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Pramiracetam

Status: Approved (prescription in some European countries)
Evidence: Not graded on a research bench yet

Pramiracetam is a racetam nootropic developed at Parke, Davis and Company, which gave it the investigational code CI-879 after screening a series of pyrrolidineacetamides for the ability to reverse amnesia in mice.

Reviewed 27 October 2026

01Overview

What Pramiracetam is

A United States patent covering that chemical series, granted on 20 March 1979, names Parke, Davis and Company as the assignee and two of those chemists as inventors (PubChem patent record US-4145347-A). Pramiracetam reached the market in Europe rather than the United States: Italy authorised a 600 mg tablet under the name Pramistar by a ministerial decree published on 16 January 1993, for disorders of attention and memory in older patients of degenerative or vascular origin (Gazzetta Ufficiale della Repubblica Italiana n. 12, 16 January 1993). The human literature is small and old, the largest retrieved study being a 108-patient comparison with piracetam after head injury, while most of what is known about how pramiracetam acts in the brain comes from rats (PMID: 19145827, PMID: 1786500, PMID: 2987637).

How it works

Choline uptake in rat brain

The step most often reported for pramiracetam is sodium-dependent high-affinity choline uptake (HACU), the rate-limiting step for making acetylcholine. In rat hippocampal synaptosomes measured 30 minutes after dosing the animal, pramiracetam at 44 and 88 mg/kg raised HACU, while higher and lower doses did not (PMID: 2987637). A single dose raised choline uptake in rat cortex and hippocampus, and increases seen after repeated dosing had disappeared within 24 hours (PMID: 3149192). Six days of 100 mg/kg a day raised hippocampal HACU in rats without changing striatal dopamine or homovanillic acid (PMID: 3035858). None of this work was done in people.

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Choline transport across the blood-brain barrier

In Wistar rats given scopolamine for 14 days, choline extraction and the permeability-surface area product for choline rose across nine brain regions; co-injection of piracetam or pramiracetam at 100 mg/kg a day prevented that change, and both compounds raised cerebral blood flow (PMID: 2610714). The author proposed that cholinergic innervation of brain endothelial cells regulates choline transport.

Nitric oxide synthase

Pramiracetam at 300 mg/kg by injection raised nitric oxide synthase activity about 20 percent in rat cortical homogenates but not in hippocampal homogenates, with no change in the enzyme's messenger RNA; a 100 mg/kg dose did nothing, and pretreatment with lithium chloride raised the cortical effect to about 40 percent (PMID: 8557218).

A dependence on adrenal steroids seen in mice

A group at Ciba-Geigy in Basel reported repeatedly that the memory effects of piracetam-like compounds disappear without the adrenal glands. Doses of 1, 10, 100, 1,000 and 3,000 mg/kg of piracetam, oxiracetam, aniracetam or pramiracetam were all inactive in adrenalectomised mice, so the loss is not a question of dose (PMID: 2765169). Blocking steroid synthesis with aminoglutethimide, or blocking aldosterone receptors, also removed the memory effect, while the same blockade did not remove the memory effect of cholinomimetic drugs (PMID: 2137359, PMID: 2690149). Oral aldosterone or corticosterone given before training blocked the memory effect of all four compounds in a dose-related way without impairing learning itself (PMID: 1410129).

A cell-free enzyme target

Pramiracetam and aniracetam inhibited prolyl endopeptidase in cell-free tests with inhibition constants in the nanomolar to micromolar range, alongside peptide inhibitors that prevented scopolamine-induced amnesia in rats (PMID: 3330562).

What has not been established

A review covering 407 references on piracetam-like compounds found no affinity at adrenergic, muscarinic, serotonin, dopamine, adenosine A1, opioid, GABA, benzodiazepine or glutamate receptors, and reported that no generally accepted mechanism had emerged for the class (PMID: 8061686). A 1995 review of drugs studied in Alzheimer's disease noted that of the three nootropic agents it covered, only pramiracetam penetrates the central nervous system poorly (PMID: 7586900). BodyHackGuide's guides to piracetam, aniracetam and oxiracetam cover the same open question for the rest of the family.

Studied for

Nootropic pharmacology
Cholinergic neurotransmission
Memory and learning
Traumatic brain injury
Geriatric cognition
Pharmacokinetics

Benefits listed

Delayed recall in a double-blind placebo-controlled trial in men with memory problems after head injury or anoxia (PMID: 1786500)
Partial reduction of scopolamine-induced memory impairment in two groups of 12 healthy men (PMID: 15374306)
Objective memory scores in a 35-person open-label pilot of drug therapy with and without memory training (PMID: 18653001)
Reference memory in a 16-arm radial maze in rats (PMID: 3088666)

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Object recognition at a 24-hour interval in rats (PMID: 2765166)
High-affinity choline uptake in rat hippocampus (PMID: 2987637)
Slow-wave pattern of the aged rat electroencephalogram (PMID: 4065299)

02Research

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What the research shows

No research bench grades Pramiracetam yet. Benches compare compounds people pair, with the evidence for each.

Key research findings

Controlled human studies

McLean 1991, double-blind placebo-controlled study in young men with memory and cognitive problems after head injury and anoxia (PMID: 1786500). Participants received 400 mg of pramiracetam sulfate three times a day. The authors report clinically significant improvements in memory measures, especially delayed recall, against placebo, maintained through an 18-month open-label period and a 1-month follow-up after the drug was stopped. The abstract does not give the number of participants or name a single primary endpoint, and the paper is not indexed with a trial registration.
Claus 1991, two-phase placebo-controlled enrichment trial in 10 patients with probable Alzheimer's disease, National Institute of Neurological Disorders and Stroke (PMID: 2011259). Eight patients showed a best dose during the dose-finding phase, but only two improved again to a similar degree in the replication phase. Fluorodeoxyglucose PET in two individuals showed no definite change. The authors concluded that doses up to 4,000 mg are unlikely to confer symptomatic benefit in Alzheimer's disease.
Mauri 1994, randomised placebo-controlled scopolamine challenge in two groups of 12 healthy men aged 18 to 42 and 55 to 65 (PMID: 15374306). Participants took 600 mg twice a day for 10 days, then received 0.5 mg of scopolamine hydrobromide by intramuscular injection on day 11, with psychometric tests before and 1, 3 and 6 hours after. Scopolamine impaired episodic memory and selective attention in both groups, and pramiracetam partially reduced that impairment in both the young and the older men. Visuo-motor and incidental learning measures were unaffected by scopolamine.
De Vreese 1996, four-arm open-label pilot in 35 non-depressed, non-demented healthy elderly volunteers with a mean age of 64.8 years (PMID: 18653001). Participants were randomly assigned to memory training (10), drug therapy with pramiracetam (8), both (10) or control (7). Objective memory gains in the two groups that received pramiracetam were significantly larger than in the training-only and control groups, while metamemory measures showed only a trend between groups. The study was open-label with seven to ten people per arm.

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Human pharmacokinetics

Chang 1985, double-blind randomised tolerance study in two groups of six healthy men (PMID: 4008675). Each group received alternating placebo and single oral doses of 400, 800, 1,200 and 1,600 mg after an overnight fast. Peak plasma concentrations came 2 to 3 hours after dosing and rose linearly with dose, while elimination half-life (4.5 to 6.5 hours), total body clearance, renal clearance and volume of distribution were independent of dose.
Auteri 1992, two-formulation study in 11 fasting volunteers (PMID: 1473879). A 600 mg solution and a 600 mg tablet gave similar plasma profiles, with faster absorption from the solution. Half-life varied widely between subjects (2 to 8 hours) but little within a subject.
Animal distribution (PMID: 11387954). After oral dosing in dogs, half-life was 2.3 to 3.9 hours across doses. In rats, concentrations were highest in kidney, then liver, intestine, lung, muscle, heart, gonad, spleen and sebum, with drug also detected in brain; 28.26 percent of the dose appeared in urine and 6.35 percent in faeces over 72 hours, and plasma protein binding was 20.1 to 22.2 percent.

Clinical reports from Ukraine using the European product

These reports are published as English abstracts of Ukrainian-language papers and describe comparisons rather than placebo-controlled trials.

65 patients with mild craniocerebral trauma, allocated to pramistar or piracetam within a combined treatment (PMID: 18418926). Both groups improved on headache, dizziness and nausea; the pramistar group showed better restoration of orientation and subjective state, and the author reports a larger effect in patients with amnesia.
108 people in the acute period of closed craniocerebral injury, 71 given pramistar and 37 given piracetam alongside base treatment (PMID: 19145827). Assessment used scales, questionnaires, brain magnetic resonance imaging and electroencephalography on days 1, 10 and 30, and the author reports that asthenic disorders accompanied every case of concussion.
Patients with chronic cerebrovascular insufficiency and stroke sequelae given pramiracetam as monotherapy (PMID: 14965012). The abstract reports statistically significant but heterogeneous effects on the evaluated memory symptoms and gives no group sizes.

Animal studies

Rats, radial arm maze (PMID: 3088666). Daily pramiracetam at 7.5 and 15 mg/kg before testing for 7 weeks in a 16-arm maze with nine baited arms improved the reference memory component but not the working memory component.
Rats, one-trial object recognition (PMID: 2765166). Pramiracetam at 30 mg/kg given 30 minutes before the sample trial improved retention at a 24-hour interval, with no change in overall exploratory behaviour; 400 mg/kg of piracetam did the same.
Rats, quantitative electroencephalogram (PMID: 4065299). Pramiracetam sulfate acted strongly to normalise the slow-wave pattern of the aged Fisher-344 rat electroencephalogram, while piracetam acted weakly and appeared to lose effect with repetition.
Rats, dose-response shape (PMID: 4043326, PMID: 6716406). Pramiracetam shows an inverted U-shaped dose-response at three levels of measurement: learned behaviour, cortical and hippocampal electroencephalogram, and firing rate of single hippocampal neurons. The original medicinal chemistry paper reported the same inverted U shape for amnesia reversal in mice.
Mice, cholinergic amnesia (PMID: 3786350). Pretreatment with piracetam, etiracetam or pramiracetam blocked the amnesia produced by intracerebroventricular hemicholinium-3 in a passive avoidance task. The abstract reports that piracetam and etiracetam did not prevent the fall in brain acetylcholine and says nothing about pramiracetam on that measure.
Rats, hypoxia (PMID: 9200217). In 12-day-old and 18-day-old rat pups exposed to a simulated altitude of 7,000 metres for one hour, pramiracetam did not change hippocampal afterdischarges in the younger group and only partly shortened the first afterdischarge in the older group.

Reviews

A 2010 systematic survey of piracetam and piracetam-like drugs placed pramiracetam in the subgroup that has been used in humans, reported that pramiracetam had improved cognitive deficits associated with traumatic brain injuries, and noted that oxiracetam and aniracetam were no longer in clinical use (PMID: 20166767). A 1994 review of 407 references concluded that the class has very low toxicity, lacks affinity for the classical neurotransmitter receptors, and has no commonly accepted mechanism (PMID: 8061686).

Safety and side effects

What the human studies recorded

The clinical tolerance study that measured pramiracetam pharmacokinetics gave single oral doses of 400, 800, 1,200 and 1,600 mg against placebo to two groups of six men in a double-blind randomised design and reported no significant side effects at any dose level (PMID: 4008675). The chemists who selected the compound wrote that pramiracetam showed a wide margin of safety in animals and was well tolerated in normal human volunteers (PMID: 6716406). The double-blind head injury trial was described by its authors as an evaluation of safety and efficacy, but its abstract reports no adverse event data at all. What the abstract describes as maintained through the 18-month open-label period and the 1-month follow-up is the memory improvement, not a safety finding (PMID: 1786500). None of the retrieved trials was large enough to detect uncommon events.

Read all the safety notesShow less

The one regulator-driven safety change

After assessing the periodic safety update reports for pramiracetam, the PRAC concluded that regular evaluation of creatinine clearance is needed during long-term treatment of older patients, because excretion of pramiracetam is delayed in elderly patients with renal impairment, and the CMDh agreed in June 2015. The same procedure deleted the dosing recommendations for adults aged 18 to 65 from the product information, because the medicine is indicated only in older patients, and added wording that the product is not for use under 18 years of age (EMA/536968/2015, procedure PSUSA/00002492/201409).

Animal observations

In rats with alloxan-induced chronic hyperglycaemia, pramiracetam had a strong antiaggregant effect on platelets, which the authors attributed mainly to inhibition of thromboxane A2 metabolism (PMID: 24824701); a companion survey of nootropic drugs in the same model reported that pramiracetam, entrop and Ginkgo biloba extract shared the most general antiaggregant action among the drugs tested (PMID: 22702111). No human bleeding data were retrieved. In immature rats exposed to simulated altitude, pramiracetam only partly shortened the first epileptic afterdischarge and did not change afterdischarges in unexposed animals, so the authors called its protective action moderate (PMID: 9200217).

Gaps

No human pregnancy, paediatric, long-term or overdose data for pramiracetam were retrieved from PubMed. The product information for the European medicine states that there is no relevant use in the paediatric population and that no studies have been conducted in children and adolescents (EMA/536968/2015).

On PubMed

The search pramiracetam[All Fields] OR "CI-879"[All Fields] on PubMed.

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Safety and side effects
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03Safety

Pramiracetam side effects and interactions

Side effects

Common

No significant side effects were reported at single oral doses of 400 to 1,600 mg in two groups of six healthy men (PMID: 4008675)
The chemists who selected the compound described it as well tolerated in normal human volunteers and as having a wide margin of safety in animals (PMID: 6716406)
The double-blind head injury study was described by its authors as an evaluation of safety and efficacy, but its abstract reports no adverse event data (PMID: 1786500)

Serious events

No serious adverse event was attributed to pramiracetam in the human literature retrieved here, which totals well under 300 treated people
Excretion is delayed in elderly patients with renal impairment, which is why European regulators required regular creatinine clearance checks during long-term treatment (EMA/536968/2015)
Pramiracetam reduced platelet aggregation in diabetic rats; no human bleeding data were retrieved (PMID: 24824701)
No human pregnancy, paediatric, long-term or overdose data were retrieved

Who should not use it

Contraindications

Reduced kidney function in older people. European regulators concluded that excretion of pramiracetam is delayed in elderly patients with renal impairment and required regular evaluation of creatinine clearance during long-term treatment (EMA/536968/2015).

Read all the contraindications and cautionsShow less

People under 18. The European product information was changed in 2015 to state that there is no relevant use of pramiracetam in the paediatric population for concentration and memory disorders, that no studies have been conducted in children and adolescents, and that use in these groups is not recommended (EMA/536968/2015).

Bleeding tendency. Pramiracetam reduced platelet aggregation in diabetic rats through thromboxane A2 metabolism (PMID: 24824701, PMID: 22702111). No human study of bleeding with pramiracetam was retrieved, so this is a mechanism-based caution drawn from animals.

Anticholinergic drugs. The human evidence for pramiracetam is strongest against a cholinergic blocker: in 24 men, 10 days of pramiracetam partially reduced the memory impairment produced by intramuscular scopolamine (PMID: 15374306). Animal work puts choline uptake at the centre of its action (PMID: 2987637), so drugs that block cholinergic transmission act against the mechanism studied.

Research-use-only status in the United States. Pramiracetam is not an approved drug in the United States, and FDA has told at least one seller that its pramiracetam product is not a dietary supplement or a conventional food and is an unapproved new drug (FDA warning letter MARCS-CMS 557887, 4 February 2019).

Interactions

5 pairings in our record: 3 with a caution and 2 to monitor.

Scopolamine and other anticholinergics
Caution

In 24 healthy men, 10 days of pramiracetam partially reduced the episodic memory and attention impairment produced by a single 0.5 mg intramuscular dose of scopolamine (PMID: 15374306). Anticholinergic drugs act against the cholinergic mechanism that the animal work describes.
Antiplatelet and anticoagulant drugs
Caution

Pramiracetam reduced platelet aggregation in rats with chronic alloxan-induced hyperglycaemia, which the authors linked to thromboxane A2 metabolism (PMID: 24824701, PMID: 22702111). No human study of pramiracetam with an antiplatelet or anticoagulant drug was retrieved.
Piracetam
Caution

Pramiracetam and piracetam were compared head to head after head injury in two Ukrainian reports, with the authors favouring pramiracetam on some measures (PMID: 18418926, PMID: 19145827). No study of the two taken together was retrieved.
Corticosteroids and aldosterone
Monitor

In mice, aldosterone or corticosterone given before training blocked the memory effect of pramiracetam and of three other racetams in a dose-related way, and blocking steroid synthesis with aminoglutethimide did the same (PMID: 1410129, PMID: 2137359). These are mouse findings with no human counterpart.
Drugs that reduce renal function
Monitor

European regulators required regular evaluation of creatinine clearance during long-term treatment of older patients because excretion of pramiracetam is delayed in elderly patients with renal impairment (EMA/536968/2015). Drugs that reduce kidney function would be expected to slow its clearance further.

This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.

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04Dosing

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Dosing

No dose on record

Our record lists no dose for Pramiracetam. This section holds what it does list.

Dosing summary

Route: Oral, Intraperitoneal (animal studies only)

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Route

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05Prices

Pramiracetam prices

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06Chemistry

Chemistry and structure

Molecular formula: C14H27N3O2
Molecular mass: 269.38 g/mol
CAS number: 68497-62-1
Half-life: About 4.5 to 6.5 hours as a harmonic mean after single oral doses of 400, 800, 1,200 and 1,600 mg in two groups of six healthy men, with clearance and volume of distribution independent of dose (PMID: 4008675). In 11 fasting volunteers given 600 mg as a tablet or as a solution, the half-life averaged 4.3 and 4.7 hours and ranged from 2 to 8 hours between subjects (PMID: 1473879).

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08Questions

Frequently asked questions

What is pramiracetam?

Pramiracetam is a racetam nootropic developed at Parke, Davis and Company under the code CI-879, chosen from a series of pyrrolidineacetamides screened for reversal of amnesia in mice (PMID: 6716406). Pramiracetam has a molecular formula of C14H27N3O2 and a molecular weight of 269.38 g/mol as the free base, and the European medicine contains the sulfate salt (PubChem CID 51712, CID 51711). Pramiracetam is sold in parts of Europe as a prescription tablet under the name Pramistar and is not an approved medicine in the United States.

Is pramiracetam approved anywhere?

Pramiracetam was authorised in Italy as the prescription tablet Pramistar by a ministerial decree published on 16 January 1993, for disorders of attention and memory in older patients of degenerative or vascular origin (Gazzetta Ufficiale n. 12, 16 January 1993). The European Medicines Agency's 2025 list of nationally authorised pramiracetam products names Pramistar 600 mg tablets in Latvia, Romania and Lithuania, while earlier lists from 2015 and 2020 also named Italy (EMA/169859/2025, EMA/270645/2015, EMA/268260/2020). Pramiracetam has never been approved by the United States Food and Drug Administration, and a search of Drugs@FDA on 25 October 2026 returned no product containing it.

What does the human research on pramiracetam show?

The strongest published result for pramiracetam is a double-blind placebo-controlled study in young men with memory problems after head injury and anoxia, in which 400 mg three times a day improved delayed recall against placebo (PMID: 1786500). In 10 patients with probable Alzheimer's disease, pramiracetam produced a best dose in eight during dose-finding but reproduced the improvement in only two, and the authors concluded that doses up to 4,000 mg are unlikely to help in that disease (PMID: 2011259). In 24 healthy men given 600 mg twice a day for 10 days, pramiracetam partially reduced the memory impairment caused by scopolamine (PMID: 15374306).

How does pramiracetam work?

The best-documented action of pramiracetam is on sodium-dependent high-affinity choline uptake, the rate-limiting step for acetylcholine synthesis, which rose in rat hippocampal synaptosomes at 44 and 88 mg/kg but not at higher or lower doses (PMID: 2987637). Pramiracetam also prevented a scopolamine-induced change in choline transport across the blood-brain barrier in rats and raised cerebral blood flow (PMID: 2610714), and raised nitric oxide synthase activity about 20 percent in rat cortex at 300 mg/kg (PMID: 8557218). A review of 407 papers on piracetam-like compounds, pramiracetam among them, found no affinity at the classical neurotransmitter receptors and no commonly accepted mechanism for the class (PMID: 8061686).

How long does pramiracetam stay in the body?

Pramiracetam had an elimination half-life of about 4.5 to 6.5 hours in two groups of six healthy men given single oral doses of 400 to 1,600 mg, with peak plasma levels 2 to 3 hours after dosing (PMID: 4008675). In 11 fasting volunteers given 600 mg, the half-life of pramiracetam averaged 4.3 to 4.7 hours and ranged from 2 to 8 hours between people (PMID: 1473879). A 1995 review of antidementia drug pharmacokinetics stated that of the three nootropics it covered, pramiracetam penetrates the central nervous system poorly (PMID: 7586900).

What is known about the safety of pramiracetam?

The double-blind tolerance study of pramiracetam in two groups of six men reported no significant side effects at single doses of 400, 800, 1,200 or 1,600 mg (PMID: 4008675). European regulators changed the product information for pramiracetam in 2015 to require regular evaluation of creatinine clearance during long-term treatment of older patients, because excretion is delayed in elderly patients with renal impairment, and to state that the medicine is not for use under 18 years of age (EMA/536968/2015). No human pregnancy, paediatric, long-term or overdose data for pramiracetam were retrieved from PubMed, and the published trials are too small to detect uncommon events.

Is pramiracetam a dietary supplement in the United States?

Pramiracetam is not a dietary supplement in the United States. In a warning letter dated 4 February 2019, the Food and Drug Administration told a nootropics seller that its pramiracetam, piracetam, oxiracetam, aniracetam, phenylpiracetam, noopept, adrafinil and phenibut products are not dietary supplements or conventional foods, and that the claims made for them made the products unapproved new drugs (FDA warning letter MARCS-CMS 557887). FDA also granted pramiracetam sulfate an orphan designation in November 1991 for cognitive dysfunction associated with electroconvulsive therapy, and that designation was later withdrawn or revoked without approval (FDA Orphan Drug Designations and Approvals database).

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