The anticonvulsants (also commonly known as antiepileptic drugs) are a diverse group of pharmaceuticals used in the treatment of epileptic seizures. Anticonvulsants are also increasingly being used in the treatment of bipolar disorder, since many seem to act as mood stabilizers, and for the treatment of neuropathic pain. The goal of an anticonvulsant is to suppress the rapid and excessive firing of neurons that start a seizure. Failing this, an effective anticonvulsant would prevent the spread of the seizure within the brain and offer protection against possible excitotoxic effects, that may result in brain damage. Some studies have cited that anticonvulsants themselves are linked to lowered IQ in children.[1] However these adverse effects must be balanced against the significant risk epileptiform seizures pose to children and the distinct possibility of death and devastating neurological sequela secondary to seizures. Anticonvulsants are more accurately called antiepileptic drugs (abbreviated "AEDs"), and are sometimes referred to as antiseizure drugs. While the term 'anticonvulsant' is a fair description of AEDs, the use of this term tends to lead to confusion between epilepsy and non-epileptic convulsions. Convulsive seizures non-epileptic seizures are quite common, and these types of seizures do not respond to antiepileptic drugs. In epilepsy, an area of the cortex is typically hyper-irritable. This condition can often be confirmed by completing a diagnostic EEG. Antiepileptic drugs function to help reduce this area of irritability and thus prevent epileptiform seizures.
Conventional antiepileptic drugs block sodium channels or enhance g-aminobutyric acid function. Several antiepileptic drugs have multiple or uncertain mechanisms of action.[2] Next to the voltage-gated sodium channels and components of the GABA system, their targets include GABAA receptors, the GAT-1 GABA transporter, and GABA transaminase.[3] Additional targets include voltage-gated calcium channels, SV2A, and α2δ.[4][5] The drug class was the US's 5th-best-selling in 2007.[6]
Some anticonvulsants have shown antiepileptogenic effects in animal models of epilepsy. That is, they either prevent the expected development of epilepsy or can halt or reverse the progression of epilepsy. However, no drug has been shown to prevent epileptogenesis (the development of epilepsy after an injury such as a head injury) in human trials.[7]
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Contents
- 1 Approval
- 2 Drugs
- 2.1 Aldehydes
- 2.2 Aromatic allylic alcohols
- 2.3 Barbiturates
- 2.4 Benzodiazepines
- 2.5 Bromides
- 2.6 Carbamates
- 2.7 Carboxamides
- 2.8 Fatty acids
- 2.9 Fructose derivatives
- 2.10 GABA analogs
- 2.11 Hydantoins
- 2.12 Oxazolidinediones
- 2.13 Propionates
- 2.14 Pyrimidinediones
- 2.15 Pyrrolidines
- 2.16 Succinimides
- 2.17 Sulfonamides
- 2.18 Triazines
- 2.19 Ureas
- 2.20 Valproylamides (amide derivatives of valproate)
- 3 Non-medical anticonvulsants
- 4 Treatment guidelines
- 5 History
- 5.1 Marketing approval history
- 6 Use in pregnancy
- 7 See also
- 8 References
- 9 External links
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Approval
The usual method of achieving approval for a drug is to show it is effective when compared against placebo, or that it is more effective than an existing drug. In monotherapy (where only one drug is taken) it is considered unethical by most to conduct a trial with placebo on a new drug of uncertain efficacy. This is because untreated epilepsy leaves the patient at significant risk of death. Therefore, almost all new epilepsy drugs are initially approved only as adjunctive (add-on) therapies. Patients whose epilepsy is currently uncontrolled by their medication (i.e., it is refractory to treatment) are selected to see if supplementing the medication with the new drug leads to an improvement in seizure control. Any reduction in the frequency of seizures is compared against a placebo.[7] The lack of superiority over existing treatment, combined with lacking placebo-controlled trials, means that few modern drugs have earned FDA approval as initial monotherapy. In contrast, Europe only requires equivalence to existing treatments, and has approved many more. Despite their lack of FDA approval, the American Academy of Neurology and the American Epilepsy Society still recommend a number of these new drugs as initial monotherapy.[7]
Drugs
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This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (October 2010) |
In the following list, the dates in parentheses are the earliest approved use of the drug.
Aldehydes
Main article: Aldehyde
- Paraldehyde (1882). One of the earliest anticonvulsants. Still used to treat status epilepticus, particularly where there are no resuscitation facilities.
Aromatic allylic alcohols
- Stiripentol (2001 - limited availability). Indicated for the treatment of severe myoclonic epilepsy in infancy (SMEI).
Barbiturates
Main article: Barbiturate
Barbiturates are drugs that act as central nervous system (CNS) depressants, and by virtue of this they produce a wide spectrum of effects, from mild sedation to anesthesia. The following are classified as anticonvulsants:
- Phenobarbital (1912). See also the related drug primidone.
- Methylphenobarbital (1935). Known as mephobarbital in the US. No longer marketed in the UK
- Barbexaclone (1982). Only available in some European countries.
Phenobarbital was the main anticonvulsant from 1912 till the development of phenytoin in 1938. Today, phenobarbital is rarely used to treat epilepsy in new patients since there are other effective drugs that are less sedating. Phenobarbital sodium injection can be used to stop acute convulsions or status epilepticus, but a benzodiazepine such as lorazepam, diazepam or midazolam is usually tried first. Other barbiturates only have an anticonvulsant effect at anaesthetic doses.
Benzodiazepines
Main article: Benzodiazepine
The benzodiazepines are a class of drugs with hypnotic, anxiolytic, anticonvulsive, amnestic and muscle relaxant properties. Benzodiazepines act as a central nervous system depressant. The relative strength of each of these properties in any given benzodiazepine varies greatly and influences the indications for which it is prescribed. Long-term use can be problematic due to the development of tolerance to the anticonvulsant effects and dependency.[8][9][10][11] Of the many drugs in this class, only a few are used to treat epilepsy:
- Clobazam (1979). Notably used on a short-term basis around menstruation in women with catamenial epilepsy.
- Clonazepam (1974).
- Clorazepate (1972).
The following benzodiazepines are used to treat status epilepticus:
- Diazepam (1963). Can be given rectally by trained care-givers.
- Midazolam (N/A). Increasingly being used as an alternative to diazepam. This water-soluble drug is squirted into the side of the mouth but not swallowed. It is rapidly absorbed by the buccal mucosa.
- Lorazepam (1972). Given by injection in hospital.
Nitrazepam, temazepam, and especially nimetazepam are powerful anticonvulsant agents, however their use is rare due to an increased incidence of side effects and strong sedative and motor-impairing properties.
Bromides
Main article: Bromide
- Potassium bromide (1857). The earliest effective treatment for epilepsy. There would not be a better drug until phenobarbital in 1912. It is still used as an anticonvulsant for dogs and cats.
Carbamates
Main article: Carbamate
- Felbamate (1993). This effective anticonvulsant has had its usage severely restricted due to rare but life-threatening side effects.
Carboxamides
Main article: Carboxamide
The following are carboxamides:
- Carbamazepine (1963). A popular anticonvulsant that is available in generic formulations.
- Oxcarbazepine (1990). A derivative of carbamazepine that has similar efficacy but is better tolerated and is also available generically.
- Eslicarbazepine acetate (2009)
Fatty acids
Main article: Fatty acid
The following are fatty-acids:
- The valproates — valproic acid, sodium valproate, and divalproex sodium (1967).
- Vigabatrin (1989).
- Progabide
- Tiagabine (1996).
Vigabatrin and progabide are also analogs of GABA.
Fructose derivatives
Main article: Fructose
GABA analogs
- Gabapentin (1993).
- Pregabalin (2004).
Hydantoins
Main article: Hydantoin
The following are hydantoins:
- Ethotoin (1957).
- Phenytoin (1938).
- Mephenytoin
- Fosphenytoin (1996).
Oxazolidinediones
Main article: Oxazolidinedione
The following are oxazolidinediones:
- Paramethadione
- Trimethadione (1946).
- Ethadione
Propionates
Main article: Propionate
Pyrimidinediones
Main article: Pyrimidinedione
Pyrrolidines
Main article: Pyrrolidine
- Brivaracetam
- Levetiracetam (1999).
- Seletracetam
Succinimides
Main article: Succinimide
The following are succinimides:
- Ethosuximide (1955).
- Phensuximide
- Mesuximide
Sulfonamides
Main article: Sulfonamide (medicine)
- Acetazolamide (1953).
- Sultiame
- Methazolamide
- Zonisamide (2000).
Triazines
Main article: Triazine
Ureas
Main article: Urea
Valproylamides (amide derivatives of valproate)
Main article: Amide
Non-medical anticonvulsants
This article focuses on anticonvulsant drugs. Non-medical "anticonvulsants" are further described in Epilepsy#Other treatment
Sometimes, ketogenic diet or vagus nerve stimulation are described as "anticonvulsant" therapies as well.
Treatment guidelines
According to guidelines by the AAN and AES,[12] mainly based on a major article review in 2004,[13] patients with newly diagnosed epilepsy who require treatment can be initiated on standard anticonvulsants such as carbamazepine, phenytoin, valproic acid/valproate semisodium, phenobarbital, or on the newer anticonvulsants gabapentin, lamotrigine, oxcarbazepine or topiramate. The choice of anticonvulsants depends on individual patient characteristics.[12] Both newer and older drugs are generally equally effective in new onset epilepsy.[12] The newer drugs tend to have fewer side effects.[12] For newly diagnosed partial or mixed seizures, there is evidence for using gabapentin, lamotrigine, oxcarbazepine or topiramate as monotherapy.[12] Lamotrigine can be included in the options for children with newly diagnosed absence seizures.[12]
History
The first anticonvulsant was bromide, suggested in 1857 by Charles Locock who used it to treat women with "hysterical epilepsy" (probably catamenial epilepsy). Bromides are effective against epilepsy, and also cause impotence, which is not related to its anti-epileptic effects. Bromide also suffered from the way it affected behaviour, introducing the idea of the 'epileptic personality' which was actually a result of medication. Phenobarbital was first used in 1912 for both its sedative and antiepileptic properties. By the 1930s, the development of animal models in epilepsy research led to the development of phenytoin by Tracy Putnam and H. Houston Merritt, which had the distinct advantage of treating epileptic seizures with less sedation.[14] By the 1970s, an National Institutes of Health initiative, the Anticonvulsant Screening Program, headed by J. Kiffin Penry, served as a mechanism for drawing the interest and abilities of pharmaceutical companies in the development of new anticonvulsant medications.
Marketing approval history
The following table lists anticonvulsant drugs together with the date their marketing was approved in the US, UK and France. Data for the UK and France are incomplete. In recent years, the European Medicines Agency has approved drugs throughout the European Union. Some of the drugs are no longer marketed.
| Drug |
Brand |
US |
UK |
France |
| acetazolamide |
Diamox |
1953-07-2727 July 1953[15] |
1988[16] |
|
| carbamazepine |
Tegretol |
1974-07-1515 July 1974[17][18] |
1965[16] |
1963[19] |
| clobazam |
Frisium |
|
1979[16] |
|
| clonazepam |
Klonopin/Rivotril |
1975-06-044 June 1975[20] |
1974[16] |
|
| diazepam |
Valium |
1963-11-1515 November 1963[21] |
|
|
| divalproex sodium |
Depakote |
1983-03-1010 March 1983[22] |
|
|
| eslicarbazepine |
|
Data needed |
|
|
| ethosuximide |
Zarontin |
1960-11-022 November 1960[23] |
1955[16] |
1962[19] |
| ethotoin |
Peganone |
1957-04-2222 April 1957[24] |
|
|
| felbamate |
Felbatol |
1993-07-2929 July 1993[25] |
|
|
| fosphenytoin |
Cerebyx |
1996-08-055 August 1996[26] |
|
|
| gabapentin |
Neurontin |
1993-12-3030 December 1993[27] |
1993-05May 1993[16][19] |
1994-10October 1994[19] |
| lamotrigine |
Lamictal |
1994-12-2727 December 1994[28] |
1991-10October 1991[16][19] |
1995-05May 1995[19] |
| lacosamide |
Vimpat |
2008-10-2828 October 2008[29] |
|
|
| levetiracetam |
Keppra |
1999-11-3030 November 1999[30] |
2000-09-2929 September 2000[16][31] |
2000-09-2929 September 2000[31] |
| mephenytoin |
Mesantoin |
1946-10-2323 October 1946[32] |
|
|
| metharbital |
Gemonil |
1952[33][34] |
|
|
| methsuximide |
Celontin |
1957-02-088 February 1957[35] |
|
|
| methazolamide |
Neptazane |
1959-01-2626 January 1959[36] |
|
|
| oxcarbazepine |
Trileptal |
2000-01-1414 January 2000[37] |
2000[16] |
|
| phenobarbital |
|
|
1912[16] |
1920[19] |
| phenytoin |
Dilantin/Epanutin |
1938[19][38] |
1938[16] |
1941[19] |
| phensuximide |
Milontin |
1953[39][40] |
|
|
| pregabalin |
Lyrica |
2004-12-3030 December 2004[41] |
2004-07-066 July 2004[16][42] |
2004-07-066 July 2004[42] |
| primidone |
Mysoline |
1954-03-088 March 1954[43] |
1952[16] |
1953[19] |
| sodium valproate |
Epilim |
|
1977-12December 1977[19] |
1967-06June 1967[19] |
| stiripentol |
Diacomit |
|
2001-12-055 December 2001[44] |
2001-12-055 December 2001[44] |
| tiagabine |
Gabitril |
1997-09-3030 September 1997[45] |
1998[16] |
1997-11November 1997[19] |
| topiramate |
Topamax |
1996-12-2424 December 1996[46] |
1995[16] |
|
| trimethadione |
Tridione |
1946-01-2525 January 1946[47] |
|
|
| valproic acid |
Depakene/Convulex |
1978-02-2828 February 1978[48] |
1993[16] |
|
| vigabatrin |
Sabril |
2009-08-2121 August 2009[49] |
1989[16] |
|
| zonisamide |
Zonegran |
2000-03-2727 March 2000[50] |
2005-03-1010 March 2005[16][51] |
2005-03-1010 March 2005[51] |
Use in pregnancy
During pregnancy, the metabolism of several anticonvulsants is affected. There may be an increase in the clearance and resultant decrease in the blood concentration of lamotrigine, phenytoin, and to a lesser extent carbamazepine, and possibly decreases the level of levetiracetam and the active oxcarbazepine metabolite, the monohydroxy derivative.[52] Therefore, these drugs should be monitored during use in pregnancy.[52] Taking valproic acid or divalproex sodium during pregnancy should be cautioned against, as this class of medications has been linked to birth defects (teratogenic).
There is inadequate evidence to determine if newborns of women with epilepsy taking anticonvulsants have a substantially increased risk of hemorrhagic disease of the newborn.[52]
Regarding breastfeeding, some anticonvulsants probably pass into breast milk in clinically significant amounts, including primidone and levetiracetam.[52] On the other hand, valproate, phenobarbital, phenytoin, and carbamazepine probably are not transferred into breast milk in clinically important amounts.[52]
In animal models, several anticonvulsant drugs have been demonstrated to induce neuronal apoptosis in the developing brain. [53] [54] [55] [56] [57]
See also
References
- ^ Loring, David W (1 September 2005). "Cognitive Side Effects of Antiepileptic Drugs in Children". Psychiatric Times XXII (10).
- ^ https://www.neurology.wisc.edu/publications/2010%20pubs/stafstrom-4.pdf
- ^ Rogawski MA, Löscher W (July 2004). "The neurobiology of antiepileptic drugs". Nat. Rev. Neurosci. 5 (7): 553–64. doi:10.1038/nrn1430. PMID 15208697.
- ^ Rogawski MA, Bazil CW (July 2008). "New molecular targets for antiepileptic drugs: alpha(2)delta, SV2A, and K(v)7/KCNQ/M potassium channels". Curr Neurol Neurosci Rep 8 (4): 345–52. doi:10.1007/s11910-008-0053-7. PMC 2587091. PMID 18590620.
- ^ Meldrum BS, Rogawski MA (January 2007). "Molecular targets for antiepileptic drug development". Neurotherapeutics 4 (1): 18–61. doi:10.1016/j.nurt.2006.11.010. PMC 1852436. PMID 17199015.
- ^ http://www.joacp.org/index.php?option=com_content&view=article&id=188&catid=1 "According to the Washington Post who quoted research from IMS Health, AEDs were the fifth best selling class of drugs in the US in 2007, with sales topping 10 billion dollars. "
- ^ a b c Abou-Khalil BW (2007). "Comparative Monotherapy Trials and the Clinical Treatment of Epilepsy". Epilepsy currents / American Epilepsy Society 7 (5): 127–9. doi:10.1111/j.1535-7511.2007.00198.x. PMC 2043140. PMID 17998971.
- ^ Browne TR (May 1976). "Clonazepam. A review of a new anticonvulsant drug". Arch Neurol 33 (5): 326–32. doi:10.1001/archneur.1976.00500050012003. PMID 817697.
- ^ Isojärvi, JI; Tokola RA (December 1998). "Benzodiazepines in the treatment of epilepsy in people with intellectual disability". J Intellect Disabil Res 42 (1): 80–92. PMID 10030438.
- ^ Tomson T; Svanborg E, Wedlund JE (May-Jun 1986). "Nonconvulsive status epilepticus". Epilepsia 27 (3): 276–85. doi:10.1111/j.1528-1157.1986.tb03540.x. PMID 3698940.
- ^ Djurić, M; Marjanović B, Zamurović D (May-Jun 2001). "[West syndrome--new therapeutic approach]". Srp Arh Celok Lek 129 (1): 72–7. PMID 15637997.
- ^ a b c d e f AAN Guideline Summary for CLINICIANS EFFICACY AND TOLERABILITY OF THE NEW ANTIEPILEPTIC DRUGS, I: TREATMENT OF NEW ONSET EPILEPSY Retrieved on June 29, 2010
- ^ French JA, Kanner AM, Bautista J, et al. (May 2004). "Efficacy and tolerability of the new antiepileptic drugs, I: Treatment of new-onset epilepsy: report of the TTA and QSS Subcommittees of the American Academy of Neurology and the American Epilepsy Society". Epilepsia 45 (5): 401–9. doi:10.1111/j.0013-9580.2004.06204.x. PMID 15101821.
- ^ Eadie MJ, Bladin PF (2001). A Disease Once Sacred: a History of the Medical Understanding of Epilepsy.
- ^ NDA 008943
- ^ a b c d e f g h i j k l m n o p q r Epilepsy Action: Druglist. Retrieved on 1 November 2007.
- ^ NDA 016608 (Initial approval on 11 March 1968 was for trigeminal neuralgia.)
- ^ Schain, Richard J. (1 March 1978). "Pediatrics—Epitomes of Progress: Carbamazepine (Tegretol®) in the Treatment of Epilepsy". Western Journal of Medicine 128 (3): 231–232. PMC 1238063. PMID 18748164.
- ^ a b c d e f g h i j k l m Loiseau, Pierre Jean-Marie (June 1999). "Clinical Experience with New Antiepileptic Drugs: Antiepileptic Drugs in Europe" (PDF). Epilepsia 40 (Suppl 6): S3–8. doi:10.1111/j.1528-1157.1999.tb00925.x. PMID 10530675. Retrieved 26 March 2007.
- ^ NDA 017533
- ^ NDA 013263
- ^ NDA 018723
- ^ NDA 012380
- ^ NDA 010841
- ^ NDA 020189
- ^ NDA 020450
- ^ NDA 020235
- ^ NDA 020241
- ^ NDA 022253
- ^ NDA 021035
- ^ a b EPAR: Keppra. Retrieved on 1 November 2007.
- ^ NDA 006008
- ^ NDA 008322
- ^ Dodson, W. Edwin; Giuliano Avanzini; Shorvon, Simon D.; Fish, David R.; Emilio Perucca (2004). The treatment of epilepsy. Oxford: Blackwell Science. xxviii. ISBN 0-632-06046-8.
- ^ NDA 010596
- ^ NDA 011721
- ^ NDA 021014
- ^ NDA 008762 (Marketed in 1938, approved 1953)
- ^ NDA 008855
- ^ Kutt, Henn; Resor, Stanley R. (1992). The Medical treatment of epilepsy. New York: Dekker. p. 385. ISBN 0-8247-8549-5. (first usage)
- ^ NDA 021446
- ^ a b EPAR: Lyrica Retrieved on 1 November 2007.
- ^ NDA 009170
- ^ a b EPAR: Diacomit. Orphan designation: 5 December 2001, full authorisation: 4 January 2007 Retrieved on 1 November 2007.
- ^ NDA 020646
- ^ NDA 020505
- ^ NDA 005856
- ^ NDA 018081
- ^ Lundbeck Press Release
- ^ NDA 020789
- ^ a b EPAR: Zonegran. Retrieved on 1 November 2007
- ^ a b c d e Harden CL, Pennell PB, Koppel BS, et al. (May 2009). "Management issues for women with epilepsy--focus on pregnancy (an evidence-based review): III. Vitamin K, folic acid, blood levels, and breast-feeding: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Epilepsy Society". Epilepsia 50 (5): 1247–55. PMID 19507305.
- ^ Bittigau P, Sifringer M, Genz K,et al. (May 2002). "Antiepileptic drugs and apoptotic neurodegenereation in the developing brain". Proc Natl Acad SCI USA 99 (23): 15089–94. doi:10.1073/pnas.222550499. PMC 137548. PMID 12417760.
- ^ Manthey D, Asimiadou S, et al. (Jun 2005). "Sulthiame but not levetiracetam exerts neurotoxic effect in the developing rat brain.". Exp Neurol 193 (2): 497–503. doi:10.1016/j.expneurol.2005.01.006. PMID 15869952.
- ^ Katz I, Kim J, et al. (Aug 2007). "Effects of lamotrigine alone and in combination with MK-801, phenobarbital, or phenytoin on cell death in the neonatal rat brain.". J Pharmacol Exp Ther 322 (2): 494–500. doi:10.1124/jpet.107.123133. PMID 17483293.
- ^ Kim J, Kondratyev A, and Gale K (Oct 2007). "Antiepileptic drug-induced neuronal cell death in the immature brain: effects of carbamazepine, topiramate, and levetiracetam as monotherapy versus polytherapy.". J Pharmacol Exp Ther 323 (1): 165–73. doi:10.1124/jpet.107.126250. PMC 2789311. PMID 17636003.
- ^ Forcelli PA, Kim J "et al." (Dec 2011). "Pattern of antiepileptic drug-induced cell death in limbic regions of the neonatal rat brain". Epilepsia 52 (12): e207–11. doi:10.1111/j.1528-1167.2011.03297.x. PMID 22050285.
- Drug Reference for FDA Approved Epilepsy Drugs
- Epilepsy Action: UK Anti-Epileptic Drugs List
External links
- eMedicine: Antiepileptic Drugs: an overview
- NINDS: Anticonvulsant Screening Program
- Use of Anticonvulsants in Pharmacotherapy of Bronchial Asthma
- MDNG: Anticonvulsants and Bone Health
- Miami Children's Brain Institute - Anticonvulsants
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Anticonvulsants (N03)
|
|
| GABAA receptor agonist |
|
Barbiturates
|
- Barbexaclone
- Metharbital
- Methylphenobarbital
- Pentobarbital
- Phenobarbital#
- Primidone
|
|
|
Benzodiazepines
|
- Clobazam
- Clonazepam
- Clorazepate
- Diazepam#
- Flutoprazepam
- Lorazepam
- Midazolam
- Nimetazepam
- Nitrazepam
- Temazepam
|
|
|
| Other GABA agents |
|
Aromatic allylic alcohols
|
|
|
|
| Carbonic anhydrase inhibitor |
|
Sulfa drugs
|
- Acetazolamide
- Ethoxzolamide
- Sultiame
- Topiramate
- Zonisamide
|
|
|
| Channel blockers |
|
Primarily sodium
|
|
Hydantoins
|
- Ethotoin
- Fosphenytoin
- Mephenytoin
- Phenytoin#
|
|
|
Carboxamides
|
- Carbamazepine#
- Eslicarbazepine acetate
- Oxcarbazepine
- Oxitriptyline
- Rufinamide
|
|
|
|
Primarily calcium
|
|
Succinimides
|
- Ethosuximide#
- Mesuximide
- Phensuximide
|
|
|
|
AMPA receptor
|
|
|
|
Unknown/ungrouped
|
- Phenyltriazine (Lamotrigine), Oxazolidinediones (Ethadione
- Paramethadione
- Trimethadione), Ureas (Phenacemide
- Pheneturide), Monosaccharide (Topiramate)
|
|
|
| Channel openers |
|
|
| Indirect GABA agents |
|
Carboxylic acids/
Fatty acid derivatives
|
- GABA transaminase inhibitor: Valproic acid# (Sodium valproate & Valproate semisodium)
- Valpromide
- Valnoctamide
- Valproate pivoxil
GABA reuptake inhibitor: Tiagabine
|
|
|
GABA analogs
|
- Gabapentin
- Pregabalin
- Progabide
- Tolgabide
- Vigabatrin
|
|
|
Unknown/multiple/
unsorted |
|
Carbamates
|
- Emylcamate
- Felbamate
- Meprobamate
- Carisbamate
|
|
|
Pyrrolidines
|
- Brivaracetam
- Levetiracetam
- Nefiracetam
- Seletracetam
|
|
|
Propionates
|
|
|
|
Aldehydes
|
|
|
|
Bromides
|
- Potassium bromide
- Sodium bromide
|
|
|
- #WHO-EM
- ‡Withdrawn from market
- Clinical trials:
- †Phase III
- §Never to phase III
|
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anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp
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noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr
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proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
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