Α5IA

α₅IA (LS-193,268) is a nootropic drug invented in 2004 by a team working for Merck, Sharp and Dohme, which acts as a subtype-selective inverse agonist at the benzodiazepine binding site on the GABA_A receptor. It binds to α₁, α₂, α₃ and α₅ -containing subtypes, with functional selectivity for α₅-containing subtypes.^[1][2]

α₅IA

Clinical data
Other names	LS-193,268
ATC code	None
Pharmacokinetic data
Elimination half-life	2-2.5h
Identifiers
IUPAC name 3-(5-methylisoxazol-3-yl)-6-[(1-methyl-1H-1,2,3-triazol-4-yl)methoxy][1,2,4]triazolo[3,4-a]phthalazine
CAS Number	215874-86-5
PubChem CID	6918451
ChemSpider	5293648
UNII	1M7NI1A92L
CompTox Dashboard (EPA)	DTXSID10175950
Chemical and physical data
Formula	C17H14N8O2
Molar mass	362.353 g·mol−1
3D model (JSmol)	Interactive image
SMILES CC1=CC(=NO1)C2=NN=C3N2N=C(C4=CC=CC=C43)OCC5=CN(N=N5)C
InChI InChI=1S/C17H14N8O2/c1-10-7-14(22-27-10)16-20-19-15-12-5-3-4-6-13(12)17(21-25(15)16)26-9-11-8-24(2)23-18-11/h3-8H,9H2,1-2H3 Key:NZMJFRXKGUCYNP-UHFFFAOYSA-N

Clinical research

Administration of α₅IA following alcohol consumption was found to reverse memory impairments induced by alcohol.^[3]

In vitro electrophysiology

Recordings of local field potentials indicate that oral administration of α5IA increases the amplitude of sharp wave ripples which are implicated in memory function in adult wild type rats. The increase in ripple amplitude is not seen in adult male TgF344-AD rats which express human β-amyloid precursor protein (with the Swedish mutation) and human presenilin-1 (with a Δ exon 9 mutation).^[4]

See also

• GABA_A receptor negative allosteric modulator
• GABA_A receptor § Ligands