Endogenous Metabolite Inducer

Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC).

Dexbrompheniramine ((+)-Brompheniramine; (S)-Brompheniramine) is a dual inhibitor of histamine H1 receptor and TRPV1 receptor that can cross the blood-brain barrier. Dexbrompheniramine exerts its effects by functionally blocking H1 receptor activity and dose-dependently inhibiting TRPV1-mediated calcium responses, including Capsaicin (HY-10448)-induced responses. The combination of Dexbrompheniramine with Cimetidine (HY-14289) eliminates histamine-induced and sham-feeding-induced drinking behavior, whereas Dexbrompheniramine alone does not induce thirst or alter sham-feeding behavior in rats. Dexbrompheniramine can be used in the research of chronic cough and related pathological mechanisms.

Glycochenodeoxycholic acid (Standard) is the analytical standard of Glycochenodeoxycholic acid. This product is intended for research and analytical applications. Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC)[1][2][3][4].

Adipokinetic hormone II (Locusta migratoria) (Lom-AKH-II) is a insect adipokinetic hormone (AKH), enhances fat body cAMP levels in vitro. Insect adipokinetic hormones (AKHs) controls flight-directed mobilization of carbohydrate and lipid from fat body stores, which depends on AKH receptor(s) coupling to cAMP formation and glycogen phosphorylase activation via the stimulatory guanine nucleotide-binding protein (Gs).

Adipokinetic hormone I (Locusta migratoria) (Lom-AKH-I) is a insect adipokinetic hormone (AKH), enhances fat body cAMP levels in vitro. Insect adipokinetic hormones (AKHs) controls flight-directed mobilization of carbohydrate and lipid from fat body stores, which depends on AKH receptor(s) coupling to cAMP formation and glycogen phosphorylase activation via the stimulatory guanine nucleotide-binding protein (Gs).

Antibiofilm agent-8 (compound Ru2) enhances antimicrobial activity on visible-light exposure (400-700 nm, 10 J cm-2). Antibiofilm agent-8 generates of oxidative stress via NADH oxidation and ROS generation and compromises bacterial wall.