Chenodiol is the non-proprietary name for chenodeoxycholic acid, a naturally occurring human bile acid. It is a bitter-tasting white powder consisting of crystalline and amorphous particles freely soluble in methanol, acetone and acetic acid and practically insoluble in water. Chenodiol suppresses hepatic synthesis of both cholesterol and cholic acid, gradually replacing the latter and its metabolite, deoxycholic acid in an expanded bile acid pool. These actions contribute to biliary cholesterol desaturation and gradual dissolution of radiolucent cholesterol gallstones in the presence of a gall-bladder visualized by oral cholecystography. Bile acids may also bind the the bile acid receptor (FXR) which regulates the synthesis and transport of bile acids. Chenodiol is indicated for patients with radiolucent stones in well-opacifying gallbladders, in whom selective surgery would be undertaken except for the presence of increased surgical risk due to systemic disease or age. The likelihood of successful dissolution is far greater if the stones are floatable or small. For patients with nonfloatable stones, dissolution is less likely and added weight should be given to the risk that more emergent surgery might result form a delay due to unsuccessful treatment.

Cefuroxime is a semisynthetic, broad-spectrum, cephalosporin antibiotic. Cefuroxime is a bactericidal agent that acts by inhibition of bacterial cell wall synthesis. Cefuroxime has activity in the presence of some beta-lactamases, both penicillinases and cephalosporinases, of Gram-negative and Gram-positive bacteria. Cefuroxime has been shown to be active against most isolates of the following bacteria, both in vitro and in clinical infection: Enterobacter spp., Escherichia coli, Klebsiella spp., Haemophilus influenzae, Neisseria meningitidis, Neisseria gonorrhoeae, Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes. Cefuroxime is indicated for the treatment of patients with septicemia, meningitis, gonorrhea, lower respiratory tract, urinary tract, skin and skin-structure, bone and joint infections caused by susceptible strains of the designated organisms.

Succimer is an analogue of dimercaprol, and has replaced dimercaprol as one of the main antidotes used in the management of poisoning by lead and other heavy metals. The advantages of succimer are that it is effective by oral administration because it is soluble in water, it is well-tolerated, has relatively low toxicity and can be given at the same time as iron supplements to treat iron deficiency anaemia. It does not cause significant increase in urinary excretion of essential minerals unlike the other widelyused lead chelating agent, sodium calcium EDTA.

Malathion is an organophosphate insecticide, an inhibitor of cholinesterase. In low doses (0.5%) malathion is used for treatment of pediculosis and scabies.

Etomidate (AMIDATE®) is an imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It is intended for the induction of general anesthesia by intravenous injection. Etomidate (AMIDATE®) is also indicated for the supplementation of subpotent anesthetic agents, such as nitrous oxide in oxygen, during maintenance of anesthesia for short operative procedures such as dilation and curettage or cervical conization. It also produces a unique toxicity among anesthetic drugs - inhibition of adrenal steroid synthesis that far outlasts its hypnotic action and that may reduce survival of critically ill patients. The major molecular targets mediating anesthetic effects of etomidate (AMIDATE®) in the central nervous system are specific gamma-aminobutyric acid (GABA) type A receptor subtypes. The R(+) isomer of etomidate is 10 times more potent than its S(-) isomer at potentiating GABA-A receptor activity.

Diflunisal is a salicylic acid derivative with analgesic and anti-inflammatory activity. It was developed by Merck Sharp & Dohme in 1971 after showing promise in a research project studying more potent chemical analogs of aspirin. Diflunisal is an aspirin-like nonsteroidal anti-inflammatory drug that inhibits cyclooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis.In animals, prostaglandins sensitize afferent nerves and potentiate the action of bradykinin in inducing pain. Since prostaglandins are known to be among the mediators of pain and inflammation, the mode of action of diflunisal may be due to a decrease of prostaglandins in peripheral tissues.

Nifedipine has been formulated as both a long- and short-acting 1,4-dihydropyridine calcium channel blocker. Nifedipine is sold under the brand names Adalat and Procardia among others. Nifedipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the influx of calcium ions through L-type calcium channels. Calcium ions entering the cell through these channels bind to calmodulin. Calcium-bound calmodulin then binds to and activates myosin light chain kinase (MLCK). Activated MLCK catalyzes the phosphorylation of the regulatory light chain subunit of myosin, a key step in muscle contraction. Signal amplification is achieved by calcium-induced calcium release from the sarcoplasmic reticulum through ryanodine receptors. Inhibition of the initial influx of calcium inhibits the contractile processes of smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. The vasodilatory effects of nifedipine result in an overall decrease in blood pressure. Nifedipine is used for the management of vasospastic angina, chronic stable angina, hypertension, and Raynaud's phenomenon. May be used as a first line agent for left ventricular hypertrophy and isolated systolic hypertension (long-acting agents).

Gemfibrozil, a fibric acid antilipemic agent similar to clofibrate, is used to treat hyperlipoproteinemia and as a second-line therapy for type IIb hypercholesterolemia. It acts to reduce triglyceride levels, reduce VLDL levels, reduce LDL levels (moderately), and increase HDL levels (moderately). Gemfibrozil increases the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis. It does so by activating Peroxisome proliferator-activated receptor-alpha (PPARα) 'transcription factor ligand', a receptor that is involved in metabolism of carbohydrates and fats, as well as adipose tissue differentiation. This increase in the synthesis of lipoprotein lipase thereby increases the clearance of triglycerides. Chylomicrons are degraded, VLDLs are converted to LDLs, and LDLs are converted to HDL. This is accompanied by a slight increase in secretion of lipids into the bile and ultimately the intestine. Gemfibrozil also inhibits the synthesis and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. Gemfibrozil is most commonly sold as the brand name, Lopid. Other brand names include Jezil and Gen-Fibro.

Ecraprost [AS 013, Circulase] is a prodrug of prostaglandin E(1) within lipid microspheres that is being developed in Japan by Mitsubishi Pharma Corporation and Asahi Glass. It was originally in development with Welfide Corporation. On 1 October 2001, Welfide Corporation (formerly Yoshitomi) merged with Mitsubishi-Tokyo Pharmaceuticals to form Mitsubishi Pharma Corporation. The new company is a subsidiary of Mitsubishi Chemical. Taisho and Seikagaku Corporation had been involved in the development of ecraprost but discontinued their licences to do so. The effects of ecraprost on reperfusion injury, in preclinical studies, had been reported by Taisho. Ecraprost is in phase II in Japan and was in phase II in Europe for the treatment of peripheral arterial disease. It was also in a phase II study in the treatment of diabetic neuropathies. However, this is no longer an active indication. A phase III trial using a lipid emulsion of ecraprost [Circulase] is underway with Mitsubishi Pharma Corporation in the US, using ecraprost for the treatment of patients with severe peripheral arterial disease, which, because of decreased blood flow to the extremities, can lead to painful ulcers on the legs and feet and subsequent amputation. Alpha Therapeutic Corporation (a former subsidiary of Mitsubishi Pharma) was initially involved in trials of ecraprost in the US, but this responsibility has been taken over by the parent company.