Naratriptan 2.5mg tablets
Requires a prescription from a doctor or prescriber
Naratriptan is a triptan drug that is selective for the 5-hydroxytryptamine1 receptor subtype.
Genetic variations that may affect drug response
1 known genetic variation may influence how your body responds to Naratriptan 2.5mg tablets.Gene involved: GNB3
These are known genetic variations. They don't mean the medicine won't work for you — speak to your doctor or a pharmacogenomics specialist for personalised advice. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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Drug safety updates
MHRA alerts for Naratriptan
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 Naratriptan
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Interactive Drug Analysis Profiles for all medicines
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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
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.
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Suspected adverse reactions reported for Naratriptan
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.
26 branded products available
MHRA licensed products
View all licensed products for Naratriptan on the MHRA register
Naramig 2.5mg tablets
Naramig 2.5mg tablets
Naramig 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
Naratriptan 2.5mg tablets
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)
2.5 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
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Supply & safety information
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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: 4 · Randomised trials: 2 · 1997–2026
Showing the 50 most relevant studies, sorted by most relevant.
Karlsson WK, Ostinelli EG, Zhuang ZA, et al.
2024
- Migraine Disorders
- Tryptamines
ObjectiveTo compare all licensed drug interventions as oral monotherapy for the acute treatment of migraine episodes in adults.DesignSystematic review and network meta-analysis.Data sourcesCochrane Central Register of Controlled Trials, Medline, Embase, ClinicalTrials.gov, EU Clinical Trials Register, WHO International Clinical Trials Registry Platform, as well as websites of regulatory agencies and pharmaceutical companies without language restrictions until 24 June 2023.MethodsScreening, data extraction, coding, and risk of bias assessment were performed independently and in duplicate. Random effects network meta-analyses were conducted for the primary analyses. The primary outcomes were the proportion of participants who were pain-free at two hours post-dose and the proportion of participants with sustained pain freedom from two to 24 hours post-dose, both without the use of rescue drugs. Certainty of the evidence was graded using the confidence in network meta-analysis (CINeMA) online tool. Vitruvian plots were used to summarise findings. An international panel of clinicians and people with lived experience of migraine co-designed the study and interpreted the findings.Eligibility criteria for selecting studiesDouble blind randomised trials of adults (≥18 years) with a diagnosis of migraine according to the International Classification of Headache Disorders.Results137 randomised controlled trials comprising 89 445 participants allocated to one of 17 active interventions or placebo were included. All active interventions showed superior efficacy compared with placebo for pain freedom at two hours (odds ratios from 1.73 (95% confidence interval (CI) 1.27 to 2.34) for naratriptan to 5.19 (4.25 to 6.33) for eletriptan), and most of them also for sustained pain freedom to 24 hours (odds ratios from 1.71 (1.07 to 2.74) for celecoxib to 7.58 (2.58 to 22.27) for ibuprofen). In head-to-head comparisons between active interventions, eletriptan was the most effective drug for pain freedom at two hours (odds ratios from 1.46 (1.18 to 1.81) to 3.01 (2.13 to 4.25)), followed by rizatriptan (1.59 (1.18 to 2.17) to 2.44 (1.75 to 3.45)), sumatriptan (1.35 (1.03 to 1.75) to 2.04 (1.49 to 2.86)), and zolmitriptan (1.47 (1.04 to 2.08) to 1.96 (1.39 to 2.86)). For sustained pain freedom, the most efficacious interventions were eletriptan and ibuprofen (odds ratios from 1.41 (1.02 to 1.93) to 4.82 (1.31 to 17.67)). Confidence in accordance with CINeMA ranged from high to very low. Sensitivity analyses on Food and Drug Administration licensed doses only, high versus low doses, risk of bias, and moderate to severe headache at baseline confirmed the main findings for both primary and secondary outcomes.ConclusionsOverall, eletriptan, rizatriptan, sumatriptan, and zolmitriptan had the best profiles and they were more efficacious than the recently marketed drugs lasmiditan, rimegepant, and ubrogepant. Although cost effectiveness analyses are warranted and careful consideration should be given to patients with a high risk cardiovascular profile, the most effective triptans should be considered as preferred acute treatment for migraine and included in the WHO List of Essential Medicines to promote global accessibility and uniform standards of care.Systematic review registrationOpen Science Framework https://osf.io/kq3ys/.
Abstract licence: CC BY
C Barrows, W Saunders, R Austin, et al.
Cephalalgia, 2004
JosephMakram Botros, AtefMohammed Sayed
Anesthesia: Essays and Researches, 2019
Darren M. Ashcroft, David Millson
Pharmacoepidemiology and Drug Safety, 2003
Peer Tfelt-Hansen
Cephalalgia, 2021
Ninan T. Mathew, Mahnaz Asgharnejad, Margaret Peykamian, et al.
Neurology, 1997
Volker Limmroth, Zaza Kazarawa, Gunther Fritsche, et al.
The Lancet, 1999
Martin Bomhof, Jose Paz, Nigel Legg, et al.
European Neurology, 1999
Arthur Klassen, Arthur Elkind, Mahnaz Asgharnejad, et al.
Headache: The Journal of Head and Face Pain, 1997
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
35 found
Half-life
5-8 hours
Mechanism
Three distinct pharmacological actions have been implicated in the antimigraine…
Food interactions
1 warning
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
74%
Half-life
5-8 hours
Protein binding
28%
Volume of distribution
170 L
Metabolism
Clearance
6.6 mL/min/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1091 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:22957663 PMID:3138543 PMID:33762731 PMID:37935376 PMID:37935377 PMID:8138923 PMID:8393041
Also functions as a receptor for various drugs and psychoactive substances .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:38552625 PMID:8138923 PMID:8393041
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:8138923 PMID:8393041
HTR1A is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission: signaling inhibits adenylate cyclase activity and activates a phosphatidylinositol-calcium second messenger system that regulates the release of Ca(2+) ions from intracellular stores .
PMID:33762731 PMID:35610220
Beta-arrestin family members regulate signaling by mediating both receptor desensitization and resensitization processes .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of 5-hydroxytryptamine release and in the regulation of dopamine and 5-hydroxytryptamine metabolism .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of dopamine and 5-hydroxytryptamine levels in the brain, and thereby affects neural activity, mood and behavior .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the response to anxiogenic stimuli PMID:18476671 PMID:20363322 PMID:20945968
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
Also functions as a receptor for ergot alkaloid derivatives, various anxiolytic and antidepressant drugs and other psychoactive substances .
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
HTR1D is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission by inhibiting adenylate cyclase activity .
PMID:33762731
Regulates the release of 5-hydroxytryptamine in the brain, and thereby affects neural activity .
PMID:18476671 PMID:20945968
May also play a role in regulating the release of other neurotransmitters .
PMID:18476671 PMID:20945968
May play a role in vasoconstriction PMID:18476671 PMID:20945968
PMID:10452531 PMID:1315531 PMID:1328844 PMID:1348246 PMID:1351684 PMID:1559993 PMID:1565658 PMID:1610347 PMID:23519210 PMID:23519215 PMID:29925951 PMID:8218242
Also functions as a receptor for ergot alkaloid derivatives, various anxiolytic and antidepressant drugs and other psychoactive substances, such as lysergic acid diethylamide (LSD) .
PMID:23519210 PMID:23519215 PMID:29925951
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:10452531 PMID:1315531 PMID:1328844 PMID:1348246 PMID:1351684 PMID:1559993 PMID:1565658 PMID:1610347 PMID:23519210 PMID:23519215 PMID:29925951 PMID:8218242
HTR1B is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission by inhibiting adenylate cyclase activity .
PMID:29925951 PMID:35610220
Arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways .
PMID:29925951
Regulates the release of 5-hydroxytryptamine, dopamine and acetylcholine in the brain, and thereby affects neural activity, nociceptive processing, pain perception, mood and behavior .
PMID:18476671 PMID:20945968
Besides, plays a role in vasoconstriction of cerebral arteries PMID:15853772
PMID:21422162 PMID:34239069 PMID:8380639 PMID:8384716
Also functions as a receptor for various alkaloids and psychoactive substances .
PMID:21422162 PMID:8380639 PMID:8384716
Receptor for lasmiditan, a drug for the treatment of acute migraine .
PMID:34239069
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:34239069
HTR1F is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission by inhibiting adenylate cyclase activity PMID:34239069 PMID:35610220
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N02CC02
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Naratriptan
Additional database identifiers
Drugs Product Database (DPD)
11770
ChemSpider
4287
BindingDB
50073682
Guide to Pharmacology
45
ZINC
ZINC000000004076
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5286
GenAtlas
HTR1A
GeneCards
HTR1A
GenBank Gene Database
M28269
GenBank Protein Database
189928
Guide to Pharmacology
1
UniProt Accession
5HT1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5289
GenAtlas
HTR1D
GeneCards
HTR1D
GenBank Gene Database
M89955
GenBank Protein Database
177772
Guide to Pharmacology
3
UniProt Accession
5HT1D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5287
GenAtlas
HTR1B
GeneCards
HTR1B
GenBank Gene Database
D10995
GenBank Protein Database
219679
Guide to Pharmacology
2
UniProt Accession
5HT1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5292
GenAtlas
HTR1F
GeneCards
HTR1F
GenBank Gene Database
L05597
GenBank Protein Database
307420
Guide to Pharmacology
5
UniProt Accession
5HT1F_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6833
GenAtlas
MAOA
GeneCards
MAOA
GenBank Gene Database
M68840
GenBank Protein Database
187353
Guide to Pharmacology
2489
UniProt Accession
AOFA_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