A nine-amino-acid peptide your brain makes naturally, first found in the blood of sleeping rabbits in the 1970s. Despite its name, DSIP is better understood as a sleep regulator than a sedative — it appears to deepen slow-wave (delta) sleep and calm the body's stress system rather than knock you out. Its boldest human results are not in sleep but in addiction medicine: in an early series, roughly 97% of opioid-dependent and 87% of alcohol-dependent patients improved or cleared their withdrawal symptoms after DSIP. It is not FDA-approved; in April 2026 it was removed from the FDA's Category-2 list and is awaiting a compounding-review decision.
Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (WAGGDASGE) — an amphiphilic endogenous nonapeptide isolated by the Schoenenberger–Monnier group in Basel in 1977 from the cerebral venous blood of rabbits during hypnogenic thalamic stimulation. It promotes delta-EEG / spindle activity on intraventricular infusion and is distributed across hypothalamus, limbic system, and pituitary as well as gut and pancreas. Mechanistically multifunctional: HPA-axis / ACTH attenuation, GH and LH modulation, antioxidant and opioid-system effects, and neuroprotection. It behaves as a sleep-promoting regulator with greatest activity when sleep is disturbed and minimal effect in undisturbed sleepers — not a bedtime sedative. Plasma half-life is very short (minutes) owing to an N-terminal-Trp-cleaving aminopeptidase.
DSIP (C₃₅H₄₈N₁₀O₁₅, MW 848.81 Da, CAS 62568-57-4, UniProt P01158; FDA designation Emideltide) is a pleiotropic neuromodulatory nonapeptide whose endogenous gene, receptor, and precursor remain unidentified. First characterized as a "delta-electroencephalogram-(sleep)-inducing peptide" (Schoenenberger & Monnier, PNAS 1977). Reported actions span HPA modulation, antioxidant defense (↑SOD/catalase/GPx, ↓lipid peroxidation), mitochondrial respiration, and stress protection; intranasal DSIP improves motor recovery after focal stroke in rats without significantly shrinking infarct volume. The human evidence base is small, largely pre-1995, and contradictory on sleep — the best-controlled double-blind trial found near-null sleep effects — while the withdrawal and stress-protection signals are more consistent. CAS [Asn5]-DSIP analog 80064-67-1.
The numbers that define DSIP across five decades of literature — a peptide whose name promises sleep induction but whose most consistent human signal is in stress and withdrawal, whose controlled sleep evidence is modest, and whose mechanism remains incompletely mapped. DSIP is best read as a multifunctional regulator with intriguing preclinical breadth, a small and largely pre-1995 human dataset, and an unsettled but improving regulatory position.
DSIP doesn't act like a sleeping pill that switches the brain off. Instead it seems to nudge several systems toward "rest and recover" mode: it quiets the stress hormone cascade (cortisol/ACTH), supports the natural growth-hormone pulse that comes with deep sleep, taps into the body's own pain-and-calm (opioid) signals, and boosts antioxidant defenses. The catch is that the exact machinery — which receptor it binds, which gene makes it — is still unknown, and the human evidence is thin and mixed.
Six loosely connected mechanistic arms, none fully resolved. First — HPA-axis attenuation: reduced basal ACTH and blunted CRF-induced corticosterone in animal paradigms, though a controlled human CRH-infusion study found no difference vs placebo. Second — slow-wave-sleep modulation with delta/spindle EEG enhancement, strongest when sleep is disturbed. Third — neuroendocrine effects: GH and LH release, somatostatin inhibition, and α1-adrenergic modulation of pineal N-acetyltransferase linking DSIP to melatonin synthesis. Fourth — antioxidant / mitochondrial protection (↑SOD, catalase, GPx; ↓lipid peroxidation). Fifth — opioid-system interaction underlying analgesia and the withdrawal data. Sixth — neuroprotection in ischemia models.
DSIP is a pleiotropic regulator without an identified cognate receptor, gene, or precursor, which is the central mechanistic problem: its effects are reproducible in some paradigms and absent in others, and its rapid aminopeptidase degradation complicates exposure-response inference. The Graf–Kastin reviews catalog distribution and endocrine actions across species. Anti-stress effects include raised hypothalamic substance P and increased resistance to emotional stress in rats; stress protection is mirrored at the mitochondrial level through modulation of MAO-A, hexokinase, creatine kinase and oxidative phosphorylation. A delta-sleep / sleep-related-GH coupling has been described, contrasted by null results on injection into the raphe. Claims of direct GABA-A or NMDA receptor action are frequently repeated commercially but rest on weak primary evidence.
This is a speculative, evidence-anchored dosing engine — every ladder, threshold, and titration rule is layered on top of (1) the small set of human clinical-study doses (IV withdrawal at ~25 nmol/kg; IV/SC sleep-study ranges), (2) preclinical exposures (e.g. intranasal 120 µg/kg in rats), and (3) current practice-pattern SC ranges (≈100–500 µg, most commonly 100–250 µg) that are not trial-validated. No standardized, modern, controlled human dose ladder exists for any DSIP indication as of 2026. DSIP is dosed in micrograms (µg). Each protocol is built to the same skeleton — starting dose, escalation cadence, dose ladder, maintenance target, cycle structure, reconstitution math, monitoring overlay, and explicit evidence grade — and is backed below by global dose bands, weight-band interpolation, engine-ready titration logic, and a borrowed biomarker scaffold, so the section can drive a protocol engine rather than read as static prose.
100 µg SC, given in the evening (commonly 1–2 h before intended sleep, though strict pre-bedtime timing is not required). Reconstitute and rotate abdominal SC sites. Start low to gauge next-day grogginess and dream intensity.5–7 nights. Because effects accrue over a series of doses rather than acutely, do not judge a single night; DSIP's human effect emerged over repeated administration, not as an acute hit.100 µg → 150 µg → 200 µg → 250 µg nightly (or every-other-night). 250 µg is a reasonable practice ceiling for the sleep indication; higher doses raise next-day grogginess without clear added benefit and are not better-supported.100–250 µg on the nights it is used. An open series normalized sleep in 6 of 7 severe insomniacs over 3–7 months using a course of 10 injections — supporting intermittent courses rather than indefinite nightly use. Many users dose only on poor-sleep nights.2–4 weeks on, then reassess / pause. The regulatory (vs sedative) profile and minutes-long half-life argue against chronic continuous dosing; cycling is the conservative default.5 mg vial + 2 mL BAC water = 2,500 µg/mL; a 200 µg dose = 0.08 mL = 8 units on a U-100 syringe; 25 doses per vial. See the calculator below.100 µg/day SC × 7 days, evening. The stress / recovery use leans on DSIP's animal antioxidant and anti-stress biology and stress-resilience data — not on human outcome trials.day 8 if well tolerated and stress / sleep / recovery markers are sub-target. Hormonal effects (GH/LH/ACTH) argue for conservatism.100 µg → 200 µg → 300 µg/day. 300 µg/day is a practice ceiling for this use; there is no human dose-response curve to justify higher.100–200 µg/day within a finite block. Consider 5-on/2-off to limit cumulative exposure of an agent with unmapped long-term endocrine effects.2–4 weeks on / 1–2 weeks off. The geroprotective signal is animal-only (long-term murine lifespan / tumor-rate study) and does not justify indefinite human use.~25 nmol/kg IV. At DSIP's 848.8 g/mol, 25 nmol/kg ≈ 21 µg/kg → ≈ 1.5 mg for a 70-kg adult — roughly 6–15× the SC sleep dose. Doses were given as part of an inpatient detox program.~100–300 µg intranasally per administration in practice-pattern use; no validated human intranasal dose exists. Bioavailability and nose-to-brain transfer are not quantified for DSIP in humans.DSIP is dosed in micrograms. The SC practice band converges on ≈ 1.5–4 µg/kg per dose (≈100–250 µg for most adults). A separate, much higher anchor governs the supervised IV withdrawal model: ~25 nmol/kg ≈ 21 µg/kg ≈ 1.5 mg / 70 kg. All SC values are grade C/D (small-clinical + practice-pattern); the IV anchor is grade C from one open series. None is validated by a modern controlled dose-response trial.
| Band | Per-dose (adult) | ≈ µg/kg | Basis / use | Grade |
|---|---|---|---|---|
| Low (entry) | 100 µg SC | ~1.5 µg/kg | Sensitive individuals, first exposure, sleep onset. Standard starting dose. | C/D |
| Standard | 150–250 µg SC | ~2–3.5 µg/kg | The convergent practice band for sleep and stress / recovery use. Default working range. | C/D |
| High ceiling (SC) | 300–500 µg SC | ~4–7 µg/kg | Upper practice bound; rising next-day grogginess without clear added benefit. Flag >500 µg as off-protocol. | D |
| Clinical IV anchor | ~1.5 mg IV / 70 kg | ~21 µg/kg (25 nmol/kg) | Supervised withdrawal model only (Dick 1984). Not for SC or self-use. | C |
| Body weight | Low | Standard | High ceiling | IV withdrawal anchor (supervised) |
|---|---|---|---|---|
| ~55 kg (120 lb) | 100 µg | 150 µg | 250–300 µg | ~1.16 mg (25 nmol/kg) |
| ~68 kg (150 lb) | 100 µg | 200 µg | 300–400 µg | ~1.44 mg |
| ~82 kg (180 lb) | 150 µg | 250 µg | 400–500 µg | ~1.74 mg |
| ~91 kg (200 lb) | 150 µg | 250 µg | 500 µg (cap) | ~1.93 mg |
| ~105 kg (230 lb) | 200 µg | 300 µg | 500 µg (cap) | ~2.23 mg |
SC weight bands are interpolated from practice-pattern ranges and a µg/kg heuristic; they are not anchored to any human dose-response trial. The IV column reproduces the 25 nmol/kg withdrawal anchor for reference only and applies solely to supervised detox settings. No pediatric DSIP dosing exists — pediatric use is off-protocol by default. DSIP's minutes-long half-life means body weight scales the bolus signal, not a steady-state level.
Generic heuristics mirroring how clinicians titrate CNS-active agents — explicitly marked unvalidated for DSIP. Escalation requires both a response floor (sub-target sleep / stress endpoint) and a safety floor (no flags). Because DSIP effects accrue over a series of doses, do not escalate on a single night. Hard stops are precautionary and reflect regulatory / ethical caution and the absence of long-term human data rather than observed DSIP toxicity.
| Decision node | Rule template (generic — not DSIP-validated) | Grade |
|---|---|---|
| Escalate | If nights_on_therapy ≥ 5–7 at current dose AND no next-day grogginess / headache / mood change AND sleep or stress endpoint below target → step one band (+50–100 µg), not exceeding the 500 µg SC ceiling. | C/D |
| De-escalate | Next-day grogginess, headache, dizziness, vivid/disturbing dreams, or mood change temporally linked to a dose step → return to the prior band, move dosing earlier in the evening, or switch to every-other-night. | D |
| Hold | New or worsening mood instability, daytime sedation impairing function, suspected hormonal symptom, or any planned use with sedatives / opioids / alcohol → hold and reassess; do not stack CNS depressants without supervision. | D |
| Non-response | No benefit after a 2–4-week course at standard dose → stop rather than chase higher doses; the controlled evidence predicts many non-responders. Re-evaluate the underlying sleep / stress diagnosis. | C |
| Permanent stop (hard) | Pregnancy / lactation; minors; active severe psychiatric instability; active substance dependence outside a supervised program; product from an unverified source; patient preference after disclosure. Encode as non-editable red hard-stops. | D |
Special populations — hepatic, renal, elderly, pregnancy: no PK/PD data stratified by organ function exists for DSIP. Small peptides are cleared renally and hepatically; the distinctive consideration is DSIP's broad endocrine reach (GH/LH/ACTH) and unstudied drug interactions with CNS depressants. Conservative default: avoid in pregnancy, lactation, minors, and in anyone on sedatives / opioids without physician oversight.
No DSIP trial defines a validated biomarker endpoint or MCID. Each bundle is imported from the standard of care for the analogous context and flagged validated_for_DSIP = false. The engine drives escalation / de-escalation off the direction of change and whether the borrowed threshold is met — not off any DSIP-specific cut-off. Sleep bundles lean on EEG / actigraphy / scales; the endocrine bundle reflects DSIP's HPA and GH reach.
| Bundle | Labs / tests | Interpretation (borrowed) | Validated for DSIP? |
|---|---|---|---|
| Sleep endpoint | Sleep diary, Insomnia Severity Index (ISI), PSQI, actigraphy; polysomnography (SWS %, sleep efficiency, latency) where available | Track over 2–4 wk; ≥ a few-point ISI drop or improved efficiency = response. Expect modest / variable effects per controlled data; direction of change drives titration. | No |
| HPA / stress (baseline + periodic) | Morning cortisol, late-night / diurnal cortisol, ACTH; perceived-stress scale; optional HRV | Animal data predict ACTH attenuation but a controlled human study showed no CRH-stimulated cortisol change — interpret cautiously and trend rather than spot-check. | No |
| Neuroendocrine (extended) | IGF-1 (GH-pulse proxy), LH / sex-hormone panel if symptomatic, TSH | DSIP's GH / LH effects are animal-derived; obtain only if there is a clinical question. No DSIP-specific thresholds. | No |
| Safety (all routes) | CBC, CMP (LFTs, renal), hs-CRP at baseline and end-of-course | General safety screen; clinically significant abnormality = hold. Borrowed from generic peptide-safety practice. | No |
| Withdrawal (supervised IV only) | COWS / CIWA-Ar, vitals, the detox program's own labs | Symptom-driven titration within a physician-led detox; DSIP is an adjunct hypothesis, not stand-alone therapy. | No |
Architecture note: store each biomarker with a source_context tag and a validated_for_DSIP boolean (currently false across the board). Flip to true only when an actual DSIP trial supports the specific endpoint. The cortisol / ACTH axis is the most mechanistically relevant bundle, but the controlled human CRH result means even that is unproven as a DSIP response marker.
For reference only. Not medical dosing advice. DSIP is dosed in micrograms (µg); common research vials are 2–10 mg. Verify peptide purity (≥98% HPLC), sterility, endotoxin limits, identity, and storage, and use only product from a licensed / verified source for any injection.
DSIP is paired in practice with circadian, sleep-architecture, geroprotective, and recovery agents — and, historically, deployed inside supervised detoxification protocols. No controlled trial has evaluated any DSIP combination; every pairing below is a mechanistic or clinical-reasoning model drawn from DSIP's neuroendocrine, antioxidant, and withdrawal literature, not trial-validated synergy. The defining engine rules: DSIP is a regulator, not a sedative, so it does not reliably add depth to a hypnotic stack; treat any combination with CNS depressants — opioids, alcohol, benzodiazepines, Z-drugs — as additive-risk rather than synergistic; and route all withdrawal and dependence applications through medical supervision, never self-directed.
| Component | Role | Evidence |
|---|---|---|
| DSIP | Delta-EEG / circadian-amplitude regulator | Mixed human (C) |
| Melatonin | Phase-setting · sleep-onset signal | RCTs (A) |
| Combination | Phase + depth circadian model | Mechanistic only (D/P) |
| Component | Mechanism | Status |
|---|---|---|
| DSIP | Delta / circadian regulation | Mixed human (C) |
| Magnesium | NMDA modulation · relaxation | Small RCTs (B/C) |
| Glycine | Core-temp drop · sleep latency | Small RCTs (B/C) |
| Component | Mechanism | Evidence |
|---|---|---|
| DSIP | Pineal NAT · antioxidant defenses | Preclinical (P) |
| Epitalon | Pineal rhythm · telomerase (proposed) | Preclinical (P) |
| Combination | Geroprotective pineal model | No data (P) |
| Component | Role | Status |
|---|---|---|
| DSIP | Delta sleep · sleep-GH coupling | Preclinical / mixed (P/C) |
| Ipamorelin | GHS-R1a agonist · GH pulse | No human RCT (P) |
| Combination | Sleep-driven recovery model | No data (P) |
| Component | Role | Evidence |
|---|---|---|
| DSIP | Withdrawal-symptom attenuation | Open series, n≈107 (C) |
| Detox protocol | Monitoring · symptomatic care | Standard of care (A) |
| Combination | Adjunctive withdrawal model | Uncontrolled (C) |
⛔ CNS-depressant additivity & supervision. Do not self-combine DSIP with opioids, alcohol, benzodiazepines, or Z-drugs outside a supervised setting — DSIP's documented use is inside withdrawal management, and combining a research peptide with active CNS depressants stacks unpredictable additive and sedative risk. DSIP/Emideltide was placed on FDA's significant-safety-risk list partly over potential immunogenicity and the absence of identified safety data, so combination use compounds an already-uncharacterized profile. Because DSIP exerts broad endocrine and antioxidant modulation and carries an unresolved tumor-biology signal, avoid stacking it with other growth-axis or proliferative-signaling agents in anyone with active malignancy or high cancer-risk concern. Any dependence, narcolepsy, or insomnia application belongs with a clinician, not a self-directed stack.
DSIP's safety picture is dominated by what is missing rather than by alarming signals. Across four decades of small studies it has generally been described as well tolerated, with no consistent serious toxicity reported even in the IV withdrawal series. But FDA classed Emideltide as a significant-risk compounding substance citing potential immunogenicity and the fact that no safety-related information had been identified — the defining caveat. There is no modern controlled adverse-event dataset, no validated human PK beyond an extremely short half-life, and no long-term human safety, reproductive, or oncologic data. The honest grade is "apparently benign in short courses, formally uncharacterized."
DSIP has no FDA label, so these are precautionary extrapolations from its endocrine activity, the absence of safety data, and general unapproved-injectable-peptide principles — not label-grade contraindications.
| Condition / factor | Risk level | Applies to | Rationale |
|---|---|---|---|
| Pregnancy | Avoid | All use | No reproductive/developmental data; broad neuroendocrine activity — precautionary absolute. |
| Breastfeeding | Avoid | All use | Unknown excretion and infant exposure; no data. |
| Active malignancy | Caution | All use | Endocrine modulation in active cancer is uncharacterized; an animal tumor signal does not establish human safety. |
| Concurrent CNS depressants (opioids, alcohol, benzodiazepines, Z-drugs) | Caution | All use | DSIP's documented use is inside supervised withdrawal; unsupervised combination stacks additive sedative/CNS risk. |
| Opioid / alcohol withdrawal management | Supervised only | IV / clinical | The withdrawal application is under formal PCAC review and is an inpatient, physician-directed use — never self-directed. |
| Known peptide-drug hypersensitivity | Caution | All use | Potential immunogenicity was FDA's cited concern; prior peptide reactions warrant avoidance. |
| Minors / adolescents | Avoid | All use | No pediatric safety data; developing neuroendocrine axis. |
| Competitive athlete / tested pool | Caution | All use | Not named on the WADA list, but as an unapproved substance it may fall under the S0 catch-all and research-grade products risk contamination — treat as high-caution, not cleared. |
| Reliance on research-grade product | Caution | All use | Variable purity/sterility; source verification essential for any injectable use. |
Sleep assessment (ISI / PSQI ± actigraphy or PSG where available); cortisol / ACTH if endocrine effects are a concern; CBC / CMP; pregnancy test if reproductive potential; malignancy history review. Confirm product source / purity.
Symptom / sleep diary; watch for headache, daytime sluggishness, mood or sleep-quality change. Injection-site review and site rotation each administration.
Optional periodic cortisol / ACTH, IGF-1, LH, TSH if a hormonal effect is suspected or a GH-axis agent is co-used — interpret cautiously given conflicting human endocrine data.
COWS (opioid) or CIWA-Ar (alcohol) symptom scales, vitals, hydration, and standard detox monitoring — within an inpatient, physician-run protocol only.
hs-CRP and CBC/CMP if longer or repeated courses are pursued; no validated DSIP-specific biomarker exists, so these are general-safety, not response, markers.
Any systemic hypersensitivity, new neurological or mood symptoms, pregnancy, suspected product-quality problem, or — in a withdrawal setting — clinical deterioration. Discontinue and reassess; there is no validated long-term protocol.
DSIP's evidence base is the inverse of its evocative name. The discovery work and animal mechanism studies are genuine and repeatedly cited, but the controlled human sleep evidence is small and, where best-blinded, near-null. The most striking human signal is in withdrawal, not sleep — and it is an uncontrolled open series. Below is the pivotal record: discovery, the 1980s clinical sleep series, the decisive double-blind result, the withdrawal data, and the preclinical mechanism studies that keep the molecule interesting.
The founding paper: DSIP was isolated and characterized from the cerebral venous blood of rabbits during low-frequency ('hypnogenic') thalamic stimulation, defining the WAGGDASGE nonapeptide and its delta-EEG-promoting activity on intraventricular infusion. It established the molecule, its sequence, and the original "delta sleep" framing that the name still carries.
Clinical study of DSIP in chronic insomnia describing improved sleep and a regulatory rather than sedative effect. Together with the companion open trial — a series of 10 DSIP injections in 7 patients with severe insomnia, with sleep normalized in all but one case over 3–7 months of follow-up and improved daytime mood — it represents the optimistic early-1980s clinical signal, all of it uncontrolled.
The most rigorous controlled DSIP sleep trial: under proper blinding in chronic insomniac patients, the sleep effects shrank to near-null on most measures. This is the result that defines the gap between the peptide's name and its controlled human evidence, and is reinforced by a short-term study in chronic insomniacs reporting only limited therapeutic benefit. The honest read: the controlled sleep case is weak.
An open clinical series of ~107 patients in which intravenous DSIP (≈25 nmol/kg) improved or cleared withdrawal symptoms in roughly 97% of opioid-dependent and 87% of alcohol-dependent patients, with rapid relief of somatic signs and anxiety. It is DSIP's strongest historical efficacy signal and the empirical root of the current PCAC opioid-withdrawal review — but it is open-label, decades old, and never replicated in a modern controlled trial.
Intranasal DSIP at 120 µg/kg, given before middle-cerebral-artery occlusion and for 7 days after reperfusion, significantly improved rotarod motor recovery in rats; infarct volume trended smaller but was not significantly reduced. A modern, methodologically cleaner preclinical signal — and a demonstration that a non-injection route can deliver a functional effect — keeping the neuroprotection thread alive alongside antioxidant work showing DSIP raises SOD, catalase, and glutathione-system activity and modulates mitochondrial enzymes under stress.
A clinical review summarizing DSIP's sleep-promoting (vs sedative) profile, neuroprotection, stress attenuation, and withdrawal use — and noting the controlled study in which ACTH and cortisol responses to CRH were identical on DSIP and placebo, the principal caveat against direct HPA-axis suppression. Read alongside the standard reviews — Graf & Kastin's comprehensive synthesis of distribution, endocrine actions, and stress protection and work showing DSIP raises hypothalamic substance-P and behavioral stress resistance in rats — it frames DSIP as a real but small, multifunctional neuromodulator rather than a proven hypnotic.
A polygraphically controlled inpatient case: a 47-year-old woman with chronic delayed-sleep-phase insomnia and low-dose benzodiazepine dependence advanced her main sleep phase by ~5 hours, achieved abrupt complete benzodiazepine withdrawal, and restored a normal sleep profile sustained on follow-up. A single case, but a vivid illustration of the circadian-amplitude and dependence-bridging effects that recur in the DSIP literature.
Overall evidence strength for human use is LOW to very low. The discovery and mechanistic work is real and repeatedly cited, and there are intriguing preclinical signals in neuroprotection, antioxidant defense, and stress resilience. But the best-controlled human sleep trial was near-null, and the strongest efficacy signal — withdrawal — rests on an uncontrolled 1980s open series. The missing pieces are decisive: modern double-blind RCTs, validated human PK and dosing, a formal safety and immunogenicity dataset, and reproductive/oncologic data. This is why the dosing protocols above are framed as a practice-pattern / historical-evidence layer, not a validated clinical regimen — and why the July 2026 PCAC review will be a genuine inflection point for the molecule's legal and evidentiary status.
| Parameter | DSIP | Melatonin | Epitalon | Z-drugs / benzodiazepines |
|---|---|---|---|---|
| Class | Endogenous nonapeptide (WAGGDASGE) | Endogenous indoleamine hormone | Synthetic tetrapeptide (AEDG) | Small-molecule GABA-A modulators |
| Primary frame | Delta / circadian regulator; withdrawal adjunct | Circadian phase / sleep-onset signal | Pineal rhythm · geroprotection | Hypnotic sedation |
| Mechanism on sleep | Modulator, not sedative | Phase-setting via MT1/MT2 | Indirect (pineal melatonin rhythm) | Direct CNS depression |
| Best human evidence | C — mixed; double-blind near-null | A — multiple RCTs / meta-analyses | P/C — mostly Russian preclinical/clinical | A — extensive RCTs |
| Half-life | Very short (~minutes; aminopeptidase) | ~30–60 min | Short | Hours (agent-dependent) |
| Dependence / hangover | Low reported; used in withdrawal | Very low | Very low | ⚠ Dependence + next-day impairment |
| Distinct non-sleep signal | Withdrawal, neuroprotection, anti-stress | Antioxidant; limited | Telomerase / longevity (proposed) | None therapeutic |
| FDA status | ❌ Not approved · PCAC review July 2026 | ✅ OTC supplement (US) | ❌ Not approved | ✅ Approved (Rx, scheduled) |
| Doping status | S0 catch-all risk (not named) | Permitted | S0 catch-all risk (not named) | Permitted (some monitored) |