Rizatriptan 5mg orodispersible tablets sugar free
Requires a prescription from a doctor or prescriber
Genetic variations that may affect drug response
1 known genetic variation may influence how your body responds to Rizatriptan 5mg orodispersible tablets sugar free.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).
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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 Rizatriptan
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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.
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Suspected adverse reactions reported for Rizatriptan
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4 branded products available
Part of the Maxalt brand family (generic: Rizatriptan)
MHRA licensed products
View all licensed products for Rizatriptan on the MHRA register
Rizatriptan 5mg orodispersible tablets sugar free
Rizatriptan 5mg orodispersible tablets sugar free
Rizatriptan 5mg orodispersible tablets sugar free
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)
10 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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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 the 50 most relevant studies.
Reviews & meta-analyses: 11 · Randomised trials: 4 · 1996–2026
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
Kira Ahonen, Mathias Hämäläinen, Mervi Eerola, et al.
Neurology, 2006
- Ambulatory Care
- Finland
- Migraine Disorders
Michel D. Ferrari, Elizabeth Loder, KA McCarroll, et al.
Cephalalgia, 2001
- Migraine Disorders
- Triazoles
- Tryptamines
Jeffrey P. Staab, Scott D. Eggers, Joanna C. Jen, et al.
JAMA neurology, 2025
- Vestibular Diseases
- Tryptamines
- Triazoles
Tony W. Ho, Eric Pearlman, Donald W. Lewis, et al.
Cephalalgia, 2012
- Migraine Disorders
- Triazoles
- Tryptamines
Pringsheim
Patient Preference and Adherence, 2009
Farnaz Amoozegar, Tamara PringsheimCalgary Headache Assessment and Management Program, Department of Clinical Neurosciences, University of Calgary, Calgary, AB, CanadaAbstract: Rizatriptan is a 5HT (IB/ID) agonist with proven efficacy in the acute treatment of migraine headache. We performed a systematic review of the literature for clinical trials of rizatriptan incorporating important patient outcomes including consistency of response, preference, satisfaction, and quality of life. We found evidence that rizatriptan provides consistent relief of migraine attacks and that patients prefer rizatriptan over other treatments because of its speed of relief. Patient satisfaction with rizatriptan is significantly higher than placebo, but appears equivalent to most other triptans. Migraine-specific quality of life at 24 hours is significantly better in patients treated with rizatriptan compared to placebo, while overall long-term quality of life is less affected. The published clinical trials included in this systematic review are subject to bias due to the open-label nature of preference trials and the doses chosen for comparison in head-to-head trials.Keywords: migraine, rizatriptan, patient preference
Abstract licence: CC BY-NC 3.0
Peer Tfelt‐Hansen, Judith Teall, Francisco Javier Rodríguez‐Gómez, et al.
Headache The Journal of Head and Face Pain, 1998
- Migraine Disorders
- Triazoles
- Tryptamines
U. K. Misra, Jayantee Kalita, Rama Kant Yadav
The Journal of Headache and Pain, 2007
- Acute Disease
- Anti-Inflammatory Agents, Non-Steroidal
- Ibuprofen
Jerome Goldstein, Robert Ryan, Kaihong Jiang, et al.
Headache The Journal of Head and Face Pain, 1998
- Migraine Disorders
- Triazoles
- Tryptamines
Amelia M. Avachat, Kishore N. Gujar, Kishor V. Wagh
Carbohydrate Polymers, 2012
- Drug Delivery Systems
- Adhesives
- Administration, Buccal
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
136 found
Half-life
Not available
Mechanism
There are several physiological and molecular processes implicated in the pathophysiology of migraine.
Food interactions
1 warning
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
90%
Half-life
[L46018]
Protein binding
14%
[L46018]
Volume of distribution
140 L
[L46018]
Metabolism
14%
Elimination
10 mg
Clearance
1042 mL/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L46018][L46023][L46038][L46043]
Rizatriptan is not indicated for the prophylactic therapy of migraine nor the treatment of cluster headache.
[L46018]
In Canada, rizatriptan is approved in adults.
[L46038][L46043]
In the US, the oral tablet formulations are used in patients six years of age and older [L46018] and the oral film formation is approved for patients 12 years of age and older weighing 40 kg or more.
[L46023]
Rizatriptan, in combination with [Meloxicam] is indicated for the acute treatment of migraine with or without aura in adults.
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1226 interactions
[L46028]
No overdoses of rizatriptan were reported in clinical trials. Some adult patients who received 40 mg of rizatriptan either a single dose or as two doses with a two-hour interdose interval had dizziness and somnolence. Syncope, dizziness, bradycardia including third degree AV block, vomiting, and/or incontinence were experienced by two adults who received a total cumulative doses of 80 mg (given within four hours) in a clinical pharmacology study.
Some adolescent patients (aged 12 to 17 years old) receiving two 10-mg doses of orally disintegrating tablets of rizatriptan experienced abdominal discomfort, fatigue, and dyspnea.
[L46018]
Based on the pharmacological properties of rizatriptan, hypertension and myocardial ischemia are possible after overdosage. Gastrointestinal decontamination, (i.e., gastric lavage followed by activated charcoal) should be considered in patients suspected of an overdose with rizatriptan. Clinical and electrocardiographic monitoring should be continued for at least 12 hours, even if clinical symptoms are not observed.
The effects of hemo- or peritoneal dialysis on serum concentrations of rizatriptan are unknown.
[L46018]
Rizatriptan is a selective agonist at the 5-HT1B and 5-HT1D receptors on intracranial blood vessels and sensory nerves of the trigeminal system. It binds to these receptors with high affinity.[L46018] The exact mechanism of action of rizatriptan has not been fully elucidated; however, several documented pharmacological actions of rizatriptan may contribute to its antimigraine effects. Rizatriptan causes vasoconstriction of intracranial extracerebral blood vessels, which is thought to occur primarily via 5-HT1B receptors. Rizatriptan also inhibits nociceptive neurotransmission in trigeminal pain pathways. It attenuates the release of vasoactive neuropeptides by the trigeminal nerve, which is thought to occur via neurogenic and central 5-HT1D receptors.[A1460][A258918][A258928] Rizatriptan inhibited neurogenic dural vasodilation and plasma protein extravasation in animal studies.[A1460][A5971][A258918][A258928]
Rizatriptan has a weak affinity for other 5-HT1 receptor subtypes (5-HT1A, 5-HT1E, 5-HT1F) and the 5-HT7 receptor but has no significant activity at 5-HT2, 5-HT3, alpha- and beta-adrenergic, dopaminergic, histaminergic, muscarinic or benzodiazepine receptors.[L46038]
How the body processes this drug — absorption, distribution, metabolism, and elimination
Food has no significant effect on the bioavailability of rizatriptan but delays the time to reach peak concentration by an hour. In clinical trials, rizatriptan was administered without regard to food.
[L46018]
The bioavailability and Cmax of rizatriptan were similar following the administration of rizatriptan tablets and rizatriptan orally disintegrating tablets. Still, the absorption rate is somewhat slower with orally disintegrating tablets, with Tmax delayed by up to 0.7 hours.
The AUC of rizatriptan is approximately 30% higher in females than males. No accumulation occurred on multiple dosing.
[L46018]
[L46018]
[L46018]
[L46018]
Other pharmacologically inactive minor metabolites include the N-oxide, the 6-hydroxy compound, and the sulfate conjugate of the 6-hydroxy metabolite.
[A1460][A258963][L46018]
[L46018]
[A258918][A258923]
Proteins and enzymes this drug interacts with in the body
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: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: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
PMID:35714614 PMID:8226867
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:35714614 PMID:8226867
HTR7 is coupled to G(s) G alpha proteins and mediates activation of adenylate cyclase activity PMID:35714614
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
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N02CC04
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)
Rizatriptan
Additional database identifiers
Drugs Product Database (DPD)
11899
ChemSpider
4900
BindingDB
50033437
Guide to Pharmacology
51
ZINC
ZINC000000005895
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: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: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:5302
GenAtlas
HTR7
GeneCards
HTR7
GenBank Gene Database
U68487
GenBank Protein Database
1857143
Guide to Pharmacology
12
UniProt Accession
5HT7R_HUMAN
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:5291
GenAtlas
HTR1E
GeneCards
HTR1E
GenBank Gene Database
M91467
GenBank Protein Database
177774
Guide to Pharmacology
4
UniProt Accession
5HT1E_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
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_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 (Q212171), 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.