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· 7 min read
Named in 1977 and still something of an enigma, DSIP - delta sleep-inducing peptide - carries one of the more misleading names in the neuropeptide literature. The name comes from the isolation paradigm, not from any confirmed mechanism of action, a distinction that matters considerably when reading the preclinical literature on this compound. Supplied strictly as a research reagent; everything below describes what published studies have investigated, not any human use.
| Compound | DSIP (delta sleep-inducing peptide) |
|---|---|
| Synonyms / sequence | H-WAGGDASGE-OH; Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu |
| Class / mechanism | Endogenous linear nonapeptide; preclinical neuromodulatory characterisation only |
| Molecular formula | C35H48N10O15 (free acid) |
| Molecular weight | 848.8 g/mol (free acid) |
| CAS number | 62568-57-4 (free acid; alternate salt/registry form 69431-45-4) |
| PubChem CID | 68816 |
| Supply status | Research use only - not for human or veterinary use |
DSIP is an endogenous linear nonapeptide, nine residues in the sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (single-letter notation H-WAGGDASGE-OH), first isolated in 1977 from the cerebral venous blood of rabbits under a specific physiological preparation. The IUPAC name runs to the expected mouthful: L-tryptophyl-L-alanylglycylglycyl-L-alpha-aspartyl-L-alanyl-L-serylglycyl-L-glutamic acid. It carries PubChem CID 68816, CAS 62568-57-4 (free acid), molecular formula C35H48N10O15, and a molecular weight of 848.8 g/mol.
A word on the name before anything else. 'Delta sleep-inducing peptide' describes the experimental context of the 1977 isolation - it is not a claim of any sleep, insomnia, sedative, stress, anxiety, or wellbeing effect. No such effect is asserted, implied, or supported anywhere on this page. The study descriptions below name only the study design and the pre-specified endpoint; none asserts a result, direction of effect, effect size, benefit, or human-relevant outcome. Kovalabs supplies DSIP as a research chemical for laboratory research use only, not for human or veterinary use.
The identifiers have been adversarially cross-checked and are mutually consistent. A forward lookup of CID 68816 in PubChem returns the formula C35H48N10O15, molecular weight 848.8, and the nine-residue sequence above. The synonym list for that CID independently contains CAS 62568-57-4 (the free acid) alongside 69431-45-4, an alternate salt or registry form; 62568-57-4 is the primary free-acid CAS adopted here. Independent supplier and chemical-registry records - ChemicalBook, the Biosynth catalogue entry PDS-4054-V, and CPC Scientific - report the same CAS, formula, molecular weight of 848.81 g/mol, and sequence. The CID, CAS, formula, molecular weight, and nine-residue count all resolve to one molecule with no collision found. One arithmetic note: all values correspond to the free acid, not a salt form, and the nine-residue count includes the unprotected N- and C-termini.
There is, however, a genuine naming collision worth flagging in any laboratory record. The phrase 'delta sleep-inducing peptide immunoreactor' appears in some circadian-biology literature as a name for glucocorticoid-induced leucine zipper (GILZ), a transcription factor. That protein is a different molecule entirely - unrelated to the DSIP nonapeptide CID 68816 - and any endpoints from GILZ research must never be attributed to, or conflated with, DSIP-peptide data. The collision is purely terminological, but it is the sort of thing that will quietly ruin a literature cross-reference if no one catches it.
| Identifier | Value | Independent corroboration |
|---|---|---|
| Sequence (three-letter) | Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu | PubChem CID 68816; supplier registries |
| Sequence (single-letter) | H-WAGGDASGE-OH | PubChem CID 68816 |
| Residue count | Nonapeptide (9 residues, free N- and C-termini) | PubChem CID 68816 |
| Molecular formula | C35H48N10O15 (free acid) | PubChem CID 68816; ChemicalBook / Biosynth / CPC Scientific |
| Molecular weight | 848.8 g/mol (free acid) | PubChem CID 68816; registries report 848.81 g/mol |
| CAS number | 62568-57-4 (free acid) | PubChem synonym list; ChemicalBook / Biosynth / CPC Scientific |
| PubChem CID | 68816 | NCBI PubChem Compound |
DSIP is grouped here by molecular and structural pharmacology - as an endogenous neuromodulatory research peptide - rather than by any therapeutic indication. The nine-residue sequence is glycine-, glutamate- and aspartate-rich, with an N-terminal tryptophan and a single serine, which gives the molecule its amphiphilic character. The two glycine residues and the acidic aspartate and glutamate side chains account for ready solubility in water and aqueous buffers; the N-terminal tryptophan and the serine residue are the positions most relevant to handling stability, discussed in the laboratory-handling section below.
At the level of proposed mechanism, the literature is explicit that the pharmacology of DSIP remains a matter of preclinical characterisation, not established action. The narrative review by Graf and Kastin (Peptides, 1986; PMID 3550726) collated the isolation, structural characterisation, and tissue distribution of DSIP-like immunoreactivity mapped by immunohistochemical and radioimmunochemical methods. That review records that a candidate mechanism framed around modulation of adrenergic transmission, along with various proposed physiological functions, remained to be established. No confirmed receptor has been identified, and no human outcome is asserted in that source or on this page. The mechanism studies below are reported strictly as molecular-pharmacology characterisations, grouped by probe and readout.
The investigations described here are reported by study design and named endpoint only. None is reproduced with a result, effect size, benefit, or human-relevant outcome, and none asserts that DSIP produces any physiological, behavioural, therapeutic, or disease-relevant effect in animals or humans.
Serotonergic (5-HT1A) pharmacology, preclinical in vivo. Tsunashima and colleagues (Peptides, 1994; PMID 8015981) reported a rat pharmacology study in Wistar animals using serotonergic agonists - including 5-MeO-DMT and the 5-HT1A agonist 8-OH-DPAT - with DSIP pretreatment, the beta-blocker and 5-HT1A antagonist pindolol, and an intracerebroventricular anti-DSIP antibody as a neutralisation control. The pre-specified endpoint was a change in body (core) temperature, a thermoregulatory readout. The authors discuss a 5-HT1A-linked mechanism. Named here to identify the molecular-pharmacology probe and measured endpoint; no clinical or human-relevant effect is asserted.
Dopaminergic mechanism, in-vitro neuroendocrine assay. Iyer and McCann (Neuroendocrinology, 1987; PMID 2886936) reported an in-vitro incubation of rat median eminence tissue, with DSIP applied across a concentration range and the dopamine D2 antagonist pimozide used as a pharmacological blocker. The pre-specified endpoint was somatostatin (SRIF) release into the incubation medium, attributed in the source to a dopaminergic mechanism. The biochemical endpoint name and in-vitro design are cited; no human outcome is asserted.
Central neuronal excitability, electrophysiology. Grigorchuk and Umriukhin (Bulletin of Experimental Biology and Medicine, 2012; PMID 23113238) reported extracellular single-unit recording from dorsal hippocampus neurons in Wistar rats during lateral hypothalamus electrical stimulation, with microiontophoretic application of DSIP. The pre-specified endpoint was the proportion and responsiveness of recorded hippocampal neurons to lateral-hypothalamic stimulation. The electrophysiological design and endpoint name are cited only; no behavioural or human-relevant effect is asserted.
The published work below is described by design and named endpoint only. All studies are in vitro or preclinical animal work, grouped by biochemical or neuroendocrine readout rather than by any indication. Study design only; no effect of the compound is asserted for any entry.
Neuropeptide and hormone-cascade biochemistry, preclinical. Sudakov and colleagues (Annals of the New York Academy of Sciences, 1995; PMID 8597403) reported a rat study across two strains (Wistar and August), administering DSIP at a single pre-specified preclinical dose level at defined pre-decapitation intervals, with quantification by radioimmunoassay. The pre-specified biochemical endpoints, named here only, were substance P and beta-endorphin immunoreactivity in hypothalamus and plasma, and plasma corticosterone concentration. A residual-risk note applies: this study sits within an emotional-state behavioural paradigm in its source literature. That paradigm and any associated behavioural endpoint are deliberately not reproduced, summarised, or claimed here. The study is cited solely for the named biochemical readouts - substance P, beta-endorphin, and corticosterone - as molecular-pharmacology endpoints; no effect, benefit, or outcome is asserted, and no human dose is implied.
Proposed neuromodulatory mechanism, narrative review. Graf and Kastin (Peptides, 1986; PMID 3550726), introduced above, serves additionally as the consolidated review of the isolation, tissue-distribution mapping of DSIP-like immunoreactivity, and the adrenergic-modulation hypothesis. It is cited as the standard reference framing all of the above as proposed mechanisms that remain to be established, not confirmed pharmacology.
No registered clinical-trial (NCT) record is cited because none was retrieved within the lookup budget; none has been invented to fill the gap. Taken together, none of the studies above is presented as evidence of a physiological, behavioural, therapeutic, or disease-relevant effect of DSIP. Each is a discrete characterisation of a research compound, named by design and endpoint.
The notes below are general peptide-laboratory practices for a research-use-only material in an in-vitro or preclinical context. They are not a use protocol and not a preparation method for any use in humans or animals.
Physical form. DSIP is typically supplied as a white lyophilised powder, as the free acid or a trifluoroacetate salt. Confirm whether a given lot is the free acid or a salt before computing concentrations, because net peptide content differs between forms; the molecular weight of 848.8 g/mol used for molar calculations corresponds to the free acid.
Reconstitution. Given its amphiphilic, glycine-, glutamate- and aspartate-rich sequence, DSIP is soluble in water and aqueous buffers. Deionised water or an appropriate aqueous laboratory buffer is the conventional vehicle for in-vitro work - used within a defined working window for analysis, not as a preparation method for any use in humans or animals. See the reconstitution guide for general laboratory handling under clean technique.
Stability and storage. Store the lyophilised powder desiccated at -20 C and protect it from light. The serine and N-terminal tryptophan residues make solutions susceptible to oxidative and hydrolytic degradation, so prepare working solutions fresh, aliquot to avoid repeated freeze-thaw cycles, and keep reconstituted material refrigerated for short-term laboratory use only. The unprotected N- and C-termini make the peptide sensitive to proteases, so avoid contamination when weighing and reconstituting.
Identity and purity. Peptide identifiers are easy to get wrong on paper, and a vial that says one thing is not the same as a vial that is one thing. That gap is exactly what a certificate of analysis closes: every Kovalabs batch ships with one, so the mass and purity in hand can be checked against the documented identifiers (formula C35H48N10O15, CAS 62568-57-4, PubChem CID 68816) rather than taken on trust. Researchers working across endogenous neuropeptides may also wish to review the neuropeptides research category for mechanistically related compounds.
The chemistry is the firm ground. The identifiers resolve cleanly and were cross-checked - CID 68816, CAS 62568-57-4, formula C35H48N10O15, the nine-residue sequence - and DSIP is a genuinely endogenous nonapeptide first isolated in 1977. The mechanism work is real but indirect, spanning in-vitro neuroendocrine assays, rat electrophysiology and preclinical pharmacology against serotonergic and dopaminergic probes; a Wistar rat preparation is not a person, and an indirect probe is not a confirmed pathway. Human evidence is the part that is barely there: no registered clinical-trial record was retrieved, no receptor has been confirmed, and the foundational review frames the pharmacology as proposed rather than established. It is not a licensed medicine, and it has not been shown to produce defined outcomes in humans.
DSIP is supplied by Kovalabs for laboratory and in-vitro research only. It is not a medicine, not a supplement, and not for human or veterinary use, and nothing on this page describes a dose, a route, a schedule, or an outcome. The name 'delta sleep-inducing peptide' is historical and is not a claim of any sleep, sedative, stress, anxiety, or wellbeing effect. DSIP has not been evaluated by the MHRA or any comparable regulator for safety or efficacy in humans or animals, and it is not for the diagnosis, treatment, cure, or prevention of any condition. Every batch is third-party tested with a certificate of analysis. See the full research disclaimer for terms.
No. DSIP (delta sleep-inducing peptide) is an endogenous research peptide. It has not been approved as a medicine by the MHRA or any comparable regulator, and Kovalabs supplies it strictly as a research reagent for laboratory use, not for human or veterinary use.
No. The name is purely historical, derived from the 1977 isolation paradigm in which the peptide was first recovered. It describes that original experimental context and is not a claim of any sleep, sedative, insomnia, stress, or wellbeing effect. No such effect is asserted, implied, or supported on this page.
DSIP is the linear nonapeptide Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (H-WAGGDASGE-OH). Its molecular formula is C35H48N10O15 with a molecular weight of 848.8 g/mol for the free acid. PubChem indexes it under CID 68816, and the primary free-acid CAS number is 62568-57-4 (an alternate salt or registry form, 69431-45-4, also appears in the synonym list).
Published preclinical and in-vitro work has characterised DSIP against several molecular-pharmacology probes, named here by design and endpoint only: serotonergic (5-HT1A) pharmacology with a thermoregulatory endpoint, a dopaminergic mechanism with a somatostatin-release endpoint, central neuronal excitability by single-unit electrophysiology, and neuropeptide and hormone immunoreactivity readouts. An older review additionally frames an adrenergic-modulation hypothesis that the literature states remains to be established. No result, effect, or human outcome is asserted for any of these.
No. The phrase 'delta sleep-inducing peptide immunoreactor' is used in some circadian-biology literature as a name for glucocorticoid-induced leucine zipper (GILZ), a transcription factor. That is a different molecule entirely and is unrelated to the DSIP nonapeptide CID 68816. It must never be presented as DSIP-peptide pharmacology.
As bench handling of a research reagent only. The lyophilised powder is typically stored desiccated at -20 C and protected from light. Because its serine and N-terminal tryptophan residues make solutions prone to oxidative and hydrolytic degradation, working solutions are prepared fresh, aliquoted to avoid freeze-thaw, and kept refrigerated for short-term laboratory use. Reconstitution is a routine dissolution step in a suitable aqueous vehicle such as deionised water or an appropriate buffer. None of this is a preparation method for any use in humans or animals; see the reconstitution guide for general laboratory handling.