Life Science

ATB-346 is a non-steroidal anti-inflammatory drug (NSAID), derived from naproxen but coupled to an H₂S-releasing moiety. At 30 &micromol/kg in rats, it suppressed COX and gastric PGE₂ synthesis to the same level as naproxen

ATB-346 is a non-steroidal anti-inflammatory drug (NSAID), derived from naproxen but coupled to an H₂S-releasing moiety. At 30 &micromol/kg in rats, it suppressed COX and gastric PGE₂ synthesis to the same level as naproxen

ATB-346 is a non-steroidal anti-inflammatory drug (NSAID), derived from naproxen but coupled to an H₂S-releasing moiety. At 30 &micromol/kg in rats, it suppressed COX and gastric PGE₂ synthesis to the same level as naproxen

A potent, selective, and competitive inhibitor of ATGL (IC₅₀ = 0.7 &muM) does not inhibit hormone-sensitive lipase, monoglyceride lipase, pancreatic lipase, lipoprotein lipase, or other lysophospholipases blocks lipolysis by ATGL in

A potent, selective, and competitive inhibitor of ATGL (IC₅₀ = 0.7 &muM) does not inhibit hormone-sensitive lipase, monoglyceride lipase, pancreatic lipase, lipoprotein lipase, or other lysophospholipases blocks lipolysis by ATGL in

A potent, selective, and competitive inhibitor of ATGL (IC₅₀ = 0.7 &muM) does not inhibit hormone-sensitive lipase, monoglyceride lipase, pancreatic lipase, lipoprotein lipase, or other lysophospholipases blocks lipolysis by ATGL in

A potent, selective, and competitive inhibitor of ATGL (IC₅₀ = 0.7 &muM) does not inhibit hormone-sensitive lipase, monoglyceride lipase, pancreatic lipase, lipoprotein lipase, or other lysophospholipases blocks lipolysis by ATGL in

An imidazole that potently antagonizes the &alpha2-adrenoceptor (Ki = 1.6 nM) shows selectivity over the &alpha1-adrenoceptor (Ki = 13,300 nM) and is a poor antagonist at a wide variety of other receptors and channels.

An imidazole that potently antagonizes the &alpha2-adrenoceptor (Ki = 1.6 nM) shows selectivity over the &alpha1-adrenoceptor (Ki = 13,300 nM) and is a poor antagonist at a wide variety of other receptors and channels.

An imidazole that potently antagonizes the &alpha2-adrenoceptor (Ki = 1.6 nM) shows selectivity over the &alpha1-adrenoceptor (Ki = 13,300 nM) and is a poor antagonist at a wide variety of other receptors and channels.

An imidazole that potently antagonizes the &alpha2-adrenoceptor (Ki = 1.6 nM) shows selectivity over the &alpha1-adrenoceptor (Ki = 13,300 nM) and is a poor antagonist at a wide variety of other receptors and channels.

An HMG-CoA reductase inhibitor that is effective in treating hypercholesterolemia and certain dyslipidemias reduces the production of LDL as well as inhibiting cholesterol synthesis metabolized by CYP3A4, prodrug several metabolites that are