Benfosformin (also known as JAV 852), a phosphorylated biguanide that was studied as a hypoglycemic and antidiabetic agent. However, the information about the studies of this compound now is not available.

Davalintide (AC-2307) is a second-generation mimetic of a pancreatic peptide hormone amylin, developed by Amylin Pharmaceuticals. In preclinical models, davalintide possessed enhanced pharmacological properties and was able to reduce food intake. Safety, tolerability, and effect on body weight of subcutaneous davalintide were investigated in obese or overweight subjects. The results of the clinical trial were not reported, but Amylin decided to discontinue davalintide in 2010.

Darglitazone is a member of the thiazolidinedione class of drugs and an agonist of peroxisome proliferator-activated receptor-γ (PPAR-γ), an orphan member of the nuclear receptor superfamily of transcription factors. It has a variety of insulin-sensitizing effects, such as improving glycemic and lipidemic control, and is used in the treatment of metabolic disorders such as type II diabetes. Darglitazone sodium had been in phase I clinical trials by Pfizer for the treatment of type 2 diabetes. However, this study has been discontinued.

Trantelinium bromide is an anticholinergic and spasmolytic drug, used for the treatment of gastric ulcers.

Tiquinamide (Wy 24081) is a potent inhibitor of gastric secretion and gives good protection in animals against gastric and duodenal erosions induced by stress and chemical stimuli. It reduces basal as well as stimulated acid secretion but has no anticholinergic activity and is only a weak histamine H2 antagonist, since it is substantially more potent in inhibiting basal acid-secretion than the established H2-receptor antagonists, metiamide and burimamide. Since no other pharmacological effect of tiquinamide has been detected in isolated tissues, it seems unlikely that the gastric antisecretory effect of the compound results from a direct action on the peripheral autonomic nervous system. The report from Dr. Szabo on the protective effect of dopamine agonists against duodenal ulceration suggests a possible mechanism of action for tiquinamide.

Gemcabene calcium (PD 72953), the monocalcium salt of a dialkyl ether dicarboxylic acid, is a lipid-regulating compound that was first described in 1998. It down-regulates apolipoprotein C-III expression, enhancing the clearance of very low density lipoprotein (LDL), and reduces plasma triglycerides. It also raises high-density lipoprotein cholesterol (HDL). Unlike fibrates (blood trygliceride level lowering drugs), its mechanism of action is not linked to agonist or antagonist activity on PPAR-α receptors. There is limited information on the exact mechanism of action, but an anti-inflammatory profile was found, associated with a lowered expression of the high-sensitivity C-reactive protein gene regulating mechanisms. Gemcabene (administered as 6, 6’-oxybis [2, 2-dimethyl-4-hexanoic acid] monocalcium salt) has been investigated for treatment in a wide range of hyperlipidaemias, as well as atherosclerosis, and cardiovascular disorders. Gemcabene is generally well tolerated. One phase 2 study testing the preliminary efficacy and safety of gemcabene in children with established nonalcoholic fatty liver disease has been stopped early due to increasing weight and a rise in liver fat content in patients. Clinical trials are still ongoing.

Linogliride is a substituted guanidine structurally unrelated to the sulphonylureas but with a similar mechanism of action. Linogliride potentiates insulin release in isolated islets and in the perfused pancreas. In islets, linogliride is reported to stimulate insulin secretion in the presence of glucose but not in its absence. Linogliride and the sulphonylureas act via closely related mechanisms. Possible extrapancreatic effects of the agent have also been suggested. Linogliride produces hypoglycaemic effects in various non-diabetic and diabetic animals. In normal rats and dogs, it improves glucose tolerance and in fasted rats or mice, linogliride lowers blood glucose. Linogliride showed modest effects in the db/db mice but significantly lowered fasting blood glucose in neonatal streptozotocin-treated rats. Clinical studies with non-insulin-dependent diabetes patients have shown linogliride to be effective at lowering fasting and postprandial plasma glucose levels in non-insulin-dependent diabetes patients. linogliride leads to a decrease in the activity of ATP-sensitive K+ channels.

Edaglitazone have a clear PPAR-gamma agonist profile, with predominant PPAR-gamma activity and little PPAR-alpha activity. Edaglitazone was reported to significantly improve insulin sensitivity and enhance the rate of glucose oxidation in both the presence and absence of insulin. Additional studies have shown that edaglitazone affects muscle glucose metabolism by additional mechanisms other than PPAR-gamma activation. Phase I clinical studies have revealed that edaglitazone is well-tolerated and capable of significantly improving glucose homeostasis. Edaglitazone had been in phase II clinical trials for the treatment if type 2 diabetes. 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.

Etintidine is a potent competitive antagonist of histamine H2-receptors. It has a low level of antiandrogenic activity. Etintidine was being investigated in the treatment of peptic ulcer, however, its development has been discontinued.