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BMS 299897

Catalog No. T14673 CAS 290315-45-6

BMS 299897 is a sulfonamide γ-secretase inhibitor. It has an IC50 of 7 nM for Aβ production inhibition in HEK293 cells stably overexpressing amyloid precursor protein (APP).

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BMS 299897, CAS 290315-45-6

Pack Size	Availability	Price/USD
5 mg	In stock	$ 52.00
10 mg	In stock	$ 97.00
25 mg	In stock	$ 178.00
50 mg	In stock	Inquiry
1 mL * 10 mM (in DMSO)	In stock	$ 59.00

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Purity: 100%

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Description	BMS 299897 is a sulfonamide γ-secretase inhibitor. It has an IC50 of 7 nM for Aβ production inhibition in HEK293 cells stably overexpressing amyloid precursor protein (APP).
Targets&IC50	β-Amyloid (HEK293 cells):7 nM, β-Amyloid (HEK293 cells):7 nM
In vitro	BMS-299897 (1 μM) decreases these peptides to levels ranging from 20 to 50% of the vehicle control. Furthermore, it leads to a reduction in the proportion of QD-BDNF signals moving in the retrograde direction (p=0.0198) while concurrently increasing the proportion of signals moving in the anterograde direction (p=0.0147).[2]
In vivo	BMS-299897 (0.1-1 nmol/mouse; male Swiss mice; one week) blocks the increase in Aβ1-42 content and decreases Aβ1-40 levels significantly. The compound does not affect the Aβ25-35-induced increase in hippocampal lipid peroxidation. Behaviorally, BMS-299897 blocks the Aβ25-35-induced deficits in spontaneous alternation or novel object recognition, using a 1 h intertrial time interval. The co-administration of the γ-secretase inhibitor BMS-299897, in the 0.1-1 μmol/mouse dose range, completely blocks the Aβ25-35-induced increase in Aβ1-42 content.[1]

Molecular Weight	511.94
Formula	C24H21ClF3NO4S
CAS No.	290315-45-6

Storage

store at low temperature,keep away from direct sunlight

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 27.0 mg/mL (52.7 mM)

References and Literature

1. Meunier J, et al. The γ-secretase inhibitor 2-[(1R)-1-[(4-chlorophenyl)sulfonyl](2,5-difluorophenyl) amino]ethyl-5-fluorobenzenebutanoic acid (BMS-299897) alleviates Aβ1-42 seeding and short-term memory deficits in the Aβ25-35 mouse model of Alzheimer's disease. Eur J Pharmacol. 2013;698(1-3):193-199. 2. Weissmiller AM, et al. A γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APP. PLoS One. 2015;10(2):e0118379. 3. Zheng M, et al. Studies on the pharmacokinetics and metabolism of a gamma-secretase inhibitor BMS-299897, and exploratory investigation of CYP enzyme induction. Xenobiotica. 2009;39(7):544-555. 4. Xue YJ, et al. Liquid-liquid extraction of strongly protein bound BMS-299897 from human plasma and cerebrospinal fluid, followed by high-performance liquid chromatography/tandem mass spectrometry. J Pharm Biomed Anal. 2007;43(5):1728-1736. 5. Anderson JJ, et al. Reductions in beta-amyloid concentrations in vivo by the gamma-secretase inhibitors BMS-289948 and BMS-299897. Biochem Pharmacol. 2005;69(4):689-698. 6. Zhang D, et al. In vitro and in vivo metabolism of a gamma-secretase inhibitor BMS-299897 and generation of active metabolites in milligram quantities with a microbial bioreactor. Curr Drug Metab. 2006;7(8):883-896.

Related compound libraries

This product is contained In the following compound libraries：

Anti-Neurodegenerative Disease Compound Library Inhibitor Library Bioactive Compounds Library Max Bioactive Compound Library

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Keywords

BMS 299897 290315-45-6 Neuroscience Proteases/Proteasome Stem Cells Beta Amyloid Gamma-secretase BMS299897 BMS-299897 inhibitor inhibit

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