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Systematic (IUPAC) name
CAS number 298-46-4
85756-57-6 (dihydrate)
ATC code N03AF01
PubChem 2554
DrugBank APRD00337
Chemical data
Formula C15H12N2O 
Mol. mass 236.269 g/mol
Pharmacokinetic data
Bioavailability 80%
Protein binding 76%
Metabolism Hepatic—by CYP3A4, to active epoxide form (carbamazepine-10,11 epoxide)
Half life 25–65 hours
Excretion 2–3% excreted unchanged in urine
Therapeutic considerations
Pregnancy cat.


Legal status


Routes Oral

Carbamazepine ("CBZ") is an anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy and bipolar disorder. It is also used to treat ADD, ADHD, schizophrenia and trigeminal neuralgia.


Trade names

Carbamazepine has been sold under the names Tegretol, Biston, Calepsin, Carbatrol, Epitol, Equetro, Finlepsin, Sirtal, Stazepine, Telesmin,Teril, Timonil, Trimonil, Epimaz, and Degranol (in South Africa)[1].


Carbamazepine was discovered by chemist Walter Schindler at J.R. Geigy AG (now part of Novartis) in Basel, Switzerland, in 1953.[2] Schindler then synthesized the drug in 1960, before its anti-epileptic properties had been discovered.

Carbamazepine was first marketed as a drug to treat trigeminal neuralgia in 1962. It has been used as an anticonvulsant in the UK since 1965, but only approved in the U.S. since 1974.

In 1971, Drs. Takezaki and Hanaoka first used carbmazepine to control mania in patients refractory to antipsychotics (lithium was not available in Japan at that time). Dr. Okuma, working independently, did the same thing with success. As they were also epileptologists, they had some familiarity with the anti-aggression effects of this drug. Carbamazepine would be studied for bipolar disorder throughout the 1970's.[3]

Adverse effects

Carbamazepine is known to render many hormonal contraception products ineffective, due to its action as a cytochrome P450 enzyme inducer, which is the system that metabolizes many oral contraceptives. Carbamazepine causes more cytochrome P450 enzyme to be produced, which hastens removal of the contraceptive from the blood plasma although the clinical significance of this effect is debatable.

Common side effects include drowsiness, motor coordination impairment and/or upset stomach. Carbamazepine preparations may also greatly decrease a person's alcohol tolerance.

Less common side effects include cardiac arrhythmias, blurry or double vision and/or the temporary loss of blood cells or platelets. With normal use, small reductions in white cell count and serum sodium are common, however, in rare cases, the loss of platelets may become life-threatening. This occurs commonly enough that a doctor may recommend frequent blood tests during the first few months of use, followed by three to four tests per year for established patients. In the UK, testing is generally performed much less frequently for long-term carbamazepine patients -typically once per year. Additionally, carbamazepine may exacerbate preexisting cases of hypothyroidism, so yearly thyroid function tests are advisable for persons taking the drug.

There are also reports of an auditory side effect for carbamazepine use, whereby patients perceive sounds about a semitone lower than their actual pitch. Thus, middle C would be heard as the note B3 just below it, etc. This unusual side-effect is usually not noticed by most people, and quickly disappears after the the person stops taking carbamazepine.

Oxcarbazepine, a derivative of carbamazepine, reportedly has fewer and less serious side effects.

Carbamazepine may cause SIADH (syndrome of inappropriate anti-diuretic hormone), since it both increases the release and potentiates the action of ADH (vasopressin).

Carbamazepine may aggravate juvenile myoclonic epilepsy, so it is important to mention any history of jerking, especially in the morning, before starting to take this drug.

Pregnant women taking carbamazepine put their fetuses at increased risk for teratogenic effects. As a result, they should be given folic acid supplementation and undergo prenatal ultrasonography for diagnosis.

In addition, carbamazepine has been linked to serious adverse cognitive anomalies, including EEG slowing[4] and cell apoptosis.[5]

The FDA informed healthcare professionals that dangerous or even fatal skin reactions (Stevens Johnson syndrome and toxic epidermal necrolysis), that can be caused by carbamazepine therapy, are significantly more common in patients with a particular human leukocyte antigen (HLA) allele, HLA-B*1502. This allele occurs almost exclusively in patients with ancestry across broad areas of Asia, including South Asian Indians. [6]

Mechanism of Action

The mechanism of action of carbamazepine and its derivatives is relatively well understood. Voltage-gated sodium channels are the molecular pores that allow brain cells (neurons) to generate action potentials, the electrical events that allow neurons to communicate over long distances. After the sodium channels open, to start the action potential, they inactivate, essentially closing the channel. Carbamazepine stabilizes the inactivated state of sodium channels, meaning that fewer of these channels are available to open, making brain cells less excitable.


Valproic acid and valnoctamide both interact with carbamazepine, as they inhibit microsomal epoxide hydrolase (mEH), the enzyme responsible for the breakdown of carbamazepine-10,11 epoxide into inactive metabolites.[7] By inhibiting mEH, valproic acid and valnoctamide cause a buildup of the active metabolite, prolonging the effects of carbamazepine and delaying its excretion.

Carbamazepine,as CYP 450 inducer, may increase clearance of many drugs, decreasing their blood levels.

See also


  1. ^
  2. ^ Schindler W, Häfliger F (1954). "Über Derivate des Iminodibenzyls". Helvetica Chimica Acta 37 (2): 472–83.. doi:10.1002/hlca.19540370211.
  3. ^ Okuma T, Kishimoto A (February 1998). "A history of investigation on the mood stabilizing effect of carbamazepine in Japan". Psychiatry Clin. Neurosci. 52 (1): 3–12. PMID 9682927.
  4. ^ Salinsky MC, Binder LM, Oken BS, Storzbach D, Aron CR, Dodrill CB (2002). "Effects of gabapentin and carbamazepine on the EEG and cognition in healthy volunteers". Epilepsia 43 (5): 482–90. doi:10.1046/j.1528-1157.2002.22501.x. PMID 12027908.
  5. ^ Gao XM, Margolis RL, Leeds P, Hough C, Post RM, Chuang DM (1995). "Carbamazepine induction of apoptosis in cultured cerebellar neurons: effects of N-methyl-D-aspartate, aurintricarboxylic acid and cycloheximide". Brain Res. 703 (1-2): 63–71. PMID 8719616.
  6. ^ MedWatch (December 12, 2007). Carbamazepine. 2007 Safety Alerts for Drugs, Biologics, Medical Devices, and Dietary Supplements. FDA.
  7. ^ Gonzalez, Frank J.; Robert H. Tukey (2006). "Drug Metabolism", in Laurence Brunton, John Lazo, Keith Parker (eds.): Goodman & Gilman's The Pharmacological Basis of Therapeutics, 11th ed., New York: McGraw-Hill, p. 79. ISBN 978-0071422802. 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Carbamazepine". A list of authors is available in Wikipedia.
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