Chlorcyclizine is a first generation phenylpiperazine class antihistamine used to treat urticaria, rhinitis, pruritus, and other allergy symptoms. Chlorcyclizine also has some local anesthetic, anticholinergic, and antiserotonergic properties, and can be used as an antiemetic. Chlorcyclizine temporarily relieves the symptoms due to hay fever or other upper respiratory allergies. It has also being shown to possess in vitro and in vivo activity against hepatitis C virus.

The small molecule PF-429242 was developed as a hypolipidemic agent based on high throughput screening in a Pfizer compound library. PF-429242 is a competitive inhibitor of sterol regulatory element-binding protein (SREBP) site 1 protease (IC50 = 0.175 uM). It is selective for site 1 protease against a panel of serine proteases. PF-429242 inhibits rate of cholesterol synthesis in CHO cells (IC50 = 0.53 uM). PF-429242 inhibits the activity of S1P reversibly and competitively and suppresses the expression level of SREBP target genes, consequently decreasing cellular lipid levels. It has been shown that PF-429242 suppresses hepatic SREBP target genes and inhibits cholesterol and fatty acid synthesis in a mouse model. It also has been reported that PF-429242 suppresses viral replication in cells infected with hepatitis C virus (HCV), Lassa virus, lymphocytic choriomeningitis virus, New World arenaviruses and Dengue virus.

GS-9851 (formerly PSI 7851) is an orally available, second generation uridine nucleoside analog polymerase inhibitor of hepatitis C treatment. GS-9851 is a nucleotide prodrug of the nucleoside analog GS-331007 (formerly PSI-6206). GS-9851 potently inhibits HCV NS5B polymerase and has demonstrated pan-genotypic activity in vitro. Preclinical studies of GS-9851 demonstrated a favorable profile in terms of antiviral potency, distribution, and metabolism. GS-9851 is first hydrolyzed to the intermediate GS-566500 (formerly PSI-352707), which is then metabolized to either the inactive metabolite, GS-331007, or the monophosphate GS-606965 (formerly PSI-7411). Inside the hepatocyte, GS-606965 is further phosphorylated by a series of enzymatic steps to an active triphosphate metabolite, GS-461203 (formerly PSI-7409), that selectively inhibits recombinant NS5B. A first-time-in-human study demonstrated that GS-9851 (25 to 800 mg) is generally safe and well tolerated in patients chronically infected with HCV. GS-9851 has a pharmacokinetic profile consistent with once-daily dosing. Administration of GS-9851 led to significant reductions in plasma HCV RNA levels without the evolution of known resistance mutations.

Verbenalin is an iridoid glycoside, and an alkaloid as well, found in Verbena officinalis. Verbenalin has demonstrated cardioprotection against experimental myocardial ischemic injury. It attenuated hypoxia-induced cytotoxicity significantly in H9c2 cells in a concentration-dependent manner. Treatment of H9c2 cells with Verbenalin blocked the reduction of expression of phospho-CREB and phospho-Akt in a hypoxic condition. Verbenalin can protect myocardial function in rats during myocardial I/R injury, suggesting the therapeutic potential of Verbenalin against myocardial I/R injury. Verbenalin also exhibited significant anti-HCV entry and anti-infectivity activities.

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.