Delta Sleep-Inducing Peptide (DSIP) — nonapeptide; sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu
DSIP (Delta Sleep-Inducing Peptide) is a nonapeptide with a plasma elimination half-life of approximately 30–40 minutes following intravenous administration in humans[1], based on pharmacokinetic data reported by Graf and Kastin. The peptide promotes slow-wave (delta) sleep and is cleared primarily by proteolytic degradation across multiple tissues. DSIP is not approved by the FDA or any major regulatory body and has no approved clinical indication.
| Parameter | Value | Source |
|---|---|---|
| Elimination Half-Life (IV) | ~30–40 min | Graf & Kastin, Peptides 1986 (PMID 3520839)[1] |
| Elimination Half-Life (SC) | No published human data | — |
| Tmax (IV) | End of infusion (immediate) | Graf & Kastin 1986[1] |
| Route(s) | Intravenous (human PK data); Subcutaneous (animal data) | — |
| Molecular Weight | ~850 Da (nonapeptide) | Schoenenberger & Monnier 1977[2] |
| Full Clearance (5 × t½, IV) | ~2.5–3.5 hours | Calculated from PMID 3520839 |
| Primary Clearance Route | Proteolytic degradation (multi-tissue) | Graf & Kastin 1986[1] |
| Dosing Frequency (research) | Single evening dose or short course (3–5 days) | Schneider-Helmert 1985[3] |
| Data Quality | Human PK Study (limited) — no large RCT; primary reference is Graf & Kastin review (Peptides 1986) | |
DSIP has an elimination half-life of approximately 30–40 minutes following intravenous administration in humans, as reported by Graf and Kastin in their 1986 comprehensive review of DSIP pharmacokinetics and pharmacology.[1] This short half-life is characteristic of small neuropeptides, which are susceptible to rapid proteolytic cleavage by plasma and tissue peptidases.
No formal subcutaneous pharmacokinetic study in humans has been published in peer-reviewed English-language literature. Animal data suggest subcutaneous absorption extends the effective plasma presence compared to IV, but precise half-life values from human SC studies are not available as of the 2026 literature review date.
The half-life data available for DSIP comes from pharmacokinetic studies following intravenous bolus or infusion administration, where plasma concentration is sampled serially and the terminal elimination slope is used to calculate t½. The principal reference — Graf and Kastin 1986 — consolidated data from multiple earlier investigations into DSIP kinetics in animal and human subjects.[1]
DSIP's plasma half-life of ~30–40 minutes describes how quickly the nonapeptide clears from circulation. This is distinct from the duration of its biological effects. Schneider-Helmert's human clinical studies (1985) demonstrated that intravenous DSIP at 25 µg/kg produced measurable changes in sleep EEG architecture — specifically increases in delta-wave (slow-wave) sleep — that persisted across multiple nights following a short administration course.[3] This suggests that DSIP initiates a cascade of neurochemical events that outlast plasma presence — a common pattern among neuropeptides that act on central sleep-regulatory systems.
| Half-Lives Elapsed | Time After IV Dose | % Remaining | Note |
|---|---|---|---|
| 1 | ~30–40 min | 50% | Still within first hour post-dose |
| 2 | ~60–80 min | 25% | Substantial reduction |
| 3 | ~90–120 min | 12.5% | Approaching negligible |
| 4 | ~2–2.7 hours | 6.25% | Near-complete plasma clearance |
| 5 (clinical threshold) | ~2.5–3.5 hours | ~3% | Pharmacologically negligible in plasma |
Note: Biological sleep effects may persist well beyond plasma clearance. The table above describes plasma concentration kinetics only.
Because DSIP modulates the sleep-regulatory system rather than requiring continuous receptor occupancy, research protocols use single evening doses or short multi-day courses (typically 3–5 consecutive evenings). Schneider-Helmert's 1985 human study used IV administration at approximately 25 µg/kg in the evening before intended sleep onset.[3] The rationale is that a single acute dose is sufficient to trigger the downstream neurochemical cascade, with effects persisting into subsequent nights.
| Compound | Half-Life | Route | Approval Status | Mechanism |
|---|---|---|---|---|
| DSIP | ~30–40 min (IV) | IV / SC | Not approved | Neuropeptide; SWS promotion |
| Melatonin (endogenous) | ~40–50 min | Oral / SL | OTC supplement (US) | MT1/MT2 receptor agonist |
| Selank | ~1–2 min (estimated, IV) | Intranasal / IV | Not FDA approved | Anxiolytic neuropeptide |
| Semax | ~Minutes (estimated) | Intranasal | Not FDA approved | ACTH analog; BDNF modulation |
| Route | Half-Life | Human Data? | Notes |
|---|---|---|---|
| Intravenous (IV) | ~30–40 min | Yes — limited human PK study (PMID 3520839) | Reference pharmacokinetic route; 100% bioavailability |
| Subcutaneous (SC) | No published human data | No human PK data | Animal data only; SC absorption expected to extend presence vs IV |
| Intranasal | No published data | No | Speculative; no human PK study available |
| Oral | Not applicable | No | Degraded by GI proteases; oral bioavailability expected to be negligible |
DSIP is not included in standard WADA anti-doping panels or routine workplace drug testing immunoassays. No regulatory body has prohibited its use in sport or occupational contexts as of the 2026 literature review date.
No published forensic pharmacokinetic study characterises the urinary or serum detection window for DSIP in humans. Specialised LC-MS/MS assays can theoretically detect the DSIP nonapeptide sequence, but no validated reference method has been published in peer-reviewed literature.
DSIP is a nonapeptide (9 amino acids; sequence Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) with a molecular weight of approximately 850 Da.[2] Small peptides of this size are inherently susceptible to rapid proteolytic degradation by plasma and tissue peptidases — including aminopeptidases, endopeptidases, and serum proteases — which cleave the peptide backbone at multiple sites. This distributed proteolytic clearance, occurring across plasma, kidney, liver, and brain tissue, produces the short ~30–40 minute half-life observed following IV administration.
Unlike larger therapeutic peptides (e.g. semaglutide, ~7 days) that have been engineered with fatty acid side chains or backbone modifications to resist proteolysis, DSIP retains a native, unmodified sequence. No half-life–extending structural modifications have been applied to DSIP in published research formulations.
DSIP appears to modulate slow-wave sleep through interaction with multiple central neurochemical systems. Early research proposed involvement in GABA, opioid, and corticotropin-releasing hormone (CRH) pathways, though the precise receptor-level mechanism remains incompletely characterised.[1] The sleep-promoting effects are generally attributed to DSIP's central actions, particularly in hypothalamic and brainstem sleep-regulatory circuits, where peptide concentrations may be sustained longer than peripheral plasma measurements suggest due to blood-brain barrier transport dynamics.
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