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Rufinamide

Rufinamide

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Rufinamide
Rufinamide.svg
Clinical data
Trade names Banzel, Inovelon
AHFS/Drugs.com Monograph
MedlinePlus a609001
License data
Pregnancy
category
  • AU: B3
Routes of
administration
By mouth
ATC code
Legal status
Legal status
  • UK: POM (Prescription only)
  • US: ℞-only
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 85% (under fed conditions); tmax = 4–6 hours
Protein binding 34%
Metabolism Carboxylesterase-mediated hydrolysis (CYP not involved)
Metabolites Inactive
Elimination half-life 6–10 hours
Excretion Urine (85%)
Identifiers
  • 1-(2,6-Difluorobenzyl)-1H-1,2,3-triazole-4-carboxamide
CAS Number
PubChem CID
IUPHAR/BPS
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
Formula C10H8F2N4O
Molar mass 238.198 g·mol−1
3D model (JSmol)
  • O=C(c1nnn(c1)Cc2c(F)cccc2F)N
  • InChI=1S/C10H8F2N4O/c11-7-2-1-3-8(12)6(7)4-16-5-9(10(13)17)14-15-16/h1-3,5H,4H2,(H2,13,17) checkY
  • Key:POGQSBRIGCQNEG-UHFFFAOYSA-N checkY
 ☒NcheckY (what is this?)  (verify)

Rufinamide is an anticonvulsant medication. It is used in combination with other medication and therapy to treat Lennox–Gastaut syndrome and various other seizure disorders. Rufinamide, a triazole derivative, was developed in 2004 by Novartis Pharma, AG, and is manufactured by Eisai.

Rufinamide was approved by the US Food and Drug Administration (FDA) in November 2008, as adjunctive treatment of seizures associated with Lennox-Gastaut syndrome in children four years and older and adults. Its official FDA-approved labeling does not mention use in the treatment of partial seizures inasmuch as clinical trials submitted to the FDA were marginal. However, several recent clinical trials suggest that the drug has efficacy for partial seizures It is marketed under the brand name Banzel. It is also marketed in the European Union under the brand name Inovelon. It is available as a generic medication.

The mechanism of action of rufinamide is not fully understood. There is some evidence that rufinamide can modulate the gating of voltage-gated sodium channels, a common target for antiepileptic drugs. A recent study indicates subtle effects on the voltage-dependence of gating and the time course of inactivation in some sodium channel isoforms that could reduce neuronal excitability. However, this action cannot explain the unique spectrum of activity of rufinamide.

External links

  • "Rufinamide". Drug Information Portal. U.S. National Library of Medicine.

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