Topiramate clinical pharmacology: Difference between revisions
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==Clinical Pharmacology== | ==Clinical Pharmacology== | ||
==Pharmacodynamics== | |||
Chemically, topiramate is a [[sulfamic acid|sulfamate]]-substituted [[monosaccharide]], related to [[fructose]], a rather unusual chemical structure for an [[anticonvulsant]]. Topiramate is quickly absorbed after oral use. Most of the drug (70%) is excreted in the urine as unchanged drug. The remainder is extensively metabolized by [[hydroxylation]], [[hydrolysis]], and [[glucuronidation]]. Six [[metabolite]]s have been identified in humans, none of which constitutes more than 5% of an administered dose. Topiramate enhances [[GABA]]-activated chloride channels. In addition, topiramate inhibits excitatory neurotransmission, through actions on [[kainic acid|kainate]] and [[AMPA receptor]]s. There is evidence that topiramate has a specific effect on GluR5 kainate receptors. It is also an inhibitor of [[carbonic anhydrase]], particularly subtypes II and IV, but this action is weak and unlikely to be related to its anticonvulsant actions, but may account for the bad taste and the development of [[Kidney stone|renal stones]] seen during treatment. Its possible effect as a [[mood stabilizer]] seems to occur before [[anticonvulsant]] qualities at lower dosages. Topiramate inhibits maximal electroshock and [[pentylenetetrazol]]-induced seizures as well as partial and secondarily generalized [[tonic-clonic seizures]] in the kindling model, findings predictive of a broad spectrum of activities clinically. | |||
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<ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = TOPIRAMATE (TOPIRAMATE ) TABLET, FILM COATED [AUROBINDO PHARMA LIMITED] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=32b48ea0-a215-43b8-83b4-a5435a686d68 | publisher = | date = | accessdate = 6 February 2014 }}</ref> | <ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = TOPIRAMATE (TOPIRAMATE ) TABLET, FILM COATED [AUROBINDO PHARMA LIMITED] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=32b48ea0-a215-43b8-83b4-a5435a686d68 | publisher = | date = | accessdate = 6 February 2014 }}</ref> | ||
==References== | ==References== | ||
Revision as of 03:30, 7 February 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]
For patient information, click here.
Clinical Pharmacology
Pharmacodynamics
Chemically, topiramate is a sulfamate-substituted monosaccharide, related to fructose, a rather unusual chemical structure for an anticonvulsant. Topiramate is quickly absorbed after oral use. Most of the drug (70%) is excreted in the urine as unchanged drug. The remainder is extensively metabolized by hydroxylation, hydrolysis, and glucuronidation. Six metabolites have been identified in humans, none of which constitutes more than 5% of an administered dose. Topiramate enhances GABA-activated chloride channels. In addition, topiramate inhibits excitatory neurotransmission, through actions on kainate and AMPA receptors. There is evidence that topiramate has a specific effect on GluR5 kainate receptors. It is also an inhibitor of carbonic anhydrase, particularly subtypes II and IV, but this action is weak and unlikely to be related to its anticonvulsant actions, but may account for the bad taste and the development of renal stones seen during treatment. Its possible effect as a mood stabilizer seems to occur before anticonvulsant qualities at lower dosages. Topiramate inhibits maximal electroshock and pentylenetetrazol-induced seizures as well as partial and secondarily generalized tonic-clonic seizures in the kindling model, findings predictive of a broad spectrum of activities clinically.
References
- ↑ "TOPIRAMATE (TOPIRAMATE ) TABLET, FILM COATED [AUROBINDO PHARMA LIMITED]". Retrieved 6 February 2014.