Nuclear transport modulators are disclosed. The compounds can inhibit nuclear transporters such as the exportin-1 transporter. The compounds and pharmaceutical compositions comprising the compounds can be used to treat neurological diseases and cancer.

The present invention relates to ether-linked triazole compounds, methods of making them, pharmaceutical compositions containing them and their use as NRF2 activators. In particular, the invention relates to compounds of Formula (I), and pharmaceutically acceptable salts thereof:

##STR00001##

The present invention relates to ether-linked triazole compounds, methods of making them, pharmaceutical compositions containing them and their use as NRF2 activators. In particular, the invention relates to compounds of Formula (I), and pharmaceutically acceptable salts thereof:

##STR00001##

Provided is a novel compound capable of improving the luminous efficiency, stability and life span of a device, an organic electric element using the same, and an electronic device thereof.

The present invention relates to bisaryl amide analogs, pharmaceutical compositions containing them and their use as NRF2 activators. In particular, the invention relates to bisaryl heterocycles of Formula (I), ##STR00001##

The present invention provides non-peptide compounds that mimic the streptococcal SspB Adherence Region (BAR) and function as inhibitors of P. gingivalis adherence to streptococci. The invention also provides methods of making and using the inhibitors.

The present invention provides non-peptide compounds that mimic the streptococcal SspB Adherence Region (BAR) and function as inhibitors of P. gingivalis adherence to streptococci. The invention also provides methods of making and using the inhibitors.

Provided are a compound capable of improving the luminous efficiency, stability and life span of a device, an organic electric element using the same, and an electronic device thereof.

Irreversible inhibitors of G12C mutant K-Ras protein are provided. Also disclosed are methods to modulate the activity of G12C mutant K-Ras protein and methods of treatment of disorders mediated by G12C mutant K-Ras protein.

Irreversible inhibitors of G12C mutant K-Ras protein are provided. Also disclosed are methods to modulate the activity of G12C mutant K-Ras protein and methods of treatment of disorders mediated by G12C mutant K-Ras protein.