DSIP (emideltide) – what is the sleep-inducing peptide and what do scientific studies say?

Delta sleep-inducing peptide (DSIP), also known as emideltide, is an experimental peptide composed of nine amino acids. It was first identified in material isolated from the venous blood flowing from the brain of rabbits. Since then, scientists have studied its possible relationship with sleep, stress responses, neuroendocrine regulation, and neuroprotective processes. However, DSIP is not an approved drug or recognized treatment method for sleep disorders.

The name of this substance may suggest that it is a natural hormone responsible for inducing sleep. However, available scientific evidence presents a much more complex picture. DSIP was synthesized and tested under laboratory conditions in animals, healthy volunteers, and small groups of people suffering from insomnia. Some early studies showed changes in sleep parameters and electroencephalographic (EEG) activity. Other controlled studies yielded results that were weak, inconsistent, or devoid of any clinically significant meaning.

Several basic biological issues have also not been elucidated. The natural source of DSIP, its precursor protein, its specific receptor, or its exact physiological function in the human body have not been unequivocally established [1–3].

The article presents the structure of DSIP, the history of its discovery, differences between the native peptide and related compounds, and the results of clinical and preclinical studies. Particular attention is paid to what was actually demonstrated in the studies, and which properties remain only hypotheses.

What is DSIP peptide?

DSIP is a nonapeptide, which is a molecule composed of nine amino acid residues. Its sequence is Trp–Ala–Gly–Gly–Asp–Ala–Ser–Gly–Glu.

The name delta sleep-inducing peptide comes from the first experiments on rabbits. The material isolated from the venous blood flowing out of the brain of these animals, and then synthetically reproduced peptide, increased the activity of delta waves and sleep spindles in the EEG recording after direct administration to the brain [1].

The term „DSIP peptide” often appears in search engines. From a chemical point of view, it is partially redundant, because the letter „P” in the abbreviation DSIP already stands for peptide, i.e., a peptide.

DSIP should be described primarily as an experimental peptide with biological activity, rather than as a confirmed sleep hormone.

Its amino acid sequence is well defined. Therefore, it is possible to synthesize a molecule with a defined structure and study its chemical and biological properties.

Much greater uncertainty concerns the natural occurrence of DSIP in the body.

In an extensive scientific review it was indicated that the gene directly encoding DSIP, the typical precursor protein, nor the specific receptor of this peptide had not been identified. The authors also pointed out that some historical measurements may have concerned substances structurally similar to DSIP, recognized by antibodies exhibiting cross-reactivity [3].

This means that although DSIP was originally isolated from biological material, its natural synthesis, distribution, and function in humans have not been unequivocally confirmed.

What does the abbreviation DSIP mean?

DSIP stands for delta sleep-inducing peptide, which can be translated as „delta sleep-inducing peptide”.

The word „delta” refers to the free brain waves recorded on the EEG. Activity in this band is particularly characteristic of the deep stages of NREM sleep.

In the original scientific publication, a more detailed name, delta-electroencephalogram (-sleep)-inducing peptide [1], was also used.

The name therefore refers to the activity observed under certain experimental conditions. It does not constitute proof that DSIP reliably induces sleep in humans.

This distinction is important because scientific nomenclature often remains unchanged even when later research leads to a more cautious interpretation of earlier discoveries.

In subsequent animal experiments, it was not always possible to reproduce the effects conducive to sleep. In a review published in 2006, the hypothesis that DSIP is a physiological factor inducing sleep was assessed as poorly documented [3].

Clinical studies also did not provide consistent confirmation of the sedative effect.

Therefore, the name DSIP is primarily of historical and descriptive significance. It does not indicate confirmed therapeutic efficacy.

How was the delta sleep-inducing peptide discovered?

The history of DSIP dates back to the sleep research conducted by Swiss scientists Günther A. Schoenenberger and Marcel Monnier in Basel.

The researchers collected venous blood flowing from the brains of mice subjected to electrical stimulation associated with inducing sleep. Subsequently, they isolated material whose presence was associated with increased activity of free EEG waves.

In 1977 Schoenenberger and Monnier described the chemical characteristics and synthesis of a peptide composed of nine amino acids.

In a double-blind experiment involving 58 rabbits, synthetic DSIP was compared with its fragments and analogs with altered amino acid sequence.

After administration of synthetic DSIP directly to brain cells, significant increases in delta wave and sleep spindles activity were observed in the EEG.

The examined fragments and analogs with a rearranged amino acid sequence did not produce the same effect [1].

This was an interesting discovery, but the scope of its interpretation remains limited.

The experiments were conducted on rabbits, and the substance was administered directly to the central nervous system. The main endpoints were changes in EEG activity under controlled laboratory conditions.

The results did not prove that DSIP circulating in the blood functions as a sleep hormone in humans. They also did not confirm that intravenous administration provides a similar exposure in the brain, nor that the substance can effectively treat insomnia.

Subsequent reviews have shown significant variability in the results depending on the species of animal, the experimental model, the route of administration, the exposure, and the analog used [2,3].

The English term rabbit cerebral venous blood is often used in descriptions of the discovery, meaning the venous blood that flows from the rabbit's brain.

This term refers exclusively to the biological material used in the original isolation experiments.

The modern DSIP for research purposes is usually obtained by chemical methods of peptide synthesis.

The ability to reproduce the same sequence does not, however, determine whether free DSIP naturally occurs in human tissues at concentrations of physiological significance.

Is DSIP a peptide, a protein, a supplement, or a medication?

DSIP is a peptide, not a protein.

Both peptides and proteins are composed of amino acids linked by peptide bonds. DSIP, however, contains only nine amino acid residues, making it much smaller than most molecules classified as proteins.

It is also not a vitamin, mineral, nutrient, or a typical component of dietary supplements.

In the context of pharmacological studies, DSIP is best described as an experimental substance or an unapproved drug candidate.

The peptide was administered to clinical trial participants. This means that there is some data regarding its activity in humans, but this is not equivalent to approval for medical use.

DSIP does not have a specific indication approved by the FDA or the EMA for the treatment of insomnia, stress, pain, epilepsy, stroke, withdrawal-related disorders, or the aging process.

The term research peptide, or „research peptide”, describes the context of its use. However, it is not a guarantee of pharmaceutical quality, safety, or efficacy.

On the internet, you can find markings such as DSIP 2 mg, DSIP 5 mg or DSIP 10 mg.

They usually refer to the total amount of substance declared by the seller in the vial. They do not indicate different molecules or clinically confirmed doses.

The label itself does not confirm the chemical identity, purity, absence of impurities, stability, or the actual content of the intact peptide.

In published studies in humans, exposure was often described in nanomoles per kilogram of body weight. Controlled experimental preparations were used, sometimes administered intravenously.

Such protocols cannot be directly converted into instructions for the self-administration of products available for sale.

The declared vial content is a product parameter and not a confirmation of the appropriate clinical dose.

Structure, Sequence, and Molecular Identity of the DSIP Peptide

The native amino acid sequence of DSIP is:

Trp–Ala–Gly–Gly–Asp–Ala–Ser–Gly–Glu

In the one-liter amino acid code, it is written as:

WAGGDASGE

DSIP contains nine amino acid residues, therefore it is classified as a nonapeptide.

At the amino end is tryptophan, while at the carboxyl end is glutamic acid.

Asparaginic acid is also present in the sequence. Both of these amino acids contain acidic side chains that are important for the physicochemical properties of the molecule.

According to PubChem data, the free, neutral peptide referred to as emideltide has a molecular formula of C₃₅H₄₈N₁₀O₁₅ and a molecular mass of approximately 848.8 g/mol [4].

These values refer to a specific chemical form.

DSIP salts, such as DSIP acetate, contain additional anti-oxidants. This can affect the molecular weight, the way the substance is calculated, and the properties of the formulation.

Depending on the method of declaring the product’s content, water, solvent residues, and other ingredients may also be taken into account.

Therefore, the information itself about the number of milligrams does not allow one to unequivocally determine the amount of chemically intact DSIP.

It is also necessary to distinguish between native DSIP and its analogues and complex preparations.

Phospho-DSIP, also known as P-DSIP, is a phosphorylated analogue. The KND peptide is structurally related to the nonapeptide with amino acid residues at the base.

Deltaran, on the other hand, is a preparation containing DSIP and glycine.

The results of the DeltaRNA research cannot be automatically attributed to DSIP itself.

Similarly, peptide fragments, analogs with D-amino acids, cyclic derivatives, and fusion proteins constitute separate research units.

It is also important to distinguish between intact DSIP and material exhibiting immunoreactivity similar to DSIP. A positive result of an immunological test does not always mean the detection of exactly the same molecule.

What is emideltide and is it the same as DSIP?

Emideltide is an unassigned name referring to the same nine-amino acid molecule that is commonly known as the delta sleep-inducing peptide.

PubChem lists emideltide, DSIP and delta sleep-inducing peptide as synonyms for the same chemical substance [4].

Emideltide is therefore not a separate peptide with a different amino acid sequence.

However, the name of a substance must be distinguished from its specific chemical form.

For example, emideltide acetate represents the salt form, and the finished preparation may also contain excipients or other active ingredients.

When comparing the results of the studies, the sequence, the salt form, the formulation composition, and the route of administration are therefore important factors.

The mere presence of a formal chemical name or non-registered name does not also indicate obtaining regulatory approval.

What was DSIP studied for?

DSIP is most commonly associated with sleep, but the scope of scientific research regarding this substance is much broader.

In studies involving humans, insomnia, sleep architecture, hormonal parameters, pain, withdrawal-related conditions, and interactions with medications used during anesthesia were analyzed among other things.

In animal experiments and laboratory systems, the response to stress, seizures, oxidative stress, neurotransmitter signaling, ischemic damage, metabolism, and aging-related changes were also studied.

However, the wide range of research does not mean equally strong evidence for each of these areas.

A significant portion of the literature is based on small, older or exploratory studies, rather than on large contemporary clinical trials.

DSIP and sleep research

In some early studies in humans, a reduction in the time required to fall asleep or an improvement in sleep efficiency were observed.

In a 1986 publication involving 18 people with psychophysiological chronic insomnia, improvement in selected sleep parameters was described during a week-long experimental administration of DSIP and in the subsequent period of observation [5].

Another controlled cross-sectional study on chronic insomnia yielded much more cautious conclusions.

Some of the changes were not significant compared to placebo or could be due to differences that existed before the study began. The authors assessed the clinical significance of the improvement as being minor [6].

In a subsequent double-blind study involving 16 participants, only limited changes in objective sleep parameters were observed, and no significant improvement in subjective sleep quality was observed.

Researchers concluded that a significant therapeutic effect is unlikely [7].

These results do not unequivocally confirm the effectiveness of DSIP in the treatment of insomnia.

DSIP and neuroendocrine activity

11 healthy men participated in a randomized, double-blind study.

After experimental intravenous administration of DSIP, a short-term reduction in immunoreactivity similar to ACTH was observed in plasma compared to the group receiving physiological salt.

At the same time, the concentration of cortisol in the blood and urine remained unchanged [8].

The result indicates a possible influence of DSIP on a specific hormonal biomarker.

However, it does not prove to be effective in treating stress, anxiety, adrenal gland disorders, or other endocrine diseases.

By comparison, other peptides that act on hormonal regulation may have a different mechanism and a much more extensive clinical documentation. An example is Tessamorelina, a synthetic analog of GHRH, studied for its effect on the GH–IGF-1 axis.

However, this does not mean that DSIP and tesamorelina act on the same receptors or have similar applications.

DSIP and GABA and NMDA signaling

In ex vivo studies on rat neurons, the effect of DSIP on neurotransmission mechanisms was analyzed.

An increase in currents activated by gamma-aminobutyric acid (GABA), changes in signaling related to NMDA receptors, and an effect on calcium uptake in the synapses of the cerebral cortex have been observed [9].

GABA is one of the main inhibitory neurotransmitters in the central nervous system.

NMDA receptors, on the other hand, are involved in excitatory neurotransmission and synaptic plasticity processes.

The results suggest that DSIP may affect selected mechanisms related to the balance between neuronal excitation and inhibition.

However, studies on isolated cells and tissues do not allow determining the therapeutic efficacy in humans.

DSIP and experimental models of seizures

In studies in rats, the effect of DSIP on experimentally induced seizures was evaluated.

In some models, a reduction in behavioral symptoms of seizures was observed.

However, this was not always accompanied by a complete disappearance of the epileptic activity in the EEG recording [10].

This means that the improvement in the animal's behavior does not necessarily correspond to a complete inhibition of the abnormal electrical activity of the brain.

These studies are preliminary in nature and do not confirm the efficacy of DSIP in the treatment of epilepsy in humans.

DSIP and cerebral ischemia and neuroprotection

In a study conducted in 2021 in rats, DSIP was evaluated in a model of focal ischemia of the brain.

Improved performance of selected motor function parameters was observed after experimental ischemic injury [11].

In other experiments, peptides related to DSIP were also analyzed in models of cerebral and cardiac ischemia.

Additional studies in rodents described changes in markers of oxidative stress, the activity of antioxidant enzymes, the properties of cell membranes, and responses to stress.

These results may help in formulating hypotheses regarding the mechanisms of cell protection.

However, they do not provide evidence that DSIP improves stroke treatment outcomes in humans, prevents neurodegeneration, or slows biological aging.

Human studies and clinical trials of DSIP

DSIP was the subject of intervention studies involving humans, but the available evidence base remains small and comes from a significant portion of the studies that took place several decades ago.

Most sleep research was conducted in the 1980s and the early 1990s of the 20th century.

The trials included relatively small groups of participants, used different experimental designs, and often relied on intravenous administration of the peptide.

Some studies were conducted using a double-blind trial and were controlled by a placebo.

Such solutions reduce the risk of methodological errors, but do not eliminate the problems associated with small sample sizes, differences in baseline characteristics, inconsistent results, and limited replication.

Study by Schneider-Helmert et al. (1981)

Six healthy volunteers participated in a double-blind cross-over study.

The researchers analyzed behavioral changes during sleep after experimental intravenous administration of DSIP.

Increased sleep pressure and some immediate and delayed changes in its parameters have been observed [12].

Due to the very small number of participants, the study should be considered a physiological experiment.

It does not allow to conclude that DSIP is an effective treatment for diagnosed sleep disorders.

Schneider-Helmert study (1986)

In the study published in 1986, 18 people with psychophysiological chronic insomnia participated.

During experimental exposure to DSIP and during observation, improvements in some sleep parameters were described [5].

The results suggested the possibility of the peptide influencing the course of sleep in this group.

However, the limitation was the small number of trials and the lack of sufficient independent replication.

Study by Montiego et al. (1987)

Monti and colleagues conducted a controlled cross-sectional study on the short-term effects of DSIP in people with chronic insomnia.

The study involved five nights of observation.

Some sleep parameters changed, but the observed effects were small or difficult to distinguish clearly from placebo.

The researchers also drew attention to the importance of the differences that existed between the participants before the experiment began.

The overall assessment indicated limited clinical value of the observed changes [6].

Study by Bes et al. (1992)

In a double-blind study based on matched pairs, 16 people with chronic insomnia participated.

The researchers analyzed both objective sleep parameters and subjective assessment of its quality.

Only limited changes in objective parameters were observed.

However, no significant improvement in subjective well-being was demonstrated.

The authors concluded that the significant therapeutic value of DSIP in chronic insomnia is unlikely [7].

The results of this study are particularly important because they do not unequivocally confirm the main action suggested by the name of the peptide.

DSIP study during general anesthesia (2009)

DSIP was also studied in the context of interactions with anesthetics.

24 women undergoing gynecological surgeries participated in a randomized study.

Twelve participants received physiological salt, while the remaining twelve received one of three experimental doses of DSIP.

The substance was evaluated during wakefulness and during anesthesia using propofol and isoflurane.

Changes in EEG activity, the bispectral index BIS, heart rate variability and heart rate variability were observed.

Some observations suggested a deeper rather than a shallower level of anesthesia [13].

The study shows that the name „sleep-inducing peptide” does not mean a substance with the same effects as classic sedative or anesthetic agents.

List of the most important DSIP studies

The term „clinical trials DSIP” is justified because intervention experiments involving humans have been conducted.

However, this should not be interpreted as proof of the existence of a complete drug development program.

The available studies do not provide the appropriate scale of independent replication, standardized endpoints, long-term safety assessment, or confirmatory multicenter studies that are usually required before a new sleep medication can be approved for routine clinical practice.

What do current evidence confirm, and what do they not confirm?

Available publications confirm that DSIP is a chemically defined nonapeptide capable of inducing measurable biological effects under certain experimental conditions.

The substance was synthesized and evaluated in studies involving humans, animals, and laboratory models.

Changes in sleep parameters, EEG activity, hormonal biomarkers, autonomic indicators, receptor responses, and results in animal models of disease have been observed in certain experiments [1,5–13].

This justifies the designation of DSIP as a biologically active substance of interest from a scientific point of view.

However, it was not confirmed that DSIP is a natural human sleep hormone.

Neither a specific receptor has been identified nor has it been shown that the peptide reliably reaches biologically significant concentrations in the human brain via various peripheral administration routes.

There is a lack of convincing clinical evidence confirming the effectiveness of DSIP in the treatment of insomnia, anxiety, epilepsy, stroke, pain, withdrawal symptoms, or other conditions.

Its anti-aging or improving athletic performance effects in humans have also not been established.

The literature does not provide sufficient data to determine a standardized therapeutic dose, long-term safety, stability after reconstitution, or the equivalence of different preparations.

The variety of the substances tested also remains an important limitation.

DSIP, phospho-DSIP, KND, Deltaran, and material with immunoreactivity similar to DSIP are not mutually interchangeable units.

Changes in EEG activity and biomarker concentrations are also indirect indicators. They do not automatically mean an improvement in patients' well-being or a reduction in the risk of diseases.

The inconsistency of sleep outcomes is particularly significant, because even the main effect suggested by the peptide’s name has not been reliably confirmed in repeated clinical trials [3,6,7].

The availability of products labeled as DSIP for sale online does not constitute proof of their approval, pharmaceutical quality, or medical acceptance.

Regulatory information should be verified from the official sources of the FDA, EMA and the UK’s MHRA.

Most common questions about the DSIP peptide

Is DSIP really a sleep-inducing peptide?

DSIP was named because of the increased delta wave activity and REM sleep activity observed in the original experiments in mice. However, later studies in humans yielded inconsistent results. Some showed improvements in selected sleep parameters, while others did not confirm significant clinical benefits. The name of the peptide therefore describes a historical discovery, but does not constitute evidence of efficacy in the treatment of insomnia [1,3,6,7].

Does DSIP occur naturally?

DSIP was originally isolated from the venous blood draining from the brains of rabbits. Material with immunoreactivity similar to DSIP was also detected in various tissues and biological fluids. However, the specific gene, the precursor protein, or the specific receptor have not been unequivocally identified. Therefore, the natural origin and function of DSIP in humans remain unclear. It is more accurate to refer to the peptide isolated from biological material as a confirmed human sleep hormone [3].

What is the amino acid sequence of DSIP?

The DSIP sequence is Trp–Ala–Gly–Gly–Asp–Ala–Ser–Gly–Glu. In a single-letter amino acid code, it is written as WAGGDASGE. Since the molecule contains nine amino acid residues, it is classified as a nonapeptide. This sequence forms the basis for the chemical identification of native DSIP and distinguishes it from analogs containing substituents or additional modifications [1,4].

Is emideltide the same as DSIP?

Yes. Emideltide is the name referring to the same native molecule that is known as delta sleep-inducing peptide. Both names appear as synonyms in the PubChem database [4]. However, it is important to distinguish the free peptide from its salts, such as emideltide acetate, and from preparations containing additional ingredients. The name of the substance does not automatically mean equivalence of all formulations.

What are DSIP 2 mg, DSIP 5 mg, and DSIP 10 mg?

The designations DSIP 2 mg, DSIP 5 mg and DSIP 10 mg usually refer to the declared total amount of the substance in the vial. They do not describe the various amino acid sequences or the clinically confirmed doses. The label itself does not confirm the purity, identity, sterility, stability or safety of the product. The published clinical studies do not establish these designations as validated regimens for self-administration.

Is phospho-DSIP the same as DSIP?

No. Phospho-DSIP is a phosphorylated analog of the native DSIP. Phosphorylation is a chemical modification that can affect the properties of the molecule, including its stability, molecular interactions, and biological activity. Therefore, the results of studies regarding phospho-DSIP should not be automatically attributed to the unmodified peptide. Each of these substances requires a separate experimental evaluation.

Is Deltaran the same as DSIP?

No. Deltaran is a complex preparation containing DSIP and glycine. The results of the studies regarding Deltaran refer to the entire formulation, not just the native peptide. Without appropriate control groups, it is not possible to determine which part of the observed effect results from the action of DSIP, glycine, or their combination. Therefore, the data regarding these two substances should not be considered equivalent.

Does DSIP cross the blood–brain barrier?

It has not been unequivocally established whether DSIP, when administered peripherally, reliably reaches significant biological concentrations in the human brain. Earlier animal studies and in vitro transport models suggested the possibility of the interaction of some DSIP-related materials with the blood-brain barrier. However, this does not confirm similar behavior in contemporary preparations in humans. Differences in formulation, route of administration, peptide degradation, protein binding, and analytical methods complicate interpretation.

Are there clinical trials of DSIP in humans?

Yes. Several small intervention studies involving humans were conducted in the 80s and early 90s of the 20th century. In 2009, a study on the interaction of DSIP with anesthesia was also published [5–8,12,13]. However, the results were inconsistent and the trials involved small groups of participants. The available data do not confirm clinical efficacy, standardized treatment, or long-term safety.

Is DSIP approved by the FDA, EMA, or in the UK?

DSIP does not have an established approved FDA or EMA therapeutic indication and is not a standard approved insomnia medication in the UK. The presence of DSIP products on the internet does not mean that they are registered as medicinal products. Since the regulatory status of a substance can change over time, the current information should be checked directly in the official databases of the FDA, EMA and MHRA, rather than relying on vendor claims.

Limitations of the evidence base regarding DSIP

The most important problem with research on DSIP is not the complete lack of publications, but the large discrepancy between the range of properties attributed to it and the actual strength of scientific evidence.

Literature includes many experiments on animals, isolated tissues, cell models, and biochemical systems.

Part of the studies also concerns structural analogues or complex preparations, the results of which cannot be directly related to native DSIP.

Studies involving humans are usually small, old, and methodologically diverse.

Independent replication remains limited.

Most studies on insomnia were conducted during a period when the standards for designing and reporting clinical trials differed from those of today.

This makes it difficult to assess randomization, previously defined endpoints, the method of collecting data on adverse effects, and the risk of selective reporting of results.

An important limitation is also the availability of full publications. Some older studies can only be analyzed based on abstracts.

The absence of reported adverse effects in a small experiment is not evidence of the substance's complete safety.

The available studies also do not allow for a clear assessment of the authenticity, stability, purity, or accuracy of the declared DSIP content in products sold online.

Applications

DSIP, also known as emideltide, is a synthetically produced nonapeptide with a defined amino acid sequence WAGGDASGE.

Its name comes from experiments in which an increased activity of delta waves and spindles of sleep were observed in the EEG of rabbits.

Later studies have shown that the biological interpretation of DSIP is much more complex.

Its role as a natural sleep hormone in humans has not been unequivocally confirmed. Neither has a specific receptor, a typical precursor protein, nor a complete physiological mechanism been established.

Studies involving humans indicated possible changes in selected sleep parameters and hormonal activity, but their results were small, inconsistent, and insufficiently replicated.

Preclinical experiments provided additional observations regarding GABA and NMDA signaling, seizures, oxidative stress, and brain ischemia.

However, they do not constitute confirmation of therapeutic efficacy in humans.

The current state of knowledge justifies further research into the biological properties of DSIP, but does not allow it to be presented as an approved treatment for insomnia, a neuroprotective agent, or a substance with proven anti-aging effects.

Disclaimer

The article is purely educational and scientifically informative. It does not constitute medical advice, diagnosis, therapeutic recommendations, dosage instructions, reconstitution, or administration of DSIP.

Delta sleep-inducing peptide is not an FDA- or EMA-approved drug for the uses discussed in the article and is not the standard treatment for insomnia in the UK.

The evidence presented includes small human studies, animal experiments, ex vivo experiments, and mechanistic studies.

They do not confirm clinical efficacy, long-term safety, a standardized method of use, or the equivalence of DSIP products available on the market.

References

1. Schoenenberger, G. A., & Monnier, M. (1977). Characterization of a delta-electroencephalogram (-sleep)-inducing peptide. Proceedings of the National Academy of Sciences of the United States of America, 74(3), 1282–1286. https://doi.org/10.1073/pnas.74.3.1282
2. Graf, M. V., & Kastin, A. J. (1986). Delta-sleep-inducing peptide (DSIP): An update. Peptides, 7(6), 1165–1187. https://doi.org/10.1016/0196-9781(86)90148-8
3. Kovalzon, V. M., & Strekalova, T. V. (2006). Delta sleep-inducing peptide (DSIP): A still unresolved riddle. Journal of Neurochemistry, 97(2), 303–309. https://doi.org/10.1111/j.1471-4159.2006.03693.x
4. National Center for Biotechnology Information. (2026). PubChem Compound Summary for CID 68816, Emideltide. PubChem. Retrieved August 22, 2026, from https://pubchem.ncbi.nlm.nih.gov/compound/68816
5. Schneider-Helmert, D. (1986). Efficacy of DSIP to normalize sleep in middle-aged and elderly chronic insomniacs. European Neurology, 25(6), 448–453. https://doi.org/10.1159/000116050
6. Monti, J. M., Debellis, J., Alterwain, P., Pellejero, T., & Monti, D. (1987). Study of delta sleep-inducing peptide efficacy in improving sleep on short-term administration to chronic insomniacs. International Journal of Clinical Pharmacology Research, 7(2), 105–110. https://pubmed.ncbi.nlm.nih.gov/3583493/
7. Bes, F., Hofman, W., Schuur, J., & Van Boxtel, C. (1992). Effects of delta sleep-inducing peptide on sleep of chronic insomniac patients: A double-blind study. Neuropsychobiology, 26(4), 193–197. https://doi.org/10.1159/000118919
8. Bjartell, A., Ekman, R., Bergquist, S., & Widerlöv, E. (1989). Reduction of immunoreactive ACTH in plasma following intravenous injection of delta sleep-inducing peptide in man. Psychoneuroendocrinology, 14(5), 347–355. https://doi.org/10.1016/0306-4530(89)90004-8
9. Grigor’ev, V. V., Ivanova, T. A., Kustova, E. A., Petrova, L. N., Serkova, T. P., & Bachurin, S. O. (2006). Effects of delta sleep-inducing peptide on pre- and postsynaptic glutamate and postsynaptic GABA receptors in neurons of the cortex, hippocampus, and cerebellum in rats. Bulletin of Experimental Biology and Medicine, 142(2), 186–188. https://doi.org/10.1007/s10517-006-0323-9
10. Stanojlović, O., Hrncić, D., Zivanović, D., Rasić, A., & Susić, V. (2006). Valproate and delta-sleep peptide display high efficacy against metaphit-induced audiogenic seizure in rats. Acta Physiologica Hungarica, 93(4), 303–314. https://doi.org/10.1556/APhysiol.93.2006.4.6
11. Tukhovskaya, E. A., Ismailova, A. M., Shaykhutdinova, E. R., Slashcheva, G. A., Prudchenko, I. A., Mikhaleva, I. I., Khokhlova, O. N., Murashev, A. N., & Ivanov, V. T. (2021). Delta sleep-inducing peptide recovers motor function in SD rats after focal stroke. Molecules, 26(17), 5173. https://doi.org/10.3390/molecules26175173
12. Schneider-Helmert, D., Gnirss, F., Monnier, M., Schenker, J., & Schoenenberger, G. A. (1981). Acute and delayed effects of DSIP (delta sleep-inducing peptide) on human sleep behavior. International Journal of Clinical Pharmacology, Therapy, and Toxicology, 19(8), 341–345. https://pubmed.ncbi.nlm.nih.gov/6895513/
13. Pomfrett, C. J. D., Dolling, S., Anders, N. R. K., Glover, D. G., Bryan, A., & Pollard, B. J. (2009). Delta sleep-inducing peptide alters bispectral index, the electroencephalogram and heart rate variability when used as an adjunct to isoflurane anaesthesia. European Journal of Anaesthesiology, 26(2), 128–134. https://doi.org/10.1097/EJA.0b013e32831c8644