Chemistry:Clocapramine

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Short description: Antipsychotic medication
Clocapramine
Clinical data
Trade namesClofekton, Padrasen
AHFS/Drugs.comInternational Drug Names
Routes of
administration		Oral
ATC code
  • None
Legal status
Legal status
  • In general: ℞ (Prescription only)
Identifiers
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
Chemical and physical data
FormulaC28H37ClN4O
Molar mass481.08 g·mol−1
3D model (JSmol)

Clocapramine (Clofekton, Padrasen), also known as 3-chlorocarpipramine, is an atypical antipsychotic of the iminostilbene class which was introduced in Japan in 1974 by Yoshitomi for the treatment of schizophrenia.[1][2][3][4][5] In addition to psychosis, clocapramine has also been used to augment antidepressants in the treatment of anxiety and panic.[6]

Clocapramine has been reported to act as an antagonist of the D2, 5-HT2A, α1-adrenergic, and α2-adrenergic receptors, and does not inhibit the reuptake of either serotonin or norepinephrine.[4][7][8][9][10] It has also been shown to have affinity for SIGMAR1.[11] Clocapramine's affinity for the 5-HT2A receptor is greater than that for the D2 receptor and it has a lower propensity for inducing extrapyramidal symptoms compared to typical antipsychotics, thus underlying its atypical nature.[4][5][10]

Clinical trials

In several clinical trials, clocapramine has been compared to other neuroleptic agents. Against haloperidol, though there was no significant difference in efficacy at the end of the study, clocapramine tended to be superior in alleviating motor retardation, alogia, and thought disorder, and also produced fewer side effects.[12] Against sulpiride, clocapramine demonstrated more favorable effects in the treatment of both positive and negative symptoms, including motor retardation, delusions, hallucinations, and social isolation, though it produced more side effects.[13] Against timiperone, clocapramine showed lower efficacy against both positive and negative symptoms and produced more side effects such as dyskinesia, insomnia, constipation, and nausea.[14]

Clocapramine has been implicated in at least one fatality, a suicide in which there were two self-inflicted stab wounds and an overdose of clocapramine as well as three other antipsychotics was taken.[15] The stab wounds could not explain the death, and thus, it was attributed to multiple drug toxicity instead.[15]

See also

References

  1. ↑ David J. Triggle (1997). Dictionary of pharmacological agents. London: Chapman & Hall. ISBN 978-0-412-46630-4. 
  2. ↑ Swiss Pharmaceutical Society (2000). Index Nominum 2000: International Drug Directory (Book with CD-ROM). Boca Raton: Medpharm Scientific Publishers. pp. 1932. ISBN 978-3-88763-075-1. https://books.google.com/books?id=5GpcTQD_L2oC&q=clocapramine&pg=PA253. 
  3. ↑ Sittig, Marshall (1988). Pharmaceutical manufacturing encyclopedia. Park Ridge, N.J., U.S.A: Noyes Publications. pp. 1756. ISBN 978-0-8155-1144-1. https://archive.org/details/pharmaceuticalma0002sitt. "clocapramine." 
  4. ↑ 4.0 4.1 4.2 "Atypicality of several antipsychotics on the basis of in vivo dopamine-D2 and serotonin-5HT2 receptor occupancy". Neuropsychopharmacology 12 (1): 57–64. February 1995. doi:10.1016/0893-133X(94)00064-7. PMID 7766287. 
  5. ↑ 5.0 5.1 "Atypical properties of several classes of antipsychotic drugs on the basis of differential induction of Fos-like immunoreactivity in the rat brain". Life Sciences 76 (2): 225–37. November 2004. doi:10.1016/j.lfs.2004.08.009. PMID 15519367. http://ousar.lib.okayama-u.ac.jp/8313. 
  6. ↑ "Augmentation of paroxetine with clocapramine in panic disorder". Psychiatry and Clinical Neurosciences 61 (4): 449. August 2007. doi:10.1111/j.1440-1819.2007.01690.x. PMID 17610675. 
  7. ↑ "A study on the pharmacological and biochemical profile of clocapramine". International Pharmacopsychiatry 17 (2): 73–90. 1982. doi:10.1159/000468561. PMID 6125486. 
  8. ↑ "Interaction of neuroleptics and antidepressants with rat brain alpha 2-receptors: a possible relationship between alpha 2-receptor antagonism and antidepressant action". Biological Psychiatry 19 (9): 1283–91. September 1984. PMID 6149771. 
  9. ↑ "Effects of iminodibenzyl antipsychotic drugs on cerebral dopamine and alpha-adrenergic receptors". European Journal of Pharmacology 112 (3): 313–22. June 1985. doi:10.1016/0014-2999(85)90776-9. PMID 2862053. 
  10. ↑ 10.0 10.1 "In vitro receptor binding and in vivo receptor occupancy in rat and guinea pig brain: risperidone compared with antipsychotics hitherto used". Japanese Journal of Pharmacology 69 (4): 399–412. December 1995. doi:10.1254/jjp.69.399. PMID 8786644. 
  11. ↑ "Characterization of the currents induced by sigma ligands in NCB20 neuroblastoma cells". Brain Research 637 (1–2): 190–6. February 1994. doi:10.1016/0006-8993(94)91232-7. PMID 7910100. 
  12. ↑ Yamagami S (1985). "A crossover study of clocapramine and haloperidol in chronic schizophrenia". The Journal of International Medical Research 13 (6): 301–10. doi:10.1177/030006058501300601. PMID 4076529. 
  13. ↑ "A single-blind study of clocapramine and sulpiride in hospitalized chronic schizophrenic patients". Drugs Under Experimental and Clinical Research 14 (11): 707–13. 1988. PMID 3246215. 
  14. ↑ "Comparison of efficacy of timiperone, a new butyrophenone derivative, and clocapramine in schizophrenia: a multiclinic double-blind study". The Journal of International Medical Research 11 (5): 247–58. 1983. doi:10.1177/030006058301100501. PMID 6139317. 
  15. ↑ 15.0 15.1 "Clocapramine-related fatality. Postmortem drug levels in multiple psychoactive drug poisoning". Forensic Science International 122 (1): 48–51. October 2001. doi:10.1016/S0379-0738(01)00442-X. PMID 11587865. 



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