DSIP
Delta Sleep-Inducing Peptide — a nine-amino-acid neuropeptide originally isolated from rabbit brain tissue during sleep research. Promotes deep delta wave (stage 3) sleep, the most restorative sleep phase, while also modulating stress responses, pain perception, and oxidative stress. One of the few peptides specifically targeting sleep architecture rather than sedation.
Typical Dosage
Standard: 100-200 mcg subcutaneous or intranasal 30 minutes before bed. Often cycled 2-4 weeks on, 1-2 weeks off.
Administration
Subcutaneous injection or intranasal spray
Mechanism of Action
Delta Sleep-Inducing Peptide is a nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) first isolated from rabbit cerebral venous blood during electrically induced sleep in 1977. Despite decades of research, its precise molecular receptor has not been definitively identified, making DSIP unusual among well-studied peptides. However, its physiological effects have been extensively characterized.
DSIP's sleep-promoting mechanism involves modulation of the balance between excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmission in sleep-regulating brain regions. It enhances GABAergic tone in the ventrolateral preoptic area (VLPO) — the brain's primary sleep-promoting nucleus — while reducing glutamatergic excitatory drive in wake-promoting areas like the lateral hypothalamus and locus coeruleus. The net effect is promotion of slow-wave (delta) sleep, characterized by high-amplitude, low-frequency (0.5-4 Hz) EEG oscillations. This is the deepest, most restorative sleep stage, during which growth hormone secretion peaks, memory consolidation occurs, and cellular repair processes are most active.
Beyond sleep, DSIP has significant neuroendocrine effects. It reduces cortisol secretion by suppressing corticotropin-releasing hormone (CRH) and ACTH release, lowering the activity of the hypothalamic-pituitary-adrenal (HPA) stress axis. This stress-reducing effect may itself contribute to sleep quality, as HPA axis hyperactivity is a common cause of insomnia and fragmented sleep. DSIP also modulates endogenous opioid signaling — it has been studied in opiate withdrawal protocols for its ability to normalize disturbed endorphin/enkephalin balance. Some research suggests it may regulate somatostatin release and interact with the orexin/hypocretin system, though these mechanisms are less well established. The paradox of DSIP is that despite its very short plasma half-life (15-25 minutes), sleep-promoting effects persist for hours, suggesting it triggers sustained changes in neural network activity or gene expression rather than requiring continuous receptor occupancy.
Regulatory Status
Not FDA approved. Research primarily from European studies (1970s–1990s). Available through research peptide suppliers.
Risks & Safety
Common: morning grogginess, vivid dreams, mild next-day drowsiness. Serious: very limited human research data, long-term safety unknown, mechanism not fully understood — effects may involve modulation of GABA, opioid, and serotonin systems. Rare: allergic reactions. Not FDA approved.
Research Papers
1Published: December 31, 2025
Abstract
Therapeutic peptides are emerging as promising adjuncts in the management of orthopaedic injuries, grounded in their ability to modulate molecular signaling networks central to cellular medicine. By acting on key pathways such as PI3K/Akt, mTOR, MAPK, TGF-β, and AMPK, peptides exert influence over tissue regeneration, inflammation resolution, and neuromuscular recovery. Wound-healing peptides such as BPC-157, TB-500, and GHK-Cu promote angiogenesis, integrin-mediated extracellular matrix remodeling, and fibroblast activation, whereas growth hormone secretagogues like ipamorelin, CJC-1295, tesamorelin, sermorelin, and AOD-9604 activate IGF-1 signaling and satellite cell repair. Recovery-enhancing agents such as epithalon, delta sleep-inducing peptide, and pinealon target circadian and mitochondrial regulators, and neuroactive peptides like selank, semax, and dihexa enhance brain-derived neurotrophic factor and HGF/c-Met pathways critical to neuroplasticity. Although preclinical studies are promising, there is a current lack of clinical trials. This review integrates current mechanistic insights with orthopaedic relevance, emphasizing safety, efficacy, and future directions for responsible integration into musculoskeletal care.
Related Peptides
AEDG Peptide
A tetrapeptide (Ala-Glu-Asp-Gly) identical to Epithalon's core active sequence — effectively the same compound. Studied for telomerase activation and pineal gland regulation, promoting melatonin production and potentially slowing cellular aging through telomere maintenance. Part of the Khavinson bioregulator peptide family developed at the Institute of Bioregulation and Gerontology in St. Petersburg.
CJC-1295 (no DAC)
A synthetic GHRH analogue (also called Mod GRF 1-29) consisting of the first 29 amino acids of native GHRH with four amino acid substitutions for increased enzymatic stability. Stimulates natural, pulsatile growth hormone release while preserving the body's somatostatin feedback regulation. One of the most commonly prescribed GH peptides, often combined with Ipamorelin for synergistic effects.
CJC-1295 + Ipamorelin
The most commonly prescribed peptide combination in anti-aging and regenerative medicine. Pairs the GHRH analogue CJC-1295 (Mod GRF 1-29) with the selective ghrelin-mimetic Ipamorelin for synergistic, pulsatile growth hormone release. Exploits two complementary signaling pathways — cAMP (GHRH) and calcium/PLC (ghrelin receptor) — to amplify GH pulses while maintaining minimal side effects.
CJC-1295 with DAC
CJC-1295 with Drug Affinity Complex — the same core GHRH analogue as Mod GRF 1-29 but with a reactive succinimide linker that covalently binds to circulating albumin after injection. This albumin binding dramatically extends the half-life from 30 minutes to nearly a week, allowing weekly dosing. Produces sustained rather than pulsatile GH elevation, which some practitioners consider less physiological.