Noopept

Areas of active research — not promised effects

Each tag links to other compounds with research into that goal. Research use only: these are areas of study, not human-use claims.

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Noopept is not FDA-approved and is not classified as a controlled substance under the Controlled Substances Act. The FDA treats it as an unapproved new drug (a piracetam analog / Active Pharmaceutical Ingredient) and has issued import alerts against it. It cannot lawfully be marketed as a dietary supplement, food ingredient, or drug for human use. It is not on the FDA Category 2 'do not compound' list (fda19 = false), but it is also not on the Category 1 authorized compounding list; no compounding authorization exists. Sale for in vitro / laboratory research purposes only.

Transparent blend · bci-1.0 · never paid-placement

Primary name

Noopept

Origin

Fully synthetic compound developed in Russia at the Zakusov Institute of Pharmacology, designed as a stabilized analog of the endogenous neuropeptide cycloprolylglycine. It bears a phenylacetyl group and a prolylglycine ethyl ester backbone and is approved as a prescription nootropic in Russia (INN: omberacetam) for vascular and traumatic cognitive disorders.

Registry IDs

PubChem CID

180496

CAS

157115-85-0

InChIKey

PJNSMUBMSNAEEN-AWEZNQCLSA-N

DrugBank

DB19956

ChEMBL

CHEMBL4303687

Molecular formula

C17H22N2O4

Molar mass

318.4 g/mol

Monoisotopic

318.15795719 Da

InChIKey

PJNSMUBMSNAEEN-AWEZNQCLSA-N

Appearance

White to off-white crystalline powder

Solubility

Poorly soluble in water; soluble in ethanol and DMSO; solubility in aqueous medi…

Sequence not available in current seed.

Stability: Susceptible to hydrolysis of the ethyl ester moiety under aqueous conditions; hydrolysis yields the active metabolite cycloprolylglycine. Stability is reduced i

Vial sizes

null mg · 10 mg

Purity grades

≥98% HPLC / ≥99% HPLC

Salt forms

Free base (primary)

• GHS hazard class on file
• PPE & spill response
• Disposal guidance
• Not-for-human-consumption posture

How much research exists, and of what maturity — never a verdict on whether it works.

Mechanism of action

• Noopept acts primarily as a prodrug: after oral or parenteral administration it is rapidly hydrolyzed to its active metabolite cycloprolylglycine, which functions as a positive allosteric modulator of AMPA-type glutamate receptors and activates TrkB signaling downstream of BDNF
• In rodent hippocampus, both acute and repeated administration have been associated with increased mRNA expression of NGF and BDNF, supporting synaptic plasticity and neuronal survival
• Additional mechanistic actions documented in preclinical models include inhibitory modulation of α7 nicotinic acetylcholine receptors on hippocampal GABAergic interneurons (PMID 36195298), attenuation of TRPV1 calcium channel activity with consequent reduction of oxidative hippocampal stress (PMID 34241806), and neuroprotective effects against amyloid-beta-induced tau hyperphosphorylation and apoptosis in cell-culture Alzheimer's models
• The parent compound itself may also modulate HIF-1 transcription factor activity and exhibits direct antioxidant and anti-inflammatory properties independent of cycloprolylglycine

Pharmacokinetics (ADME)

Half-life

~15–20 minutes (parent compound, estimated from rodent data; formal human PK characterization not published as of 2026)

PK–PD note: Oral bioavailability is approximately 10% due to extensive first-pass hydrolysis by hepatic esterases and peptidases. The active metabolite cycloprolylglycine has a longer plasma residence time than t…

Reading the evidence

• Evidence quality and gaps vary by application — see the cited grades above.
• Indexed-article counts span all evidence tiers, not only completed human trials.
• No first-party human-dosing, efficacy, or benefit claims are made here.

Key reviews & evidence-gap sources

• Vakhitova et al. 2016 — Molecular Mechanism Underlying the Action of Substituted Pro-Gly Dipeptide Noopept (Acta Naturae 8(1):82-89; PMID 27099787) — A >100-receptor panel (run by CEREP) did NOT identify a confirmed direct receptor target; molecular docking instead proposes Noopept (and its active L-phenylacetylprolylglycine metabolite) inhibits prolyl hydroxylase 2 (PHD2), stabilizing HIF-1α, which the authors call the likely primary mechanism. [Verification: the widely-repeated 'confirmed AMPA/NMDA modulation' claim is unconfirmed lore — glutamate receptors fell within the negative panel; PHD2 binding is docking-proposed, not definitively proven.]
• Alzheimer's Drug Discovery Foundation — Cognitive Vitality "Noopept" evidence report (updated Mar 20, 2020) — Independent, non-commercial secondary synthesis: 'little clinical evidence supports its use.' Logs the Neznamov/Teleshova study as an OPEN-LABEL clinical study and flags that nearly all preclinical work comes from a single laboratory using non-standardized animal models.
• Neznamov & Teleshova 2009 — comparative Noopept vs piracetam in mild cognitive disorders (Neurosci Behav Physiol 39(3):311-21; DOI 10.1007/s11055-009-9128-4; Engl. translation of the 2008 Russian original) — The principal published human study — an OPEN-LABEL, active-comparator (piracetam) design, NOT placebo-controlled, NOT blinded, NOT registered; ~53 patients total (Noopept arm ~31), 20 mg/day (10 mg BID) for 56 days; MMSE improvement reported. [Verification: the PubMed record has NO abstract, so design specifics are cited from the Springer full text + independent reviews (ADDF / Examine), not the abstract-less PMID page; PubMed classifies it 'Comparative Study', not an RCT.]
• Noopept in mild cognitive impairment after stroke (Zh Nevrol Psikhiatr Im S S Korsakova 2011;111(10 Pt 1):44-6) — Independent OPEN prospective study, n=60 stroke patients, 20 mg/day; cognitive improvement reported vs an unchanged comparison group at 2 months. Open/uncontrolled — not randomized, not registered.
• Neznamov et al. 2008 — clinical and EEG characteristics of Noopept in mild cognitive impairment (Zh Nevrol Psikhiatr Im S S Korsakova 108(11):47-54) — Companion EEG sub-analysis of the same open-label cohort; nootropic-pattern EEG shifts (increased alpha/beta, reduced delta), most pronounced in vascular-origin patients. Not a registered trial.

No registered human trials found for this compound.

Status

No registered trials found

Summary (literature)

In the principal Russian clinical observation (n=31, 20 mg/day for 56 days), the most frequently reported adverse effects were elevated blood pressure (7/31, 22.6%), sleep disturbance (5/31, 16.1%), and irritability (3/31, 9.7%); no treatment discontinuations were reported. Precl…

WADA status

Not specifically listed on the WADA 2026 Prohibited List. Noopept (omberacetam) does not appear to fall under currently defined prohibited categories (peptide h…

Dominant research route: Oral (peroral) is the dominant marketed and studied human route — Noopept is formulated as a 10 mg oral tablet in Russia (see below), and the core human/PK literature is built around oral (and IV) dosing. In rodent laboratory pharmacology, intraperitoneal injection is the dominant systemic route; intranasal has been compared to intraperitoneal in two mouse studies. Sublingual and human intranasal ('nasal spray') use are commercially marketed and community-reported but have no dedicated pharmacokinetic study in any species. [Verification corrected: the Russian tablet is OVER-THE-COUNTER, not prescription — see the Oral route note.]

Rat oral-dosing PK established GI absorption and BBB penetration (Boiko et al. 2000). A rat–rabbit–human interspecies PK comparison examined oral/IV dosing and reported human elimination as slower and more variable than in rats/rabbits, with no parent-drug metabolites detected in human plasma. A 2009 Russian OPEN-LABEL comparative study (Neznamov & Teleshova) dosed patients with mild vascular/traumatic cognitive complaints on oral Noopept vs. piracetam; PubMed classifies it 'Comparative Study', NOT a randomized/blinded RCT. Noopept is also marketed as an OVER-THE-COUNTER oral 10 mg tablet in Russia (ГРЛС reg. ЛС-001577; manufactured by CJSC LEKKO; marketing-authorization holder Otisifarm PAO) — a foreign marketing authorization, not FDA approval.

Bioavailability: Preclinical rat values (RUO, not human PK): at 50 mg/kg oral in rats, secondary summaries citing Boiko et al. 2000 report serum Tmax ~7 min (0.116 h), Cmax ~0.82 µg/mL (with near-identical brain levels ⇒ rapid BBB equilibration), oral bioavailability of the parent compound ~10% (first-pass metabolism), and a short rat half-life (~16 min). [Verification: these numbers are secondary-sourced (peptideinsight.com, corroborated by Examine.com) attributing to the paywalled Boiko 2000; the PubMed abstract independently confirms ONLY the qualitative GI-absorption/BBB finding. Always dose-qualify (50 mg/kg) and label rat/preclinical.] The interspecies study reports progressively slower elimination rat → rabbit → human with large individual variability in humans.

The only route with both formal PK characterization (animal) and a completed, published human comparative study; described from the literature's own study design, not as a dosing recommendation.

No dedicated pharmacokinetic or clinical study of sublingual Noopept was found. Sublingual dosing (powder held under the tongue) is a community- and content-site-promoted variant of oral use, not a route examined in any published pharmacology paper located this pass.

Bioavailability: Community/content-site sources claim faster onset and higher bioavailability from bypassing first-pass hepatic metabolism, but cite no pharmacokinetic study — the claim is reasoned from general absorption theory, not measured for Noopept specifically.

A community-promoted variant of oral administration; framed here as reported claims, not an established pharmacokinetic property or a protocol.

Minimal formal study: two published mouse behavioral/receptor-pharmacology papers (BALB/c and C57BL/6) dosed noopept 1 mg/kg/day intranasally vs. intraperitoneally for 5 days, comparing anxiolytic/nootropic endpoints and cortical GABA-A receptor density. No pharmacokinetic study of intranasal Noopept exists in any species. Separately, it is widely sold to humans as an unapproved 'research' nasal spray by US vendors.

Bioavailability: No published pharmacokinetic data exist for intranasal Noopept in any species — the mouse papers measured behavior and receptor density, not plasma/brain kinetics. The vendor/community 'nose-to-brain' rationale used to market nasal-spray products is extrapolated from other molecules and has not been demonstrated for Noopept.

Predominantly a marketed/community route in humans (nasal-spray products sold as research chemicals); the limited animal work assessed behavior and receptor density, not kinetics, and establishes neither human nasal absorption nor a benefit.

The dominant systemic dosing route in rodent laboratory pharmacology — used across memory, anxiolytic, neuroprotection and receptor-density studies in rats and mice (commonly ~0.5–1 mg/kg/day). Not a human administration route.

Bioavailability: Used as a laboratory dosing route for efficacy/behavioral endpoints rather than characterized in a dedicated IP pharmacokinetic study. A direct intraperitoneal-vs-intranasal comparison in BALB/c mice found IP dosing produced a stronger anxiolytic behavioral effect while intranasal produced a stronger nootropic behavioral effect.

A laboratory-animal administration route, cited only to describe how preclinical pharmacology/behavior studies were conducted; no human dosing implied.

Characterized in rat and rabbit pharmacokinetic studies, including a lyophilized (mannitol-based) IV formulation developed and evaluated in rats as a potential future medicinal preparation. Also the reference route in the rat–rabbit–human interspecies-comparison literature. Not a marketed human route — clinically Noopept is sold to humans only as oral tablets/capsules (plus unapproved nasal-spray research products).

Bioavailability: 100% bioavailable by definition in the species dosed. Very intensive metabolism was observed after IV dosing in rats, forming a hydroxylated (phenyl-ring) metabolite not seen in rabbits, which showed slower biotransformation and longer circulation of unchanged drug; the interspecies literature reports progressively slower elimination rat < rabbit < human, though no confirmed human IV PK dataset was located.

An investigational/laboratory route — the lyophilized IV form was developed and characterized in rats as a candidate future medicinal preparation, not a marketed human product.

Animal & human figures are kept visibly separate so studied animal doses are never misread as human guidance.

Sorted A–Z by vendor — never by price

Weekly median $/mg from the live vendor crawl.

Researched storefront prices, bucketed

p25 $0.002 · median $0.003 · p75 $0.107 · 7 researched vendors

Legit, COA-backed band: $0.002–$0.005/mg.

Value rule: don't just buy the cheapest — a price under $3/mg is a red flag. Pair price with COA and independent-test grade.

Estimated cost of research (10 mg)

Vial (best researched price)

$0

Bacteriostatic water (generic estimate)

$6

Syringes / supplies (generic estimate)

$12

What each test proves — general guidance, plus this compound's researched purity data

Purity on the current market (researched)

US vendor pages near-universally advertise ~98–99%+ HPLC purity/identity claims for Noopept (CAS 157115-85-0) — e.g. Chemyo, Nootropic Source, PureRawz, Limitless — several naming Janoshik as an independent verifying lab. No independent cross-vendor purity aggregate (the Finnrick / MZ Biolabs kind used for injectable research peptides) was located specifically for Noopept this pass; Noopept was NOT among the 10 compounds in the Jan-2026 MZ Biolabs / thepeptidelist.com investigation (confirmed by direct check). The one independent peer-reviewed analytical dataset located (Cohen et al. 2021, LC-QTOF-MS) measured delivered-dose accuracy rather than chromatographic purity — see underdosingNote.

Independent labs cited for this compound

No product recall specific to Noopept was found (2019–2026 search window). As an ingredient sold outside the regulated dietary-supplement/drug supply chain and treated by FDA as an unapproved new drug, enforcement has taken the form of warning letters, import controls and importer debarment rather than a Class I/II/III recall. Reported honestly as an empty recall result, not invented.

Buyer red-flag checklist

• Marketing that claims or implies FDA approval, dietary-supplement/GRAS status, or disease-treatment/cognitive-therapy benefits — the exact pattern cited in the 2019 (Peak Nootropics) and 2022 (Crystal Clear Supplements) FDA warning letters.
• No current, batch-matched third-party COA verifying both identity (CAS 157115-85-0) and purity provided on request.
• Undisclosed 'proprietary blend' dosing that conceals the actual per-serving omberacetam amount — the labeling-accuracy failure mode documented by Cohen et al. 2021.
• Injectable-format or reconstitution-instruction listings for Noopept — an orally-active small molecule, not an injectable peptide; buyer guides flag this framing as atypical.
• Price far below the prevailing market band for the stated purity/quantity, consistent with an underfilled or off-spec product.

GMP vs research-grade: the chemistry (SPPS + HPLC + MS) is identical — the difference is the quality system.

Underdosing / mislabeling: From the only independent analytical dataset located: Cohen et al. 2021 (Neurol Clin Pract, LC-QTOF-MS) purchased 10 commercial products declaring omberacetam (Noopept) and detected it in all 10, at 5.1–40.6 mg/serving against a ~10 mg pharmacologic reference dose (up to ~4× over). Across the declared unapproved-drug ingredients in that sample, 9 of 12 (75%) declared quantities were inaccurate, spanning 0–135% of the labeled amount. The study did NOT publish an omberacetam-isolated breakdown, so this is reported at the whole-sample level, not isolated to Noopept — flagged for human review. Direction skews toward over-labeling/mislabeling more than pure underdosing, but the field covers 'underdosing/mislabeling' jointly.

• FDA Import Alert 66-66 authorizes detention-without-physical-examination of bulk drug substances (APIs) that appear misbranded under FD&C Act §502(f)(1) / 21 CFR 201.122 because they fail the labeling exemption for research/industrial (non-human-use) chemicals — an API is released only when tied to an approved/pending NDA/ANDA/BLA/IND, and an RUO 'not for human consumption' label is not itself an exemption. Its application to omberacetam/Noopept (as a piracetam-family unapproved-new-drug API) is corroborated via Wikipedia's citation of the alert plus FDA's parallel §502(f)(1) charge against Noopept in the 2019 Peak Nootropics warning letter — but NOT via a directly-verified Red-List entry naming omberacetam (the live accessdata page and Red List could not be opened this pass). Flagged for human re-confirmation against a current FDA source before publish.66-66 (misbranded-API detention; specific omberacetam attribution unconfirmed)
• An RUO label is not an import exemption — CBP judges actual intended use.
• Lyophilized powder is ambient-stable in transit; temperature control needed for > 7-day transit.
• US-warehouse vendors dodge import scrutiny — they cost more but ship more reliably.

Every item dated & sourced

Not listed by name on the WADA Prohibited List (2026 or earlier), USADA's list, or GlobalDRO. It is structurally/pharmacologically related to phenylpiracetam (carphedon), which is explicitly prohibited under S6 (stimulants); consequently noopept could in principle be captured by the List's catch-all 'similar chemical structure or biological effect(s)' provision — but WADA has issued no explicit ruling or schedule tag naming it, and it is not a routine testing target. Its framing as a potential clandestine doping agent derives from anti-doping/industry commentary (Banned Substances Control Group; a 2023 Drug Testing and Analysis review by Jedrejko et al.), NOT an official WADA determination. Sporting status is separate from jurisdiction-specific legal status (e.g. controlled in Hungary since 2020; unscheduled in US/Canada).

No granted patents identified in current seed. Composition-of-matter coverage is limited given the peptide's synthetic origin.

• IACUC / IRB research context
• RUO buyer responsibilities & documentation
• Veterinary / alternative-use where lawful
• Jurisdiction-aware "who may lawfully obtain"

What people discuss

Reported concerns — discussion, not established effects

Reading caveats

• Self-experimentation confounding — individual reports carry no blinding or placebo control.
• Survivorship / positivity bias — dramatic 'game changer' stacking posts over-shared vs quiet non-responders.
• Vendor-affiliate 'best nootropic' / 'where to buy' blog content blends into organic community tone reads.
• Non-responder vs counterfeit-product ambiguity — 'felt nothing' reports conflate true non-response with fake/underdosed material.
• Skeptic / mainstream-media framing (e.g. 'Genius pill or placebo?') pulls some video-platform tone toward neutral rather than purely positive.
• Individual-variation is repeatedly self-reported as a confound by the sources themselves, not resolved by any blinded comparison.

Manually researched from reddit, youtube— theme weights are research estimates, not live counts; aggregated & de-identified. No individual posts, quotes, or usernames are ever shown.

Relative research / market volume — populated once the activity stream is wired

Inline tooltips for lyophilized, RUO, EU/mg, SPPS, 503A and more.

Toggle plain-language ↔ scientific in the header.

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Synthetic dipeptide prodrug of cycloprolylglycine studied for cognitive enhancement and neuroprotection; approved in Russia, RUO in most other jurisdictions. Approximately 83 articles are indexed (literature last scanned 2026-05-29). US regulatory status: Unapproved new drug — Research Use Only. Research use only.

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