Ezetimibe is an anti-hyperlipidemic medication which is used to lower cholesterol levels. Specifically, it appears to bind to a critical mediator of cholesterol absorption, the Niemann-Pick C1-Like 1 (NPC1L1) protein on the gastrointestinal tract epithelial cells as well as in hepatocytes. Ezetimibe is in a class of lipid-lowering compounds that selectively inhibits the intestinal absorption of cholesterol and related phytosterols. Ezetimibe, administered alone is indicated as adjunctive therapy to diet for the reduction of elevated total-C, LDL-C, and Apo B in patients with primary (heterozygous familial and non-familial) hypercholesterolemia. It is also used in combination therapy with HMG-CoA reductase inhibitors. Ezetimibe has a mechanism of action that differs from those of other classes of cholesterol-reducing compounds (HMG-CoA reductase inhibitors, bile acid sequestrants, fibric acid derivatives, and plant stanols). Ezetimibe does not inhibit cholesterol synthesis in the liver, or increase bile acid excretion but instead localizes and appears to act at the brush border of the small intestine and inhibits the absorption of cholesterol, leading to a decrease in the delivery of intestinal cholesterol to the liver. This causes a reduction of hepatic cholesterol stores and an increase in clearance of cholesterol from the blood; this distinct mechanism is complementary to that of HMG-CoA reductase inhibitors.

Avasimibe (CI 1011) is a potent ACAT (Acyl-CoA:cholesterol acyltransferase) inhibitor. Avasimibe inhibits both ACAT1 and ACAT2 isoforms. Avasimibe was in development by Parke-Davis (now Pfizer) in the US for the treatment of atherosclerosis and hyperlipidaemia. Avasimibe was in phase III studies and more than 1300 patients had been treated for up to one year, however, in October 2003, Pfizer announced that development had been discontinued.

Eflucimibe is a new and potent Acyl coenzyme A:cholesterol acyltransferases inhibitor. Eflucimibe effectively decreased plasma cholesterol in cholesterol-fed animals. In animal models, drug restores normolipodemia in endogenous hypercholesterolemic rabbits and prevents the progression of atherosclerosis by decreasing the number of macrophages in the foam cells. Eflucimibe has been in phase II clinical trials for the treatment of atherosclerosis and hyperlipidemia. However, this research has been discontinued.

Cetaben has been identified as an anti-atherosclerotic hypolipidaemic substance. Cetaben is a unique, PPARα-independent peroxisome proliferator with hypolipidemic activity that inhibits cholesterol synthesis in the human hepatoma Hep-G2 cells resulting in reversible changes in Golgi morphology. Cetaben represents an exceptional type of peroxisome proliferator, specifically affecting peroxisomes, without having a negative influence on the processes of peroxisome biogenesis. Cetaben raised only the peroxisomal enzymes, acyl-CoA oxidase, glycerone-phosphate acyltransferase, D-amino-acid oxidase, catalase, and urate oxidase. Cetaben sodium has being shown to be an antiatherosclerotic agent.

Methylene di-t-butylcresol (GERI-BP002-A) is a hindered phenolic antioxidant and thermal stabilizer providing effective stabilization in adhesives, ABS, polyolefins, and other substrates. GERI-BP002-A is a novel inhibitor of SOAT (Acyl-CoA Cholesterol Acyltransferase (ACAT)) which is produced by Aspergillus fumigatus F93. GERI-BP002-A also exhibits antioxidant activity.

Protopanaxadiol (PPD, Yuxintine) is an organic compound characterizing a group of ginsenosides. It is a dammarane-type tetracyclic terpene sapogenin found in ginseng (Panax ginseng) and in notoginseng (Panax pseudoginseng). Protopanaxadiol has a wide range of pharmacologic activities, including antiestrogen, anti-inflammatory, antitumor, vasodilating, cardioprotection, and antidepressant effects. The antidepressant effect of oral Protopanaxadiol had been confirmed by several different animal models, such as forced swimming test tail suspension test, and rat olfactory bulbectomy depression models. Protopanaxadiol was found to have much fewer adverse drug reactions than currently-used first-line antidepressants. It is almostdevoid of sedation, sexual dysfunction, weight gain, cardiovascular complications, and anticholinergic effects. Protopanaxadiol was in phase II clinical trials as a novel antidepressant in China.

Echinocystic acid (EA) is a pentacyclic triterpene isolated from the fruits of Gleditsia sinensis Lam, has potent antioxidant, anti-inflammatory and anti-tumor properties. Echinocystic acid (EA) inhibit the formation of osteoclast. EA inhibit RANKL-induced NF-κB activation and ERK phosphorylation in BMMs. Echinocystic acid inhibits IL-1β-induced COX-2 and iNOS expression in human osteoarthritis chondrocytes. Echinocystic acid also inhibited TPA-induced myeloperoxidase activity, as well as COX-2, iNOS, TNF-α and IL-1β expressions. Echinocystic acid inhibited NF-κB in TPA-treated mouse ears, as well as in lipopolysaccharide-stimulated peritoneal macrophages. Its potency is comparable with that of dexamethasone. These findings indicate that echinocystic acid may ameliorate inflammatory diseases, such as dermatitis. EA inhibited ACAT and DGAT, with IC50 values of 103 and 139  uM, respectively, and exhibited no significant effect on HMG-CoA reductase activity. The present findings suggest that EA may exert hypolipidemic effect by inhibiting the activity of ACAT and DGAT.

Folipastatin is a depsone metabolite first isolated from Aspergillus unguis by researchers at Sankyo, Japan in 1992 as an inhibitor of phospholipase A2. Folipastatin also possesses moderate antibiotic activity as against Gram positive bacteria. It is a component of a mixture of unguinol-related metabolites produced by A. unguis and A. nidulins patented as growth promotants in livestock. More recently, folipastatin was reported as an inhibitor of sterol O-acyltransferase (SOAT) 1 and 2 iso-enzymes in cell-based and enzyme assays.