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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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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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
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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 BNF/ATC 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
Official UK regulator monitoring and safety alerts
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. 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 all 12 studies.
Reviews & meta-analyses: 1 · Randomised trials: 1 · 1997–2026
Showing all 12 studies, sorted by most relevant.
Carl H. Göbel, Axel Heinze, Anna Cirkel, et al.
Pain and Therapy, 2024
Around 91% of migraine patients use over-the-counter medicines to treat attacks, often without further treatment or medical consultation. This therapeutic principle is established in most countries, regardless of how the healthcare system is otherwise structured or financed. Using Germany as an example, the basis for an expansion of attack therapy with rizatriptan as an over-the-counter triptan is described. To achieve the best possible tolerability and safety in the context of self-medication, the lowest possible dose should be selected to provide the most favourable tolerability and safety profile in the context of self-medication through low dosages. The lowest approved dose of rizatriptan is 5 mg. This was investigated in three randomized controlled trials with 752 patients. The results show that rizatriptan at a dose of 5 mg is more effective than the triptans naratriptan 2.5 mg, almotriptan 12.5 mg and sumatriptan 50 mg, which were previously available for self-medication in Germany. There was no significant difference in the frequency of adverse events with rizatriptan 5 mg compared to placebo. Rizatriptan 5 mg does not have a higher side effect potential than sumatriptan 50 mg, which is already exempt from the prescription requirement. The reasons given show that rizatriptan in a dose of 5 mg for the treatment of acute migraine attacks fulfils the requirements for a transfer from prescription to pharmacy-only status at least as well as sumatriptan 50 mg, naratriptan 2.5 mg and almotriptan 12.5 mg. From a clinical care perspective, it is desirable for affected patients to have other options available for self-medication. Non-responders to other substances also have a further treatment option with rizatriptan 5 mg, with the same or even better risk-benefit profile, to treat migraine attacks safely, effectively and in a tolerable manner as part of self-medication.
Abstract licence: CC BY-NC
P. Tfelt-Hansen
Cephalalgia, 2021
- Migraine Disorders
- Sumatriptan
- Piperidines
Ninan T. Mathew, Mahnaz Asgharnejad, Margaret Peykamian, et al.
Neurology, 1997
- Gastrointestinal Diseases
- Hyperesthesia
- Indoles
Kim Y, Yook Y, Rhee SJ
2025
- Migraine Disorders
- Tinnitus
- Tryptamines
Tinnitus, a distressing condition that can significantly impair quality of life, has been associated with several medications, including triptans. This study aimed to explore the relationship between tinnitus and specific migraine treatments, focusing on triptans and calcitonin gene-related peptide (CGRP) inhibitors. Data from the FDA Adverse Event Reporting System (FAERS) through the third quarter of 2023 were analyzed to calculate proportional reporting ratios (PRR) and reporting odds ratios (ROR) for migraine treatments, specifically triptans and CGRP inhibitors. Positive tinnitus signals were identified when PRRs or RORs were greater than 2.0, the lower bound of the 95% confidence interval exceeded 1.0, and at least three cases were reported. Intra- and inter-class analyses were conducted to compare tinnitus reports among individual drugs and drug classes. Among 47,615 tinnitus-related adverse events, 345 were associated with CGRP inhibitors and 183 with triptans. Positive tinnitus signals were observed for several CGRP inhibitors, except eptinezumab and atogepant, and for all triptans except sumatriptan. Inter-class analysis revealed no significant differences between triptans and CGRP inhibitors. However, intra-class analysis identified naratriptan, almotriptan, and frovatriptan as having notable tinnitus signals among triptans, while CGRP inhibitors did not exhibit strong signals for any specific drug. Using real-world data from FAERS and pharmacovigilance methods, this study identified tinnitus signals related to migraine treatments, particularly among certain triptans. These findings provide preliminary evidence for further investigation into the relationship between migraine medications and tinnitus.
Abstract licence: CC BY
Moskatel LS, Linfield RY, Zhang N
2025
Background: Understanding all factors that affect a patient's acute migraine treatment care is crucial. We sought to determine the impact of headache specialist density and the introduction of the gepants and lasmiditan on the prescription of acute treatments for migraine. Methods: We analyzed three scenarios: first, we performed linear regression analysis with the percentage of patients with migraine prescribed an acute medication in 2023, obtained via Epic Cosmos, and the density of headache specialists at the state level. Second, we conducted interrupted time-series analysis examining the change in patients prescribed the triptans before (2016-2019) and after (2020-2023) the introduction of the gepants and lasmiditan. Finally, we used regression analysis to look at the association of one pharmaceutical company, Pfizer, payments to physicians with prescriptions for that company's gepant, rimegepant. Results: We included 6,559,854 patients with migraine and found that increased headache specialist density was associated with increased eletriptan, almotriptan, and naratriptan; there was no association with the other queried acute medications. In our interrupted time-series analysis, the introduction of the gepants and lasmiditan was linked to decreases in triptan utilization, except for eletriptan which remained stable, and rizatriptan which rose at a slower rate. Finally, increased Pfizer payments to physicians were associated with a higher percentage of patients prescribed rimegepant. Conclusion: Our study suggests increased headache provider availability is associated with more prescriptions for naratriptan, eletriptan, and almotriptan. Additionally, the introduction of the gepants and lasmiditan broadly decreased the utilization of triptans. Critically, there was a strong association between a pharmaceutical company's, Pfizer, payments to physicians and utilization of their medication, rimegepant.
Abstract licence: CC BY
S. Shelke, S. Shahi, S. Jalalpure, et al.
Journal of Drug Delivery Science and Technology, 2015
Kenji Sakakibara, Kenjiro Tanaka, Madoka Iida, et al.
Disease Models & Mechanisms, 2025
- Models, Biological
- Pioglitazone
- Cell Line
Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by CAG trinucleotide expansion in the androgen receptor (AR) gene. To improve the quality of in vitro cell-based assays for the evaluation of potential drug candidates for SBMA, we developed a morphology-based phenotypic analysis for a muscle cell model of SBMA that involves multiparametric morphological profiling to quantitatively assess the therapeutic effects of drugs on muscle cell phenotype. The analysis was validated using dihydrotestosterone and pioglitazone, which have been shown to exacerbate and ameliorate the pathophysiology of SBMA, respectively. Gene expression analysis revealed activation of the JNK pathway in the SBMA cells compared to the control cells. Phenotypic analysis revealed the effect of naratriptan, a JNK inhibitor, on the phenotypic changes of SBMA cells, and the results were confirmed by LDH assays. We then trained a predictive machine learning model to classify the drug responses, and it successfully discriminated between pioglitazone-type and naratriptan-type morphological profiles based on their morphological characteristics. Our morphology-based phenotypic analysis provides a noninvasive and efficient screening method to accelerate the development of therapeutics for SBMA.
Abstract licence: CC BY
Wen-Hui Liu, Hui-Min Hu, Chen Li, et al.
The Journal of Headache and Pain, 2024
- Migraine Disorders
- Tryptamines
- Piperidines
BACKGROUND: Triptans selectively agoniste 5-Hydroxytryptamine(5-HT) receptors and are widely used in the treatment of migraine. Nevertheless, there is a dearth of comprehensive real-world clinical research on the safety of triptans. In light of the growing prevalence of migraine, it is imperative to gain a deeper understanding of the true extent of adverse events (AEs) associated with triptans in the clinical management of migraine. METHODS: A database query of AEs reported to the U.S. Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) database for triptans was performed using the online platform Open Vigil 2.1. The query spanned the period from 1 January 2018 to 31 December 2023 and extracted all AEs for 'sumatriptan', 'zolmitriptan', 'rizatriptan', and 'naratriptan' from the 15-49 years old population and retrospective quantitative analyses. A proportional reporting ratio (PRR), reporting odds ratio (ROR), and Bayesian Confidence Propagation Neural Network (BCPNN) methodology were utilized to contrast AEs across the four triptans. RESULTS: A total of 1.272 AEs reports for sumatriptan, 114 for zolmitriptan, 162 for rizatriptan, and 15 for naratriptan were identified. The ratio of females to males was approximately three times higher in all cases, with the highest number of reports originating from the Americas. A review of the FAERS database revealed that nervous system disorders were the primary SOC category for four drugs, with all four drugs exhibiting the AE indicative of reversible cerebral vasoconstriction syndrome, also classified as Nervous system disorders. The most frequently reported AE signal for sumatriptan was dyspnea, which is classified as respiratory, thoracic and mediastinal disorders. The most frequently reported AEs signals for the remaining three drugs were nausea, vomiting and terminal ileitis, all of which are classified as gastrointestinal disorders. CONCLUSION: Analyses have demonstrated that AEs are present in a range of systems, including cardiac, nervous, gastrointestinal, and musculoskeletal disorders. It should be noted, however, that the incidence and signal intensity of these AEs vary depending on the specific drug in question. In clinical practice, the selection of an appropriate drug and the monitoring of AEs should be tailored to the individual patient's and specific characteristics.
Abstract licence: CC BY-NC-ND
Kyohei Otani, Nobuyasu Imbe, Ryota Shindo
PCN Reports, 2025
Abstract Aim Headache is one of the most frequent somatic complaints in psychiatric practice and is often attributed to underlying mental disorders. However, primary headache disorders—particularly migraine and tension‐type headache (TTH)—commonly coexist with psychiatric conditions. Evidence from psychiatric outpatient settings remains limited. Methods We conducted a retrospective chart review of all psychiatric outpatients who visited our 600‐bed regional general hospital between April 1, 2023, and March 31, 2024. Among 2525 patients, we identified 360 individuals with headache‐related insurance diagnoses and extracted data on headache labels, treating departments, and prescribed medications. For calcitonin gene–related peptide (CGRP)‐targeted monoclonal antibodies, we extended the observation period to March 31, 2025, to describe an exploratory case series including additional prescriptions. Results Of 2525 psychiatric outpatients, 360 (14.3%) carried a headache‐related insurance diagnosis. The most frequent labels were “headache” (203/360, 56.4%), migraine (92/360, 25.6%), and TTH (46/360, 12.8%); cluster headache and medication‐overuse headache (MOH) were each recorded in 1/360 (0.3%). Headache care was most often delivered within psychiatry (153/360, 42.5%), followed by neurology (42/360, 11.7%), neurosurgery (40/360, 11.1%), general internal medicine (28/360, 7.8%), and rheumatology/collagen‐vascular disease (15/360, 4.2%). Commonly documented agents included nonsteroidal anti‐inflammatory drug (NSAIDs) (40/360, 11.1%), acetaminophen (38/360, 10.6%), triptans (23/360, 6.4%), Japanese Kampo formulas (16/360, 4.4%), and CGRP monoclonal antibodies (6/360, 1.7%). At the agent level, acetaminophen ( n = 38), loxoprofen ( n = 33), zolmitriptan ( n = 14), goreisan ( n = 8), sumatriptan ( n = 6), kakkonto ( n = 6), diclofenac ( n = 4), valproic acid ( n = 4), and naratriptan ( n = 3) were among the most frequently listed. In the exploratory CGRP analysis (total seven patients through March 31, 2025), six were women; the mean age was 48.4 ± 9.2 years. Psychiatric comorbidities were heterogeneous, including eating disorder, bipolar disorder, post‐traumatic stress disorder, dysthymia with social anxiety disorder, schizophrenia, autism spectrum disorder, and neurotic depression. All cases experienced headache improvement; two required switching to another CGRP agent for recurrent attacks yet maintained benefit. One patient temporarily discontinued due to a rash before resuming a different CGRP agent. In contrast, medium‐term changes in mood/anxiety were limited. Conclusion In a psychiatric outpatient cohort, primary headaches were common and frequently managed within psychiatry. CGRP‐targeted therapy yielded headache relief even under psychiatric comorbidity, while psychiatric symptoms did not uniformly improve, underscoring the need for parallel mental‐health interventions alongside headache‐specific care. Strengthening cross‐specialty pathways and early headache evaluation within psychiatry are warranted.
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
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 medications. 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
Show
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 the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q421315), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.