Seletracetam

Seletracetam

Clinical data
Routes of administration	Oral
ATC code	none
Legal status
Legal status	US: Unscheduled
Pharmacokinetic data
Bioavailability	>90%
Biological half-life	8 hours
Identifiers
IUPAC name (2S)-2-[(4R)-4-(2,2-Difluoroethenyl)-2-oxo-pyrrolidin-1-yl]butanamide
CAS Number	357336-74-4 N
PubChem CID	9856063
ChemSpider	8031763 Y
UNII	RFR2CH3QZK
KEGG	D05817 Y
Chemical and physical data
Formula	C10H14F2N2O
Molar mass	232.227
3D model (Jmol)	Interactive image
SMILES F\C(F)=C/[C@H]1CC(=O)N([C@H](C(=O)N)CC)C1
InChI InChI=1S/C10H14F2N2O2/c1-2-7(10(13)16)14-5-6(3-8(11)12)4-9(14)15/h3,6-7H,2,4-5H2,1H3,(H2,13,16)/t6-,7-/m0/s1 Y Key:ANWPENAPCIFDSZ-BQBZGAKWSA-N Y
NY (what is this?)

Seletracetam (UCB 44212) is a pyrrolidone-deriveddrug of the racetam family that is structurally related to levetiracetam (trade name Keppra). It was under development by UCB Pharmaceuticals as a more potent and effective anticonvulsant drug to replace levetiracetam but its production has been halted.

There are two main mechanisms of action for seletracetam. The first is its high-affinity stereospecific binding to synaptic vesicle glycoprotein 2A (SV2A). Seletracetam has shown potent seizure suppression in models of acquired and genetic epilepsy, and has been well tolerated by various animal models. The second is its binding to N-type calcium channels and preventing influx of Ca²⁺ during high-voltage activation that is typical of epilepsy.

While similar in structure to nootropic drugs, it is not expected to have cognitive enhancing properties. Seletracetam was in Phase II clinical trials under the supervision of the U.S. Food and Drug Administration (FDA) but its production is on hold.

Seletracetam's molecular structure contains elements common to other anticonvulsants, including levetiracetam and brivaracetam, such as a nitrogen heterocyclic system. Like brivaracetam, seletracetam is a derivative of levetiracetam.

Structure and activity relationship studies have concluded that the most potent anticonvulsant activity was at the imide nitrogen atom and that this activity was further enhanced by nearby electronegative functional groups such as the di-fluoro group on seletracetam.