DSIP Nasal Spray 10MG

Delta Sleep-Inducing Peptide (DSIP) is a small endogenous peptide isolated in the 1970s by the Monnier laboratory in Zurich from cerebral venous blood of rabbits in a state of induced "EEG delta-wave" sleep. The peptide has been studied for nearly five decades in published preclinical and exploratory clinical literature in contexts including sleep regulation, stress-axis modulation, opioid-system interaction, and seizure research. The mechanism by which DSIP produces its various reported effects remains incompletely characterized, and the peptide has not advanced to approved-medicine status for any indication.

This product is an intranasal research formulation of DSIP at 10 mg per spray bottle. The intranasal format is studied in the context of nose-to-brain peptide delivery, where the relevant research rationale is direct or partial direct access of nasally administered peptide to central nervous system tissue via the olfactory and trigeminal pathways, bypassing first-pass hepatic metabolism that limits oral peptide bioavailability and partially circumventing the blood-brain barrier limitations on systemic peptide delivery to CNS.

This page is a research-only educational reference. The preparation is supplied as a research-supply product and is not intended for human consumption or any therapeutic application. No medical claims are made on this page.

DSIP is a nonapeptide with the amino-acid sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE), molecular weight approximately 849 Da. The peptide is one of the smallest characterized putative neuropeptides and its compact size is one of the factors that has supported intranasal-research interest, as smaller peptides may achieve more favorable nasal-mucosal permeation than larger peptide molecules.

The 10 mg per bottle DSIP intranasal research formulation provides per-spray exposure consistent with research-supply nasal preparations. Specific volume per spray, peptide concentration, and excipient profile appear on the supplier's certificate of analysis. Typical nasal-spray preparations deliver approximately 50-100 μL per spray, with the total bottle volume distributed across many actuations.

DSIP is endogenous to mammals — it has been detected in brain, peripheral tissues, and plasma at low concentrations — but the specific receptor or molecular target through which DSIP produces its reported physiological effects has not been definitively identified. Published mechanistic work has implicated effects on opioid systems, GABAergic signaling, corticotropin-releasing-hormone (CRH) axis modulation, and other neurotransmitter systems, but no single receptor or signaling pathway has emerged as the established DSIP mechanism of action.

This is a peptide research compound in an intranasal format intended for laboratory and research-supply use. It is not a sleep aid, not a medicine, and not labeled or supplied for human consumption. The intranasal format is provided for the research-supply context relevant to nose-to-brain peptide delivery research.

DSIP was identified by Marcel Monnier, Guido Schoenenberger, and colleagues at the University of Zurich in the mid-1970s through perfusion experiments in rabbits. The investigators induced "EEG delta-wave" sleep states in donor rabbits by electrical stimulation of intralaminar thalamic nuclei and collected cerebral venous blood, which was then administered to recipient rabbits and produced EEG patterns characteristic of delta-wave sleep. Fractionation of the active material yielded a small peptide subsequently named "delta sleep-inducing peptide" with the WAGGDASGE sequence. The original publications appeared in the 1977-1979 timeframe.

Subsequent decades produced a substantial preclinical literature on DSIP in models of sleep regulation, stress-axis function, opioid-system interaction, seizure threshold, and other neuro-endocrine endpoints. Several open-label exploratory clinical reports examined DSIP administration in human subjects in contexts including chronic insomnia, opioid-withdrawal management, and chronic pain; the clinical literature has remained limited in scale and has not advanced to controlled trial-based regulatory approval for any indication.

Interest in DSIP has waxed and waned over the decades. The peptide is included in research-supply peptide catalogs because of its historical position as the prototype "sleep peptide," its small size that supports straightforward synthesis and characterization, and its continued research-context use in neuropeptide and sleep-research literature. Intranasal research formats are a more recent introduction reflecting growing research interest in nose-to-brain peptide delivery as a tool for CNS-targeted neuropeptide research.

Despite five decades of published research, the molecular target through which DSIP produces its reported physiological effects has not been definitively identified. The peptide does not have a characterized high-affinity receptor in the manner of well-characterized neuropeptide systems. Proposed mechanisms in the published literature include:

Opioid-system interaction. Effects of DSIP on endogenous opioid signaling, on β-endorphin release, on opioid-receptor expression, and on opioid-withdrawal phenotypes have been reported in multiple published studies. The opioid-system interaction is one of the more frequently invoked mechanism-of-action hypotheses for DSIP-mediated effects.

GABAergic and inhibitory neurotransmitter effects. Effects on GABA receptor function and on inhibitory neurotransmission have been reported in some published work and proposed as the substrate for the sleep-related and seizure-threshold effects.

Stress-axis (HPA) modulation. Effects of DSIP on corticotropin-releasing hormone (CRH) release, on ACTH, and on cortisol have been reported in published rodent and primate work. Modulation of stress-axis activity is one of the more reproducible findings in the DSIP literature.

Antioxidant and cytoprotective effects. Some published work has reported antioxidant activity and protective effects in models of oxidative stress and excitotoxicity.

Sleep-regulation effects. The original characterization context — EEG delta-wave sleep — has been investigated in multiple subsequent rodent and primate sleep-research studies with mixed reproducibility. The "sleep-inducing" label attached to DSIP from its original characterization is arguably stronger than the current state of the published evidence supports; effects on sleep parameters in subsequent work have been inconsistent across study designs and species.

Intranasal nose-to-brain peptide delivery is a research-context delivery strategy in which peptide administered to the nasal cavity reaches central nervous system tissue via two principal routes: the olfactory pathway (olfactory mucosa → olfactory nerve fascicles → olfactory bulb → CNS) and the trigeminal pathway (respiratory and olfactory mucosa → trigeminal nerve branches → brainstem entry). Both pathways bypass the blood-brain barrier and can deliver small peptides to brain regions at concentrations higher than would be predicted from systemic-administration pharmacokinetics. The research strategy is well-established for insulin (extensive published work including the "intranasal insulin and cognition" research literature), oxytocin (the basis for the substantial intranasal-oxytocin research literature), and several other neuropeptides.

For DSIP specifically, intranasal research formats are studied in contexts where central-nervous-system DSIP exposure is the research-relevant variable. The pharmacokinetic and biodistribution characterization of intranasal DSIP in published rodent work remains more limited than for intranasal oxytocin or intranasal insulin, but the formulation strategy follows the same nose-to-brain delivery rationale.

DSIP is a linear nonapeptide with the unmodified sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu. Molecular formula: C35H48N10O15. Molecular weight: approximately 849 Da. The peptide contains no cysteine residues (no disulfide bond), no proline residues, and no aromatic residues other than the N-terminal tryptophan. The overall character is small, acidic (two glutamic-acid-family residues), and relatively unstructured in solution — typical of a small linear neuropeptide.

Research-grade DSIP is produced by solid-phase peptide synthesis (Fmoc chemistry), purified by reversed-phase HPLC, and verified by mass spectrometry and HPLC analysis. Research-grade specifications typically include peptide content, HPLC purity (commonly >97%), mass-spectrometric identity, and residual counterion content. Specifications are reported on the supplier's certificate of analysis.

For the nasal-spray formulation, the peptide is dissolved in an aqueous vehicle compatible with intranasal administration. Typical excipients in nasal-spray formulations include sodium chloride for isotonicity, sodium phosphate or citrate for pH buffering, and a preservative system (commonly benzalkonium chloride or phenylethyl alcohol) to support multi-use functionality of the bottle. Specific formulation details appear on the supplier's certificate of analysis or product specification documentation.

Storage of intranasal peptide preparations is typically refrigerated (2-8°C) when in use and protected from light, with the relevant in-use period specified on supplier documentation. The compact size and lack of disulfide bonds in DSIP support reasonable solution-phase stability under appropriate storage conditions.

Published research using DSIP and the analogous research-supply applications for intranasal DSIP formats include:

Sleep-research models. EEG-recording rodent and primate sleep-research models are the original context for DSIP characterization and continue to be used in published mechanistic studies. Sleep-architecture endpoints (slow-wave-sleep duration, REM and NREM phase characterization, sleep-onset latency) are studied with various administration routes including intracerebroventricular, intraperitoneal, intravenous, and increasingly intranasal.

Stress-axis research. Effects of DSIP on HPA-axis function in rodent and primate stress models — including restraint stress, swim stress, and pharmacological stress challenges — have been studied with attention to ACTH, cortisol, CRH, and behavioral stress endpoints.

Opioid-system interaction research. The opioid-withdrawal models in rodents and the effects of DSIP co-administration on withdrawal phenotypes are a research-context category with a clinical-history motivation from the original exploratory opioid-withdrawal clinical reports.

Seizure-threshold research. DSIP effects on chemoconvulsant-induced seizures (PTZ, kainate, others) and electroconvulsive-threshold endpoints have been studied in rodent seizure-research models.

Neuroprotection and excitotoxicity research. Models of excitotoxic neuronal injury (NMDA-receptor-mediated, glutamate-mediated, ischemia-reperfusion) have been used to characterize the reported antioxidant and cytoprotective effects of DSIP.

Intranasal pharmacokinetic and biodistribution research. The intranasal nasal-spray format is particularly well-suited to characterization of nose-to-brain peptide delivery — pharmacokinetic measurement of CSF and brain-region peptide levels following intranasal administration, comparison with systemic administration, and identification of the olfactory versus trigeminal contributions to CNS delivery.

Comparative-route research. Studies comparing intranasal, intravenous, and intracerebroventricular DSIP administration in matched rodent models provide research-context information on the relative CNS exposure achieved by different routes.

All applications are research-supply context: laboratory and research-supply use in cells, isolated tissues, and rodent or primate in-vivo studies. The preparation is not for human consumption. Nothing on this page describes a clinical protocol or therapeutic use.

DSIP nasal spray sits within the family of intranasal neuropeptide research formats and within the broader sleep-research peptide category.

Delta Sleep-Inducing Peptide (DSIP) is a small nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu, ~849 Da) isolated in 1977 by the Monnier laboratory in Zurich from cerebral venous blood of rabbits in EEG delta-wave sleep states. The peptide has been studied for five decades in preclinical research on sleep regulation, stress-axis function, opioid-system interaction, seizure threshold, and neuroprotection. The molecular target through which DSIP produces its reported effects has not been definitively identified.

This 10 mg intranasal research formulation provides DSIP in a nose-to-brain delivery format. Intranasal administration delivers peptide to central nervous system tissue via the olfactory and trigeminal pathways, bypassing the blood-brain barrier and producing CNS-region exposure that supports CNS-targeted neuropeptide research. The intranasal format is distinct from the lyophilized injectable DSIP research format, which provides systemic exposure for non-CNS-targeted research applications.

DSIP is not an approved medicine for any indication. The intranasal preparation is supplied for laboratory and research-supply use only and is not intended for human consumption. The educational content on this page provides scientific and historical context for the research-supply application.