Results for Enzymes ( 22555 )
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ND-630 (NDI 010976) is a highly specific, reversible inhibitor of ACC1 (IC50 = 2 nM) and ACC2 (IC50 = 6 nM). ND-630 interacts within the ACC phosphopeptide acceptor and dimerization site to prevent dimerization of ACC. Because the dimerization site is not conserved among other mammalian carboxylases, ND-630 lacks the ability to inhibit other mechanistically-related enzymes. In rats with diet-induced obesity, ND-630 reduced hepatic steatosis, improved insulin sensitivity, and reduced weight gain, suggesting ACC inhibition may be useful in treating metabolic disorders, including type 2 diabetes mellitus, and fatty liver disease.
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ND-630 (NDI 010976) is a highly specific, reversible inhibitor of ACC1 (IC50 = 2 nM) and ACC2 (IC50 = 6 nM). ND-630 interacts within the ACC phosphopeptide acceptor and dimerization site to prevent dimerization of ACC. Because the dimerization site is not conserved among other mammalian carboxylases, ND-630 lacks the ability to inhibit other mechanistically-related enzymes. In rats with diet-induced obesity, ND-630 reduced hepatic steatosis, improved insulin sensitivity, and reduced weight gain, suggesting ACC inhibition may be useful in treating metabolic disorders, including type 2 diabetes mellitus, and fatty liver disease.
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Celastrol is a naturally occurring triterpenoid antioxidant compound with anti-inflammatory activity. Inhibits NFkappaB (IC50 = 270 nM). It induces heat shock response and cytoprotection in various cells. Celastrol inhibits 20S proteasome chymotrypsin-like activity (IC50 = 2.5 µM). Cell permeable.
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Celastrol is a naturally occurring triterpenoid antioxidant compound with anti-inflammatory activity. Inhibits NFkappaB (IC50 = 270 nM). It induces heat shock response and cytoprotection in various cells. Celastrol inhibits 20S proteasome chymotrypsin-like activity (IC50 = 2.5 µM). Cell permeable.
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DBeQ is cell permeable, potent, selective and reversible inhibitor of the AAA-ATPase p97 (ATPase associated with diverse cellular activities). Ki=3.2 µM. DBeQ blocks both ubiquitin dependent and endoplasmic reticulum-associated degradation pathways, protein clearance pathways, and activates caspases -3 and -7 inducing apoptosis.