Systematic (IUPAC) name
Clinical data
Pregnancy cat.  ?
Legal status Unscheduled (US)
Routes Oral
CAS number 77191-36-7 N
ATC code None
PubChem CID 71157
ChemSpider 64299 YesY
Chemical data
Formula C14H18N2O2 
Mol. mass 246.305 g/mol
SMILES eMolecules & PubChem
 N(what is this?)  (verify)

Nefiracetam is a nootropic antidementia drug of the racetam family.[1]

Nefiracetam's cytoprotective actions are mediated by enhancement of GABAergic, cholinergic, and monoaminergic neuronal systems that give antiamnesia effects to the Alzheimer's type and cerebrovascular type of dementia.[2][3]

Nefiracetam has reduced testicular testosterone in both rats and dogs. To investigate mechanisms of the testicular toxicity of nefiracetam and to find sensitive parameters to predict the toxicity, male beagle dogs were orally administered 180 or 300mg/kg per day of the drug once and for 1 and 4 weeks. Time-course changes in serum and/or testicular hormone levels and semen parameters, and testicular morphology were examined. The testicular testosterone level was decreased 4h after single administration of nefiracetam at 300mg/kg per day, but the progesterone level showed no change at that time. The serum testosterone level was decreased after single, 1-week or 2-week treatment. In contrast, the serum estradiol level was increased from 1- to 4-week treatment. No changes in serum LH, FSH and inhibin B levels were observed throughout the experimental period. Decreased sperm motility and increased number of malformed sperms were first observed in semen after 4-week treatment. Histopathological examination of the testis revealed moderate and severe seminiferous atrophy with multinucleated giant cell formation at 180 and 300mg/kg per day, respectively, after 4-week treatment, but not 1-week treatment. These results show that nefiracetam decreases testicular testosterone level in dogs following single oral administration of a high dose, and induces severe morphologic changes after 4-week treatment. This reduction is shown to be a sensitive parameter to detect the toxicity, and is suggested to be induced by the impaired conversion of progesterone to testosterone in Leydig cells of rats [4] and dogs.[5] Although the dosages used in the studies were 1500 mg/kg and 300 mg/kg, respectively.

See also

  • Racetams


  1. ^ Murphy, Keith (22 July 2004). "Chronic Exposure of Rats to Cognition Enhancing Drugs Produces a Neuroplastic response". Neuropsychopharmacology. Retrieved 1 September 2010. 
  2. ^ Robinson RG, Jorge RE, Clarence-Smith K, Starkstein S (2009). "Double-blind treatment of apathy in patients with poststroke depression using nefiracetam". The Journal of Neuropsychiatry and Clinical Neurosciences 21 (2): 144–51. doi:10.1176/appi.neuropsych.21.2.144. PMID 19622685. 
  3. ^ Robinson RG, Jorge RE, Clarence-Smith K (2008). "Double-blind randomized treatment of poststroke depression using nefiracetam". The Journal of Neuropsychiatry and Clinical Neurosciences 20 (2): 178–84. doi:10.1176/appi.neuropsych.20.2.178. PMID 18451188. 
  4. ^ Shimada, M; Shikanai, Y; Shimomura, K; Harada, S; Watanabe, G; Taya, K; Kato, M; Furuhama, K (2003). "Investigation of testicular toxicity of nefiracetam, a neurotransmission enhancer, in rats". Toxicology letters 143 (3): 307–15. PMID 12849691. 
  5. ^ Shimomura, K; Shimada, M; Hagiwara, M; Harada, S; Kato, M; Furuhama, K (2004). "Testicular toxicity induced in dogs by nefiracetam, a neutrotransmission enhancer". Reproductive toxicology (Elmsford, N.Y.) 18 (3): 423–30. doi:10.1016/j.reprotox.2004.01.008. PMID 15082078.