Sultosilic acid is a benzenesulfonate ester. Sultosilic acid has been shown to be a hypolipidaemic drug both in animal experiments and in human clinical studies, chemically unrelated to other such drugs. The compound is being developed as a human drug (Mimedran ®) and is formulated as the piperazine salt (A-585). The recommended daily dose is three times one tablet containing 500 mg of Sultosilic acid.

Pirozadil (Pemix), a hypolipidemic agent that improves cerebral blood flow and Inhibits platelet aggregation. This drug was studied for the treatment of patients with Type IIa hyperlipoproteinemia.

Xenyhexenic acid is a biphenyl organic compound, discovered in 1958. When fed to rats, xenyhexenic acid inhibited hypercholesterolemia and hyperlipemia that been induced by the administration of Triton.

Reglitazar is a dual agonist of PPAR alpha/PPAR gamma receptors. The drug was tested in phase II clinical trial, however, its development was terminated.

Binifibrate is an anti-arteriosclerotic and hypolipidaemic agent. It was used under the name Biniwas in patients with hyperlipidemia, however, it is currently withdrawn from the market.

Tenatoprazole, also known as TU-199 and STU-Na, is a proton pump inhibitor drug candidate that was undergoing clinical testing. The compound was invented by Mitsubishi Tanabe Pharma and was licensed to Negma Laboratories (part of Wockhardt as of 2007). Mitsubishi reported that tenatoprazole was still in Phase I clinical trials in 2007 and again in 2012. STU-Na will be used for treatment of acid related diseases (gastroduodenal ulcers, erosive or ulcerative esophagitis due to gastroesophageal reflux disease). Tenatoprazole has an imidazopyridine ring in place of the benzimidazole moiety found in other proton pump inhibitors; the binding sites of tenatoprazole were in the TM5/6 region at Cys813 and Cys822 as shown by tryptic and thermolysin digestion of the ATPase labeled by tenatoprazole. It has a half-life about seven times longer than other PPIs.

Glyparamide is the chlorophenyl-containing oral hypoglycemic sulfonamide. Glyparamide rarely causes hepatic injury.

Glymidine (Glycodiazine ) is a hypoglycaemic agent which has been introduced as a possible alternative to the sulphonylurea as and biguanides for the oral treatment of diabetes mellitus. It is one of a group of lipid soluble sulphapyrimidine derivatives synthesized by Gutsche et al. and bears some structural resemlance to tolbutamide. Its mode of action is similar to that of the sulphonylureas in that it appears to stimulate insulin release from the pancreas. Glycodiazine likely binds to ATP-sensitive potassium channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Membrane depolarization stimulates calcium ion influx through voltage-sensitive calcium channels. This increase in intracellular calcium ion concentration induces the secretion of insulin. It is used for the concomitant use with insulin for the treatment of noninsulin-dependent (type 2) diabetes mellitus. Glycodiazine is used concomitantly with insulin for the treatment of noninsulin-dependent (type 2) diabetes mellitus.

Glurenorm is an anti-diabetic drug in the sulfonylurea class. It is used in the treatment of diabetes mellitus type 2. It is an ATP-dependent K+ (KATP) channel blocker. This block causes a depolarization which leads to activation of voltage-dependent Ca channels and Ca2+ influx, and eventually increases insulin release. Minor skin allergies, gastric upsets and other non-specific side effects have been reported. Hypoglycaemic reactions have been reported but they are infrequent. Glurenorm effect increase butadion, chloramphenicol, tetracycline, coumarin derivatives, cyclophosphamide, sulfonamides, MAO inhibitors, thiazide diuretics, beta-blockers, salicylates, alcohol.

Glisoxepide (BS 4231) is a sulfonylurea compound with glucose-lowering activity. Glisoxepide is a specific inhibitor of the L- aspartate/L-glutamate antiport system. Glisoxepide also inhibits transport of bile acids into hepatocytes