levetiracetam reference
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(levetiracetam · DailyMed)
Registered Kenya · PPB

LEVE-Q ORAL SOLUTION 100MG/ML

LEVETIRACETAM

H2022/CTD9902/22352 LEVETIRACETAM 100MG/ML GENERIC/BIOSIMILARS nervous system INN generic

What it does

Levetiracetam is a medication used to help control seizures in people with epilepsy.

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.

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Registration & product details

Registration no.
H2022/CTD9902/22352
Registration date
-
Expiry date
2028 March 10
Status
Registered
Active ingredient
LEVETIRACETAM
Strength
-
Pack size
THE FINAL PRODUCT IS PACKED IN AMBER GLASS BOTTLE OF 60ML WITH ALUMINUM CAP PACKED IN UNIT CARTON ALONG WITH LEAFLET.
Therapeutic class
GENERIC/BIOSIMILARS
ATC class (WHO)
N03AX - Other antiepileptics
Drug group
NERVOUS SYSTEM
RxNorm RxCUI
114477
Manufacturer / MAH
Cintana Healthcare
Applicant / LTR
Q PHARMA DMCC
Country of origin
FOREIGN

Source: Pharmacy and Poisons Board · fetched 2026-01-28 19:30:31 · updated 2026-09-15 02:23:15

Drug Interactions

65
Check interactions

Pharmacodynamic Warnings

Levetiracetam appears in TABLE 11: Drugs with CNS depressant effects

Severe (7)

Antiepileptics - decreases absorption

Iron chelators (dexrazoxane) might decrease the absorption of antiepileptics (fosphenytoin, phenytoin). Avoid.

Severe Theoretical

Antiepileptics - decreases exposure

Lumacaftor is predicted to decrease the exposure to antiepileptics (carbamazepine, fosphenytoin, phenobarbital, phenytoin, primidone). Avoid.

Severe Theoretical

Antiepileptics - decreases concentration

St John’s wort is predicted to decrease the concentration of antiepileptics (fosphenytoin, phenobarbital, phenytoin, primidone). Avoid.

Severe Theoretical

Antiepileptics - increases risk of overheating and dehydration

Hydroxyzine potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.

Severe Theoretical

Antiepileptics - increases risk of overheating and dehydration

Haloperidol potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.

Severe Theoretical

Antiepileptics - decreases absorption

Dexrazoxane might decrease the absorption of antiepileptics (fosphenytoin, phenytoin). Avoid.

Severe Theoretical

Antiepileptics - increases risk of overheating and dehydration

Oxybutynin potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.

Severe Theoretical

Moderate (25)

Antiepileptics - increases concentration

Intravenous chloramphenicol increases the concentration of antiepileptics (fosphenytoin, phenytoin) and antiepileptics (fosphenytoin, phenytoin) affect the concentration of intravenous chloramphenicol

Moderate Study

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

Moderate Anecdotal

Antiepileptics - increases concentration

Disulfiramincreasestheconcentrationofantiepileptics (fosphenytoin,phenytoin).Monitorconcentrationandadjust dose.rStudy →AlsoseeTABLE12p.1520

Moderate Study

Antiepileptics - increases concentration

Fluorouracilincreasestheconcentrationofantiepileptics (fosphenytoin,phenytoin).Monitorconcentrationandadjust dose.rAnecdotal 1xidneppA|snoitcaretnI A1 https://www.facebook.c (Books-Courses-Medic

Moderate Anecdotal

Antiepileptics - decreases concentration

Folates are predicted to decrease the concentration of antiepileptics (fosphenytoin, phenobarbital, phenytoin, primidone). Monitor concentration and adjust dose.

Moderate Study

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.

Unknown Theoretical

Antiepileptics - increases risk of visual disturbances

Alcohol potentially increases the risk of visual disturbances when given with antiepileptics (retigabine).

Unknown Study

Antiepileptics - decreases exposure

Enzalutamide is predicted to slightly decrease the exposure to antiepileptics (brivaracetam).

Unknown Theoretical

Antiepileptics - decreases exposure

Apalutamidepotentiallydecreasestheexposureto antiepileptics(valproate).nTheoretical

Unknown Theoretical

Antiepileptics - increases concentration

Capecitabine increases the concentration of antiepileptics (fosphenytoin, phenytoin).

Unknown Anecdotal

Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: class

Disclaimer: This information is sourced from Pharmacy and Poisons Board (Kenya). Always consult a qualified healthcare professional before using any medication.

About this medicine

Levetiracetam is a medication used to help control seizures in people with epilepsy.

What it treats

  • epilepsy
  • seizure disorders

How it works

It helps to stabilize electrical activity in the brain, reducing the chance of seizures.

Who it's for

It is for people diagnosed with epilepsy who experience seizures.

Drug class

Antiepileptics

Cautions

  • • Be cautious if taking other medications that affect the brain, as they may increase side effects.

AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.

Clinical monograph: Levetiracetam

BNF-referenced

Levetiracetam is an antiepileptic drug primarily used in the management of epilepsy and other seizure disorders. It is recognized for its unique mechanism of action, which distinguishes it from other antiepileptic medications. Levetiracetam is typically well tolerated and has a wide therapeutic index, making it a preferred choice in various clinical settings. Its ability to modulate synaptic transmission without affecting normal neuronal activity contributes to its efficacy in seizure control.

Indications

  • Epilepsy
  • Focal seizures
  • Generalized tonic-clonic seizures
  • Myoclonic seizures in juvenile myoclonic epilepsy

Mechanism of action

Levetiracetam exerts its antiepileptic effects by binding to synaptic vesicle protein 2A (SV2A), a protein found on synaptic vesicles within the central nervous system. This binding is thought to play a crucial role in vesicle exocytosis and the modulation of synaptic transmission. By stimulating pre-synaptic SV2A, levetiracetam may inhibit the release of neurotransmitters during pathological conditions without interfering with normal neurotransmission. Additionally, it has been shown to indirectly affect GABAergic transmission and may inhibit N-type calcium channels, although the implications of these actions for its antiepileptic effects remain to be fully understood.

Pharmacodynamics

Levetiracetam prevents seizure activity primarily by selectively inhibiting hypersynchronized epileptiform burst firing, while preserving normal neuronal transmission. It has a wide therapeutic index, which implies a lower risk of toxicity compared to other antiepileptic drugs. However, it is important to monitor patients for potential emergence or worsening of depressive symptoms, suicidal ideation, and behavioral changes, as there is an associated increased risk of such effects with the use of antiepileptic medications, including levetiracetam.

Pharmacokinetics

Levetiracetam is rapidly absorbed after oral administration, with peak plasma concentrations typically achieved within 1 to 1.5 hours. It is primarily eliminated by the kidneys, with approximately 66% of an administered dose excreted unchanged in the urine. The half-life of levetiracetam is approximately 7 to 8 hours in adults, and it does not undergo significant metabolism, which limits drug-drug interactions. Dose adjustments may be necessary in patients with renal impairment.

Adverse effects

  • Drowsiness
  • Fatigue
  • Irritability
  • Dizziness
  • Nausea
  • Vomiting
  • Aseptic meningitis
  • Suicidal behaviour
  • Severe cutaneous adverse reactions
  • Hypersensitivity reactions

Interactions

  • Other antiepileptic drugs
  • Alcohol
  • CNS depressants

Precautions

  • Cautions in patients with renal impairment
  • Monitor for signs of depression or suicidal ideation
  • Consider withdrawal if rash or signs of hypersensitivity occur

Pregnancy

Limited data suggest no harmful effects, but caution is advised.

Breast-feeding

Present in breast milk, but limited data indicate no harmful effects on the infant.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

  • Oral solution
  • Tablets
  • Dispersible tablets
  • Injection
BNF 85 (British National Formulary) p.371 BNF for Children 2019-2020 p.230 PubChem / pathway

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: Levetiracetam

PubChem CID 5284583

Molecular formula: C8H14N2O2

Mechanism of action

The exact mechanism through which levetiracetam exerts its anti-epileptic effects is unclear, but is thought to be unique amongst other anti-epileptic medications. Current knowledge suggests that levetiracetam’s binding to synaptic vesicle protein 2A (SV2A) is a key driver of its action. SV2A is a membrane-bound protein that is found on synaptic vesicles and is ubiquitous throughout the CNS - it appears to play a role in vesicle exocytosis and in the modulation of synaptic transmission by increasing the available amount of secretory vesicles available for neurotransmission. Stimulation of pre-synaptic SV2A by levetiracetam may inhibit neurotransmitter release, but this action does not appear to affect normal neurotransmission. This has led to the suggestion that levetiracetam exclusively modulates the function of SV2A only under pathophysiological conditions. Levetiracetam and related analogues showed a correlation between affinity for SV2A and anti-epileptic potency, further suggesting that action at this site contributes to the anti-epileptic activity of the drug. Levetiracetam has also been shown to indirectly affect GABAergic neurotransmission (despite having no direct effect on GABAergic or glutamatergic receptors) and modulate ionic currents. Similarly, levetiracetam has been shown in vitro to inhibit N-type calcium channels. How, or even if, these actions are implicated in its anti-epileptic action have yet to be elucidated. The precise mechanism by which levetiracetam exerts its antiepileptic effect is unknown. The antiepileptic activity of levetiracetam was assessed in a number of animal models of epileptic seizures. Levetiracetam did not inhibit single seizures induced by maximal stimulation with electrical current or different chemoconvulsants and showed only minimal activity in submaximal stimulation and in threshold tests. Protection was observed, however, against secondarily generalized activity from focal seizures induced by pilocarpine and kainic acid, two chemoconvulsants that induce seizures that mimic some features of human complex partial seizures with secondary generalization. Levetiracetam also displayed inhibitory properties in the kindling model in rats, another model of human complex partial seizures, both during kindling development and in the fully kindled state. The predictive value of these animal models for specific types of human epilepsy is uncertain. In vitro and in vivo recordings of epileptiform activity from the hippocampus have shown that levetiracetam inhibits burst firing without affecting normal neuronal excitability, suggesting that levetiracetam may selectively prevent hypersynchronization of epileptiform burst firing and propagation of seizure activity. Levetiracetam at concentrations of up to 10 muM did not demonstrate binding affinity for a variety of known receptors, such as those associated with benzodiazepines, GABA (gammaaminobutyric acid), glycine, NMDA (N-methyl-D-aspartate), re-uptake sites, and second messenger systems. Furthermore, in vitro studies have failed to find an effect of levetiracetam on neuronal voltage-gated sodium or T-type calcium currents and levetiracetam does not appear to directly facilitate GABAergic neurotransmission. However, in vitro studies have demonstrated that levetiractem opposes the activity of negative modulators of GABA- and glycine-gated currents and partially inhibits N-type calcium currents in neuronal cells. A saturable and stereoselective neuronal binding site in rat brain tissue has been described for levetiracetam. Experimental data indicate that this binding site is the synaptic vesicle protein SV2A, thought to be involved in the regulation of vesicle exocytosis. Although the molecular significance of levetiracetam binding to synaptic vesicle protein SV2A is not understood, levetiracetam and related analogs showed a rank order of affinity for SV2A which correlated with the potency of their antiseizure activity in audiogenic seizure-pro

Pharmacodynamics

Levetiracetam appears to prevent seizure activity via the selective inhibition of hypersynchronized epileptiform burst firing without affecting normal neuronal transmission, though the exact mechanism through which this occurs is unclear. The therapeutic index of levetiracetam is wide, making it relatively unique amongst other anti-epileptic medications. Anti-epileptic drugs, including levetiracetam, may increase the risk of suicidal ideation or behaviour - patients taking levetiracetam should be monitored for the emergence or worsening of depressive symptoms, suicidal ideation, and behavioural abnormalities.

Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.

This drug in other countries

The same active ingredient registered across other registries we cover - including different brands.