An article LMP2 Inhibitors as a Potential Treatment for Alzheimer’s Disease WOS:000526405300024 published article about ANTIINFLAMMATORY DRUGS; IMMUNOPROTEASOME; DESIGN; CELLS; RISK in [Bhattarai, Deepak; Lee, Min Jae; Miller, Zachary; Kim, Kyung Bo] Univ Kentucky, Dept Pharmaceut Sci, Lexington, KY 40536 USA; [Baek, Ahruem; Baek, Yu Mi; Kim, Dong-Eun] Konkuk Univ, Dept Biosci & Biotechnol, Seoul 05029, South Korea; [Yeo, In Jun; Hong, Jin Tae] Chungbuk Natl Univ, Coll Pharm, Cheongju 28160, Chungbuk, South Korea; [Lee, Sukyeong] Baylor Coll Med, Verna & Marrs McLean Dept Biochem & Mol Biol, Houston, TX 77030 USA in 2020, Cited 43. The Name is Pyrazine-2-carboxylic acid. Through research, I have a further understanding and discovery of 98-97-5. Application In Synthesis of Pyrazine-2-carboxylic acid
The immunoproteasome (iP), an inducible proteasome variant harboring three immunosubunits, low molecular mass polypeptide-2 (LMP2), multicatalytic endopeptidase complex subunit-1, and low molecular mass polypeptide-7 (LMP7), is involved in multiple facets of inflammatory responses. We recently reported that YU102, a dual inhibitor of the iP subunit LMP2 and the constitutive proteasome catalytic subunit beta 1, ameliorates cognitive impairments in mouse models of Alzheimer’s disease (AD) independently of amyloid deposits. To investigate whether inhibition of LMP2 is sufficient to improve the cognitive functions of AD mice, here we prepared 37 YU102 analogues and identified a potent LMP2 inhibitor DB-310 (28) (IC50: 80.6 nM) with improved selectivity and permeability in cells overexpressing ABCB1 transporters. We show that DB-310 induces suppression of IL-1 alpha production in microglia cells and improves cognitive functions in the Tg2576 transgenic mouse model of AD. This study supports that inhibition of LMP2 is a promising therapeutic strategy for treatment of AD.
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Reference:
Patent; Chevron Research Company; US4732894; (1988); A;,
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