DSIP increased the release of immunoreactive Met-enkephalin. This was an isolated-tissue biochemical endpoint, not a measurement of sleep or pain in a person. A separate sheep experiment examined passage of labeled DSIP from blood into cerebrospinal fluid and reported limited transport under the tested conditions.
These studies can inform hypotheses about biochemical interactions and disposition. They do not establish a human mechanism, clinical effect, or safety profile.
Animal evidence
The original characterization work associated a peptide fraction with delta-electroencephalogram activity in rabbits. Later rat experiments reported longer sleep duration in one model and antinociceptive behavior in another. The experiments differed in species, design, endpoint, and exposure context.
Animal findings are not human efficacy evidence. They do not show that DSIP improves insomnia, pain, recovery, or another health outcome in people.
Observational human evidence
One study repeatedly measured plasma DSIP-like immunoreactivity in seven healthy men during nocturnal sleep, sleep deprivation, and recovery sleep. The assay signal decreased near the transition from wakefulness to sleep but was not specific to a sleep stage.
This was an observational association. It does not show that DSIP caused sleep onset, that the assay detected intact emideltide, or that administering a synthetic peptide improves sleep.
Interventional human evidence
The most decision-relevant sleep paper used a double-blind, matched-pairs design in 16 people with chronic insomnia. It reported higher sleep efficiency and shorter sleep latency than placebo, but the authors described the statistically significant effects as weak and potentially influenced by an incidental change in the placebo group. Subjective sleep quality and most other measures did not change. The paper concluded that short-term DSIP exposure was unlikely to offer major therapeutic benefit.
Two earlier controlled studies each enrolled six people. One involved chronic insomnia and reported changes in selected sleep measures; the other involved healthy volunteers and reported acute and delayed sleep-related differences. An open report in seven people with severe insomnia had no control group. Small sample sizes, inconsistent findings, and limited reporting prevent reliable conclusions about effectiveness or uncommon harms.
Historical open reports also described small pain and alcohol- or opioid-withdrawal cohorts. Those studies lacked randomized placebo controls, relied heavily on clinical judgment, and in one case lost a substantial share of enrolled participants from evaluation. Small endocrine studies reported an ACTH-related signal but did not establish a patient-centered benefit.
Negative and null findings
The 16-person double-blind insomnia study is the clearest check on the compound’s name-driven narrative. Most measured outcomes did not change, subjective sleep quality did not improve, and the authors judged the positive findings weak. FDA’s 2026 evidence review likewise characterized the insomnia literature as preliminary or inconclusive and noted that later studies did not consistently reproduce early positive conclusions.
The human literature is old, sparse, and not a modern confirmatory development program. No study in this source set establishes durable benefit, long-term safety, immunogenicity risk, reproductive safety, carcinogenic risk, or clinically meaningful interactions. Findings from one form or preparation cannot be transferred to another without comparability evidence.
Current U.S. status
Status checked August 27, 2026. No FDA-approved drug containing emideltide free base or emideltide acetate was identified. FDA’s July 2026 staff briefing states that neither form is a component of an FDA-approved drug and neither has an applicable USP or National Formulary drug-substance monograph.
The original section 503A nominations were withdrawn, but FDA evaluated the substances on its own initiative and proposed that neither be added to the section 503A Bulks List. A staff proposal or advisory-committee recommendation is not a final rule. FDA’s meeting page states that committee recommendations are non-binding and that FDA makes the final determination.
FDA’s current compounding safety-risk page identifies potential concerns involving peptide aggregation, immunogenicity, peptide-related impurities, and inadequate safety information for the proposed exposure context. No exact emideltide or DSIP intervention record was identified in the ClinicalTrials.gov audit.
What the evidence does not establish
The evidence does not establish DSIP as a proven sleep, pain, or withdrawal intervention. It does not establish a safe or effective exposure method, long-term human safety, or equivalence between a study material and any commercially listed material. The word “sleep” in the compound’s common name should not be used as a substitute for controlled evidence.
Frequently asked questions
Is DSIP the same as emideltide?
DSIP is the common abbreviation for delta sleep-inducing peptide; FDA’s preferred substance name is emideltide. A complete identity still needs to distinguish the free base from an acetate form and document the actual material tested.
What is the DSIP sequence?
The free-base peptide has the one-letter sequence WAGGDASGE. Sequence alone does not identify the salt form, counterion amount, impurity profile, aggregation state, or stability.
Does DSIP have strong human sleep evidence?
No. The human studies were very small and mostly conducted decades ago. The largest controlled insomnia study in this source set enrolled 16 people, found only weak objective changes, found no subjective sleep-quality improvement, and concluded that major therapeutic benefit was unlikely.
Do the animal studies prove DSIP works in people?
No. Animal and isolated-tissue experiments can generate hypotheses, but they do not establish human effectiveness or safety.
Is DSIP FDA approved?
No FDA-approved emideltide product was identified in this audit. In July 2026, FDA staff proposed not adding emideltide free base or acetate to the section 503A Bulks List. That proposal should not be described as a final rule without a later FDA record.
Primary and official sources
- NIH PubChem, “Delta Sleep-Inducing Peptide,” CID 68816: https://pubchem.ncbi.nlm.nih.gov/compound/Delta-Sleep-Inducing-Peptide
- FDA UNII, emideltide, UNII YN28Z5YZ73: https://precision.fda.gov/uniisearch/srs/unii/yn28z5yz73
- FDA, July 2026 emideltide Pharmacy Compounding Advisory Committee briefing document: https://www.fda.gov/media/193344/download
- FDA, July 23–24, 2026 Pharmacy Compounding Advisory Committee meeting record: https://www.fda.gov/advisory-committees/advisory-committee-calendar/july-23-24-2026-meeting-pharmacy-compounding-advisory-committee-07232026
- FDA, current compounding safety-risk page: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks
- Schoenenberger GA, Monnier M. “Characterization of a delta-electroencephalogram (-sleep)-inducing peptide.” PMID 265572. DOI 10.1073/pnas.74.3.1282: https://pubmed.ncbi.nlm.nih.gov/265572/
- Schoenenberger GA, et al. “The delta EEG (sleep)-inducing peptide (DSIP). XI. Amino-acid analysis, sequence, synthesis and activity of the nonapeptide.” PMID 568769. DOI 10.1007/BF00581575: https://pubmed.ncbi.nlm.nih.gov/568769/
- Nakamura S, et al. “Delta-sleep-inducing peptide (DSIP) stimulates the release of immunoreactive Met-enkephalin from rat lower brainstem slices in vitro.” PMID 2706459. DOI 10.1016/0006-8993(89)90498-8: https://pubmed.ncbi.nlm.nih.gov/2706459/
- Kafi S, et al. “The delta-sleep inducing peptide (DSIP) increases duration of sleep in rats.” PMID 530466. DOI 10.1016/0304-3940(79)90036-3: https://pubmed.ncbi.nlm.nih.gov/530466/
- Bes F, et al. “Effects of delta sleep-inducing peptide on sleep of chronic insomniac patients. A double-blind study.” PMID 1299794. DOI 10.1159/000118919: https://pubmed.ncbi.nlm.nih.gov/1299794/
- Schneider-Helmert D, Schoenenberger GA. “The influence of synthetic DSIP on disturbed human sleep.” PMID 7028502. DOI 10.1007/BF01971753: https://pubmed.ncbi.nlm.nih.gov/7028502/
- Schneider-Helmert D. “Acute and delayed effects of DSIP on human sleep behavior.” PMID 6895513: https://pubmed.ncbi.nlm.nih.gov/6895513/
- Seifritz E, et al. “Human plasma DSIP decreases at the initiation of sleep at different circadian times.” PMID 8745061. DOI 10.1016/0196-9781(95)02027-6: https://pubmed.ncbi.nlm.nih.gov/8745061/
- Bjartell A, et al. “Reduction of immunoreactive ACTH in plasma following intravenous injection of delta sleep-inducing peptide in man.” PMID 2554357. DOI 10.1016/0306-4530(89)90004-8: https://pubmed.ncbi.nlm.nih.gov/2554357/
- ClinicalTrials.gov intervention search, emideltide: https://clinicaltrials.gov/search?intr=emideltide