Pranlukast is an antagonist of cysteinyl leukotriene receptor-1 antagonist. It is marketed in Japan by Ono Pharmaceuticals under trademark ONON for the treatment of bronchial asthma and allergic rhinitis as capsules and dry syrup for pediatric use.

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.

GW-501516 is a peroxisome proliferator-activator receptor-delta agonist for the potential treatment of dyslipidemia, hyperlipidemia, metabolic diseases and cardiovascular diseases. GW501516 treatment is associated with significant improvements in multiple lipid profile components (TG, LDL-C, HDL-C, free fatty acids and apoB, apoA-I and apoA-II) and a shift in LDL particle size from small dense to larger, less dense particles. Despite these promising early results, the further investigation and development of GW501516 was discontinued after observations in animal studies of its association with the rapid induction of cancers in several organs (liver, stomach, tongue, skin, bladder, ovaries, womb and testes).

Pittsburgh compound B (PiB) is a radioactive analog of thioflavin T, which can be used in positron emission tomography scans to image beta-amyloid plaques in the brains of patients with Alzheimer’s disease. 11C-PIB specifically binds to Aβ40 and Aβ42 fibrils and insoluble plaques containing the aforementioned Aß peptides with no detectable binding to soluble Aβ forms or neurofibrillary tangles under PET study conditions. Furthermore, this radiotracer does not bind to neurofibrillary tangles (NFTs) in the neuronal regions of the brain during postmortem autopsies. A typical injected dose ranges from 250-450 MBq and the imaging time normally varies between 40 and 90 minutes. The quantification of 11C-PIB has demonstrated to elicit a profound difference in neuronal cortical binding between individuals recognized with Alzheimer's disease and age-matched cognitively normal controls.

Ridaforolimus (Deforolimus, MK-8669) is an investigational oral mTOR inhibitor in development for the treatment of metastatic soft-tissue or bone sarcomas. Ridaforolimus is being co-developed by Merck and ARIAD Pharmaceuticals. Ridaforolimus (Deforolimus, MK-8669) is a selective mTOR inhibitor with IC50 of 0.2 nM in HT-1080 cell line; while not classified as a prodrug, mTOR inhibition and FKBP12 binding is similar to rapamycin. mTOR is a protein kinase that controls cell growth by regulating many cellular processes, including protein synthesis and autophagy. Compared with other mTOR inhibitors, ridaforolimus is not a prodrug and has shown in vivo stability. Both intravenous and oral formulations of the compound are being tested in clinical trials for the treatment of various solid tumors and hematologic malignancies. The initial indication is soft-tissue and bone sarcomas. Ridaforolimus was indicated to treat patients with metastatic soft tissue sarcoma or bone sarcoma whose disease has not progressed after at least 4 cycles of chemotherapy. In June 2012, Merck & Co., Inc. announced the receipt of a Complete Response Letter from the U.S. Food and Drug Administration (FDA), advising the company that the New Drug Application (NDA) for ridaforolimus had not been approved. Currently Ridaforolimus is in phase III clinical trials for the treatment of Coronary artery restenosis.

Endralazine (6-benzoyl-3-hydrazino-5,6,7,8-tetrahydropyrido-(4,3-c)-pyridazine mesylate) is a peripheral vasodilator drug, which acts by direct relaxation of the smooth muscle fibres of the peripheral arterial vessels. Endralazine has been used as an antihypertensive agent.

Hepronicate is a nicotinic acid derivative, developed and used in Japan under the name Megrin for the treatment of peripheral circulatory disorders. The therapeutic effect of the drug is explained by its vasodilation properties.

Glafenine is a non-steroidal anti-inflammatory drug (NSAID). Glafenine was withdrawn due to the risk of anaphylaxis and acute kidney failure.