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Pramiracetam is a nootropic drug that is believed to promote memory, focus and executive function. A detailed discussion of the molecule was published in 2008. [2]
Pramiracetam is a member of the racetam family and shares the group’s characteristic pyrrolidone nucleus.
It is structurally similar to its parent molecule, piracetam, and prepared by substituting piracetam’s amide group with a dipropan-2-ylaminoethyl group. [1]
Unlike its parent molecule, piracetam, only preliminary evidence is available about the therapeutic effects of pramiracetam. Although human studies exist, they are limited and often with small sample sizes.
Further, the exact mechanism of action is unknown; however, there is evidence to suggest the drug enhances acetylcholine synthesis, which may explain some of its observed therapeutic effects.
Product Name: Pramiracetam, Pramistar
Chemical Name: N-[2-(Diisopropylamino)ethyl]-2-(2-oxopyrrolidin-1-yl)acetamide
Formula: C14H27N3O2
Molecular Weight: 269.383 g/mol
CAS Number: 68497-62-1
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Pramiracetam Mechanisms of Action
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- Comparison to Piracetam
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Pramiracetam’s exact mechanism of action remains unknown; however, evidence suggests that it may affect the central cholinergic system. [3] Further studies have indicated pramiracetam may increase the turnover of acetylcholine in hippocampal cholinergic nerve terminals. [4]
Experimental evidence indicates that pramiracetam (100 mg/kg) does not impact the concentration of norepinephrine, dompamine (DA), serotonin (5-HT), 5-hydroxyindoleacetic, and homovanillic acid in the brain.
Further, in vitro tests indicate pramiracetam does not have an affinity for the binding sites of dopaminergic, adrenergic, serotoninergic, GABAergic, muscarinic, adenosine, and benzodiazepine receptors. [3]
In contrast, pramiracetam (44 and 88 mg/kg) did lead to an increase in the rate of sodium dependent high-affinity choline uptake (HACU) in rat hippocampal synaptosomes in vitro, but not in the cerebral cortex or the corpus striatum. [3]
In the same study piracetam did not significantly alter HACU into the hippocampus, even at significantly higher doses compared to pramiracetam (up to five times the administered dose of pramiracetam). [3]
Thus, pramiracetam seems to exhibit a unique ability to affect hippocampal acetylcholine turnover compared to piracetam. [3] The exact mechanism that leads to the stimulation of HACU is unknown.
However, it is unlikely that pramiracetam directly stimulates HACU in the hippocampus because the direct addition of pramiracetam to hippocampal preparations was not observed to alter choline uptake. [3]
The observation that pramiracetam impacts the cholinergic system was reinforced in a 1991 radial arm task study, in which researchers observed that pramiracetam improved long-term memory in rats.
The authors cite previous studies to illustrate that manipulation of the central cholinergic system can affect rat performance in radial arm task tests; they hypothesize that the increase in long-term memory observed in their study may be “due to the drug’s influence on central cholinergic systems.” [5]
It is of note that researchers have observed a therapeutic window for pramiracetam administration. Generally, the term therapeutic window is used to describe a dose range where therapeutic effects are observed without significant toxic side effects; however, pramiracetam is not known to exhibit toxic side effects. [6]
Instead, researchers examined whether or not there was a dose range where pramiracetam was most therapeutically effective, and beyond that range therapeutically ineffective. Researchers observed that pramiracetam did have a therapeutic window for behavior, EEG changes, and single neuron firing rates.
Consequently, and depending on the situation, therapeutic efficacy may be hampered by too high a dosage of pramiracetam. The mechanism underlying this therapeutic window is unknown, but researchers hypothesize it could be due to a negative feedback system. [6]
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Pramiracetam Pharmacokinetics
Pramiracetam has a high-degree of bioavailability, but a variable half-life depending on the animal model used. [1]
In a study of orally ingested carbon-14-labeled pramiracetam, 90% of the radioactive was excreted in the urine. [7]
In animal studies, the half life of 14C-labeled pramiracetam ranged from one to four hours depending on the species.
In all cases, oral pramiracetam was observed to be completely absorbed and distributed throughout the tissues of the organism. [7]
Pramiracetam Therapeutic Effects
In a test using a radial arm maze task, three groups of rats were injected with saline, 7.5 mg/kg pramiracetam, or 15 mg/kg pramiracetam, respectively.
The rats administered pramiracetam were observed to have improved long-term memory, but similar short-term memory compared to the placebo. Performance of the 15 mg/kg and 7.5mg/kg groups were not statistically different. [5]
Pramiracetam was observed to improve memory, particularly delayed recall, in a double-blind placebo-controlled study of four human males who had sustained brain injury. [4]
Over the course of 12 weeks, each subject received two 3-week blocks of pramiracetam or placebo. Observations based on the Wechsler Memory Scale (WMS) and Selective Reminding Test (SRT) indicate improved memory function during pramiracetam treatment, particularly in areas of delayed recall, long-term retrieval and long term storage. [4]
Despite the positive outcome, there is large variability in the test results; [1] however, the authors note that the same pattern of improvement was observed in all four subjects. [4]
In a small study conducted in the Ukraine, researchers observed that pramiracetam was more effective than piracetam in restoring memory loss and disorientation in individuals with craniocereberal traumas. [1, 9]
65 patients with mild craniocereberal trauma were given a complex treatment including piracetam or pramiracetam. Both groups experienced improvement over the course of treatment, including reduction or disappearance in headache, dizziness and nausea) but the pramiracetam group also experienced improved orientation and feeling compared to the piracetam group. [9]
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Pramiracetam for Amnesia
In an Italian study, researchers observed pramiracetam reduced the effects of scopolamine-induced amnesic effects in otherwise healthy volunteers.
In the study, two groups of twelve males sorted according to age (18-42 and 55-65, respectively) were randomly assigned to receive placebo or pramiracetam (600 mg twice a day) for a period of ten days.
On day 11 participants were given an injection of scopolamine and tested for impacts on short- and long-term verbal memory.
Scopolamine was observed to impair performance of episodic memory and selective attention tests; however, individuals who had received pramiracetam experienced partially reduced amnesic effects compared to the placebo group. [8]
Pramiracetam Safety and Side Effects
Pramiracetam seems well tolerated by humans. In a study published in 1991, normal volunteer subjects were administered individual pramiracetam doses up to 1600 mg/day and multiple doses up to 1500 mg/day for 28 days.
The high levels of pramiracetam were well tolerated by subjects. [4] This is particularly notably given that pramiracetam is thought to be 100 times more potent than piracetam. [4]
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- Malykh AG, Sadaie MR. Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders. Drugs. 2010 Feb 12;70(3):287-312.
- Bambagiotti-Alberti M, Bartolucci G, Bruni B, Coran SA, Di Vaira M. Diisoprop-yl{2-[2-(2-oxopyrrolidin-1-yl)acetamido]eth-yl}ammonium hydrogen sulfate. Acta Crystallogr Sect E Struct Rep Online. 2008 May 30;64(Pt 6):o1160.
- Pugsley, T. A., Shih, Y. H., Coughenour, L., & Stewart, S. F. Some neurochemical properties of pramiracetam (CI?879), a new cognition?enhancing agent. Drug development research. 1983;3(5), 407-420.
- McLean A Jr, Cardenas DD, Burgess D, Gamzu E.Placebo-controlled study of pramiracetam in young males with memory and cognitive problems resulting from head injury and anoxia. Brain Inj. 1991 Oct-Dec;5(4):375-80.
- Murray CL, Fibiger HC The effect of pramiracetam (CI-879) on the acquisition of a radial arm maze task. Psychopharmacology (Berl). 1986;89(3):378-81.
- Poschel BP, Ho PM, Ninteman FW, Callahan MJ. Pharmacologic therapeutic window of pramiracetam demonstrated in behavior, EEG, and single neuron firing rates. Experientia. 1985 Sep 15;41(9):1153-6.
- Chang T, Young RM, Goulet JR, Yakatan GJ. Pharmacokinetics of oral pramiracetam in normal volunteers. J Clin Pharmacol. 1985 May-Jun;25(4):291-5.
- Mauri, Marco, Elena Sinforiani, Fabio Reverberi, Paola Merlo, and Giorgio Bono. Pramiracetam effects on scopolamine-induced amnesia in healthy volunteers. Arch Gerontol Geriatr. 1994 Mar-Apr;18(2):133-9.
- Tkachev AV. [Application of nootropic agents in complex treatment of patients with concussion of the brain]. [Article in Russian] Lik Sprava. 2007 Jul-Sep;(5-6):82-5.
- Butler, D. E., et al. Amnesia-reversal activity of a series of N-[(disubstituted-amino) alkyl]-2-oxo-1-pyrrolidineacetamides, including pramiracetam. J Med Chem. 1984 May;27(5):684-91.
Article last updated on: July 24th, 2018 by Nootriment