DSIP
● In Stock & Ready to Ship from USA
FREE shipping on orders over $200
Secure checkout via encrypted payment processor
Research Use Only
These products are for laboratory research only and not intended for medical use. They are not FDA-approved to diagnose, treat, cure, or prevent any disease. By purchasing, you certify they will be used solely for research and not for human or animal consumption.
Research Summary
Research Overview DSIP (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) was first isolated in 1974 by the Schoenenberger-Monnier group at the University of Basel, Switzerland, from the cerebral venous blood of rabbits in electrically induced slow-wave sleep. DSIP-like immunoreactivity has since been detected in the hypothalamus, limbic system, pituitary gland, and human breast milk.[1][17] DSIP remains neuroscience's "unresolved riddle": despite 50+ years of study, no specific gene coding for a DSIP precursor has been identified, and no dedicated receptor has been cloned. Sequence analysis suggests homology with the 324–332 fragment of human lysine-specific histone demethylase 3B (KND peptide, JMJD1B gene).[1] Originally pursued as a "somnogenic molecule" to cure insomnia, the therapeutic rationale shifted to that of a "programming modulator" or adaptogen — stabilizing neuronal activity and restoring homeostasis under stress or disrupted circadian rhythms. Research spans 8+ indication categories across neurology, addiction medicine, oncology, cardiology, and gerontology.[9]
DSIP — Research Data at a Glance
| Property | Value |
|---|---|
| Contributing Researchers | 3 |
| Purity Standard | ≥99% (HPLC verified, 3rd-party COA) |
| Research Use Only | Not for human consumption. RUO only. |
Overview
Research Overview
DSIP (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) was first isolated in 1974 by the Schoenenberger-Monnier group at the University of Basel, Switzerland, from the cerebral venous blood of rabbits in electrically induced slow-wave sleep. DSIP-like immunoreactivity has since been detected in the hypothalamus, limbic system, pituitary gland, and human breast milk.[1][17]
DSIP remains neuroscience's "unresolved riddle": despite 50+ years of study, no specific gene coding for a DSIP precursor has been identified, and no dedicated receptor has been cloned. Sequence analysis suggests homology with the 324–332 fragment of human lysine-specific histone demethylase 3B (KND peptide, JMJD1B gene).[1]
Originally pursued as a "somnogenic molecule" to cure insomnia, the therapeutic rationale shifted to that of a "programming modulator" or adaptogen — stabilizing neuronal activity and restoring homeostasis under stress or disrupted circadian rhythms. Research spans 8+ indication categories across neurology, addiction medicine, oncology, cardiology, and gerontology.[9]
Mechanism of Action
Mechanism of Action
DSIP's exact mechanism remains partially obscure — the "unresolved riddle" stems from the absence of a cloned receptor or identified gene. However, extensive research characterizes its interactions across multiple receptor systems and signaling cascades.[1]
Receptor Targets
| Target | Interaction | Evidence |
|---|---|---|
| NMDA Receptors | Antagonist / modulator — blocks NMDA-activated potentiation | Reduces glutamate/NMDA-stimulated Ca²⁺ uptake in synaptosomes |
| Opioid Receptors | Agonistic activity — SWS induction reversed by naloxone | Antinociceptive effects blocked by naloxone |
| α₁-Adrenergic Receptors | Stimulates pineal N-acetyltransferase via α₁ interaction | Graf & Schoenenberger (1987) |
| Specific ³H-DSIP Binding Sites | Found on pineal membrane fractions and neurons (not glia) | Brain stem cultures — radioimmunoassay |
Downstream Signaling
| Pathway | Effect | Consequence |
|---|---|---|
| MAPK/ERK | Prevents Raf-1 activation via GILZ homology → inhibits ERK phosphorylation | Anti-inflammatory / stress-limiting |
| MAO-A | Increases monoamine oxidase A activity in brain mitochondria | Reduced serotonin levels (paradoxical) |
| Antioxidant Enzymes | Stimulates SOD, catalase, glutathione peroxidase | Cytoprotection / reduced lipid peroxidation |
| c-Fos Expression | Prevents c-fos in paraventricular nucleus during stress | Stress resistance — modulated via NMDA pathway |
| Mitochondrial Respiration | Stabilizes NADH-dehydrogenase; enhances oxidative phosphorylation | Protection against hypoxia |
Dose-Response: Bell-Shaped Curve
| Parameter | Optimal Dose | Notes |
|---|---|---|
| Delta-wave induction (rabbits) | ~30 nmol/kg IV | Higher and lower doses less effective |
| Infusion duration (humans) | 2.5–7.5 min | 1 min or 20 min less effective than mid-range |
| Motor activity (mice) | Biphasic: 30 nmol ↑ / 120 nmol ↓ | Low dose enhances, high dose suppresses |
Key analog: KND peptide (WKGGNASGE) — differs by single amino acid (Asn vs Asp at position 5); more potent antioxidant; greater reduction in myocardial infarction (19.1% vs 28.7%).[8]
Research Applications
Research Applications
DSIP research spans 8+ indication categories across neurology, addiction, oncology, and gerontology:
- Sleep Regulation & Insomnia — Increases delta (slow-wave) sleep 39–54% in rabbits; 59% median increase in total sleep time in humans (25 nmol/kg IV); 7-night treatment normalized chronic insomnia.[3][4]
- Withdrawal Syndrome Treatment — 97% improvement in opiate withdrawal (n=60); 87% in alcohol withdrawal (n=47); terminated delirium tremens in 6/8 cases.[2]
- Stress Adaptation & HPA Modulation — Reduces stress-induced metabolic disorders; lowers basal corticotropin; blocks cortisol release; prevents c-fos expression during emotional stress.[18]
- Pain Management — Dose-dependent antinociceptive effect (blocked by naloxone); reduced pain in 6/7 chronic pain patients.[11][5]
- Neuroprotection & Stroke Recovery — DSIP/KND reduced brain infarction volume during reperfusion; accelerated motor function recovery in focal stroke.[8][7]
- Cardioprotection — Reduces myocardial infarction size (IA/AAR 28.7% vs 42.1% control); stabilizes mitochondrial respiration. ⚠️ 100% mortality if given during occlusion phase.[8]
- Epilepsy & Anticonvulsant — Reduces seizure severity and duration; prolongs seizure latency; potentiates valproate effects.[16]
- Geroprotection & Oncology — Maximum lifespan +24.1% in SHR mice; total tumors ↓2.6-fold; mammary carcinoma ↓5-fold; chromosomal aberrations ↓22.6%.[10]
Biochemical Characteristics
| Property | Value |
|---|---|
| Molecular Formula | C₃₅H₄₈N₁₀O₁₅ |
| Molecular Weight | 848.81 Da |
| CAS Number | 62568-57-4 |
| PubChem CID | 3623358 |
| Sequence (1-Letter) | WAGGDASGE |
| Sequence (3-Letter) | Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu |
| Structure | Linear nonapeptide; 9 L-amino acids; amphiphilic; folded conformation in aqueous solution |
| Origin | Cerebral venous blood of rabbits during slow-wave sleep (1974) |
| Classification | Neuropeptide / Programming Modulator / Research Peptide |
| Half-Life | ~15 minutes (in vitro); extremely fragile in vivo |
| Dose-Response | Bell-shaped / inverted U-curve — optimal delta-wave induction at ~30 nmol/kg IV |
Identifiers
| Purity Standard | |
|---|---|
| Synonyms | |
| Gene/Precursor | |
| Analog |
Preclinical Research Summary
Preclinical Research Summary
Key Preclinical Studies
| Study | Model | Key Findings | Ref |
|---|---|---|---|
| Mu et al. (2024) | Mice — PCPA-induced insomnia | Wakefulness ↓ from 720→600 min (p<0.001); ↑ serotonin + melatonin | [1] |
| Monnier/Polc (1977–78) | Rabbits/Cats — EEG/sleep | 39–54% increase in delta activity (rabbits); enhanced REM in cats | [17] |
| Tukhovskaya et al. (2021) | SD rats — MCAO stroke, 120 µg/kg intranasal | Significant motor recovery (Rotarod p<0.01); infarct size not significantly reduced | [7] |
| Tukhovskaya et al. (2021) | SD rats — MI reperfusion, 150 µg/kg IP | IA/AAR reduced to 28.7% vs 42.1% control (p=0.01); ⚠️ 100% mortality during occlusion | [8] |
| Popovich et al. (2003) | SHR mice — 2.5 µg/mouse SC monthly | Max lifespan +24.1% (917 vs 739 d); tumors ↓2.6-fold; chromosomal aberrations ↓22.6% | [10] |
| Hrnčić et al. (2018) | Rats — lindane-induced seizures, 1 mg/kg IP | Reduced seizure intensity; prolonged seizure latency; decreased EEG ictal periods | [16] |
| Scherschlicht/Tissot (Patent) | Mice — morphine withdrawal (naloxone-precipitated) | Dose-dependent withdrawal inhibition: 0.3 mg/kg SC reduced jumping to 54% of control | [13] |
| Nakamura et al. (1988) | Mice/Rats — pain tests (tail-pinch, hot plate) | Potent dose-dependent antinociception via ICV; blocked by naloxone (opioid-mediated) | [11] |
Clinical / Human Studies
| Trial | Population | Key Results | Outcome | Ref |
|---|---|---|---|---|
| Acute Effects in Normals | n=6 healthy adults | 59% median increase in total sleep time; ↑ SWS and REM | Success | [3] |
| 7-Night Insomnia Treatment | n=14 chronic insomniacs | Normalized sleep efficiency and daytime alertness to levels of healthy controls | Success | [4] |
| Withdrawal Syndromes | n=107 (47 alcoholics, 60 opiate addicts) | Opiate: 97% improved; Alcohol: 87% improved; DTs terminated in 6/8 | Success | [2] |
| Chronic Pain Pilot | n=7 (migraine, tinnitus, psychogenic pain) | Pain reduced in 6/7 patients; simultaneous reduction in depression | Success | [5] |
| Double-Blind Insomnia | n=16 chronic insomniacs | Effects described as "weak"; authors concluded "not likely to be of major therapeutic benefit" | Failure | [3] |
Safety Summary
| Parameter | Finding |
|---|---|
| FDA Category 2 Warning | "Significant safety risks" — potential immunogenicity; "lacks sufficient information"; not approved for compounding |
| Acute Toxicity (Animals) | Oral LD50 in rats >5,000 mg/kg; MTD in dogs >2,000 mg/kg — high safety margin |
| Historical Human Trials | Mild adverse events: headache, nausea, vertigo; described as "incredibly safe" in 70+ subjects |
| ⚠️ CRITICAL TIMING | 100% mortality when given during active ischemic occlusion (MI or stroke); protective ONLY during reperfusion |
| Pharmacokinetics | Half-life ~15 min; degraded by aminopeptidases (N-terminal Trp cleavage); crosses BBB partly |
| Drug Interactions | Antagonizes morphine; reversed by naloxone; reverses amphetamine hyperthermia; incompatible with peptidase inhibitors (captopril) |
Authors & Attribution
✍️ Article Author
Marcel Monnier, M.D.
Marcel Monnier was a physiologist at the University of Basel, Switzerland, and a pioneer in demonstrating the humoral transmission of sleep. His group conducted the foundational experiments in which the cerebral venous blood of rabbits in electrically induced sleep was dialyzed and infused into recipient rabbits, inducing delta-wave sleep — leading to the first isolation of 'sleep factor delta' (DSIP) in 1974. Key publications include 'A naturally occurring delta-EEG enhancing nonapeptide in rabbits: final isolation, characterization and activity test' (1977). Marcel Monnier is referenced as the co-discoverer of DSIP. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →🎓 Scientific Journal Author
Guido A. Schoenenberger, M.D.
Guido A. Schoenenberger was a biochemist at the University of Basel, Switzerland (Research Division, Department of Surgery). Working alongside Marcel Monnier, he was responsible for the biochemical isolation, characterization, and synthesis of DSIP — determining the nonapeptide's amino acid sequence (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu). He proposed the 'programming' hypothesis, suggesting DSIP acts as a modulator of neurotransmitters rather than a direct transmitter. Key publications include 'Characterization, properties and multivariate functions of Delta-Sleep-Inducing Peptide' (1984). Guido Schoenenberger is referenced as the co-discoverer and synthesizer of DSIP. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Guido A. Schoenenberger, M.D. is being referenced as one of the leading scientists involved in the research and development of DSIP. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
🔬 Contributing Researcher
Abba J. Kastin, M.D.
Abba J. Kastin was a physician at the Veterans Administration Medical Center and Tulane University School of Medicine (New Orleans, USA). Kastin authored major reviews on DSIP and investigated its physiological distribution, metabolism, and ability to cross the blood-brain barrier. His work expanded understanding of DSIP's extra-sleep effects — circadian rhythms, locomotor activity, and hormone modulation. Key publications include 'Delta-sleep-inducing peptide (DSIP): a review' (Neuroscience & Biobehavioral Reviews, 1984) and 'Differential penetration of DSIP peptides into rat brain' (1982). Abba Kastin is referenced as a leading researcher in DSIP pharmacology. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Abba J. Kastin, M.D. is being referenced as one of the leading scientists involved in the research and development of DSIP. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
RUO Disclaimer
For Research Use Only (RUO). This product is intended solely for in-vitro research and laboratory experimentation. It is not a drug, food, cosmetic, or medical device and has not been approved by the FDA for any human or veterinary use. It must not be used for therapeutic, diagnostic, or any other non-research purpose. Pure US Peptide does not condone or encourage the use of this product for anything other than strictly defined research applications. Users assume full responsibility for compliance with all applicable regulations and guidelines.
Certificate of Analysis (COA)
Every batch is strictly tested by accredited third-party laboratories (ISO 17025) to ensure 99%+ purity.
Latest Lab Report
Related Research Compounds
ARA-290
10mg
Thy Alpha 1
10mg
Tesamorelin/Ipamorelin Blend 11mg/6mg
