2868 Carbamazepine An anticonvulsant used to control grand mal and psychomotor or focal seizures. Its mode of action is not fully understood, but some of its actions resemble those of phenytoin; although there is little chemical resemblance between the two compounds, their three-dimensional structure is similar. 298-46-4 2554 C15H12N2O 236.094960 White powder. 204-206°C 17.7 mg/L Oral. In clinical studies, carbamazepine suspension, conventional tablets, and extended-release tablets delivered equivalent amounts of drug to the systemic circulation. However, it has been observed that the suspension is somewhat faster absorbed. Furthermore, the extended-release tablet is slightly slower than the conventional tablet. The bioavailability of the extended-release tablet is 89%, compared to the suspension. Plasma levels of carbamazepine are variable. The time to peak concentration for the different formulations are as follows: Suspension = 1.5 hours; Conventional tablets = 4-5 hours; Extended-release tablets = 3-12 hours. Carbamazepine inhibits sustained repetitive firing by blocking use-dependent sodium channels. Pain relief is believed to be associated with blockade of synaptic transmission in the trigeminal nucleus and seizure control with reduction of post-tetanic potentiation of synaptic transmission in the spinal cord. Carbamazepine also possesses anticholinergic, central antidiuretic, antiarrhythmic, muscle relaxant, antidepressant (possibly through blockade of norepinephrine release), sedative, and neuromuscular-blocking properties. Hepatic. CYP3A4 is the primary isoform responsible for the formation of carbamazepine-10,11-epoxide. This metabolite is active and shown to be equipotent to carbamazepine as an anticonvulsant. Carbamazepine is more rapidly metabolized to the aforementioned metabolite in younger patients than in adults. It also undergoes glucuronidation via UGT2B7, however this finding has been disputed. Route of Elimination: 72% of the dose is in the urine while 28% is in the feces. Hydroxylated and conjugated metabolites are largely what was recovered in the urine. 3% of the dose is recovered as unchanged carbamazepine. Half Life: Initial half-life values range from 25-65 hours, decreasing to 12-17 hours on repeated doses. No indication of carcinogenicity to humans (not listed by IARC). For the treatment of epilepsy and pain associated with true trigeminal neuralgia. May cause a potentially dangerous rash that may develop into Stevens Johnson syndrome, an extremely rare but potentially fatal skin disease. Mild ingestions cause vomiting, drowsiness, ataxia, slurred speech, nystagmus, dystonic reactions, and hallucinations. Severe intoxications may produce coma, seizures, respiratory depression, and hypotension The prognosis in cases of severe poisoning is critically dependent upon prompt elimination of the drug, which may be achieved by inducing vomiting, irrigating the stomach, and by taking appropriate steps to diminish absorption. If these measures cannot be implemented without risk on the spot, the patient should be transferred at once to a hospital, while ensuring that vital functions are safeguarded. There is no specific antidote. (L1712) 2009-07-21T20:27:10Z 2014-12-24T20:25:52Z Carbamazepine C06868 3387 Carbamazepine DB00564 true OC(=N)N1C2=CC=CC=C2C=CC2=CC=CC=C12 C15H12N2O InChI=1S/C15H12N2O/c16-15(18)17-13-7-3-1-5-11(13)9-10-12-6-2-4-8-14(12)17/h1-10H,(H2,16,18) InChIKey=FFGPTBGBLSHEPO-UHFFFAOYSA-N 236.2686 236.094963016 Exogenous Solid 2.45 HMDB14704 CHEMBL108 2457 <p>Ketan Dhansukhlal Vyas, Wajid Sajjad Jafri, Ashok Krishna Kulkarni, &#8220;Process for preparing carbamazepine from iminostilbene.&#8221; U.S. Patent US6245908, issued February, 1998.</p>