BEMPEDOIC ACID has an innovative mechanism of action and works in the well-known cholesterol synthesis pathway.

孟泊酸具有創新的作用機制，可在眾所周知的膽固醇合成途徑中發揮作用。

Within the hepatocytes, endogenous cholesterol is synthesized along the cholesterol biosynthesis pathway through a series of enzymatic interactions, which include HMG-CoA reductase, the primary target of statins.

在肝細胞內，內源性膽固醇通過一系列酶的相互作用，沿著膽固醇生物合成途徑合成，其中包括他汀類藥物的主要靶點--HMG-CoA 還原酶。

BEMPEDOIC ACID has a mechanism complementary to statins.

苯乙雙胍酸的作用機制與他汀類藥物互補。

When activated in the liver, BEMPEDOIC ACID inhibits adenosine triphosphate citrate lyase, known as ACL, an enzyme two steps upstream of HMG-CoA reductase.

當在肝臟中被激活時，苯環丙酸會抑制三磷酸腺苷檸檬酸酶（又稱 ACL），這是 HMG-CoA 還原酶上游的一種酶。

By inhibiting ACL, BEMPEDOIC ACID reduces cholesterol synthesis, resulting in LDL receptor upregulation and increased clearance of LDL cholesterol from the bloodstream.

通過抑制 ACL，孟泊酸可減少膽固醇的合成，導致低密度脂蛋白受體上調，增加血液中低密度脂蛋白膽固醇的清除率。

Of note, BEMPEDOIC ACID is a prodrug converted primarily in the liver to its active moiety by ACSVL1.

值得注意的是，苯乙二酸是一種原藥，主要在肝臟中通過 ACSVL1 轉化為其活性分子。

ACSVL1 is not present in skeletal muscle.

骨骼肌中不存在 ACSVL1。

Therefore, BEMPEDOIC ACID is not converted to its active form within skeletal muscle.

是以，雙烯酸在骨骼肌內不會轉化為其活性形式。

BEMPEDOIC ACID is also available with ezetimibe in a combination tablet that brings together their complementary mechanisms of action.

本品還可與依折麥布一起製成複方片劑，將兩者互補的作用機制結合在一起。

BEMPEDOIC ACID inhibits cholesterol synthesis via ACL inhibition primarily in the liver, while ezetimibe blocks gastrointestinal cholesterol absorption via NPC1L1 inhibition, reducing cholesterol delivery to the liver.

苯乙酸主要通過抑制肝臟中的 ACL 來抑制膽固醇的合成，而依折麥布則通過抑制 NPC1L1 來阻止胃腸道對膽固醇的吸收，從而減少膽固醇向肝臟的輸送。

These complementary mechanisms result in LDL receptor upregulation and increased LDL-C clearance from the bloodstream.

這些互補機制會導致低密度脂蛋白受體上調，並增加血液中低密度脂蛋白-膽固醇的清除率。