CYP7A1 Mouse mAb (S-M0026)

CYP7A1, namely cholesterol 7α-hydroxylase, is a critically important liver-specific enzyme belonging to the cytochrome P450 superfamily. It catalyzes the first and rate-limiting step in the pathway of cholesterol catabolism into bile acids—introducing a hydroxyl group at the 7α-carbon position of cholesterol to generate 7α-hydroxycholesterol, which serves as the core regulatory node determining the overall rate of bile acid synthesis. This enzyme is predominantly expressed in the smooth endoplasmic reticulum of hepatocytes, and its activity is precisely regulated at the transcriptional level by multiple nuclear receptors (such as FXR, LXR, and PPARα) and transcription factors (such as HNF4α), as well as influenced by a complex signaling network involving hormones (such as thyroid hormone and glucocorticoids) and metabolites (such as bile acids themselves through the FXR-SHP feedback pathway), thereby achieving dynamic homeostasis of cholesterol balance and bile acid pool size in the body. The function of CYP7A1 is not limited to bile acid synthesis; it also profoundly affects systemic lipid metabolism by regulating cholesterol clearance and lipid absorption. Reduced expression activity or genetic polymorphisms of CYP7A1 are closely associated with the risk of various metabolic diseases, including hypercholesterolemia, gallstone formation, and non-alcoholic fatty liver disease; conversely, aberrant overexpression of CYP7A1 in certain hepatobiliary cancers may participate in tumorigenesis by promoting bile acid-mediated chronic inflammation and DNA damage. In clinical drug development, CYP7A1, owing to its central role in cholesterol reduction, has become an indirect or direct therapeutic target for multiple novel lipid-lowering agents (such as bile acid sequestrants and FXR agonists), while its enzymatic activity can also serve as an important biological indicator for assessing liver function and metabolic status.