International reference: 1 US FDA recall for this ingredient
Defective Container: powder may leak out of the pouch (vigabatrin)
US-market enforcement records (OpenFDA), shown for reference - not specific to this product in South Africa.
SABRIL TABLETS
Vigabatrin
What it does
Vigabatrin is a medication used to help control seizures.
Commonly used for: epilepsy, seizure disorders
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
Ask about this medicine
Answers come only from this medicine's registration record, BNF monograph and interaction data - not medical advice.
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Sourcing - Kenya onlyRegistration & product details
Source: South African Health Products Regulatory Authority · fetched 2026-04-15 21:24:36 · updated 2026-10-28 04:12:24
Drug Interactions
65Severe (7)
Antiepileptics - decreases absorption
Iron chelators (dexrazoxane) might decrease the absorption of antiepileptics (fosphenytoin, phenytoin). Avoid.
Antiepileptics - decreases exposure
Lumacaftor is predicted to decrease the exposure to antiepileptics (carbamazepine, fosphenytoin, phenobarbital, phenytoin, primidone). Avoid.
Antiepileptics - decreases concentration
St John’s wort is predicted to decrease the concentration of antiepileptics (fosphenytoin, phenobarbital, phenytoin, primidone). Avoid.
Antiepileptics - increases risk of overheating and dehydration
Hydroxyzine potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.
Antiepileptics - increases risk of overheating and dehydration
Haloperidol potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.
Antiepileptics - decreases absorption
Dexrazoxane might decrease the absorption of antiepileptics (fosphenytoin, phenytoin). Avoid.
Antiepileptics - increases risk of overheating and dehydration
Oxybutynin potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.
Moderate (25)
Antiepileptics - increases concentration
Intravenous chloramphenicol increases the concentration of antiepileptics (fosphenytoin, phenytoin) and antiepileptics (fosphenytoin, phenytoin) affect the concentration of intravenous chloramphenicol
Antiepileptics - decreases concentration
Diazoxide decreases the concentration of antiepileptics (fosphenytoin, phenytoin) and antiepileptics (fosphenytoin, phenytoin) are predicted to decrease the effects of diazoxide. Monitor concentration
Antiepileptics - increases concentration
Disulfiramincreasestheconcentrationofantiepileptics (fosphenytoin,phenytoin).Monitorconcentrationandadjust dose.rStudy →AlsoseeTABLE12p.1520
Antiepileptics - increases concentration
Fluorouracilincreasestheconcentrationofantiepileptics (fosphenytoin,phenytoin).Monitorconcentrationandadjust dose.rAnecdotal 1xidneppA|snoitcaretnI A1 https://www.facebook.c (Books-Courses-Medic
Antiepileptics - decreases concentration
Folates are predicted to decrease the concentration of antiepileptics (fosphenytoin, phenobarbital, phenytoin, primidone). Monitor concentration and adjust dose.
Unknown (33)
Antiepileptics - increases risk of overheating and dehydration
Acetazolamide potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.
Antiepileptics - increases risk of visual disturbances
Alcohol potentially increases the risk of visual disturbances when given with antiepileptics (retigabine).
Antiepileptics - decreases exposure
Enzalutamide is predicted to slightly decrease the exposure to antiepileptics (brivaracetam).
Antiepileptics - decreases exposure
Apalutamidepotentiallydecreasestheexposureto antiepileptics(valproate).nTheoretical
Antiepileptics - increases concentration
Capecitabine increases the concentration of antiepileptics (fosphenytoin, phenytoin).
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: class
About this medicine
Vigabatrin is a medication used to help control seizures.
What it treats
- epilepsy
- seizure disorders
How it works
Vigabatrin works by increasing the levels of a chemical in the brain that helps to reduce seizure activity.
Who it's for
This medication is for people diagnosed with epilepsy who have not responded well to other treatments.
Drug class
Antiepileptics
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Vigabatrin
BNF-referencedVigabatrin is an antiepileptic drug used primarily for the treatment of epilepsy and other seizure disorders. It acts as a structural analog of gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter in the central nervous system. By irreversibly inhibiting the enzyme GABA transaminase (GABA-T), vigabatrin increases the levels of GABA in the brain, which helps to suppress the excessive neuronal activity associated with seizures.
Indications
- Adjunctive treatment of focal seizures with or without secondary generalization not satisfactorily controlled with other antiepileptics
Dosage
Children: For children aged 1–23 months, the initial dose is 15–20 mg/kg twice daily (maximum per dose 250 mg), to be increased over 2–3 weeks to the usual maintenance dose. For children aged 12–17 years
Adults: Initially 1 g once daily, alternatively initially 1 g daily in 2 divided doses. Increase in steps of 500 mg every week, adjusted according to response; usual dose is 2–3 g daily, maximum 3 g per day.
Mechanism of action
Vigabatrin increases concentrations of GABA in the central nervous system by irreversibly inhibiting GABA transaminase (GABA-T), the enzyme responsible for its metabolism. This leads to enhanced GABAergic neurotransmission, which counteracts the pathologic excitatory neurotransmission seen in epilepsy.
Pharmacodynamics
Vigabatrin has unique pharmacodynamics as it is chemically unrelated to other anticonvulsants. Its main action is the irreversible inhibition of GABA-T, preventing the breakdown of GABA and thereby increasing its availability in the synaptic cleft. This increase in GABA concentration results in prolonged inhibitory effects on neuronal excitability, contributing to its anticonvulsant properties.
Pharmacokinetics
Vigabatrin is absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 1 to 2 hours after oral administration. It has a half-life of approximately 5 to 9 hours, but due to its irreversible action on GABA-T, its effects may persist much longer than its plasma levels suggest. The drug is not significantly metabolized and is eliminated primarily through renal excretion.
Contra-indications
- History of severe depression
- History of psychosis
- Uncontrolled epilepsy such as absence or myoclonic seizures
Adverse effects
- Visual field defects
- Dizziness
- Drowsiness
- Fatigue
- Weight gain
- Memory loss
- Mood alterations
- Speech disorders
- Psychotic disorders
- Abnormal thinking
- Abdominal pain
- Alopecia
- Anemia
- Anxiety
- Arthralgia
- Concentration impairment
- Depression
- Headache
- Insomnia
- Nausea
- Oedema
- Paraesthesias
- Tremor
- Vomiting
Interactions
- Other antiepileptic drugs may have additive effects on seizure control
- Drugs that affect GABAergic transmission may enhance the risk of adverse effects
Precautions
- Regular visual field testing before and during treatment
- Gradual withdrawal recommended to avoid seizure exacerbation
- Monitor for new visual symptoms
- Use with caution in patients with a history of behavioral problems
Pregnancy
Limited data available; use only if clearly needed and benefits outweigh risks.
Breast-feeding
Not recommended due to potential for serious adverse effects in the infant.
Storage
Store below 30°C, protect from light and moisture.
Formulations
- Tablets
- Oral solution
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Vigabatrin
PubChem CID 5665Molecular formula: C6H11NO2
Mechanism of action
Gamma-aminobutyric acid (GABA) is the major inhibitory transmitter throughout the central nervous system, and the potentiation of GABAergic neurotransmission is therefore a crucial mechanism through which antiepileptic agents may combat the pathologic excitatory neurotransmission seen in epilepsy. Vigabatrin increases concentrations of GABA in the central nervous system by irreversibly inhibiting the enzymes responsible for its metabolism to succinic semialdehyde: gamma-aminobutyric acid transaminase (GABA-T). Vigabatrin is a structural analog of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the CNS. Although the exact mechanism of vigabatrin's antiseizure effect is unknown, it is thought to be related to the drug's action as a preferential and irreversible inhibitor of GABA transaminase (GABA-T), which is the enzyme responsible for the degradation of GABA and the resultant increase in GABA concentrations in the CNS. Vigabatrin is commercially available as a racemic mixture of 2 enantiomers; the S enantiomer is pharmacologically active and the R enantiomer is inactive.
Pharmacodynamics
Vigabatrin is an antiepileptic agent chemically unrelated to other anticonvulsants. Vigabatrin prevents the metabolism of GABA by irreversibly inhibiting GABA transaminase (GABA-T). As vigabatrin is an irreversible inhibitor of gamma-aminobutyric acid transaminase (GABA-T), its duration of effect is thought to be dependent on the rate of GABA-T re-synthesis rather than on the rate of drug elimination.
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.