(levetiracetam · DailyMed)
Epiend
Glacial Acetic Acid 100 q.s,Glacial Acetic Acid 5.50 mg/ mL,Levetiracetam 500 mg/100ml,Sodium Chloride. 820 mg/6 mL,Sodium acetate trihydrate 164 mg/6 mL,Water for injection USP 100 q.s
What it does
Acetic acid is often used in medical settings for various purposes, including treating certain conditions.
Commonly used for: ear infections (otitis), skin infections, wound cleaning
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.
Medicine sourcing is available in Kenya only. We don't sell or dispense medicines - licensed pharmacies do.
Sourcing - Kenya onlyRegistration & product details
Source: Tanzania Medicines and Medical Devices Authority · fetched 2026-03-11 23:42:31 · updated 2026-10-19 03:00:44
Drug Interactions
65Pharmacodynamic 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.
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 acetic
Acetic acid is often used in medical settings for various purposes, including treating certain conditions.
What it treats
- ear infections (otitis)
- skin infections
- wound cleaning
How it works
Acetic acid helps to create an environment that can kill harmful bacteria and promote healing.
Who it's for
Acetic acid can be used by people suffering from specific infections or conditions as directed by a healthcare professional.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
About glacial
Glacial is a medicinal product used for specific health conditions.
How it works
The exact way glacial works in the body is not specified, but it is used in certain treatments.
Who it's for
Glacial may be suitable for individuals needing specific medical treatment.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
About levetiracetam
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-referencedLevetiracetam 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
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Clinical monograph: acetic
Acetic acid, commonly known as vinegar when diluted, is a colorless organic compound with a pungent smell and sour taste. It is primarily used in various applications including food preservation, flavoring, and as a chemical reagent. In medicine, it has antiseptic properties and is utilized in various formulations for its therapeutic effects, particularly in treating infections and as an astringent.
Indications
- Infections (topical treatment)
- Wound care (as an antiseptic)
- Ear infections (as an ear drop solution)
- Acid-base balance in metabolic acidosis
Dosage
Children: Refer to established guidelines as dosage may vary based on the formulation and indication.
Adults: Refer to established guidelines as dosage may vary based on the formulation and indication.
Mechanism of action
Acetic acid exerts its effects primarily through its ability to lower pH levels, creating an acidic environment which is inhospitable to many pathogens. It can disrupt the integrity of microbial cell membranes, leading to cell lysis and death. Additionally, acetic acid can promote the healing of wounds and enhance the absorption of certain medications when used as a solvent.
Pharmacodynamics
The pharmacodynamics of acetic acid involve its interaction with biological systems, leading to changes in cellular functions. Its acidic nature helps in the denaturation of proteins and disruption of microbial metabolism. This contributes to its antibacterial and antifungal activities, making it effective against a range of pathogens.
Pharmacokinetics
Acetic acid is rapidly absorbed in the gastrointestinal tract when ingested. It is metabolized primarily in the liver, converting to acetyl CoA and subsequently entering various metabolic pathways including the citric acid cycle. The elimination half-life varies but is generally short, with excretion occurring mainly via urine. When applied topically, absorption is minimal, and local effects are predominant.
Pregnancy
The safety of acetic acid during pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.
Breast-feeding
There is no specific information available regarding the use of acetic acid during breastfeeding. Caution is advised.
Storage
Store in a cool, dry place away from direct sunlight. Keep tightly closed in a well-ventilated area.
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Clinical monograph: glacial
Glacial acetic acid is a colorless liquid organic compound with a pungent smell. It is a key component in the production of vinegar and is used as a chemical reagent and solvent in various industrial applications. In medicine, glacial acetic acid is used for its antiseptic and astringent properties, particularly in the treatment of certain infections and as a topical treatment.
Indications
- Topical treatment of localized infections
- Antiseptic for skin and mucous membrane applications
- Astringent in certain dermatological conditions
Dosage
Children: Refer to professional resources for specific dosing information, as it can vary based on formulation and condition treated.
Adults: Refer to professional resources for specific dosing information, as it can vary based on formulation and condition treated.
Mechanism of action
Glacial acetic acid exerts its effects primarily through its acidic properties, leading to protein denaturation and cell lysis in microbial cells. This action disrupts cellular integrity, promoting the death of bacteria and fungi. Additionally, it can alter the pH of tissues, which may contribute to its antiseptic effects.
Pharmacodynamics
The pharmacodynamic effects of glacial acetic acid are largely attributed to its ability to lower the pH in the local environment, which can inhibit the growth of certain pathogens. Its astringent properties help to reduce secretions and promote tissue contraction, which can be beneficial in managing conditions that involve inflammation or excessive exudation.
Pharmacokinetics
Glacial acetic acid is absorbed through the skin and mucous membranes when applied topically. Once absorbed, it can be metabolized by the liver, with elimination primarily occurring through urine. The exact pharmacokinetic parameters can vary based on the route of administration and the formulation used, but detailed data on half-life and volume of distribution are not well-characterized in standard references.
Pregnancy
Glacial acetic acid should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is classified as a category C drug.
Breast-feeding
It is not known whether glacial acetic acid is excreted in human milk. Caution should be exercised when administering to nursing mothers.
Storage
Store in a tightly closed container, in a cool, dry place away from incompatible substances.
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 5284583Molecular 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.
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The same active ingredient registered across other registries we cover - including different brands.
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- ATROPINE · Reddys Pharma
- ASHITOX POWDER (Each gram contains: Propionic Acid/Benzoic acid/Sorbic Acid /Acetic Acid/MOS/Aluminum Silicate 5.75%/1.5%/0.63%/7.00%/0.50%/84.62%) · Advanced Agrovets Biotechnologies
- B- TOX POWDER (Each gram contains: Propionic acid/ Benzoic acid/ Sorbic acid/ Acetic acid/ Hydrated sodium calcium aluminosilicates 8.75%/ 1.5%/ 0.63%/ 10%) · Tradeon Band
- B-TOX POWDER POWDER ((Each gram contains: 8.75%/ 1.5%/ 0.63%/ 10%) · Tradeon Band
- BABY BEDIKOF COUGH SYRUP (Each 5ml contains Dilute Acetic Acid ) · Enicar Pharmaceutical
- DIPHEX INFANT COUGH SYRUP · Phyto-Riker Pharmaceuticals
- KELCUF JUNIOR COUGH · Enicar Pharmaceutical