Riluzole 25mg/5ml oral suspension sugar free
Requires a prescription from a doctor or prescriber
A glutamate antagonist (receptors, glutamate) used as an anticonvulsant (anticonvulsants) and to prolong the survival of patients with amyotrophic lateral sclerosis.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Yellow Card
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Drug safety updates
MHRA alerts for Riluzole
Safety monitoring data
Yellow Card reports
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.
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Suspected adverse reactions reported for Riluzole
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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
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Suspected adverse reactions reported for Riluzole
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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
MHRA licensed products
View all licensed products for Riluzole on the MHRA register
Teglutik 5mg/1ml oral suspension
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
100 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 the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(2)
Guidance on the use of riluzole (Rilutek) for the treatment of motor neurone disease (TA20)
Motor neurone disease: assessment and management (NG42)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 20 · Randomised trials: 24 · 1994–2026
Showing the 50 most relevant studies, sorted by most relevant.
J. Mora, A. Genge, A. Chiò, et al.
Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2019
M. Jaiswal
Medicinal Research Reviews, 2018
Luke J Weisbrod, Thomas T. Nilles-Melchert, Judith R. Bergjord, et al.
Neurotrauma Reports, 2024
Mona Ahmadi, Elmira Agah, S. Nafissi, et al.
Neurotherapeutics, 2018
M. Fehlings, A. Moghaddamjou, J. Harrop, et al.
Journal of Neurotrauma, 2023
Zarei H, Khatami S, Faghihi M, et al.
2025
- Spinal Cord Injuries
- Riluzole
- Neuroprotective Agents
Shanmukha Srinivas, A. Wali, Martin H. Pham
Neurosurgical focus, 2019
Mark C. Bellingham
CNS Neuroscience & Therapeutics, 2011
Hirtik Singh Rathore, Jashandeep Singh Brar, Srishti Gupta, et al.
2026
Abstract Amyotrophic Lateral Sclerosis (Lou Gehrig’s disease) is a progressive neurodegenerative disease affecting hundreds of thousands of people worldwide. It is characterized by the degeneration of the neurons in the brain and spinal cord of the patients, leading to a loss of control of muscles. Over time, without nerves to stimulate them muscles tend to atrophy. ALS may occur sporadically or run in families; many mutations have been identified for the latter. Treatment of ALS is mostly limited to three approved therapeutic agents: riluzole, edaravone, and tauroursidiol/ sodium phenylbutyrate. Among these, riluzole remains the most effective despite its early discovery. There are no conclusive meta-analysis comparing riluzole monotherapy to all possible co-therapies present. In this work we have attempted to address such a concern and observed that no adjunct therapy significantly improved the performance of riluzole. However, mitochondrial/ oxidative stress modulator and neuroimmune/ neuroexcitability modulator co-therapy exhibited positive trends. Surprisingly, trials were mainly confined to the USA and European countries, indicating unequal demographic representation in ASL research. We have concluded that large double blinded inter-continental RCTs to be carried out for better understanding of the scenario.
Abstract licence: CC BY 4.0
Araujo AQC
2026
- Spinal Cord Injuries
- Neuroprotective Agents
- Translational Research, Biomedical
Despite four decades of translational research, no pharmacological agent has been approved for acute traumatic spinal cord injury (SCI) based on class-I evidence. The current narrative review critically examines the seven agents evaluated in phase-II to -III clinical trials-methylprednisolone (MPSS), GM-1 monosialotetrahexosylganglioside, minocycline, riluzole, anti-Nogo-A antibody NG101, VX-210, and granulocyte colony-stimulating factor (G-CSF)-with emphasis on quantitative effect estimates, confidence intervals, and mechanisms of translational failure. Polylaminin, under phase-I evaluation approved by the Brazilian Health Regulatory Agency (Agência Nacional de Vigilância Sanitária, ANVISA, in Portuguese), is discussed in the context of disproportionate public communication relative to the stage of evidence; available human data are limited to a small, uncontrolled, unreviewed pilot study insufficient for efficacy inferences. High-dose MPSS conferred no motor recovery benefit in a meta-analysis of 1,863 participants and was significantly associated with gastrointestinal hemorrhage (odds ratio [OR] = 2.07; 95%CI: 1.02-4.20) and respiratory infections (OR = 1.73; 95%CI: 1.12-2.68). Furthermore, GM-1 ganglioside, G-CSF, and VX-210 failed to meet the prespecified primary endpoints. Minocycline produced inconclusive results in an underpowered phase-II study. Riluzole (Riluzole in Spinal Cord Injury Study [RISCIS]), which was prematurely terminated at 55% of enrollment due to the coronavirus disease 2019 (COVID-19) pandemic, showed a significant motor benefit in patients classified as grade C according to the American Spinal Injury Association (ASIA) Impairment Scale (AIS) (+8.0 points; 95%CI: 1.5-14.4; 2-tailed p = 0.034). The Nogo Inhibition in Spinal Cord Injury (NISCI) trial (2025), the most methodologically rigorous SCI trial to date, demonstrated no primary endpoint benefit but identified functional signals in motor-incomplete injuries. In total, six structural domains of translational failure are identified and methodological solutions proposed.
Abstract licence: CC BY
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
1 found
Half-life
12 hours
Mechanism
The mode of action of riluzole is unknown.
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
90%
Half-life
12 hours
Protein binding
96%
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1099 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
The influx of Na(+) ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues .
PMID:1309946 PMID:21447824 PMID:23085483 PMID:23420830 PMID:25370050 PMID:26279430 PMID:26392562 PMID:26776555
Nav1.5 is the predominant sodium channel expressed in myocardial cells and it is responsible for the initial upstroke of the action potential in cardiac myocytes, thereby initiating the heartbeat .
PMID:11234013 PMID:11804990 PMID:12569159 PMID:1309946
Required for normal electrical conduction including formation of the infranodal ventricular conduction system and normal action potential configuration, as a result of its interaction with XIRP2 (By similarity)
PMID:11133847 PMID:11417227 PMID:14722095 PMID:15151999 PMID:34880232 PMID:35245456 PMID:35352032
Provides L-cystine for the maintenance of the redox balance between extracellular L-cystine and L-cysteine and for the maintenance of the intracellular levels of glutathione that is essential for cells protection from oxidative stress (By similarity). The transport is sodium-independent, electroneutral with a stoichiometry of 1:1, and is drove by the high intracellular concentration of L-glutamate and the intracellular reduction of L-cystine .
PMID:11133847 PMID:11417227
In addition, mediates the import of L-kynurenine leading to anti-ferroptotic signaling propagation required to maintain L-cystine and glutathione homeostasis .
PMID:35245456
Moreover, mediates N-acetyl-L-cysteine uptake into the placenta leading to subsequently down-regulation of pathways associated with oxidative stress, inflammation and apoptosis .
PMID:34120018
In vitro can also transport L-aspartate .
PMID:11417227
May participate in astrocyte and meningeal cell proliferation during development and can provide neuroprotection by promoting glutathione synthesis and delivery from non-neuronal cells such as astrocytes and meningeal cells to immature neurons (By similarity). Controls the production of pheomelanin pigment directly (By similarity)
PMID:10580103 PMID:12384689 PMID:24036948 PMID:24776970 PMID:25791876 PMID:26645915
Involved in membrane depolarization during action potential in nociceptors which function as key relay stations for the electrical transmission of pain signals from the periphery to the central nervous system .
PMID:24036948 PMID:24776970 PMID:25791876 PMID:26645915
Also involved in rapid BDNF-evoked neuronal depolarization PMID:12384689
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
ATC N07XX02
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Riluzole
Additional database identifiers
Drugs Product Database (DPD)
12026
ChemSpider
4892
BindingDB
30705
PDB
657
Guide to Pharmacology
2326
ZINC
ZINC000000006481
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10593
GenAtlas
SCN5A
GeneCards
SCN5A
GenBank Gene Database
M77235
GenBank Protein Database
184039
Guide to Pharmacology
582
UniProt Accession
SCN5A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11059
GenAtlas
SLC7A11
GeneCards
SLC7A11
GenBank Gene Database
AB026891
GenBank Protein Database
5668545
Guide to Pharmacology
902
UniProt Accession
XCT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10583
GenAtlas
SCN11A
GeneCards
SCN11A
GenBank Gene Database
AF188679
GenBank Protein Database
6572950
UniProt Accession
SCNBA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2595
GeneCards
CYP1A1
GenBank Gene Database
K03191
GenBank Protein Database
181276
Guide to Pharmacology
1318
UniProt Accession
CP1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72