RESEARCH MONOGRAPH · KDC-MN-026
Aniracetam
Aniracetam is a more potent racetam approved in Europe and Asia. It modulates AMPA glutamate receptors, slowing receptor desensitization, and is reported to have anxiolytic effects beyond cognition. Fat-soluble (best absorbed with food). Not stocked by Kodiac. This monograph is provided for research and educational reference.
Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.
Pyrrolidinone racetam (anisoyl-substituted)
A more lipophilic anisoyl-substituted racetam developed by Hoffmann-La Roche, characterized by AMPA receptor positive allosteric modulation and brief plasma half-life with active metabolites.
Abstract
Aniracetam (1-(4-methoxybenzoyl)-2-pyrrolidinone; CAS 72432-10-1; molecular formula C12H13NO3; molecular weight 219.24) is a piracetam analog developed by Hoffmann-La Roche in the 1970s and marketed in Europe, Japan, and Argentina under names including Draganon and Sarpul for senile dementia and cerebrovascular insufficiency. The structural modification from piracetam is the addition of a para-methoxybenzoyl (anisoyl) group at the pyrrolidinone nitrogen, which substantially increases lipophilicity and enables blood-brain barrier penetration at lower oral doses than piracetam. The principal mechanism is positive allosteric modulation of AMPA receptors; aniracetam binds at the dimer interface of the GluA2 ligand-binding domain and slows desensitization, prolonging the AMPA current per glutamate-binding event. The compound also shows weak nicotinic acetylcholine receptor positive modulation. Pharmacokinetics: plasma half-life of the parent compound is short (1 to 2.5 hours); the major metabolites N-anisoyl-GABA, p-anisic acid, and p-methoxybenzoylpyrrolidine retain pharmacological activity and have longer half-lives. Oral bioavailability is high but the parent compound undergoes extensive first-pass metabolism. The clinical evidence base in elderly cognitive impairment, post-stroke aphasia, and Alzheimer disease is mixed; meta-analyses show modest cognitive endpoint improvement with effect sizes in the 0.2 to 0.4 range. Anxiolytic effects are reported in addition to the cognitive enhancement and are attributed to the AMPA potentiation enhancing prefrontal cortical regulation of subcortical anxiety circuits. The research literature reports dose ranges of approximately 750 to 1500 mg.
Mechanism of action
AMPA receptor positive allosteric modulator (binding at the dimer interface, slows desensitization). Weak nAChR positive modulation. Active metabolites contribute additional cholinergic and GABA-related activity.
Reported research dose ranges
Research literature reports a range of approximately 750 to 1500 mg.
References
- Pittaluga A, et al. Aniracetam, 1-BCP and cyclothiazide differentially modulate the synaptic glutamate response. Eur J Pharmacol 1999.
- Lee CR, Benfield P. Aniracetam: an overview of its pharmacodynamic and pharmacokinetic properties, and a review of its therapeutic potential. Drugs Aging 1994.
- Senin U, et al. Aniracetam (Ro 13-5057) in the treatment of senile dementia of Alzheimer type (SDAT): results of a placebo controlled multicentre clinical study. Eur Neuropsychopharmacol 1991.
Read the full monograph
The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, reported research dose ranges, sourcing and quality verification, reconstitution and handling, stack interaction considerations, and a curated reference list. Available as a research-use-only PDF download.
The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.
FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.