jnj-40418677 and Alzheimer-Disease

jnj-40418677 has been researched along with Alzheimer-Disease* in 2 studies

Reviews

1 review(s) available for jnj-40418677 and Alzheimer-Disease

Article	Year
γ-Secretase modulators as potential disease modifying anti-Alzheimer's drugs. Journal of medicinal chemistry, 2011, Feb-10, Volume: 54, Issue:3 Topics: Alzheimer Disease; Amides; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cinnamates; Clinical Trials as Topic; Ginsenosides; Humans; Isoenzymes; Stereoisomerism	2011

Other Studies

1 other study(ies) available for jnj-40418677 and Alzheimer-Disease

Article	Year
Potent benzoazepinone γ-secretase modulators with improved bioavailability. Bioorganic & medicinal chemistry letters, 2015, Sep-01, Volume: 25, Issue:17 The triazolyl amide γ-secretase modulators are potent alternatives to the cinnamyl amides that have entered the clinic for the treatment of Alzheimer's disease. Herein we build on the lead benzoazepinones described in our prior communication with imidazomethoxyarene moiety alternatives that offer opportunities to fine tune physical properties as well as address hERG binding and PK. Both half-life and bioavailability were significantly improved, especially in dog, with robust brain Aβ42 lowering maintained in both transgenic mouse and rat. Topics: Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Biological Availability; Mice; Mice, Transgenic; Rats	2015

Article

Year

Potent benzoazepinone γ-secretase modulators with improved bioavailability.

Bioorganic & medicinal chemistry letters, 2015, Sep-01, Volume: 25, Issue:17

The triazolyl amide γ-secretase modulators are potent alternatives to the cinnamyl amides that have entered the clinic for the treatment of Alzheimer's disease. Herein we build on the lead benzoazepinones described in our prior communication with imidazomethoxyarene moiety alternatives that offer opportunities to fine tune physical properties as well as address hERG binding and PK. Both half-life and bioavailability were significantly improved, especially in dog, with robust brain Aβ42 lowering maintained in both transgenic mouse and rat.

Topics: Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Biological Availability; Mice; Mice, Transgenic; Rats

2015