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Noopept

An orally active dipeptide nootropic registered in Russia that raises NGF and BDNF in the hippocampus and is used for memory, attention and post-injury cognitive recovery.

Also known as omberacetam, N-phenylacetyl-L-prolylglycine ethyl ester, Noopeptum, Noopept, GVS-111

Human trials — Studied in people, typically early phase or small — promising rather than proven.

Noopept is a registered prescription drug in Russia with a published comparative trial against piracetam in mild cognitive disorders of vascular and post-traumatic origin, showing at least equivalence at a fraction of the dose. The trials are small, Russian, and largely conducted by the developers. The NGF/BDNF mechanism is solid rodent work. No Western regulator has evaluated it.

How it works

Noopept was designed as a dipeptide analogue of piracetam and is roughly a thousand times more potent by weight. After oral dosing it is rapidly hydrolysed to cyclo-prolylglycine, a neuropeptide that occurs naturally in the brain and modulates AMPA and NMDA receptor function. Ostrovskaya's group showed chronic dosing increases NGF and BDNF mRNA in rat hippocampus, which distinguishes it from the classical racetams. It also shows antioxidant activity, reduces excitotoxicity, and has anxiolytic effects in rodents at low doses. The subjective profile in people is mild - most of its Russian clinical use is in mild cognitive impairment and post-concussion asthenia, not as a performance enhancer.

Targets: NGF expression, BDNF expression, AMPA and NMDA receptor modulation, Cycloprolylglycine system

Dosing

ProtocolDoseFrequencyRoute
Standard oral protocol (matches the Russian label)After meals, with the last dose no later than mid-afternoon - it can interfere with sleep.10 mg – 30 mg10 mg two or three times dailyoral
Sublingual protocolAs above.5 mg – 20 mgone to three times dailysublingual
  • · The Russian registration is 10 mg twice daily for 1.5-3 months, increased to 30 mg/day if needed. Higher is not better; above about 40 mg/day people commonly report headache and irritability.
  • · Bypasses some first-pass metabolism, so the effective dose is lower and onset faster. Tastes foul.

Titration

Start at 10 mg once daily for a few days. A meaningful minority of people find Noopept makes them irritable and headachy at any dose, and that shows up quickly.

Cycling

The Russian label runs 1.5-3 months continuously, then a break of at least a month, with courses repeatable after 30 days. Most users cycle far shorter than that.

Work out your exact syringe units →

Pharmacology

Half-life
Parent compound is cleared within roughly half an hour; the active metabolite cycloprolylglycine persists considerably longer and carries most of the effect.
Onset
Acute effects on clarity within 15-30 minutes; the memory and mood benefits described in Russian trials take 2-4 weeks of continuous dosing.
Routes
oral, sublingual, intranasal
Molecule
Synthetic dipeptide ester (proline-containing, piracetam-derived design)
Sequence length
2 amino acids
Molecular weight
318.4 Da

Handling

Diluent
Not applicable - taken as a tablet, capsule or weighed powder
Lyophilised
Powder kept cool, dry and sealed; it is hygroscopic and will clump.
Reconstituted
Volumetric solutions in water or propylene glycol should be refrigerated and used within a few weeks.

Intranasal — usable, with a caveat

Usually taken orally, since it is a small dipeptide derivative with real oral activity - the nasal route is a grey-market preference rather than a formulation designed for it. Nasal dosing gives a faster onset and is described as harsher on the mucosa; there is no human pharmacokinetic data comparing the two routes.

Mixing

Bulk powder is dosed in single-digit milligrams and is essentially impossible to eyeball accurately. Use a milligram scale or make a volumetric solution; guessing a 10 mg dose from a scoop is how people take 60 mg by accident.

Side effects

  • commonHeadache— The single most reported side effect; often responds to lowering the dose or adding choline.
  • commonIrritability or restlessness
  • commonInsomnia if dosed late
  • uncommonIncreased blood pressure— The Russian label flags caution in uncontrolled hypertension.
  • uncommonFatigue or brain fog on prolonged high dosing
  • rareAllergic reaction

Do not use if

  • Pregnancy and breastfeeding - contraindicated on the Russian label.
  • Severe hepatic or renal impairment.
  • Uncontrolled hypertension - it can raise blood pressure.
  • Lactase deficiency or galactose intolerance if using the Russian tablets, which contain lactose.

Combining it

  • cautionsemax — Both raise BDNF/NGF and both are stimulating; the combination is a common cause of headache.
  • synergycerebrolysin — Standard Russian pairing in post-stroke and post-TBI cognitive rehabilitation.
  • synergyselank — Selank offsets the irritability and overstimulation Noopept can cause. A well-worn combination.

What to monitor

  • · Check blood pressure if you have any history of hypertension.
  • · No routine bloodwork is established.

Legal status

Registered prescription medicine in Russia. Sold as a dietary supplement or research chemical in the US; classified as a medicine and not legally sold as a supplement in the UK, EU, Canada and Australia.

References

  • Neznamov & Teleshova 2009, comparative studies of Noopept and piracetam in mild cognitive disorders, Neuroscience and Behavioral Physiology (trial)
  • Ostrovskaya et al. 2008, the nootropic and neuroprotective proline-containing dipeptide Noopept restores spatial memory and increases NGF and BDNF expression (preclinical)

Mechanism in depth

Noopept is best understood as a delivery vehicle for an endogenous molecule. Cycloprolylglycine occurs naturally in mammalian brain, and what Noopept does is flood the system with it after oral dosing. CPG modulates AMPA and NMDA receptor function, which is the acute mechanism and explains the fast, mild clarity effect people describe within half an hour - it is a glutamatergic modulation, not a neurotrophic one. The neurotrophic arm is separate and slower: chronic dosing increases NGF and BDNF mRNA in rat hippocampus, which is what distinguishes Noopept from the classical racetams it was designed from and what the Russian claims about mild cognitive impairment rest on. Those two mechanisms operate on completely different timescales and account for the compound's odd clinical profile - something you feel a little of immediately and that the trials say takes 4-8 weeks to do anything meaningful. There is also documented antioxidant activity, reduced excitotoxicity, and anxiolytic effects in rodents at low doses. The honest framing is that Noopept is a genuinely well-characterised molecule by the standards of this class, with a plausible mechanism, real registration and a comparative human trial, and that what it does in a healthy person with no cognitive impairment is a different question that has not been answered.

What usually goes wrong

The most dangerous failure with Noopept has nothing to do with pharmacology - it is the scale. Doses are single-digit to low-double-digit milligrams, bulk powder is sold by the gram, and a 10 mg dose is physically almost invisible. People eyeball it from a scoop and take 60 mg by accident. Use a milligram scale or make a volumetric solution, and treat this as a non-negotiable rather than fussiness. Second, headache: it is common, it is the usual reason for discontinuation, and adding choline or lowering the dose fixes it more often than not. Third, the timing error - Noopept interferes with sleep and the last dose needs to be mid-afternoon at the latest. Fourth, the expectation error, which is the biggest one: the Russian clinical data are in people with mild cognitive impairment from vascular disease or head injury, over 1.5 to 3 month courses, with modest effect sizes. A healthy 30-year-old taking it for a week and expecting a stimulant is testing a hypothesis nobody has published. Fifth, and worth knowing: Noopept is a medicine, not a supplement, in the UK, EU, Canada and Australia, and importing it there is a legal problem regardless of how it is marketed in the US.

Titration ladder

  1. 10 mgDays 1-4 — 10 mg once daily after a meal, in the morning. A meaningful minority of people get headache and irritability from Noopept at any dose, and that reveals itself in the first few days.
  2. 20 mgDays 5-14 — 10 mg twice daily - morning and early afternoon. This is the Russian registered dose and where most of the clinical evidence sits. Last dose by mid-afternoon; it interferes with sleep.
  3. 30 mgWeek 3 onward — 10 mg three times daily, the label maximum, used if 20 mg/day has been inadequate after two weeks. The registered course runs 1.5-3 months at this level.
  4. 40 mgNot recommended — Included as a ceiling marker, not a step. Above roughly 40 mg/day the reliable findings are headache and irritability rather than added benefit. There is no evidence supporting higher dosing and good anecdotal reason against it.

Bloodwork worth running

MarkerWhenWhy it matters
Blood pressureBaseline, then daily for the first week, then weekly. Measure at the same time of day relative to your dose.This is the one monitoring item on Noopept with a real basis. The Russian label explicitly cautions in uncontrolled hypertension, and raised blood pressure appears in its adverse-effect profile. It is also the compound in this class most likely to be taken by someone middle-aged with untreated hypertension for cognitive complaints.Act if: A sustained rise of more than 10 mmHg systolic means stop. If your baseline is already above 140/90, treat the hypertension before you treat the cognition.
ALT, AST and creatinineBaseline and at the end of a 6-12 week course.The Russian label contraindicates severe hepatic and renal impairment, and Noopept is taken orally for 1.5-3 months at a stretch, which is far longer than most compounds in this class. Anyone running a full label-length course should know their baseline organ function.Act if: Transaminases above twice the upper limit of normal, or a meaningful fall in eGFR, mean stop and investigate.
An objective cognitive or output measureBaseline, then at 4 and 8 weeks.The Russian trial data are in mild cognitive disorders of vascular and post-traumatic origin, not in healthy performance enhancement, and the effects took weeks to emerge. Anyone using it for the latter is running an experiment with no published prior, and needs a measurement to interpret it.Act if: No measurable change at 8 weeks means stop rather than escalate. Above roughly 40 mg/day people commonly get headache and irritability with no additional benefit.

Pharmacokinetics

Tmax
0.25 h
Crosses blood-brain barrier
yes
Metabolism
Rapid hydrolysis of the ethyl ester and the phenylacetyl group to yield cyclo-prolylglycine (cycloprolylglycine, CPG), an endogenous brain neuropeptide that carries most of the activity. This is a prodrug relationship in everything but name, and it is why the parent's half-life of around 30 minutes tells you almost nothing about the duration of effect.
Elimination
Renal, following hydrolysis. Phenylacetic acid is a metabolite of the phenylacetyl group and is excreted conjugated.

Receptor targets

  • AMPA receptors (via cycloprolylglycine) — Modulatory rather than a direct binding interaction; no affinity constant published

    Altered AMPA receptor function is the proposed substrate for the acute clarity effect within 15-30 minutes.

  • NMDA receptors (via cycloprolylglycine) — Modulatory; not quantified

    Contributes to reduced excitotoxicity and to the neuroprotective effects in ischaemia and beta-amyloid injury models.

  • NGF expression — Indirect - transcriptional

    Increased NGF mRNA in rat hippocampus after chronic dosing. Part of what separates Noopept from piracetam mechanistically.

  • BDNF expression — Indirect - transcriptional

    Increased BDNF mRNA in rat hippocampus after chronic dosing, alongside restored spatial memory in impaired animals.

Trials

  • Comparative study of Noopept and piracetam in mild cognitive disorders of vascular and post-traumatic origin (Neznamov & Teleshova) Comparative clinical trial · 8 weeks · 2009

    Cognitive and asthenic symptom improvement in patients with mild cognitive disorders in organic brain disease of vascular and traumatic origin, comparing Noopept 20 mg/day against piracetam 1200 mg/day. The authors reported Noopept at least equivalent to piracetam at a fraction of the dose, with earlier onset of effect on anxiety and asthenia. Conducted by the developing institute, Russian-language, and never independently replicated in the West.

What to expect, and when

15-30 minutes to a mild subjective clarity effect after an oral dose, faster sublingually. The parent compound is cleared within roughly half an hour and the active metabolite carries the effect for several hours. The acute effect is genuinely mild - people expecting a stimulant consistently report nothing. The memory and mood benefits described in the Russian trials take 2-4 weeks of continuous dosing to appear and the registered courses run 1.5-3 months, with a break of at least a month afterwards. Headache, if it is going to happen, shows up in the first three days. Most users cycle far shorter than the label, typically 4-8 weeks.

Stacking and comparisons

Choline is the stack that actually matters, and it is a practical rather than a mechanistic point: headache is the single most reported side effect of Noopept, it responds in a large fraction of people to adding a choline source such as alpha-GPC or CDP-choline, and it is the reason most people quit the compound. Try that before abandoning it. The Cerebrolysin pairing is standard Russian practice for post-injury cognitive rehabilitation and has tradition rather than trial data behind it. Selank offsets the irritability and overstimulation that is Noopept's other main failure mode, and that combination is well worn and sensible. The one to avoid is Semax or any of its analogues: both raise BDNF and NGF, both are stimulating, the mechanisms are redundant rather than complementary, and the combination reliably generates headache in a subset of users. If you want a neurotrophic partner for Noopept, pick one that works through a different receptor family entirely.

Against piracetam, the molecule it was designed from: roughly a thousand times more potent by weight, so 20 mg replaces 1200-2400 mg, and it adds a neurotrophic mechanism the racetams do not have. The comparative trial found it at least equivalent with earlier onset on anxiety and asthenia. Against Semax: both are Russian-registered, both raise BDNF and NGF, but Noopept is oral, costs almost nothing, and is much milder subjectively; Semax is intranasal, more acutely stimulating and has stroke rather than cognitive-impairment registration. Running both is redundant and headache-prone. Against Cerebrolysin: Cerebrolysin has vastly more trial evidence and requires injection or infusion; Noopept is a tablet. Against the modern nootropic peptides in this class - the acetylated Semax and Selank analogues - Noopept has something none of them have, which is a published human comparative trial and a regulatory approval somewhere. It is also the least exciting compound here subjectively, and those two facts are probably related. Against actually treating the cause of cognitive complaints - sleep apnoea, untreated hypertension, alcohol, depression - Noopept is a small effect on top of whatever is left.

Rough cost

$5–$25/month. By a wide margin the cheapest compound in this class. Bulk powder runs roughly 20-40 USD for 10 grams, which at 20 mg/day is over a year of supply - genuinely a few dollars a month. Capsules and tablets cost more for the convenience and the dosing accuracy, typically 15-25 USD monthly, and for most people that accuracy is worth paying for. Russian pharmacy tablets are inexpensive where obtainable.

Genuinely uncertain

  • No human pharmacokinetic study has been published. The 0.5 hour half-life for the parent is from the Russian literature and the rat PK work; volume of distribution, protein binding, clearance and oral bioavailability in humans are all unmeasured.
  • Participant numbers in the Neznamov comparative trial were not stated in the abstracts I could access.
  • All clinical trials were conducted by the developing institute. No independent replication exists.
  • The trials were conducted in people with mild cognitive impairment from vascular or traumatic causes. There is no published trial in healthy people at all.
  • How much of the effect is cycloprolylglycine versus the parent compound is not fully resolved, and CPG is itself an endogenous molecule whose normal function is incompletely understood.
  • The claim of 1000-fold greater potency than piracetam is from the developers' own characterisation.
  • The mechanism of the blood pressure effect is not established, and the frequency of clinically meaningful rises is not quantified anywhere I could find.
  • The relationship between choline supplementation and Noopept headache is entirely anecdotal, though widely and consistently reported.
  • Nothing is known about use beyond the 3-month label course, or about repeated courses over years.

Papers