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Sumatriptan Source: en.wikipedia.org/wiki/Sumatriptan

Sumatriptan
Sumatriptan molecule
Clinical data
Trade namesImitrex, others
AHFS/Drugs.comMonograph
MedlinePlusa601116
License data
Routes of
administration		By mouth, subcutaneous, intranasal, transdermal
Drug classAntimigraine agent; Triptan; Serotonin 5-HT1B, 5-HT1D receptor, and 5-HT1F receptor agonist
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability15% (oral); 96% (subcutaneous)
Protein binding14–21%
MetabolismMonoamine oxidase (MAO)
Elimination half-life2.5 hours
Excretion60% urine; 40% feces
Identifiers
  • 1-[3-(2-Dimethylaminoethyl)-1H-indol-5-yl]-N-methyl-methanesulfonamide
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.130.518 Edit this at Wikidata
Chemical and physical data
FormulaC14H21N3O2S
Molar mass295.40 g·mol−1
3D model (JSmol)
  • O=S(=O)(NC)Cc1cc2c(cc1)[nH]cc2CCN(C)C
  • InChI=1S/C14H21N3O2S/c1-15-20(18,19)10-11-4-5-14-13(8-11)12(9-16-14)6-7-17(2)3/h4-5,8-9,15-16H,6-7,10H2,1-3H3 checkY
  • Key:KQKPFRSPSRPDEB-UHFFFAOYSA-N checkY
  (verify)

Sumatriptan, sold under the brand name Imitrex among others, is a medication used to treat migraine headaches and cluster headaches.[4][1] It is taken orally, intranasally, or by subcutaneous injection.[5] Therapeutic effects generally occur within three hours.[5] Sumatriptan is a serotonin (5-HT1B/1D) receptor agonist (triptan).[1]

The drug acts as a serotonin 5-HT1B, 5-HT1D, and 5-HT1F receptor agonism[6][7] and its common side effects include chest pressure, fatigue, vomiting, tingling, and vertigo. Serious side effects may include serotonin syndrome, heart attack, stroke, and seizures. With excessive use, medication overuse headaches may occur.[5] It is unclear if use during pregnancy or breastfeeding is safe.[8] The mechanism of action is not entirely clear. It is in the triptan class of medications.[5]

Sumatriptan was patented in 1982 and approved for medical use in 1992.[1][9] It is on the World Health Organization's List of Essential Medicines.[10] It is available as a generic medication.[4] In 2022, it was the 95th most commonly prescribed medication in the United States, with more than 6 million prescriptions.[11][12] It is also available as the combination product sumatriptan/naproxen.[13]

Medical uses

[edit]

Sumatriptan is indicated for the acute treatment of migraine with or without aura in adults; or the acute treatment of cluster headache in adults.[1]

Sumatriptan is effective for ending or relieving the intensity of migraine and cluster headaches.[14][14] Injected sumatriptan is more effective than other formulations.[15]

Oral sumatriptan can be used also in the treatment of post-dural puncture headache.[16]

Contraindications

[edit]

Contraindications of sumatriptan include history of coronary artery disease (atherosclerosis) or coronary artery vasospasm, Wolff–Parkinson–White syndrome or other cardiac accessory conduction pathway disorders, history of stroke, transient ischemic attack, or hemiplegic or basilar migraine, peripheral vascular disease, ischemic bowel disease, uncontrolled hypertension, use of another triptan or ergot-related medication within the last 24 hours, concomitant or recent use of a monoamine oxidase inhibitor (MAOI), hypersensitivity to sumatriptan, and severe hepatic impairment.[1]

Adverse effects

[edit]

Serious cardiac events, including some that have been fatal, have occurred following the use of sumatriptan injection or tablets. Events reported have included coronary artery vasospasm, transient myocardial ischemia, myocardial infarction, ventricular tachycardia, and ventricular fibrillation.[17] There are reports of Takotsubo cardiomyopathy and transient amnesia after sumatriptan use.[18]

The most common side effects[1] reported by at least 2% of patients in controlled trials of sumatriptan (25-, 50-, and 100-mg tablets) for migraine are atypical sensations (paresthesia and warm/cold sensations) reported by 4% in the placebo group and 5–6% in the sumatriptan groups, pain and other pressure sensations (including chest pain) reported by 4% in the placebo group and 6–8% in the sumatriptan groups, neurological events (vertigo) reported by less than 1% in the placebo group and less than 1% to 2% in the sumatriptan groups. Malaise/fatigue occurred in less than 1% of the placebo group and 2–3% of the sumatriptan groups. Sleep disturbance occurred in less than 1% in the placebo group to 2% in the sumatriptan group.

Sumatriptan has a low abuse potential;[19] however overuse is associated with medication overuse headache.[20] Moreover, prolonged sumatriptan use is associated with pronociceptive effects, resulting in allodynia. This effect's association with medication overuse headache, however, is controversial, due to the fact that animal-model studies are not consistent with typical presentation of this disorder.[21]

Overdose

[edit]

Overdose in animals produced effects including convulsions, tremor, paralysis, inactivity, ptosis, extremity erythema, abnormal breathing, cyanosis, ataxia, mydriasis, salivation, lacrimation, and death.[1] The elimination half-life of sumatriptan in humans is 2.5 hours.[1] The effect of dialysis on sumatriptan levels is unknown.[1]

Overdose of sumatriptan can cause sulfhemoglobinemia, a rare condition in which the blood changes from red to green, due to the integration of sulfur into the hemoglobin molecule. If sumatriptan is discontinued, the condition reverses within a few weeks.[22]

Interactions

[edit]

Concurrent use with other triptans or ergot-containing medications (e.g., ergotamine, dihydroergotamine) within 24 hours can result in additive vasoconstriction.[23][24] Increased systemic exposure to sumatriptan can occur if used within 2 weeks after a monoamine oxidase inhibitor (MAOI).[24] Cases of serotonin syndrome have been reported with co-administration of triptans and serotonin reuptake inhibitors.[23]

Pharmacology

[edit]

Mechanism of action

[edit]
Further information: Serotonin receptor agonist and Triptan § Mechanism of action
Sumatriptan activities
Target Affinity (Ki, nM)
5-HT1A 72–1,100 (Ki)
>10,000 (EC50Tooltip half-maximal effective concentration)
5-HT1B 0.5–62 (Ki)
12–234 (EC50)
96% (EmaxTooltip maximal efficacy)
5-HT1D 0.5–30 (Ki)
3.0–220 (EC50)
5-HT1E 1,580–2,520 (Ki)
1,020–10,000 (EC50)
5-HT1F 13.2–501 (Ki)
9.3–250 (EC50)
5-HT2A 376–>10,000 (Ki)
>10,000 (EC50)
5-HT2B 126–>10,000 (Ki)
>10,000 (EC50)
5-HT2C >10,000 (Ki)
>10,000 (EC50) (pig)
5-HT3 >10,000 (Ki) (rat)
>10,000 (EC50) (mouse)
5-HT4 1,000 (Ki) (rat)
>10,000 (EC50) (guinea pig)
5-HT5A 3,200–5,000
5-HT5B 807–7,943 (rat/mouse)
5-HT6 2,600–>10,000
5-HT7 25–1,380 (Ki)
6,030 (EC50)
α1A–α1D ND
α2 ND
α2A–α2C ND
β1–β3 ND
D1, D2 >10,000
D3–D5 ND
H1–H4 ND
M1–M5 ND
I1, I2 ND
σ1, σ2 ND
TAAR1Tooltip Trace amine-associated receptor 1 ND
SERTTooltip Serotonin transporter ND
NETTooltip Norepinephrine transporter ND
DATTooltip Dopamine transporter ND
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs: [25][26][27][28][29][30][31][32]
[33][34][35][36][37][38][39]

Sumatriptan is structurally similar to the neurotransmitter serotonin (5-HT) and acts an agonist of the serotonin 5-HT1B, 5-HT1D, and 5-HT1F receptors.[6] Sumatriptan's primary therapeutic effect is related in its inhibition of the release of calcitonin gene-related peptide (CGRP), likely through its 5-HT1D/1B receptor agonist action.[40] This has been substantiated by the efficacy of more recently developed CGRP targeting drugs and antibodies developed for the preventive treatment of migraine.[41] How agonism of the 5-HT1D/1B receptors inhibits CGRP release is not fully understood. CGRP is believed to cause sensitization of trigeminal nociceptive neurons, contributing to the pain experienced in migraine.[42]

Sumatriptan is also shown to decrease the activity of the trigeminal nerve, which presumably accounts for sumatriptan's efficacy in treating cluster headaches. The injectable form of the drug has been shown to abort a cluster headache within 30 minutes in 77% of cases.[43]

Pharmacokinetics

[edit]

Absorption

[edit]

Sumatriptan is administered in several forms: tablets, subcutaneous injection, and nasal spray. Oral administration (as succinate salt) has low bioavailability, partly due to presystemic metabolism—some of it gets broken down in the stomach and bloodstream before it reaches the target arteries. There is no simple, direct relationship between sumatriptan concentration (pharmacokinetics) per se in the blood and its anti-migraine effect (pharmacodynamics). This paradox has, to some extent, been resolved by comparing the rates of absorption of the various sumatriptan formulations, rather than the absolute amounts of drug that they deliver.[44][45]

Distribution

[edit]

Sumatriptan is a relatively hydrophilic molecule, which may limit its ability to cross the blood–brain barrier and enter the central nervous system.[46] In accordance, early animal studies found lack of indication of central penetration by sumatriptan.[46] This was in contrast to more lipophilic triptans like zolmitriptan, naratriptan, rizatriptan, and eletriptan.[46] For these reasons, it was thought for many years that sumatriptan could not cross the blood–brain barrier in significant amounts to exert central effects.[46]

However, in subsequent animal studies, sumatriptan was found to enter the brain and produce centrally mediated effects.[46] Besides animal research, clinical studies have found sumatriptan to produce centrally mediated side effects such as sleepiness, tiredness, thinking difficulty, and dizziness, among others.[46] In addition, sumatriptan has been found to be discernibly psychoactive in human drug discrimination tests, with effects like apathy, sedation, and mild dysphoria.[46] Certain other clinical findings also support centrally mediated effects of sumatriptan.[46]

A 2010 literature review concluded that sumatriptan can enter the brain to some minor extent in both animals and humans but that this minor penetration is nonetheless sufficient to cause pharmacological effects.[46] Subsequent research has found sumatriptan given during migraine attacks decreases brain serotonin 5-HT1B receptor binding in humans, with a corresponding receptor occupancy of 16%.[47][48] However, this apparent occupancy could alternatively be due to increased serotonin release during migraine attacks.[47] In contrast to receptor antagonists, it is notable that agonists like sumatriptan require only a low fractional receptor occupancy to produce central effects.[46] It is notable in this regard that the possible occupancy with sumatriptan was comparable to that with centrally acting opioids.[48] Besides the clinical findings, further animal studies have found that sumatriptan rapidly enters the brain in spite of its poor lipophilicity and was able to do so more quickly than the benzodiazepine oxazepam.[48][49]

Metabolism

[edit]
Sumatriptan metabolic pathways (MAO-A – monoamine oxidase A, CYP - cytochrome P450 isoenzymes).[50]

Sumatriptan is metabolized primarily by monoamine oxidase A into indol-3-yl-acetaldehyde and then into corresponding carboxylic acid. It is further modified by UDP-glucuronosyltransferase into a conjugate with glucuronic acid. Other pathways are mediated by cytochrome P450 isoenzymes, which give an N-oxide derivative, and N-desmethyl and N,N-didesmethyl forms (the latter can be converted into the aldehyde by monoamine oxidase A). The N-desmethyl derivative can also undergo a reaction with D-cysteine.[50]

Elimination

[edit]

The metabolites of sumatriptan are excreted in the urine and bile. Only about 3% of the active drug may be recovered unchanged.[5]

Chemistry

[edit]

The experimental log P of sumatriptan is 0.8 to 0.93 and its predicted log P is 0.46 to 1.17.[51]

History

[edit]
Sumatriptan vials

In 1991, Glaxo received approval for sumatriptan, which was the first available triptan.[citation needed]

In July 2009, the US Food and Drug Administration (FDA) approved a single-use jet injector formulation of sumatriptan. The device delivers a subcutaneous injection of sumatriptan, without the use of a needle. Autoinjectors with needles have been previously available in Europe and North America.[52]

Phase III studies with an iontophoretic transdermal patch (Zelrix/Zecuity) started in July 2008.[53] This patch uses low voltage controlled by a pre-programmed microchip to deliver a single dose of sumatriptan through the skin within 30 minutes.[54][55] Zecuity was approved by the FDA in January 2013.[56] Sales of Zecuity have been stopped following reports of skin burns and irritation.[57]

Society and culture

[edit]
[edit]

In the United States, it is available only by medical prescription. It is available over the counter in many states in Australia. The product requires labelling by a pharmacist and is only available in packs of two without a medical prescription.[58] However, it can be bought over the counter in the UK[59] and Sweden.[60]

In Russia, versions of sumatriptan which are not registered in the State Register of Medicines may be regarded as narcotic drugs (derivatives of dimethyltryptamine).[61]

Generics

[edit]

Glaxo patents for sumatriptan expired in February 2009. At that time, Imitrex sold for about $25 a pill.[62] Par Pharmaceutical then introduced generic versions of sumatriptan injection (sumatriptan succinate injection) 4- and 6-mg starter kits and 4- and 6-mg filled syringe cartridges, and 6-mg vials soon after.[63]

Mylan Laboratories Inc., Ranbaxy Laboratories, Sandoz (a subsidiary of Novartis), Dr. Reddy's Laboratories, and other companies have been producing generic versions of sumatriptan tablets in 25-, 50-, and 100-mg doses. Generic forms of the drug are available in US and European markets after Glaxo's patent protections expired in the respective countries. A nasal spray form of sumatriptan known as AVP-825 has been developed by Avanir and is generically available in some countries.[64]

Controversy

[edit]

According to the American Headache Society, "Patients frequently state that they have difficulty accessing triptans prescribed to them."[65] In the US, triptans cost from $12 to $120 each, and more than 80% of US health insurance plans place a limit on the amount of pills available to a patient per month, which has been called "arbitrary and unfair."[66]

References

[edit]
  1. ^ a b c d e f g h i j "Imitrex- sumatriptan injection". DailyMed. 8 February 2023. Retrieved 6 July 2025.
  2. ^ "Imitrex- sumatriptan spray". DailyMed. 22 March 2024. Retrieved 6 July 2025.
  3. ^ "Imitrex- sumatriptan tablet, film coated". DailyMed. 21 February 2024. Retrieved 6 July 2025.
  4. ^ a b British National Formulary: BNF 76 (76 ed.). Pharmaceutical Press. 2018. p. 474. ISBN 9780857113382.
  5. ^ a b c d e "Sumatriptan Monograph for Professionals". Drugs.com. American Society of Health-System Pharmacists. Retrieved 3 March 2019.
  6. ^ a b Rubio-Beltrán E, Labastida-Ramírez A, Villalón CM, MaassenVanDenBrink A (June 2018). "Is selective 5-HT1F receptor agonism an entity apart from that of the triptans in antimigraine therapy?". Pharmacol Ther. 186: 88–97. doi:10.1016/j.pharmthera.2018.01.005. PMID 29352859.
  7. ^ Syed YY (January 2016). "Sumatriptan/Naproxen Sodium: A Review in Migraine". Drugs. 76 (1): 111–121. doi:10.1007/s40265-015-0521-8. PMID 26628293. S2CID 25060147.
  8. ^ "Sumatriptan Use During Pregnancy". Drugs.com. Retrieved 3 March 2019.
  9. ^ Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 531. ISBN 9783527607495.
  10. ^ World Health Organization (2021). World Health Organization model list of essential medicines: 22nd list (2021). Geneva: World Health Organization. hdl:10665/345533. WHO/MHP/HPS/EML/2021.02.
  11. ^ "The Top 300 of 2022". ClinCalc. Archived from the original on 30 August 2024. Retrieved 30 August 2024.
  12. ^ "Sumatriptan Drug Usage Statistics, United States, 2013 - 2022". ClinCalc. Retrieved 30 August 2024.
  13. ^ "Treximet- sumatriptan succinate and naproxen sodium tablet, film coated". DailyMed. 23 December 2024. Retrieved 6 July 2025.
  14. ^ a b Derry CJ, Derry S, Moore RA (May 2014). "Sumatriptan (all routes of administration) for acute migraine attacks in adults - overview of Cochrane reviews". The Cochrane Database of Systematic Reviews. 2014 (5): CD009108. doi:10.1002/14651858.CD009108.pub2. PMC 6469574. PMID 24865446.
  15. ^ Dahlöf CG (2001). "Sumatriptan: pharmacological basis and clinical results". Current Medical Research and Opinion. 17 (Suppl 1): s35 – s45. doi:10.1185/0300799039117010. PMID 12463276. S2CID 2355125. Archived from the original on 17 February 2017. Retrieved 16 July 2016.
  16. ^ Shaat AM, Abdalgaleil MM (1 January 2021). "Is theophylline more effective than sumatriptan in the treatment of post-dural puncture headache? A randomized clinical trial". Egyptian Journal of Anaesthesia. 37 (1): 310–316. doi:10.1080/11101849.2021.1949195. ISSN 1110-1849.
  17. ^ Kelly KM (June 1995). "Cardiac arrest following use of sumatriptan". Neurology. 45 (6): 1211–1213. doi:10.1212/wnl.45.6.1211. PMID 7783891. S2CID 35168945.
  18. ^ Chohan A (7 March 2023). "Sumatriptan-Induced Takotsubo Cardiomyopathy". Journal of the American College of Cardiology. ACC.23. 81 (8, Supplement): 3498. doi:10.1016/S0735-1097(23)03942-6. ISSN 0735-1097.
  19. ^ Sullivan JT, Preston KL, Testa MP, Busch M, Jasinski DR (December 1992). "Psychoactivity and abuse potential of sumatriptan". Clinical Pharmacology and Therapeutics. 52 (6): 635–642. doi:10.1038/clpt.1992.202. PMID 1333934.
  20. ^ "TGA eBS - Product and Consumer Medicine Information". www.ebs.tga.gov.au. Retrieved 3 March 2025.
  21. ^ Chiarugi A, Buonvicino D (1 January 2025). "Critical reflections on medication overuse headache in patients with migraine: An unsolved riddle in nociception". Neurobiology of Pain. 17: 100179. doi:10.1016/j.ynpai.2025.100179. ISSN 2452-073X. PMC 11876746. PMID 40040782.
  22. ^ "Patient bleeds dark green blood". BBC News. 8 June 2007. Archived from the original on 5 August 2010. Retrieved 6 March 2010.
  23. ^ a b "DailyMed - SUMATRIPTAN- sumatriptan succinate tablet tablet". dailymed.nlm.nih.gov. Retrieved 3 May 2024.
  24. ^ a b "Drugs for Migraine". The Medical Letter on Drugs and Therapeutics. 65 (678). The Medical Letter Inc.: 89–96 June 2023. doi:10.58347/tml.2023.1678a. Retrieved 3 May 2024.
  25. ^ "Kᵢ Database". PDSP. 5 July 2025. Retrieved 5 July 2025.
  26. ^ Liu T. "BindingDB BDBM50005835 (3-[2-(dimethylamino)ethyl]-1H-indol-5-yl)-N-methylmethanesulfonamide::1-[3-(2-dimethylaminoethyl)-1H-indol-5-yl]-N-methyl-methanesulfonamide::1-{3-[2-(dimethylamino)ethyl]-1H-indol-5-yl}-N-methylmethanesulfonamide::3-(2-(dimethylamino)ethyl)-N-methyl-1H-indole-5-methanesulfonamide::3-[2-(dimethylamino)ethyl]-N-methylindole-5-methanesulfonamide::CHEMBL128::SUMATRIPTAN::Sumatran::Sumax". BindingDB. Retrieved 5 July 2025.
  27. ^ De Vries P, Villalón CM, Saxena PR (1999). "Pharmacology of triptans". Emerging Drugs. 4 (1): 107–125. doi:10.1517/14728214.4.1.107. ISSN 1361-9195.
  28. ^ Tfelt-Hansen P, De Vries P, Saxena PR (December 2000). "Triptans in migraine: a comparative review of pharmacology, pharmacokinetics and efficacy". Drugs. 60 (6): 1259–1287. doi:10.2165/00003495-200060060-00003. PMID 11152011.
  29. ^ Saxena PR, Tfelt-Hansen P (2001). "Success and failure of triptans". The Journal of Headache and Pain. 2 (1): 3–11. doi:10.1007/s101940170040. ISSN 1129-2369. PMC 3611827.
  30. ^ van den Brink M (22 December 1999). "Coronary Side Effects of Antimigraine Drugs From Patient to Receptor". RePub, Erasmus University Repository. Retrieved 19 June 2025. Table 1.2 Receptor binding properties (pKi values) of sumatriptan and second-generation triptans at 5-HT receptors. [...]
  31. ^ van den Broek RW (13 March 2002). "Vascular Effects of Antimigraine Drugs: pharmacology of human in vitro models in migraine". RePub, Erasmus University Repository. Retrieved 19 June 2025. Table 1.2 Receptor binding properties (pKi values) of the triptans at human 5-HT receptors. [...]
  32. ^ Perez M, Pauwels PJ, Fourrier C, Chopin P, Valentin JP, John GW, et al. (March 1998). "Dimerization of sumatriptan as an efficient way to design a potent, centrally and orally active 5-HT1B agonist". Bioorganic & Medicinal Chemistry Letters. 8 (6): 675–680. doi:10.1016/s0960-894x(98)00090-0. PMID 9871581.
  33. ^ Rubio-Beltrán E, Labastida-Ramírez A, Haanes KA, van den Bogaerdt A, Bogers AJ, Zanelli E, et al. (December 2019). "Characterization of binding, functional activity, and contractile responses of the selective 5-HT1F receptor agonist lasmiditan". British Journal of Pharmacology. 176 (24): 4681–4695. doi:10.1111/bph.14832. PMC 6965684. PMID 31418454. TABLE 1 Summary of pIC50 (negative logarithm of the molar concentration of these compounds at which 50% of the radioligand is displaced) and pKi (negative logarithm of the molar concentration of the Ki ) values of individual antimigraine drugs at 5‐HT receptors [...] TABLE 2 Summary of pEC50 values of cAMP (5‐HT1A/B/E/F and 5‐HT7), GTPγS (5‐HT1A/B/D/E/F), and IP (5‐HT2) assays of individual antimigraine drugs at 5‐HT receptors [...]
  34. ^ Perez, M., Halazy, S., Pauwels, P.J., Colpaert, F.C., John, G.W. (1999). "F-11356". Drugs of the Future. 24 (6): 0605. doi:10.1358/dof.1999.024.06.537284. Retrieved 23 June 2025.
  35. ^ Reuter U, Neeb L (2012). "Lasmiditan hydrochloride". Drugs of the Future. 37 (10): 709. doi:10.1358/dof.2012.037.010.1873629. ISSN 0377-8282. Retrieved 19 June 2025.
  36. ^ Mitsikostas DD, Ward TN (2024). "Evidence-based symptomatic treatment of migraine". Handbook of Clinical Neurology. 199: 203–218. doi:10.1016/B978-0-12-823357-3.00004-5. PMID 38307647.
  37. ^ Comer MB (April 2002). "Pharmacology of the selective 5-HT(1B/1D) agonist frovatriptan". Headache. 42 (Suppl 2): S47 – S53. doi:10.1046/j.1526-4610.42.s2.2.x. PMID 12028320.
  38. ^ Klein MT, Dukat M, Glennon RA, Teitler M (June 2011). "Toward selective drug development for the human 5-hydroxytryptamine 1E receptor: a comparison of 5-hydroxytryptamine 1E and 1F receptor structure-affinity relationships". J Pharmacol Exp Ther. 337 (3): 860–867. doi:10.1124/jpet.111.179606. PMC 3101003. PMID 21422162.
  39. ^ Boess FG, Martin IL (1994). "Molecular biology of 5-HT receptors". Neuropharmacology. 33 (3–4): 275–317. doi:10.1016/0028-3908(94)90059-0. PMID 7984267.
  40. ^ Juhasz G, Zsombok T, Jakab B, Nemeth J, Szolcsanyi J, Bagdy G (March 2005). "Sumatriptan causes parallel decrease in plasma calcitonin gene-related peptide (CGRP) concentration and migraine headache during nitroglycerin induced migraine attack". Cephalalgia. 25 (3): 179–183. doi:10.1111/j.1468-2982.2005.00836.x. PMID 15689192. S2CID 13007101.
  41. ^ Tso AR, Goadsby PJ (August 2017). "Anti-CGRP Monoclonal Antibodies: the Next Era of Migraine Prevention?". Current Treatment Options in Neurology. 19 (8): 27. doi:10.1007/s11940-017-0463-4. PMC 5486583. PMID 28653227.
  42. ^ Giniatullin R, Nistri A, Fabbretti E (February 2008). "Molecular mechanisms of sensitization of pain-transducing P2X3 receptors by the migraine mediators CGRP and NGF". Molecular Neurobiology. 37 (1): 83–90. doi:10.1007/s12035-008-8020-5. PMID 18459072. S2CID 25689799.
  43. ^ Ekbom K, Waldenlind E, Richard L, Andersson B, Boivie J, Dizdar N, et al. (Sumatriptan Cluster Headache Study Group) (August 1991). "Treatment of acute cluster headache with sumatriptan". The New England Journal of Medicine. 325 (5): 322–326. doi:10.1056/NEJM199108013250505. PMID 1647496.
  44. ^ Fox AW (February 2004). "Onset of effect of 5-HT1B/1D agonists: a model with pharmacokinetic validation". Headache. 44 (2): 142–147. doi:10.1111/j.1526-4610.2004.04030.x. PMID 14756852. S2CID 25587940.
  45. ^ Freidank-Mueschenborn E, Fox AW (June 2005). "Resolution of concentration-response differences in onset of effect between subcutaneous and oral sumatriptan". Headache. 45 (6): 632–637. doi:10.1111/j.1526-4610.2005.05129a.x. PMID 15953294. S2CID 20755695.
  46. ^ a b c d e f g h i j Tfelt-Hansen PC (February 2010). "Does sumatriptan cross the blood-brain barrier in animals and man?". J Headache Pain. 11 (1): 5–12. doi:10.1007/s10194-009-0170-y. PMC 3452191. PMID 20012125.
  47. ^ a b Deen M, Hougaard A, Hansen HD, Schain M, Dyssegaard A, Knudsen GM, et al. (July 2019). "Association Between Sumatriptan Treatment During a Migraine Attack and Central 5-HT1B Receptor Binding". JAMA Neurol. 76 (7): 834–840. doi:10.1001/jamaneurol.2019.0755. PMC 6547094. PMID 31135819.
  48. ^ a b c Holland PR, Sureda-Gibert P, Vila-Pueyo M (April 2020). "Rapid uptake of sumatriptan into the brain: An ongoing question of blood-brain barrier permeability". Cephalalgia. 40 (4): 327–329. doi:10.1177/0333102420905131. PMC 7605048. PMID 32000507.
  49. ^ Muzzi M, Zecchi R, Ranieri G, Urru M, Tofani L, De Cesaris F, et al. (April 2020). "Ultra-rapid brain uptake of subcutaneous sumatriptan in the rat: Implication for cluster headache treatment". Cephalalgia. 40 (4): 330–336. doi:10.1177/0333102419896370. PMID 31852231.
  50. ^ a b Pöstges T, Lehr M (February 2023). "Metabolism of sumatriptan revisited". Pharmacology Research & Perspectives. 11 (1): e01051. doi:10.1002/prp2.1051. PMC 9849828. PMID 36655303.
  51. ^ Tekes K, Szegi P, Hashemi F, Laufer R, Kalász H, Siddiq A, et al. (2013). "Medicinal chemistry of antimigraine drugs". Curr Med Chem. 20 (26): 3300–3316. doi:10.2174/0929867311320260012. PMID 23746273.
  52. ^ Brandes JL, Cady RK, Freitag FG, Smith TR, Chandler P, Fox AW, et al. (2009). "Needle-free subcutaneous sumatriptan (Sumavel DosePro): bioequivalence and ease of use". Headache. 49 (10): 1435–1444. doi:10.1111/j.1526-4610.2009.01530.x. PMID 19849720. S2CID 25696109.
  53. ^ Clinical trial number NCT00724815 for "The Efficacy and Tolerability of NP101 Patch in the Treatment of Acute Migraine (NP101-007)" at ClinicalTrials.gov
  54. ^ "SmartRelief -electronically assisted drug delivery (iontophoresis)". nupathe.com. Archived from the original on 7 January 2016. Retrieved 19 February 2018.
  55. ^ Pierce M, Marbury T, O'Neill C, Siegel S, Du W, Sebree T (June 2009). "Zelrix: a novel transdermal formulation of sumatriptan". Headache. 49 (6): 817–825. doi:10.1111/j.1526-4610.2009.01437.x. PMID 19438727. S2CID 205683188.
  56. ^ "Zecuity Approved by the FDA for the Acute Treatment of Migraine". nupathe.com. Archived from the original on 7 January 2016. Retrieved 19 February 2018.
  57. ^ "Teva pulls migraine patch Zecuity on reports of burning, scarring". FiercePharma. 13 June 2016. Archived from the original on 21 March 2017. Retrieved 10 April 2017.
  58. ^ "Poisons Standard June 2017". 18 May 2017. Archived from the original on 31 July 2017. Retrieved 22 July 2017.
  59. ^ "Press release: First Over The Counter (OTC) migraine pill made available". Medicines and Healthcare Products Regulatory Agency. Archived from the original on 5 December 2014. Retrieved 28 January 2015.
  60. ^ European Medicines Agency (23 November 2011). "Assessment Report: Sumatriptan Galpharm 50 mg Tablets" (PDF). European Medicines Agency. p. 20. Archived (PDF) from the original on 7 January 2016. Retrieved 28 January 2015.
  61. ^ "Постановление Правительства РФ от 30 июня 1998 г. N 681 "Об утверждении перечня наркотических средств, психотропных веществ и их прекурсоров, подлежащих контролю в Российской Федерации" (с изменениями и дополнениями)" (in Russian). Гарант. Retrieved 28 April 2019. ДМТ (диметилтриптамин) и его производные, за исключением производных, включенных в качестве самостоятельных позиций в перечень
  62. ^ "GlaxoSmithKline sets out to dupe migraine sufferers with Treximet smoke and mirrors". Community Catalyst. 24 April 2008. Retrieved 22 March 2019.
  63. ^ "Par Pharmaceutical begins shipment of sumatriptan injection". Par Pharmaceutical. 6 November 2008. Archived from the original on 10 December 2008. Retrieved 25 November 2008.
  64. ^ LaMattina J (2 March 2015). "If You 'Want To Make A Good Drug Great' Cost Must Be Factored In". Forbes. Archived from the original on 14 February 2017. Retrieved 13 February 2017.
  65. ^ Minen, M. T., Lindberg, K., Langford, A., Loder, E. (2017), "Variation in Prescription Drug Coverage for Triptans: Analysis of Insurance Formularies", Headache: The Journal of Head and Face Pain, 57 (8), Wiley: 1243–1251, doi:10.1111/head.13134, PMID 28691382, S2CID 42239120
  66. ^ Bender E (7 September 2017), "Practice Matters Wide Variation in Triptan Coverage Across Commercial and Government Health Plans", Neurology Today, 17 (17), American Academy of Neurology: 7, doi:10.1097/01.NT.0000524839.20893.03, S2CID 80167113
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