Zolmitriptan

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Template:Short description Template:Cs1 config Template:Drugbox Zolmitriptan, sold under the brand name Zomig among others, is a serotonergic medication which is used in the acute treatment of migraine attacks with or without aura and cluster headaches.<ref name="Zolmig-Label">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> It is taken by mouth as a swallowed or disintegrating tablet or as a nasal spray.<ref name="Zolmig-Label" />

Side effects include tightness in the neck or throat, jaw pain, dizziness, paresthesia, asthenia, somnolence, warm/cold sensations, nausea, chest pressure, and dry mouth.<ref name="Zolmig-Label" /> The drug acts as a selective serotonin 5-HT1B and 5-HT1D receptor agonist.<ref name="Zolmig-Label" /> Structurally, it is a triptan and a tryptamine derivative.<ref name="Zolmig-Label" /><ref name="PubChem">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

It was patented in 1990 and was approved for medical use in 1997.<ref name="Fis2006">Template:Cite book</ref><ref name="Zolmig-Label" />

Medical uses

Migraine

Zolmitriptan is used for the acute treatment of migraines with or without aura in adults.<ref name="Zolmig-Label" /> It is not intended for the prophylactic therapy of migraine or for use in the management of hemiplegic or basilar migraine.<ref name="Zolmig-Label" />

Off-label uses

Available forms

Zolmitriptan is available as a swallowed tablet, an orally disintegrating tablet, and as a nasal spray, in doses of 2.5 and 5Template:Nbspmg. People who get migraines from aspartame should not use the disintegrating tablet (Zomig ZMT) as it contains aspartame.<ref>Template:Cite journal</ref>

A 2014 Cochrane review has shown that zolmitriptan 5Template:Nbspmg nasal spray was significantly more effective than the 5Template:Nbspmg oral tablet.<ref name="BirdDerryMoore2014">Template:Cite journal</ref>

Contraindications

Zolmitriptan is contraindicated in patients with cerebrovascular or cardiovascular disease because serotonin 5-HT1B receptors are present in coronary arteries. Such conditions include, but are not limited to, coronary artery disease, stroke, and peripheral vascular disease.<ref name=statspe/> It is also contraindicated in hemiplegic migraine.<ref name=statspe/>

Side effects

Side effects include neck/throat/jaw pain/tightness/pressure, dizziness, paresthesia, asthenia, somnolence, warm/cold sensations, nausea, heaviness sensation, and dry mouth.<ref name="Zolmig-Label" />

As for cardiovascular side effects, zolmitriptan can increase systolic blood pressure in the elderly and increase diastolic blood pressure in both the elderly and young people. Additionally, there is the side effect of a dose-related increase in sedation. There is a risk for medication withdrawal headache or medication overuse headache.<ref name="statspe" />

Zolmitriptan has a weak affinity for serotonin 5-HT1A receptors; these receptors have been implicated in the development of serotonin syndrome.<ref name="statspe" />

Overdose

There is limited experience with overdose of zolmitriptan and there is no specific antidote for zolmitriptan overdose.<ref name="Zolmig-Label" /> A dose of zolmitriptan of 50Template:Nbspmg, which is 10- to 40-fold the clinically used dose range of 1.25 to 5Template:Nbspmg, commonly resulted in sedation in patients in a clinical study.<ref name="Zolmig-Label" /> Zolmitriptan has a relatively short elimination half-life of 3Template:Nbsphours, and so symptoms of overdose may be expected to resolve within around 15Template:Nbsphours post-intake.<ref name="Zolmig-Label" />

Interactions

Following administration of the non-selective cytochrome P450 inhibitor cimetidine, the elimination half-life and total exposure of zolmitriptan and its active metabolite were approximately doubled.<ref name="statspe" /> The major metabolite of zolmitriptan, N-desmethylzolmitriptan (183C91), which is active and has several-fold greater affinity for the serotonin 5-HT1B and 5-HT1D receptors than zolmitriptan, is metabolized into an inactive form by monoamine oxidase A (MAO-A).<ref name="Yu2008" /> The reversible inhibitor of MAO-A (RIMA) moclobemide combined with zolmitriptan has been found to increase N-desmethylzolmitriptan exposure and peak levels by 1.5- to 3-fold.<ref name="Yu2008" />

Pharmacology

Pharmacodynamics

Template:Nowrap
Target Affinity (Ki, nM)
5-HT1A 16–316 (Ki)
3,020–>10,000 (Template:Abbrlink)
55% (Template:Abbrlink)
5-HT1B 0.47–20 (Ki)
3.8–60 (Template:Abbr)
99–102% (Template:Abbr)
5-HT1D 0.11–4 (Ki)
0.29–1.6 (Template:Abbr)
86–106% (Template:Abbr)
5-HT1E 10–>10,000 (Ki)
6.6–62 (Template:Abbr)
101% (Template:Abbr)
5-HT1F 28–617 (Ki)
10–420 (Template:Abbr)
97% (Template:Abbr)
5-HT2A >10,000 (Ki)
>10,000 (Template:Abbr)
5-HT2B 65–>10,000 (Ki)
>10,000 (Template:Abbr)
5-HT2C 79,400 (Ki) (guinea pig)
Template:Abbr (Template:Abbr)
5-HT3 >3,160 (mouse)
5-HT4 >3,160 (guinea pig)
5-HT5A 398 (rat)
5-HT6 >3,160
5-HT7 87–96 (Ki)
525 (Template:Abbr)
α1Aα1D Template:Abbr
α2 79,000
α2Aα2C Template:Abbr
β1β3 Template:Abbr
D1, D2 >100,000
D3D5 Template:Abbr
H1H4 Template:Abbr
M1M5 Template:Abbr
I1, I2 Template:Abbr
σ1, σ2 Template:Abbr
Template:Abbrlink Template:Abbr
Template:Abbrlink Template:Abbr
Template:Abbrlink Template:Abbr
Template:Abbrlink Template:Abbr
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs: <ref name="BindingDB">{{#invoke:citation/CS1|citation CitationClass=web

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CitationClass=web

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<ref name="GlenMartinHill1995">Template:Cite journal</ref><ref name="PerezFourrierSigogneau1995">Template:Cite journal</ref><ref name="PerezPauwelsFourrier1998">Template:Cite journal</ref><ref name="NelsonPhebusJohnson2010">Template:Cite journal</ref><ref name="Rubio-BeltránLabastida-RamírezHaanes2019">Template:Cite journal</ref><ref name="PerezHalazyPauwels1999">Template:Cite journal</ref><ref name="ReuterNeeb2012">Template:Cite journal</ref><ref name="MitsikostasWard2024">Template:Cite book</ref><ref name="Comer2002">Template:Cite journal</ref>

Zolmitriptan is a selective serotonin 5-HT1B and 5-HT1D receptor agonist with weak affinity for the serotonin 5-HT1A receptor.<ref name="Tfelt-HansenDeVriesSaxena2000" /> It also has affinity for other serotonin receptors, including the serotonin 5-HT1E, 5-HT1F, 5-HT2B, 5-HT5A, and 5-HT7 receptors.<ref name="Tfelt-HansenDeVriesSaxena2000" /> Conversely, its affinities for the serotonin 5-HT2A, 5-HT2C, 5-HT3, 5-HT4, and 5-HT6 receptors are negligible or undetectable.<ref name="Tfelt-HansenDeVriesSaxena2000" /><ref name="Rubio-BeltránLabastida-RamírezHaanes2019" /> It is likewise inactive as a serotonin 5-HT2A receptor agonist.<ref name="Rubio-BeltránLabastida-RamírezHaanes2019" />

Zolmitriptan's major metabolite, N-desmethylzolmitriptan (183C91), is also active and has about 2- to 6-fold the affinity of zolmitriptan for the serotonin 5-HT1B and 5-HT1D receptors.<ref name="Yu2008">Template:Cite journal</ref>

Its action on serotonin 5-HT1B and 5-HT1D receptors causes vasoconstriction in intracranial blood vessels; as well it can inhibit the release of pro-inflammatory neuropeptides from trigeminal perivascular nerve endings. It crosses the blood–brain barrier as evidenced by the presence of radiolabeled zolmitriptan within the cells of the trigeminal nucleus caudalis and nucleus tractus solitarii.<ref name=statspe/>

Pharmacokinetics

Absorption

Zolmitriptan has a rapid onset of action and has been detected in the brain as early as within 5Template:Nbspminutes of intranasal administration. On average, zolmitriptan has an oral bioavailability of 40%, a mean volume of distribution of 8.3Template:NbspL/kg after oral administration, and 2.4Template:NbspL/kg after intravenous administration.<ref name=statspe/> According to a study of healthy volunteers, food intake seems to have no significant effect on the effectiveness of zolmitriptan in both men and women.<ref>Template:Cite journal</ref>

Distribution

Zolmitriptan is a more lipophilic compound with greater central permeability than certain other triptans like sumatriptan.<ref name="Martin1997">Template:Cite journal</ref><ref name="LionettoCasollaMastropietri2012">Template:Cite journal</ref> It has been found to cross the blood–brain barrier and enter the central nervous system both in animals and humans.<ref name="DeenChristensenHougaard2017">Template:Cite journal</ref> In a clinical pharmacokinetic study, brain concentrations were about 20% of plasma concentrations.<ref name="WallKågedalBergström2005" /> However, in another clinical study, the drug achieved relatively low occupancy of central serotonin 5-HT1B receptors (4–5%) as measured by positron emission tomography (PET) imaging.<ref name="DeenChristensenHougaard2017" /><ref name="VarnäsJučaiteMcCarthy2013">Template:Cite journal</ref><ref name="WallKågedalBergström2005">Template:Cite journal</ref>

Metabolism

Zolmitriptan is metabolized into three major metabolites by the human hepatic cytochrome P450 enzymes—primarily CYP1A2. Two-thirds of the parent compound breaks down into the active metabolite N-desmethylzolmitriptan (183C91), while the remaining one-third separates into the other two inactive metabolites: zolmitriptan N-oxide and an indole acetic acid derivative.<ref name="Yu2008" /> N-Desmethylzolmitriptan circulates at higher levels than those of zolmitriptan.<ref name="Yu2008" /> This metabolite is deaminated by monoamine oxidase A (MAO-A).<ref name="Yu2008" />

Elimination

Zolmitriptan has an elimination half-life of about 3Template:Nbsphours before it undergoes renal elimination; its clearance is greater than the glomerular filtration rate suggesting that there is some renal tubular secretion of the compound.<ref name=statspe/>

Chemistry

Zolmitriptan, also known as [(4S)-2-oxo-1,3-oxazolidin-4-yl]methyl-N,N-dimethyltryptamine, is a tryptamine derivative and a 5-substituted derivative of the psychedelic drug dimethyltryptamine (DMT).<ref name="Zolmig-Label" /><ref name="PubChem" /> It is specifically the derivative of DMT in which the hydrogen atom at position 5 of the indole ring has been substituted with a [(4S)-2-oxo-1,3-oxazolidin-4-yl]methyl group.<ref name="PubChem" />

The experimental log P of zolmitriptan is 1.6 to 1.8.<ref name="PubChem" /><ref name="TekesSzegiHashemi2013">Template:Cite journal</ref> For comparison, the experimental log P of sumatriptan is 0.8 to 0.93.<ref name="PubChem-Sumatriptan">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="TekesSzegiHashemi2013" /> Zolmitriptan is much more lipophilic than sumatriptan.<ref name="Tfelt-HansenDeVriesSaxena2000" /><ref name="TekesSzegiHashemi2013" />

Analogues of zolmitriptan include other triptans like sumatriptan, naratriptan, rizatriptan, eletriptan, almotriptan, and frovatriptan.<ref name="Tfelt-HansenDeVriesSaxena2000" /><ref name="TekesSzegiHashemi2013" />

History

Zolmitriptan was patented in 1990<ref name="Fis2006" /> and was first described in the scientific literature by 1994.<ref name="GoadsbyEdvinsson1994">Template:Cite journal</ref><ref name="Martin1994">Template:Cite journal</ref><ref name="PeckDixonSeaber1994">Template:Cite journal</ref> It was first introduced for medical use in the United States in 1997.<ref name="Fis2006" /><ref name="Zolmig-Label" /><ref name="AdisInsight">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Society and culture

Brand names

Zolmitriptan is marketed by AstraZeneca with the brand names Zomig, Zomigon (Argentina, Canada, and Greece), AscoTop (Germany) and Zomigoro (France).

Economics

In 2008, Zomig generated nearly $154 million in sales.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}  Template:Small. Drug Topics (May 26, 2009). Retrieved on August 25, 2009.</ref>

AstraZeneca's U.S. patent on Zomig tablets expired on November 14, 2012, and its pediatric exclusivity extension expired on May 14, 2013.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> The patent in certain European countries has already expired too, and generic drug maker Actavis released a generic version in those countries, starting in March 2012.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

In Russia, versions of zolmitriptan which are not registered in the National registry of medications may be regarded as narcotic drugs (derivatives of dimethyltriptamine).<ref name="Order681">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Research

Obsessive–compulsive disorder

Zolmitriptan showed no effect on obsessive–compulsive disorder (OCD) symptoms nor on mood or anxiety in a clinical study.<ref name="TigerVarnäsOkubo2018">Template:Cite journal</ref><ref name="BoshuisendenBoer2000">Template:Cite journal</ref>

Social deficits and aggression

Template:See also

Zolmitriptan, in a modified-release formulation with code name ML-004 (or ML004), is under development by MapLight Therapeutics for the treatment of pervasive developmental disorders (e.g., autism), agitation, and aggression.<ref name="AdisInsight-ML-004">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="Synapse2024">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="TheTransmitter2023">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="WangClarkHanratty2024">Template:Cite journal</ref><ref name="Cortica">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="PharmTech2024">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> The drug has been found to reduce aggression in rodents<ref name="Rasia-FilhoGiovenardide Almeida2008">Template:Cite journal</ref><ref name="deBoerKoolhaas2005">Template:Cite journal</ref><ref name="deAlmeidaNikulinaFaccidomo2001">Template:Cite journal</ref> and has also been reported to decrease aggression in humans.<ref name="TricklebankRobbinsSimmons2021">Template:Cite journal</ref><ref name="GowinSwannMoeller2010">Template:Cite journal</ref> As of June 2023, zolmitriptan is in phase 2 clinical trials for pervasive developmental disorders, phase 1 clinical trials for agitation, and is in the preclinical stage of development for aggression.<ref name="AdisInsight-ML-004" /><ref name="Synapse2024" /><ref name="TheTransmitter2023" />

References

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Further reading

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