ETC-1002

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

一种脂质和碳水化合物代谢的小分子调节剂，以 ACC（乙酰辅酶A羧化酶）为靶点，IC50 为 29 uM。

A small molecule regulator of lipid and carbohydrate metabolism that targets ACC (acetyl-CoA carboxylase) with IC50 of 29 uM without activating the AMPK pathway in vitro; reduces circulating proatherogenic lipoproteins, hepatic lipids, and body weight in a hamster model of hyperlipidemia.Diabetes Phase 2 Clinical(In Vitro):Bempedoic acid (ETC-1002) activates AMP-activated protein kinase in a Ca2+/calmodulin-dependent kinase β-independent and liver kinase β 1-dependent manner, without detectable changes in adenylate energy charge. Bempedoic acid is shown to rapidly form a CoA thioester in liver, which directly inhibits ATP-citrate lyase. In cells treated with Bempedoic acid (ETC-1002), increased levels of AMP-activated protein kinase (AMPK) phosphorylation coincide with reduced activity of MAP kinases and decreased production of proinflammatory cytokines and chemokines. (In Vivo):A marked and sustained increase in AMPK and ACC phosphorylation is found in rat livers following two weeks of treatment with Bempedoic acid (ETC-1002). Bempedoic acid is >100-fold more prevalent than the CoA thioester in rat liver and is associated with AMPK activation. Bempedoic acid (ETC-1002) suppresses thioglycollate-induced homing of leukocytes into mouse peritoneal cavity. In a mouse model of diet-induced obesity, Bempedoic acid restores adipose AMPK activity, reduces JNK phosphorylation, and diminishes expression of macrophage-specific marker 4F/80.

Bempedoic acid (ETC-1002) activates AMP-activated protein kinase in a Ca2+/calmodulin-dependent kinase β-independent and liver kinase β 1-dependent manner, without detectable changes in adenylate energy charge. Bempedoic acid is shown to rapidly form a CoA thioester in liver, which directly inhibits ATP-citrate lyase. In cells treated with Bempedoic acid (ETC-1002), increased levels of AMP-activated protein kinase (AMPK) phosphorylation coincide with reduced activity of MAP kinases and decreased production of proinflammatory cytokines and chemokines.

A marked and sustained increase in AMPK and ACC phosphorylation is found in rat livers following two weeks of treatment with Bempedoic acid (ETC-1002). Bempedoic acid is >100-fold more prevalent than the CoA thioester in rat liver and is associated with AMPK activation. Bempedoic acid (ETC-1002) suppresses thioglycollate-induced homing of leukocytes into mouse peritoneal cavity. In a mouse model of diet-induced obesity, Bempedoic acid restores adipose AMPK activity, reduces JNK phosphorylation, and diminishes expression of macrophage-specific marker 4F/80.

ESP-55016 | Bempedoic acid

Membrane Transporter/Ion Channel

AMPK

ACL

Metabolic Disease

Diabetes

738606-46-7

344.4861

C19H36O5

>98% (HPLC)

10 mM in DMSO

O=C(O)C(C)(C)CCCCCC(O)CCCCCC(C)(C)C(O)=O

Pentadecanedioic acid, 8-hydroxy-2,2,14,14-tetramethyl-

(-20℃)

With Ice Pack

≥ 2 years