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DSIP9 residuesWAGGDASGEEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: DSIP, Delta Sleep-Inducing Peptide, WAGGDASGE
Nine amino acids long, and it crosses the blood-brain barrier on its own. DSIP (Delta Sleep Inducing Peptide, Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) is a naturally occurring nonapeptide that promotes slow-wave delta sleep without sedation. The formal human evidence is small and old, all from IV studies between 1977 and 1992 with fewer than 20 subjects each. Community use runs subcutaneous at 100 to 300 mcg nightly, roughly 5 to 15 times the validated IV dose. Shift workers, athletes chasing recovery, and anyone tired of pharmaceutical sleep aids make up the core user base. No dependency. No grogginess. No FDA approval.
Fourteen chronic insomniacs. That's the largest controlled human study on DSIP, a double-blind trial from 1992 [1]. Despite that modest sample, the results showed improved delta-wave sleep architecture without the REM suppression that benzodiazepines cause. DSIP (Delta Sleep Inducing Peptide, CAS 62568-57-4) is a nonapeptide, nine amino acids, with a molecular weight of 849 Da. It crosses the blood-brain barrier through a non-competitive, non-saturable transport mechanism. In plasma, free DSIP degrades in about 7 minutes. Carrier proteins extend its functional duration to several hours, though the specific carrier has never been isolated. The mechanism touches multiple pathways. DSIP interacts with NMDA receptors in the hypothalamus, pushing the brain toward slow-wave sleep. It also stimulates pineal acetyltransferase through alpha-1 adrenergic receptors, which increases natural melatonin synthesis. On the hormonal side, it suppresses ACTH and cortisol [2] and stimulates luteinizing hormone release [3]. Community use runs subcutaneous at 100 to 300 mcg nightly, 30 to 60 minutes before bed. That's 5 to 15 times the only validated human IV dose (~21 mcg for 70 kg). No pharmacokinetic bridging study connects these two routes. Sleep tracker data from Oura and Garmin users on r/peptides consistently shows increased deep sleep percentages. Responder variability is high; a meaningful subset reports zero effect, often attributed to vendor quality problems. The research gap is real: all human trials are over 30 years old, undersized, and IV-only. A 2024 Frontiers in Pharmacology paper tested a DSIP fusion peptide in mouse models with positive results (DOI 10.3389/fphar.2024.1439536), but new human trials don't exist yet.
DSIP reaches the brain through a transport system that most peptides can't use. Blood-brain barrier crossing typically requires lipophilicity or specific receptor-mediated endocytosis. DSIP takes neither route; it uses a non-competitive, non-saturable mechanism documented by Kastin's research group. This means higher blood levels don't saturate the transport, an unusual property for a 849 Da peptide. Once inside the CNS, DSIP works through at least three distinct pathways. First, it modulates NMDA receptors in the hypothalamus and limbic system, promoting the transition into slow-wave sleep. Unlike benzodiazepines, it doesn't suppress REM sleep. Second, it stimulates pineal acetyltransferase activity via alpha-1 adrenergic receptors. This enzyme is rate-limiting for melatonin synthesis, so DSIP effectively amplifies the body's own sleep signal. Third, DSIP acts on the hypothalamic-pituitary-adrenal axis. It decreases basal corticotropin (ACTH) levels and blocks stress-induced ACTH release [2]. Lower ACTH means lower cortisol, which partly explains why users report reduced stress reactivity alongside better sleep. The half-life creates confusion. Free plasma DSIP degrades in 7 to 8 minutes via aminopeptidases. But in vivo, DSIP binds carrier proteins that shield it from degradation. Functional duration extends to an estimated 6 to 8 hours. No group has isolated the specific carrier protein or its gene, which remains one of the biggest unanswered questions in DSIP pharmacology. DSIP also stimulates hypothalamic LH-releasing hormone secretion. Measurable luteinizing hormone increases appear within 30 minutes of central administration [3]. Additional research shows suppression of lipid peroxidation and activation of endogenous antioxidant defenses, suggesting neuroprotective properties.
IV administration improved delta-wave sleep in small controlled human studies (1977-1992); effect sizes were modest and results inconsistent across labs. No human SC data exists. Most studies are >30 years old and underpowered. 2024 mouse-model work demonstrates DSIP fusion peptide efficacy but no new human trials.
PMID 1299794: "Effects of DSIP on sleep of chronic insomniac patients" (double-blind, n=14, 1992); Frontiers Pharmacology 2024 (DSIP-CBBBP fusion peptide, mouse model insomnia, DOI 10.3389/fphar.2024.1439536)
All human trials used IV administration; no human SC bioavailability data. Studies are small (n<20), >30 years old, from single research groups. Mechanism of carrier-protein binding that extends functional half-life has not been fully characterized: no carrier protein gene or precursor has been isolated. No RCTs at any community dose.
Users consistently report improved sleep architecture (deeper slow-wave sleep, faster onset, reduced night waking) without grogginess or dependency. Effect variability is high; a meaningful subset reports no effect, likely due to vendor quality issues.
Both science and community agree DSIP influences sleep architecture and may deepen slow-wave sleep. They diverge on route (IV only in science vs SC in community), dose (21 mcg IV vs 100-300 mcg SC), and confidence level. Community SC use is a pragmatic extrapolation with no PK validation. The core mechanism hypothesis is shared; the evidence quality for SC dosing is entirely community-derived.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 100mcg | Daily |
| Moderate | 200mcg | Daily |
| Aggressive | 300mcg | Daily |
Reconstitution math for the standard 5 mg vial: add 2 mL bacteriostatic water to get 2,500 mcg per mL (2.5 mg/mL). On a U-100 insulin syringe, each unit equals 25 mcg. Beginner dose (100 mcg) = 4 units. Moderate dose (200 mcg) = 8 units. Aggressive dose (300 mcg) = 12 units. These are tiny volumes. You'll want a 0.5 mL insulin syringe with half-unit markings for accuracy at the beginner dose. Inject subcutaneous 30 to 60 minutes before bed. Not at bed, not two hours before. The cascade needs time to initiate. Abdomen and upper arm are the go-to sites. Store reconstituted vials at 2 to 8 degrees Celsius. Use within 21 days. DSIP is fragile; the peptide can degrade faster than most if exposed to heat or repeated temperature swings. The one thing most beginners miss: if you feel nothing after two weeks at 100 mcg, check your vendor before bumping the dose. DSIP quality varies more than almost any other research peptide. Look for HPLC certificates of analysis from third-party labs.
Typical protocol is 2-4 weeks on, 2 weeks off. No dependence or withdrawal has been reported, but cycling preserves receptor sensitivity. Some users run 5 days on, 2 days off within each active week.
No formal receptor desensitization data exists for DSIP in humans, but community experience consistently shows diminishing returns with continuous daily use after 2-4 weeks. The pattern fits a receptor-level adaptation or downstream cascade habituation. Standard cycling protocol (2-4 weeks on, 2 weeks off) is designed to restore sensitivity.
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Expected: Improved sleep onset and modest improvement in deep sleep depth. Not all users respond: if no effect by week 2, consider vendor quality or dose uptitration.
Swab the rubber stopper with an alcohol wipe.
Inject it slowly against the vial wall (not directly onto the powder). Let it dissolve, gently swirling if needed. Don't shake. Final concentration: 2,500 mcg per mL.
Using a U-100 insulin syringe (29 to 31 gauge, 0.5 mL), draw your dose. Beginner: 4 units (100 mcg). Moderate: 8 units (200 mcg). Aggressive: 12 units (300 mcg).
Insert the needle at a 45-degree angle. Inject slowly. Release the skin fold after withdrawing the needle.
The DSIP cascade takes time to engage the sleep architecture; injecting right at lights-out reduces the window for delta-wave initiation.
Return the vial to the refrigerator (2 to 8 degrees Celsius). Mark the reconstitution date on the vial. Discard after 21 days. A single 5 mg vial provides approximately 25 doses at 200 mcg.
Human clinical dose: ~21 mcg (25 nmol/kg for 70 kg); far lower than SC community doses
All formal human studies used IV administration. This is the only route with human evidence of efficacy. Not appropriate for self-administration. SC is the de facto community standard.
Community doses of 100-300 mcg SC are 5-15x higher than validated IV human doses, partially compensating for lower bioavailability and first-pass losses
BBB penetration via non-saturable transport mechanism is documented, but no SC-to-IV PK bridging study exists. Standard home-use approach. Abdomen or upper arm preferred.
Complementary sleep and circadian normalization. Epitalon acts on the pineal gland to restore melatonin production; DSIP deepens delta-wave architecture. Often stacked in anti-aging / longevity protocols.
Epitalon 5-10 mg SC daily for 10-20 days, concurrent with or adjacent to DSIP cycle
Addresses stress-driven insomnia: Selank provides anxiolytic and cortisol-moderating effects pre-sleep; DSIP then deepens the sleep architecture. Different mechanisms, not redundant.
Selank 250-500 mcg intranasal 30-60 min before bed, same timing as DSIP injection
Neuroprotective / cognitive synergy. Semax supports BDNF and cognitive function; DSIP improves restorative sleep quality. Some users report improved memory consolidation when combining both.
Nocturnal GH pulse amplification. DSIP deepens slow-wave sleep: the phase during which GH secretion is highest. CJC-1295 no-DAC + Ipamorelin administered at bedtime amplifies this GH pulse.
CJC-1295 no-DAC 100-300 mcg + Ipamorelin 200-300 mcg SC immediately before bed; DSIP 200-250 mcg 30-60 min before bed
Both DSIP and benzodiazepines produce CNS depression. Concurrent use risks additive sedation and unpredictable CNS depression. Benzodiazepines also suppress slow-wave sleep: directly opposing DSIP's mechanism.
Do not combineSame additive CNS depression concern as benzodiazepines. Z-drugs suppress deep sleep architecture; DSIP aims to restore it: concurrent use is mechanistically counterproductive.
Do not combineDSIP is degraded by aminopeptidases. ACE inhibitors inhibit peptidase activity and may slow DSIP degradation, unpredictably extending or amplifying effects. Clinical significance unknown.
DSIP stimulates endogenous melatonin synthesis via pineal acetyltransferase. High-dose exogenous melatonin (3-10 mg) combined with DSIP risks excessive melatonin activity and may suppress natural secretion long-term. Low-dose melatonin (0.5-1 mg) is less concerning.
Pricing updated 2026-04-09
Headache is the most common complaint, and it's dose-dependent. Community reports concentrate the risk above 300 mcg, though occasional cases appear at lower doses. The mechanism isn't well understood, but reducing to 200 mcg resolves it in most users. Every human study on DSIP was conducted intravenously between 1977 and 1992. Total humans studied across all published trials is fewer than 100. Side effect data at subcutaneous doses (100 to 300 mcg) is entirely community-derived, not clinically validated. Keep that limitation in mind when reading frequency estimates. Published side effects from IV human studies include transient headache, mild nausea, and occasional vertigo. These were reported in early European clinical work and referenced in the 2006 review by Graf and Kastin [5]. Frequency data is sparse given the small sample sizes (n less than 20 per study). Community-reported side effects at subcutaneous doses: Headache (common at 300 mcg or above, uncommon at 100 to 200 mcg). Most users describe it as mild and transient. Hydration before injection helps. Persistent headache at any dose warrants stopping the protocol. Vivid or intense dreams (frequently reported, especially in the first week). Delta-wave sleep deepening can amplify dream activity. Most users consider this a feature, not a bug. If dreams become disruptive, reducing the dose to 100 mcg or injecting 90 minutes before bed (instead of 30 to 60 minutes) may help. Tolerance development with continuous daily use. Community experience consistently shows diminishing returns after 2 to 4 weeks of nightly use. Cycling is the standard solution: 2 to 4 weeks on, 2 weeks off. Some users run 5 days on, 2 days off within each active week to slow tolerance. Rebound insomnia has been occasionally reported after abrupt cessation following extended daily runs. Tapering by reducing frequency before a full break may reduce this risk. Responder variability is high. A meaningful subset of users reports zero effect. Vendor quality is the first variable to investigate before concluding non-response; DSIP peptide integrity is fragile. Injection-site reactions are uncommon but possible with any subcutaneous injection. Standard site rotation (abdomen, upper arm) applies. Contraindications: pregnancy and breastfeeding (no safety data exists for fetal or infant exposure), known hypersensitivity to DSIP, severe hypotension (DSIP may lower blood pressure through cortisol reduction), and children/adolescents (not studied in pediatric populations). Personal or family history of cancer has been cited by InnerBody's review as a precaution, cross-referencing FDA safety concerns. Drug interactions require attention. Benzodiazepines and Z-drugs risk additive CNS depression and should not be combined with DSIP. Antihypertensive medications may see amplified effects through DSIP's cortisol reduction. Exogenous corticosteroid protocols could be disrupted, since DSIP suppresses ACTH. High-dose melatonin (3 to 10 mg) creates redundant pathway stimulation; keep melatonin at 0.5 to 1 mg if combining. ACE inhibitors may slow DSIP degradation through aminopeptidase inhibition, unpredictably extending effects.
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DSIP is a nonapeptide research chemical with no FDA-approved product. Purity and authenticity vary significantly between vendors. The peptide is fragile: improper synthesis, storage, or reconstitution can render it inactive. Removed from FDA Category 2 on April 15, 2026; PCAC review begins July 2026. Compounding pharmacy oversight not yet available.
| Test | When | Target |
|---|---|---|
| Subjective sleep quality log | Nightly during protocol: rate sleep onset speed, depth, and next-day alertness on a 1-10 scale | — |
| Wearable sleep tracker (Oura Ring, Garmin, Whoop) | Continuous during protocol | — |
| AM cortisol (serum or salivary) | Optional: baseline before protocol, then at week 3 of first run | Morning serum cortisol: 10-20 mcg/dL (normal reference range) |
| LH / testosterone (optional, males) | If using DSIP alongside GH secretagogue stack for performance optimization | — |
Primary outcome measure. DSIP effect on sleep architecture is the main use case.
Objective measurement of deep/slow-wave sleep percentage. Provides data-driven evidence of response before uptitrating dose.
DSIP suppresses stress-induced ACTH and cortisol. If cortisol normalization is a protocol goal, pre/post measurement quantifies the HPA-axis effect.
DSIP stimulates hypothalamic LH-releasing hormone secretion. Baseline LH useful if tracking hormonal effects in combination protocols.
Most users notice faster sleep onset and more vivid dreams within the first few nights. Effects are subtle: this is not a sedative.
Deeper sleep becomes more consistent. Morning alertness improves. Some report reduced middle-of-the-night waking.
Sleep architecture normalizes. Cortisol patterns may improve. Cumulative recovery benefits become apparent: better mood, reduced brain fog.
Full benefits plateau. Most protocols call for cycling off at this point (2-4 weeks off) to maintain sensitivity.
Days 1 to 3: Most users notice faster sleep onset within the first few nights. Dreams may become more vivid. Don't expect sedation; DSIP initiates a sleep cascade, it doesn't knock you out. Some people feel nothing at first. Mild headache affects a minority. Morning alertness occasionally improves even on night one. Week 1: Deeper sleep becomes more consistent. Night waking reduces. If you're wearing an Oura or Garmin, check your deep sleep percentage; many users see measurable increases by day 5 to 7. Vivid dreams may persist. Occasional headache at higher doses. Weeks 2 to 3: Sleep architecture settles into a new baseline. Some users report lower daytime stress reactivity and better mood, consistent with DSIP's cortisol-suppressing mechanism [2]. Training recovery improves. Watch for tolerance signs by week 3 if running daily; diminishing returns are the signal to start your off-cycle. Week 4 and beyond (off cycle): Sleep quality typically holds for 1 to 2 weeks after stopping. No withdrawal or dependency is expected based on published data and community reports. Occasional mild rebound insomnia has been reported after long unbroken daily runs. The standard community protocol calls for a 2-week break before restarting.
Based on IV human trials, sleep architecture changes can occur within the first administration. Cascade initiation is rapid once DSIP reaches the CNS.
Most users notice faster sleep onset and somewhat more vivid dreams within the first 1-3 nights. Effects are subtle: not sedating. Some feel nothing initially.
Modulation of NMDA receptors and pineal acetyltransferase activity should produce measurable increases in slow-wave (delta) sleep proportion.
Deeper sleep becomes more consistent. Night waking reduces. Sleep tracker data (Oura, Garmin) often shows increased deep/slow-wave sleep %. Morning alertness improves.
Cortisol and ACTH modulation takes longer to manifest than direct sleep effects. LH/hormone normalization may also appear in this window.
Sleep architecture is well-normalized. Some report reduced daytime cortisol/stress reactivity and improved mood. Recovery from training improves. Tolerance beginnings may appear by week 3 with daily use.
No withdrawal or dependency expected based on mechanism and published data. Sleep improvements may persist somewhat after cessation.
Most report sleep quality holds for 1-2 weeks after stopping. Occasional mild rebound worsening reported after long daily-use runs. 2-week break is the community standard before restarting.
Source: Kastin et al.: plasma degradation studies; functional duration extended by carrier protein binding
Loading the interactive decay curve.
DSIP is not FDA-approved for any indication. It was on the FDA's Category 2 bulk drug substance list until April 15, 2026, when HHS removed it along with 11 other peptides. PCAC review begins July 2026. Compounding pharmacy access is not yet available and is projected for late 2026 to mid-2027. Research chemical vendors sell DSIP labeled "for research use only." It is not a controlled substance. DSIP is not on the WADA prohibited list. Athletes competing in tested sports should verify their governing body's current prohibited substance database. This content is for informational purposes only and does not constitute medical advice. Consult a licensed healthcare provider before using any peptide.
Peptide Schedule Research TeamReviewed Apr 20267 Citations
