Cas No.: | 357336-20-0 |
Chemical Name: | Brivaracetam |
Synonyms: | 1-Pyrrolidineacetamide,a-ethyl-2-oxo-4-propyl-, (aS,4R)-;Brivaracetam;(2S)-2-[(4R)-2-oxo-4-propylpyrrolidin-1-yl]butanamide;Rikelta;UCB 34714;UCB-34714;(alphaS,4R)-alpha-Ethyl-2-oxo-4-propyl-1-pyrrolidineacetamide;BRIVARACETAM [ORANGE BOOK];BRIVARACETAM (MART.);SCHEMBL122081;BRIVARACETAM [MART.];Brivaracetam [USAN:INN];1-Pyrrolidineacetamide, alpha-ethyl-2-oxo-4-propyl-, (alphaS,4R)-; (alphaS,4R)-alpha-Ethyl-2-oxo-4-propyl-1-pyrrolidineacetamide; Brivaracetam; Briviact; UCB 34714;(2S)-2-((4R)-2-OXO-4-PROPYLTETRAHYDRO-1H-PYRROL-1-YL) BUTANAMIDE;AKOS027324306;Briviact;GTPL9041;DB05541;AC-29289;D08879;1-PYRROLIDINEACETAMIDE, .ALPHA.-ETHYL-2-OXO-4-PROPYL (.ALPHA.S,4R)-;NS00068020;357336-20-0;AS-35277;UNII-U863JGG2IA;AE5 - Anti-epileptic drugs 5;BDBM50422531;NCGC00390779-02;CHEMBL607400;BB161996;1-Pyrrolidineacetamide, alpha-ethyl-2-oxo-4-propyl-, (alphaS,4R)-;BRIVARACETAM [JAN];(2S)-2-((4R)-2-Oxo-4-propylpyrrolidin-1-yl)butanamide;BRIVARACETAM [MI];BRIVARACETAM [INN];brivaracetamum;2-(2-oxo-4-propylpyrrolidin-1-yl)butanamide;MSYKRHVOOPPJKU-BDAKNGLRSA-N;(2s)-2-[(4r)-2-oxo-4-propylpyrrolidin-1-yl]butanamide;CS-3418;(S)-2-((R)-2-Oxo-4-propylpyrrolidin-1-yl)butanamide;CCG-266666;BRIVARACETAM [USAN];MFCD25976668;Briviact (TN);EX-A2748;U863JGG2IA;CHEBI:133013;DTXSID00905081;N03AX23;Q408099;(2S)-2-((4R)-2-oxo-4-n-propyl-1-pyrrolidinyl)butanamide;1-PYRROLIDINEACETAMIDE, alpha-ETHYL-2-OXO-4-PROPYL (alphaS,4R)-;HY-14449;BRIVARACETAM [WHO-DD];Brivaracetam (JAN/USAN/INN);compound 83alpha;UCB34714 |
SMILES: | CCC[C@@H]1CC(N([C@H](C(N)=O)CC)C1)=O |
Formula: | C11H20N2O2 |
M.Wt: | 212.2887 |
Purity: | >98% |
Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
Description: | Brivaracetam(UCB-34714) is a 4-substituted pyrrolidone butanamide as agent with significant antiepileptic activity; high affinity SV2A ligand and also shows an ability to inhibit Na+ channels. in vitro: Brivaracetam has been tested in a comprehensive safety pharmacology, toxicology, developmental toxicology, and genotoxicity program. It is of low acute toxicity, target organ for toxic effects is the hepatobiliary tract. Carcinogenicity studies are ongoing. Human pharmacology studies have shown that brivaracetam has a half-life of 8 h and nearly complete bioavailability. CSD episodes were regularly elicited on slices upon delivery of calibrated KCl drops and were recorded via two micropipette electrodes. After control CSDs, the drug was added to the perfusion and five subsequent CSDs were elicited during drug perfusion. Effects were assessed via CSD amplitude (Ampl) and duration at half-amplitude (D(1/2)). BRV, 10 and 32 microM reduced the Ampl and transiently the D(1/2). Levetiracetam, 32 and 100 microM had no effect on either Ampl or D(1/2). Brivaracetam bound selectively with 20 fold higher affinity than levetiracetam to SV2A. BRV produced a concentration-dependent inhibition of voltage-dependent Na(+) currents with IC(50) values of 41microM at the holding potential of -100mV, and of 6.5microM at the holding potential of -60mV. in vivo: BRV (2.1, 6.8 or 21.0mg/kg i.p.) was injected daily, 60min before each session. Results indicated that in both normal and amygdala-kindled rats BRV did not alter the latency to find the hidden platform or swimming speed during the four consecutive days of learning. brivaracetam (0.3 mg/kg, the minimal effective dose) was more potent than levetiracetam (3 mg/kg, the minimal effective dose) against post-hypoxic seizures.The anti-seizure activity of both compounds occurred 30 min following intraperitoneal (i.p.) administration and was maintained over the entire 150 min post-dose observation period. Both brivaracetam and levetiracetam significantly reduced auditory stimulated post-hypoxic myoclonus from a dose 0.3 mg/kg. |