Banzel

Rufinamide

Clinical data
AHFS/Drugs.com	Consumer Drug Information
MedlinePlus	a609001
License data	EU EMA: Inovelon US FDA: Rufinamide
Pregnancy category	US: C (Risk not ruled out)
Routes of administration	By mouth (tablets)
ATC code	N03AF03 (WHO)
Legal status
Legal status	In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability	85% (under fed conditions); tmax = 4–6 hours
Protein binding	34%
Metabolism	Carboxylesterase-mediated hydrolysis ( not involved)
Metabolites	Inactive
Biological half-life	6–10 hours
Excretion	Urine (85%)
Identifiers
IUPAC name 1-(2,6-Difluorobenzyl)-1H-1,2,3-triazole-4-carboxamide
CAS Number	106308-44-5 N
PubChem CID	129228
IUPHAR/BPS	7470
ChemSpider	114471 Y
UNII	WFW942PR79
ChEMBL	CHEMBL1201754 N
Chemical and physical data
Formula	C10H8F2N4O
Molar mass	238.194
3D model (Jmol)	Interactive image
SMILES O=C(c1nnn(c1)Cc2c(F)cccc2F)N
InChI 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) Y Key:POGQSBRIGCQNEG-UHFFFAOYSA-N Y
NY (what is this?)

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 on November 14, 2008 as adjunctive treatment of seizures associated with Lennox-Gastaut syndrome in children 4 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.

The mechanism of action of rufinamide is unknown. 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.