Clinical data | |
---|---|
Routes of administration | Oral[1][2] |
ATC code |
|
Legal status | |
Legal status |
|
Pharmacokinetic data | |
Bioavailability | >90%[1][2] |
Elimination half-life | 8 hours[1][2] |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
ChemSpider | |
UNII | |
KEGG | |
CompTox Dashboard (EPA) | |
Chemical and physical data | |
Formula | C10H14F2N2O |
Molar mass | 216.232 g·mol−1 |
3D model (JSmol) | |
| |
| |
(what is this?) (verify) |
Seletracetam (UCB 44212) is a pyrrolidone-derived[2] drug of the racetam family that is structurally related to levetiracetam (trade name Keppra).[2][3] It was under development by UCB Pharmaceuticals as a more potent and effective anticonvulsant drug to replace levetiracetam but its development has been halted.[1]
There are two main mechanisms of action for seletracetam. The first is its high-affinity stereospecific binding to synaptic vesicle glycoprotein 2A (SV2A).[2][3] Seletracetam has shown potent seizure suppression in models of acquired and genetic epilepsy,[3] and has been well tolerated by various animal models.[3] The second is its binding to N-type calcium channels and preventing influx of Ca2+ during high-voltage activation that is typical of epilepsy.[4][5][6]
While similar in structure to nootropic drugs, it is not expected to have cognitive enhancing properties.[7] 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.[3]
Malykh
was invoked but never defined (see the help page).Bennett
was invoked but never defined (see the help page).Martella
was invoked but never defined (see the help page).Pisani2004
was invoked but never defined (see the help page).Custer
was invoked but never defined (see the help page).Matagne
was invoked but never defined (see the help page).