Frovatriptan succinate

Modify Date: 2025-08-24 21:12:52

Frovatriptan succinate Structure
Frovatriptan succinate structure
Common Name Frovatriptan succinate
CAS Number 158930-09-7 Molecular Weight 361.39200
Density N/A Boiling Point 515.2ºC at 760 mmHg
Molecular Formula C18H23N3O5 Melting Point N/A
MSDS N/A Flash Point 265.4ºC

 Use of Frovatriptan succinate


Frovatriptan succinate ((R)-Frovatriptan succinate) is a potent, high affinity, selective and orally active 5-HT1B (pK50 of 8.2) and 5-HT1D receptor agonist. Frovatriptan succinate exhibits >10-fold selectivity for 5-HT1B and 5-HT1D over 5-HT1A, 5-HT1F, and 5-HT7 and >1000-fold selectivity over other 5-HT, dopamine, histamine H1, and α1-adrenoceptor. Frovatriptan succinate has the potential for migraine research[1][2].

 Names

Name butanedioic acid,(6R)-6-(methylamino)-6,7,8,9-tetrahydro-5H-carbazole-3-carboxamide
Synonym More Synonyms

 Frovatriptan succinate Biological Activity

Description Frovatriptan succinate ((R)-Frovatriptan succinate) is a potent, high affinity, selective and orally active 5-HT1B (pK50 of 8.2) and 5-HT1D receptor agonist. Frovatriptan succinate exhibits >10-fold selectivity for 5-HT1B and 5-HT1D over 5-HT1A, 5-HT1F, and 5-HT7 and >1000-fold selectivity over other 5-HT, dopamine, histamine H1, and α1-adrenoceptor. Frovatriptan succinate has the potential for migraine research[1][2].
Related Catalog
Target

5-HT1B Receptor:8.2 (pEC50)

5-HT1D Receptor

In Vitro Cerebral vasodilatation and neurogenic inflammation are considered to be prime movers in the pathogenesis of migraine. Activation of 5-HT1B reverses cerebral vasodilatation and activation of 5-HT1D prevents neurogenic inflammation. Frovatriptan has a high affinity for 5-HT1B and 5-HT1D receptors and a moderate affinity for the 5-HT1A and 5-HT1F receptors subtypes. Frovatriptan has a moderate affinity for the 5-HT7 receptors, an action associated with coronary artery relaxation in the dog[1].
In Vivo Oral bioavailability of Frovatriptan is 22%-30% and is not affected by food. Although the maximum concentration in the plasma is achieved in 2-3 hours, 60%-70% of this is achieved in 1 hour. A steady state is achieved in 4-5 days. Plasma protein binding is low at 15%. The most unique feature is the relative terminal long half-life of about 26 hours. Frovatriptan is chiefly metabolized by CYP1A2 and is cleared by the kidney and liver making moderate failure of either organ not a limiting factor in treatment[1]. Frovatriptan (0.1, 0.2, and 0.3 mg/kg; a single bolus intraduodenal administration) treatment produces an increase in carotid vascular resistance, which is sustained for at least 5 hours in dogs[2].
References

[1]. Kelman L. Review of frovatriptan in the treatment of migraine. Neuropsychiatr Dis Treat. 2008 Feb;4(1):49-54.

[2]. Comer MB. Et al. Pharmacology of the selective 5-HT(1B/1D) agonist frovatriptan. Headache. 2002 Apr;42 Suppl 2:S47-53.

 Chemical & Physical Properties

Boiling Point 515.2ºC at 760 mmHg
Molecular Formula C18H23N3O5
Molecular Weight 361.39200
Flash Point 265.4ºC
Exact Mass 361.16400
PSA 146.50000
LogP 2.55440
Vapour Pressure 1.01E-10mmHg at 25°C

 Synonyms

Frovatriptan succinate anhydrous
UNII-36K05YF32G
Frovatriptan Succinate
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