Do I need a prescription for Retigabine 400mg tablets?

Retigabine 400mg tablets is classified as a Valid as a prescribable product in the UK. However, always consult a pharmacist or doctor before use. (Source: NHS dm+d)

What are the brand names for Retigabine 400mg tablets?

Retigabine 400mg tablets is the generic name. It is available under brand names including: Trobalt 400mg tablets. (Source: NHS dm+d — Actual Medicinal Products)

Retigabine 400mg tablets

Tablet

400mg

Oral

Antiepileptic

Ezogabine (D23129) is a close structural analog of the centrally acting analgesic flupitrine.

Active ingredients:

Retigabine

BNF classificationBrowse formulary

Where this medicine sits in the British National Formulary — the UK's standard prescribing reference

BNF 04.08.01

ATC classificationBrowse ATC index

International classification by the WHO, grouping medicines by the organ system they act on

ATC N03AX21

Chemical classBrowse classes

Classification based on the molecule's chemical structure and properties

Primary care groupBrowse groups

NHS medication clusters used to compare prescribing patterns across GP practices

Antiepileptic

Check interactions for Retigabine

No active safety alerts

Official documents, adverse reaction reporting, and safety monitoring

Report a side effect

Submit a Yellow Card report to the MHRA

Safety monitoring data

Yellow Card reports

MHRA

The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.

View Drug Analysis Profile

Suspected adverse reactions reported for Retigabine

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Interactive Drug Analysis Profiles for all medicines

Report a side effect

Submit a Yellow Card report to the MHRA

Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.

EudraVigilance

EMA

The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.

View EudraVigilance report

Suspected adverse reactions reported for Retigabine

About EudraVigilance

Learn about EU pharmacovigilance and safety monitoring

EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.

1 branded products available

1 productsShow details

1 products

Possibly available on the UK marketDiscontinuedAvailability per NHS dm+d

MHRA licensed products

View all licensed products for Retigabine on the MHRA register

Trobalt 400mg tablets

GlaxoSmithKline UK Ltd

Discontinued

Source: NHS dm+dOGL 3.0

Updated about 1 month ago(1 Mar 2026)

Daily doseShow details

WHO defined daily dose (DDD)

900 mg

Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.

Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.

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Oral suspension

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Same therapeutic group

Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.

NHS prescribing volume and spending trends

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Clinical guidelines and formulary information

British National Formulary

Retigabine

BNF

Drug monograph — bnf.nice.org.uk

Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.

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Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.

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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.

Codes for healthcare professionals and prescribing systems

Show details

These codes are used by healthcare IT systems and prescribers to identify this medicine.

NHS UK identifiers

SNOMED CT

42136411000001107

dm+d ID

42136411000001107

VTM (Virtual Therapeutic Moiety)

777427009

VMP (Virtual Medicinal Product)

42136411000001107

BNF code

04080100

International identifiers

ATC code — Anatomical Therapeutic Chemical (WHO)

N03AX21

Browse tools

dm+d Browser

NHSBSA medicines dictionary lookup

SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).

Active and completed clinical studies from ClinicalTrials.gov

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Searching UK clinical trials...

Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.

Pharmacology and chemical data from DrugBank

go.drugbank.com

Key facts

Drug status

Approved

Major interactions

1 found

Half-life

7.5 hours

Mechanism

Ezogabine has a novel mechanism of action that involves opening of neuronal Kv7.

Food interactions

1 warning

Human targets

4 targets

Data: DrugBank · CC BY-NC 4.0

Pharmacokinetics at a glance

Absorption

60%

Rapidly absorbed and distributed, with an absolute oral bioavailability of 60%.…

Half-life

7.5 hours

Terminal half-life = 7.5 hours

Protein binding

80%

Approximately 80% protein bound.

Volume of distribution

8.7 L/kg

8.7 L/kg

Metabolism

Ezogabine is metabolized exclusively via phase II hepatic N-glucurodination and acetylation.…

Elimination

85%

Urine (85%, 36% of total dose as unchanged drug, 18% of total dose as NAMR) and feces (14%, 3% of total dose as unchanged drug)

Clearance

0.58 - 0.76 L/h

0.58 - 0.76 L/h·kg. Clearance may differ between ethnic groups with Black Americans having 20% lower clearance than Caucasian Americans.

Pharmacokinetic data: DrugBank · CC BY-NC 4.0

Status:

Approved

Withdrawn

Small molecule

About this compound

Ezogabine (D23129) is a close structural analog of the centrally acting analgesic flupitrine. It is a neuronal potassium channel opener being developed as a first-in-class antiepileptic drug (AED) and is currently being studied in Phase 3 trials as an adjunctive treatment for partial-onset seizures in adult patients with refractory epilepsy. FDA approved in June 10, 2011 under the name of ezogabine.

Properties:

solid

Avg. mass: 303.33 Da

View FDA drug label

DrugBank indication

Adjuvant treatment of partial-onset seizures.

Also known as(81)

ethyl {2-amino-4-[(4-fluorobenzyl)amino]phenyl}carbamate

Ethyl 2-amino-4-((p-fluorobenzyl)amino)carbanilate

EZG

Ezogabine

N-(2-Amino-4-(4-fluorobenzylamino)-phenyl) carbamic acid ethyl ester

N-(2-Amino-4-(4-fluorobenzylamino)phenyl)carbamic acid ethyl ester

Retigabina

Retigabine

Dosage forms(10)

Tablet, film coated (Oral) — 200 mg/1

Tablet, film coated (Oral) — 300 mg/1

Tablet, film coated (Oral) — 400 mg/1

Tablet, film coated (Oral) — 50 mg/1

Tablet, film coated (Oral) — 100 MG

Tablet, film coated (Oral) — 200 MG

Tablet, film coated (Oral) — 300 MG

Tablet, film coated (Oral) — 400 MG

Molecular properties(19)

Drug interactions(1666)

Known interactions with other medications. Always consult a healthcare professional.

Buprenorphine

Moderate

DB00921

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Buprenorphine.

Check this interaction

Doxylamine

Moderate

DB00366

Doxylamine may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Dronabinol

Moderate

DB00470

Dronabinol may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Droperidol

Moderate

DB00450

Droperidol may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Hydrocodone

Moderate

DB00956

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Hydrocodone.

Check this interaction

Magnesium sulfate

Moderate

DB00653

The therapeutic efficacy of Ezogabine can be increased when used in combination with Magnesium sulfate.

Check this interaction

Methotrimeprazine

Moderate

DB01403

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Methotrimeprazine.

Check this interaction

Metyrosine

Moderate

DB00765

Ezogabine may increase the sedative activities of Metyrosine.

Check this interaction

Minocycline

Moderate

DB01017

Minocycline may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Mirtazapine

Moderate

DB00370

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Mirtazapine.

Check this interaction

Nabilone

Moderate

DB00486

Nabilone may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Orphenadrine

Moderate

DB01173

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Orphenadrine.

Check this interaction

Paraldehyde

Moderate

DB09117

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Paraldehyde.

Check this interaction

Perampanel

Moderate

DB08883

Perampanel may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Pramipexole

Moderate

DB00413

Ezogabine may increase the sedative activities of Pramipexole.

Check this interaction

Ropinirole

Moderate

DB00268

Ezogabine may increase the sedative activities of Ropinirole.

Check this interaction

Rotigotine

Moderate

DB05271

Ezogabine may increase the sedative activities of Rotigotine.

Check this interaction

Rufinamide

Unknown severity

DB06201

The risk or severity of adverse effects can be increased when Rufinamide is combined with Ezogabine.

Check this interaction

Sodium oxybate

Moderate

DB09072

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Sodium oxybate.

Check this interaction

Suvorexant

Moderate

DB09034

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Suvorexant.

Check this interaction

Tapentadol

Moderate

DB06204

Tapentadol may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Thalidomide

Moderate

DB01041

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Thalidomide.

Check this interaction

Zolpidem

Moderate

DB00425

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Zolpidem.

Check this interaction

Mefloquine

Moderate

DB00358

The therapeutic efficacy of Ezogabine can be decreased when used in combination with Mefloquine.

Check this interaction

Mianserin

Moderate

DB06148

The therapeutic efficacy of Ezogabine can be decreased when used in combination with Mianserin.

Check this interaction

Orlistat

Moderate

DB01083

Orlistat can cause a decrease in the absorption of Ezogabine resulting in a reduced serum concentration and potentially a decrease in efficacy.

Check this interaction

Phenytoin

Unknown severity

DB00252

The serum concentration of Ezogabine can be decreased when it is combined with Phenytoin.

Check this interaction

Fosphenytoin

Unknown severity

DB01320

The serum concentration of Ezogabine can be decreased when it is combined with Fosphenytoin.

Check this interaction

Topotecan

Moderate

DB01030

Ezogabine may increase the excretion rate of Topotecan which could result in a lower serum level and potentially a reduction in efficacy.

Check this interaction

Methadone

Unknown severity

DB00333

The risk or severity of adverse effects can be increased when Methadone is combined with Ezogabine.

Check this interaction

Lamotrigine

Unknown severity

DB00555

The serum concentration of Lamotrigine can be decreased when it is combined with Ezogabine.

Check this interaction

Carbamazepine

Unknown severity

DB00564

The serum concentration of Ezogabine can be decreased when it is combined with Carbamazepine.

Check this interaction

Nelfinavir

Moderate

DB00220

The metabolism of Ezogabine can be increased when combined with Nelfinavir.

Check this interaction

Zidovudine

Moderate

DB00495

The metabolism of Ezogabine can be increased when combined with Zidovudine.

Check this interaction

Ritonavir

Moderate

DB00503

The metabolism of Ezogabine can be increased when combined with Ritonavir.

Check this interaction

Efavirenz

Moderate

DB00625

The metabolism of Ezogabine can be increased when combined with Efavirenz.

Check this interaction

Primidone

Moderate

DB00794

The metabolism of Ezogabine can be increased when combined with Primidone.

Check this interaction

Tipranavir

Moderate

DB00932

The metabolism of Ezogabine can be increased when combined with Tipranavir.

Check this interaction

Rifampin

Moderate

DB01045

The metabolism of Ezogabine can be increased when combined with Rifampicin.

Check this interaction

Phenobarbital

Moderate

DB01174

The metabolism of Ezogabine can be increased when combined with Phenobarbital.

Check this interaction

Testosterone propionate

Moderate

DB01420

The metabolism of Ezogabine can be increased when combined with Testosterone propionate.

Check this interaction

Tetracosactide

Unknown severity

DB01284

The risk or severity of liver damage can be increased when Tetracosactide is combined with Ezogabine.

Check this interaction

Azelastine

Moderate

DB00972

Ezogabine may increase the central nervous system depressant (CNS depressant) activities of Azelastine.

Check this interaction

Brimonidine

Moderate

DB00484

Brimonidine may increase the central nervous system depressant (CNS depressant) activities of Ezogabine.

Check this interaction

Fluvoxamine

Unknown severity

DB00176

The risk or severity of adverse effects can be increased when Ezogabine is combined with Fluvoxamine.

Check this interaction

Duloxetine

Unknown severity

DB00476

The risk or severity of adverse effects can be increased when Ezogabine is combined with Duloxetine.

Check this interaction

Paroxetine

Unknown severity

DB00715

The risk or severity of adverse effects can be increased when Ezogabine is combined with Paroxetine.

Check this interaction

Sertraline

Unknown severity

DB01104

The risk or severity of adverse effects can be increased when Ezogabine is combined with Sertraline.

Check this interaction

Sibutramine

Unknown severity

DB01105

The risk or severity of adverse effects can be increased when Ezogabine is combined with Sibutramine.

Check this interaction

Nefazodone

Unknown severity

DB01149

The risk or severity of adverse effects can be increased when Ezogabine is combined with Nefazodone.

Check this interaction

Showing 50 of 1666 interactions

Food & lifestyle interactions

Advice

Take with or without food. High-fat meals alter drug absorption, but not to a clinically significant extent.

Toxicity & overdose

Lethal Dose, acute, oral, rat = 100 mg/kg;
Lethal Dose, chronic, oral, rat = 5.1 mg/kg/day, 90-day;
Most common adverse effects that lead to discontinuation of therapy include dizziness and somnolence.

How it works

Mechanism of action

Ezogabine has a novel mechanism of action that involves opening of neuronal Kv7.2-7.5 (formerly KCNQ2-5) voltage activated potassium channels. These channels (primarily Kv7.2/7.3) enable generation of the M-current, a sub-threshold potassium current that serves to stabilize the membrane potential and control neuronal excitability. In addition to acting on potassium ion channels, retigabine also affects GABA neurotransmission in the GABA-A receptor, which is a key inhibitory receptor in the central nervous system and is implicated in epilepsy. Malfunctioning of the GABA-A receptor leads to hyperexcitability in the brain, which causes seizures, making this receptor an important target for antiepileptic therapeutics. Apart from increasing the concentration of GABA in the brain (by either enhancing GABA synthesis or blocking GABA metabolism), retigabine allosterically potentiates GABA-induced current in rat cortical neurons in a concentration-dependent manner. Numerous studies have demonstrated that retigabine is effective in a broad spectrum of in vivo epilepsy and seizure models.

Pharmacodynamics

As compared to other antiepileptic agents, ezogabine is unique in that it selectively activates potassium ion channels Kv 7.2-Kv7.5 and not cardiac Kv 7.1, thereby avoiding cardiac side effects. The antiepileptics, as a drug class, are routinely used in the treatment of a number of disease states in addition to epilepsy. Ezogabine is highly efficacious in a broad-spectrum of in vivo epilepsy and seizure models. A comparison of antiepileptic form activity of ezogabine with that of conventional anticonvulsants in in vitro models suggests that retigabine is especially likely to be useful in the treatment of pharmacoresistant epilepsy. Retigabine clearly attenuates pain-like behaviors in various animal models of neuropathic pain; it may also prove to be useful in treatment of clinical anxiety disorders. Clinical data obtained thus far indicate that retigabine is well tolerated in humans when titrated up to its therapeutic dose range. No tolerance, drug dependence, or withdrawal liability has been reported. Thus, retigabine may prove to be useful in the treatment of a diverse range of disease states in which neuronal hyperexcitability is a common underlying factor.

Pharmacokinetics

How the body processes this drug — absorption, distribution, metabolism, and elimination

Absorption

Rapidly absorbed and distributed, with an absolute oral bioavailability of 60%. Pharmacokinetics of ezogabine suggest first-order kinetics.
Tmax, single oral dose = 30-120 minutes;
Time to steady state = 3 days

Half-life

Terminal half-life = 7.5 hours

Protein binding

Approximately 80% protein bound.

Volume of distribution

8.7 L/kg

Metabolism

Ezogabine is metabolized exclusively via phase II hepatic N-glucurodination and acetylation. N-glucurodination is the major metabolic pathway of the two and form two major N-glucuronide metabolites. The enzymes involved are UGT1A1, 1A9, 1A4, and 1A3.

However, the product of the N-acetyl pathway is a weak, active metabolite referred to as NAMR. The enzyme that is involved in the N-acetyl pathway is called N-acetyltransferase 2. The pharmacokinetics of NAMR and ezogabine are similar.

The cytochrome P450 enzyme system is not involved with the metabolism of ezogabine.

Route of elimination

Urine (85%, 36% of total dose as unchanged drug, 18% of total dose as NAMR) and feces (14%, 3% of total dose as unchanged drug)

Clearance

0.58 - 0.76 L/h·kg. Clearance may differ between ethnic groups with Black Americans having 20% lower clearance than Caucasian Americans.

Drug targets(4)

Proteins and enzymes this drug interacts with in the body

Potassium voltage-gated channel subfamily KQT member 3

BE0002398

KCNQ3

modulator

Specific functioncalmodulin binding

Cellular location

Cell membrane

General function & pharmacology

Pore-forming subunit of the voltage-gated potassium (Kv) M-channel which is responsible for the M-current, a key controller of neuronal excitability .
PMID:16319223 PMID:27564677 PMID:28793216 PMID:9872318

M-channel is composed of pore-forming subunits KCNQ2 and KCNQ3 assembled as heterotetramers .
PMID:14534157 PMID:16319223 PMID:27564677 PMID:9872318

The native M-current has a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons as well as the responsiveness to synaptic inputs .
PMID:14534157 PMID:16319223 PMID:28793216

M-channel is selectively permeable in vitro to other cations besides potassium, in decreasing order of affinity K(+) > Rb(+) > Cs(+) > Na(+) .
PMID:28793216
M-channel association with SLC5A3/SMIT1 alters channel ion selectivity, increasing Na(+) and Cs(+) permeation relative to K(+) .
PMID:28793216
Suppressed by activation of M1 muscarinic acetylcholine receptors .
PMID:10713961
KCNQ3 also associates with KCNQ5 to form a functional channel in vitro and may also contribute to the M-current in brain PMID:11159685

Potassium voltage-gated channel subfamily KQT member 2

BE0000897

KCNQ2

Specific functionankyrin binding

Cellular location

Cell membrane

General function & pharmacology

Pore-forming subunit of the voltage-gated potassium (Kv) M-channel which is responsible for the M-current, a key controller of neuronal excitability .
PMID:24277843 PMID:28793216 PMID:9836639

M-channel is composed of pore-forming subunits KCNQ2 and KCNQ3 assembled as heterotetramers .
PMID:10781098 PMID:14534157 PMID:32884139 PMID:37857637 PMID:9836639

The native M-current has a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons as well as the responsiveness to synaptic inputs .
PMID:14534157 PMID:28793216 PMID:9836639

KCNQ2-KCNQ3 M-channel is selectively permeable in vitro to other cations besides potassium, in decreasing order of affinity K(+) > Rb(+) > Cs(+) > Na(+) .
PMID:28793216
M-channel association with SLC5A3/SMIT1 alters channel ion selectivity, increasing Na(+) and Cs(+) permeation relative to K(+) .
PMID:28793216
Suppressed by activation of the muscarinic acetylcholine receptor CHRM1 PMID:10684873 PMID:10713961

Potassium voltage-gated channel subfamily KQT member 4

BE0002399

KCNQ4

Specific functionpotassium channel activity

Cellular location

Basal cell membrane

General function & pharmacology

Pore-forming subunit of the voltage-gated potassium (Kv) channel involved in the regulation of sensory cells excitability in the cochlea .
PMID:10025409 PMID:34767770
KCNQ4/Kv7.4 channel is composed of 4 pore-forming subunits assembled as tetramers .
PMID:34767770
Promotes the outflow of potassium ions in the repolarization phase of action potential which plays a role in regulating membrane potential of excitable cells .
PMID:10025409 PMID:11245603 PMID:34767770

The channel conducts a slowly activating and deactivating current .
PMID:10025409 PMID:11245603
Current often shows some inward rectification at positive potentials .
PMID:10025409
Channel may be selectively permeable in vitro to other cations besides potassium, in decreasing order of affinity K(+) = Rb(+) > Cs(+) > Na(+) .
PMID:10025409
Important for normal physiological function of inner ear such as sensory perception of sound PMID:10025409 PMID:10369879

Potassium voltage-gated channel subfamily KQT member 5

BE0002400

KCNQ5

Specific functionvoltage-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potential

Cellular location

Cell membrane

General function & pharmacology

Pore-forming subunit of the voltage-gated potassium (Kv) channel broadly expressed in brain and involved in the regulation of neuronal excitability .
PMID:10787416 PMID:10816588 PMID:11159685 PMID:28669405

Associates with KCNQ3/Kv7.3 pore-forming subunit to form a potassium channel which contributes to M-type current, a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons .
PMID:10816588 PMID:11159685
Contributes, with other potassium channels, to the molecular diversity of a heterogeneous population of M-channels, varying in kinetic and pharmacological properties, which underlie this physiologically important current .
PMID:10816588
Also forms a functional channel with KCNQ1/Kv7.1 subunit that may contribute to vasoconstriction and hypertension .
PMID:24855057
Channel may be selectively permeable in vitro to other cations besides potassium, in decreasing order of affinity K(+) = Rb(+) > Cs(+) > Na(+) .
PMID:10816588
Similar to the native M-channel, KCNQ3-KCNQ5 potassium channel is suppressed by activation of the muscarinic acetylcholine receptor CHRM1 PMID:10816588

Metabolizing enzymes(5)

Enzymes involved in drug metabolism — important for understanding drug interactions

Enzyme activity key

substrate

inhibitor

inducer

UGT1A1UDP-glucuronosyltransferase 1A1

substrate

UGT1A3UDP-glucuronosyltransferase 1A3

substrate

UGT1A4UDP-glucuronosyltransferase 1A4

substrate

UGT1A9UDP-glucuronosyltransferase 1A9

substrate

NAT2Arylamine N-acetyltransferase 2

substrate

Scientific references(10)

Porter R.J., Nohria V., Rundfeldt C.

Retigabine.

Neurotherapeutics

20074(1):149-154. doi: 10.1016/j.nurt.2006.11.012

PMID: 17199031 DOI: 10.1016/j.nurt.2006.11.012

Hermann R., Ferron G.M., Erb K., Knebel N., Ruus P., Paul J., Richards L., Cnota H.P., Troy S.

Effects of age and sex on the disposition of retigabine.

Clinical Pharmacology & Therapeutics

200373(1):61-70. doi: 10.1067/mcp.2003.12

PMID: 12545144 DOI: 10.1067/mcp.2003.12

Hermann R., Knebel N.G., Niebch G., Richards L., Borlak J., Locher M.

Pharmacokinetic interaction between retigabine and lamotrigine in healthy subjects.

European Journal of Clinical Pharmacology

200358(12):795-802. doi: 10.1007/s00228-003-0558-6

PMID: 12698305 DOI: 10.1007/s00228-003-0558-6

Dost R., Rostock A., Rundfeldt C.

The anti-hyperalgesic activity of retigabine is mediated by KCNQ potassium channel activation.

Naunyn-Schmiedeberg's Archives of Pharmacology

2004369(4):382-390. doi: 10.1007/s00210-004-0881-1

PMID: 15007538 DOI: 10.1007/s00210-004-0881-1

Mikkelsen J.D.

The KCNQ channel activator retigabine blocks haloperidol-induced c-Fos expression in the striatum of the rat.

Neuroscience Letters

2004362(3):240-243. doi: 10.1016/s0304-3940(04)00328-3

PMID: 15158023 DOI: 10.1016/s0304-3940(04)00328-3

Punke M.A., Friederich P.

Retigabine Stimulates Human KCNQ2/Q3 Channels in the Presence of Bupivacaine.

Anesthesiology

2004101(2):430-438. doi: 10.1097/00000542-200408000-00024

PMID: 15277926 DOI: 10.1097/00000542-200408000-00024

Wuttke T.V., Seebohm G., Bail S., Maljevic S., Lerche H.

The New Anticonvulsant Retigabine Favors Voltage-Dependent Opening of the Kv7.

2 (KCNQ2) Channel by Binding to Its Activation Gate

Molecular Pharmacology. 200567(4):1009-1017. doi: 10.1124/mol.104.010793

PMID: 15662042 DOI: 10.1124/mol.104.010793

Fatope M.O.

Satellite Symposium Asta Medica.

Lung Cancer

200132:67-69. doi: 10.1016/s0169-5002(01)00220-3

PMID: 16034707 DOI: 10.1016/s0169-5002(01)00220-3

Orhan G., Wuttke T.V., Nies A.T., Schwab M., Lerche H.

Retigabine/Ezogabine, a KCNQ/K(V)7 channel opener: pharmacological and clinical data.

Expert Opinion on Pharmacotherapy

2012 Aug13(12):1807-16. doi: 10.1517/14656566.2012.706278. Epub 2012 Jul 12

PMID: 22783830 DOI: 10.1517/14656566.2012.706278

Amabile C.M., Vasudevan A.

Ezogabine: a novel antiepileptic for adjunctive treatment of partial-onset seizures.

Pharmacotherapy

2013 Feb33(2):187-94. doi: 10.1002/phar.1185

PMID: 23386597 DOI: 10.1002/phar.1185

ATC classification(1 code)

ATC N03AX21

Affected organisms(1)

Humans and other mammals

Experimental properties(1)

External resources(2)

RxList Drugs.com

Protein Data Bank entries(3)

7bym

7cr2

7cr7

Commercial products(14)

Chemical identifiers

CAS, UNII, InChI Key and database cross-references

Show

Linked compound data from DrugBank Open Data (CC BY-NC 4.0)

Ezogabine

Matched from: Retigabine

DB04953

CAS number

150812-12-7

UNII (FDA)

12G01I6BBU

InChI Key (molecular fingerprint)

PCOBBVZJEWWZFR-UHFFFAOYSA-N

Synonym match

95% confidence

Additional database identifiers

ChEBI

68584

PubChem Compound

121892

PubChem Substance

175426917

KEGG Compound

C13826

KEGG Drug

D09569

ChemSpider

108740

BindingDB

50143558

PharmGKB

PA144997862

PDB

FBX

Wikipedia

Retigabine

ChEMBL

CHEMBL41355

ZINC

ZINC000000016154

RxCUI

1112990

HUGO Gene Nomenclature Committee (HGNC)

HGNC:6297

GenAtlas

KCNQ3

GeneCards

KCNQ3

GenBank Gene Database

AF071491

IUPHAR

562

Guide to Pharmacology

562

UniProtKB

O43525

UniProt Accession

KCNQ3_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:6296

GenAtlas

KCNQ2

GeneCards

KCNQ2

GenBank Gene Database

D82346

GenBank Protein Database

1841342

IUPHAR

561

Guide to Pharmacology

561

UniProtKB

O43526

UniProt Accession

KCNQ2_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:6298

GenAtlas

KCNQ4

GeneCards

KCNQ4

GenBank Gene Database

AF105202

IUPHAR

563

Guide to Pharmacology

563

UniProtKB

P56696

UniProt Accession

KCNQ4_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:6299

GenAtlas

KCNQ5

GeneCards

KCNQ5

GenBank Gene Database

AF249278

IUPHAR

564

Guide to Pharmacology

564

UniProtKB

Q9NR82

UniProt Accession

KCNQ5_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:12530

GeneCards

UGT1A1

GenBank Gene Database

M57899

GenBank Protein Database

184473

Guide to Pharmacology

2990

UniProtKB

P22309

UniProt Accession

UD11_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:12535

GeneCards

UGT1A3

GenBank Gene Database

M84127

GenBank Protein Database

340135

UniProtKB

P35503

UniProt Accession

UD13_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:12536

GeneCards

UGT1A4

GenBank Gene Database

M57951

GenBank Protein Database

184475

UniProtKB

P22310

UniProt Accession

UD14_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:12541

GeneCards

UGT1A9

GenBank Gene Database

S55985

GenBank Protein Database

7690346

UniProtKB

O60656

UniProt Accession

UD19_HUMAN

HUGO Gene Nomenclature Committee (HGNC)

HGNC:7646

GeneCards

NAT2

GenBank Gene Database

D90040

GenBank Protein Database

219412

UniProtKB

P11245

UniProt Accession

ARY2_HUMAN

DrugBank citations

If you use DrugBank data in your research, please cite the following publications:

Knox C., Wilson M., Klinger C.M., et al

DrugBank 6.

0: the DrugBank Knowledgebase for 2024

Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275

PMID: 37953279

Wishart D.S., Feunang Y.D., Guo A.C., et al

DrugBank 5.

0: a major update to the DrugBank database for 2018

Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082

PMID: 29126136

Show earlier publications

Law V., Knox C., Djoumbou Y., et al

DrugBank 4.

0: shedding new light on drug metabolism

Nucleic Acids Res. 2014 Jan 142(1):D1091-7

PMID: 24203711

Knox C., Law V., Jewison T., et al

DrugBank 3.

0: a comprehensive resource for 'omics' research on drugs

Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41

PMID: 21059682

Wishart D.S., Knox C., Guo A.C., et al

DrugBank: a knowledgebase for drugs, drug actions and drug targets.

Nucleic Acids Research

2008 Jan36(Database issue):D901-6

PMID: 18048412

Wishart D.S., Knox C., Guo A.C., et al

DrugBank: a comprehensive resource for in silico drug discovery and exploration.

Nucleic Acids Research

2006 Jan 134(Database issue):D668-72

PMID: 16381955

Source: go.drugbank.comCC BY-NC 4.0

Updated 27 days ago(8 Mar 2026)

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Ezogabine

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