Tibric Acid is a sulfamoylbenzoic acid derivative patented by American multinational pharmaceutical corporation Pfizer Inc. as a hypolipidemic agent. In preclinical models, Tibric acid, given orally, was more effective than clofibrate in preventing the hyperlipemic and hypercholesteremic effects of various diets in rats. At high concentrations in vitro, Tibric acid moderately inhibited ADP- or thrombin-induced aggregation of rabbit blood platelets. In patients with severe type IV hyperlipoproteinemia and chylomicronemia, Tibric Acid lowered serum triglyceride and cholesterol values but administration of Tibric Acid to a normal subject did not affect serum lipid levels.

Rosiglitazone acts as a highly selective and potent agonist at peroxisome proliferator activated receptors (PPAR) in target tissues for insulin action such as adipose tissue, skeletal muscle, and liver. It is FDA approved for the treatment of as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. Inhibitors of CYP2C8 (e.g., gemfibrozil) may increase rosiglitazone levels; inducers of CYP2C8 (e.g., rifampin) may decrease rosiglitazone levels. Common adverse reactions include edema, weight gain, and headache.

Probucol is used to lower levels of cholesterol (a fat-like substance) in the blood. Probucol is a drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. This may help prevent medical problems caused by cholesterol clogging the blood vessels. Probucol was voluntarily removed from the market in the United States during 1995. The withdrawal from the market was due to safety concern. robucol lowers serum cholesterol by increasing the fractional rate of low-density lipoprotein (LDL) catabolism in the final metabolic pathway for cholesterol elimination from the body. Additionally, probucol may inhibit early stages of cholesterol biosynthesis and slightly inhibit dietary cholesterol absorption. Recent information suggests that probucol may inhibit the oxidation and tissue deposition of LDL cholesterol, thereby inhibiting atherogenesis. It appears to inhibits ABCA1-mediated cellular lipid efflux.

Tolazamide is an oral blood glucose lowering drug of the sulfonylurea class. Tolazamide appears to lower the blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. The mechanism by which tolazamide lowers blood glucose during long-term administration has not been clearly established. With chronic administration in Type II diabetic patients, the blood glucose lowering effect persists despite a gradual decline in the insulin secretory response to the drug. Extrapancreatic effects may be involved in the mechanism of action of oral sulfonylurea hypoglycemic drugs. Some patients who are initially responsive to oral hypoglycemic drugs, including tolazamide, may become unresponsive or poorly responsive over time. Alternatively, tolazamide may be effective in some patients who have become unresponsive to one or more other sulfonylurea drugs. In addition to its blood glucose lowering actions, tolazamide produces a mild diuresis by enhancement of renal free water clearance. Sulfonylureas likely bind to ATP-sensitive potassium-channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin. Tolazamide is used for use as an adjunct to diet to lower the blood glucose in patients with non-insulin dependent diabetes mellitus (Type II) whose hyperglycemia cannot be satisfactorily controlled by diet alone.

Acetohexamide (trade name Dymelor) is a first-generation sulfonylurea medication used to treat diabetes mellitus type 2, particularly in people whose diabetes cannot be controlled by diet alone. It lowers blood sugar by stimulating the pancreatic beta cells to secrete insulin and by helping the body use insulin efficiently. The pancreas must produce insulin for this medication to work. Acetohexamide binds to an ATP-dependent K+ channel on the cell membrane of pancreatic beta cells. This inhibits a tonic, hyperpolarizing out flux of potassium, which causes the electric potential over the membrane to become more positive. This depolarization opens voltage-gated Ca2+ channels. The rise in intracellular calcium leads to increased fusion of insulin granule with the cell membrane, and therefore increased secretion of (pro) insulin. Acetohexamide extensively metabolized in the liver to the active metabolite hydroxyhexamide, which exhibits greater hypoglycemic potency than acetohexamide. Hydroxyhexamide is believed to be responsible for prolonged hypoglycemic effects. Symptoms of an acetohexamide overdose include hunger, nausea, anxiety, cold sweats, weakness, drowsiness, unconsciousness, and coma. Acetohexamide has been discontinued in the US market.

Triparanol (brand and developmental code names MER/29) is a 24-dehydro cholesterol reductase inhibitor, which is an enzyme involved in the biosynthesis of cholesterol. It has antitumor properties, such as decreasing proliferation and inducing apoptosis in many cancer cell lines and slowing tumor growth in a mouse xenograft model. It can also decrease Hedgehog pathway signaling in cancer cells. Triparanol was the first synthetic cholesterol-lowering drug. It was withdrawn in 1962 due to severe adverse effects such as nausea and vomiting, vision loss due to irreversible cataracts, alopecia, skin disorders (e.g., dryness, itching, peeling, and "fish-scale" texture), and accelerated atherosclerosis and is now considered to be obsolete.

Phenformin is a biguanide hypoglycemic agent with actions and uses similar to those of metformin. It activates AMP-activated protein kinase (AMPK) and inhibits mTORC1 signaling. Phenformin used for the treatment of diabetes. Phenformin was removed from the U.S. market 20 years ago because of a high incidence of lactic acidosis. Risk factors for the development of lactic acidosis include renal deficiency, hepatic disease, cardiac disease, and drug interaction such as cimetidine. Phenformin exerts potential anti-neoplastic action.

Oxyphenisatin is a stimulant laxative that has been used by mouth and as an enema. Oxyphenisatin was introduced as Lavema by Winthrop in US in 1959. Oxyphenisatin was used as a cleansing enema apart from x-ray studies and prior to urinary, gastro-intestinal and cholecystography x-ray examination. Oxyphenisatin was also used for preoperative preparation of the large intestine and colon. May be mixed with barium for x-ray examination of the large intestine. Oxyphenisatin may cause jaundice. Oxyphenisatin-induced liver damage usually occurs when the drug has been taken for at least six months and usually two years. Oxyphenisatin was withdrawn in most countries in the early 1970s.

Bisacodyl is typically prescribed for relief of constipation and for the management of neurogenic bowel dysfunction as well as part of bowel preparation before medical examinations, such as for a colonoscopy. Some drugs (e.g., diuretics, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, or non-steroidal anti-inflammatory drugs) increase risk due to fluid and electrolyte changes. Most common adverse reactions (> 3%) are overall discomfort, abdominal fullness, abdominal cramping, nausea, and vomiting.