Pfizer developed fosdagrocorat (PF-04171327), a dissociated agonist of the glucocorticoid receptor for the treatment of rheumatoid arthritis. The drug successfully completed the phase II clinical trial; however, further study of the drug was discontinued.

AZD-2461 is an oral inhibitor of PARP-1, which was developed by AstraZeneca as a potential anti-cancer medicine. The drug was tested in phase I clinical patients against solid tumosr, but its development was discontinued.

Oprozomib (PR-047) is an orally bioavailable derivative of carfilzomib, with similar biological activity, i.e. inhibition of the chymotrypsin-like activity of the proteasome. It inhibits the activity of the proteasome, thereby blocking the targeted proteolysis normally performed by the proteasome; this may result in an accumulation of unwanted or misfolded proteins. Disruption of various cell signaling pathways may follow, eventually leading to the induction of apoptosis and inhibition of tumor growth. Oprozomib (PR-047) is being investigated for the treatment of hematologic malignancies, specifically, multiple myeloma, with Phase I/II trial ongoing.

AZD4877 was developed by AstraZeneca as a potent inhibitor of the mitotic spindle kinesin, Eg5. AZD4877 participated in clinical trials phase I/II for patients with acute myeloid leukemia, the study was terminated due to lack of efficacy. In addition, the drug was studied in Phase II in patients with previously treated advanced urothelial cancer. However, limited clinical efficacy stops the further development of AZD4877 in urothelial cancer.

GSK-1614235 (mizagliflozin) is a sodium glucose co-transporter type 1 (SGLT1) inhibitor that has been investigated for treatment in type 2 diabetes. It is thought to suppress glucose absorption from the intestine in a way that is different from conventional type 2 diabetes drugs, thereby improving postprandial hyperglycemia. Phase 1 studies have been completed.

Icopezil (previously known as CP-118,954) was developed as a selective acetylcholinesterase inhibitor for the treatment of cognitive disorders. Phase II trials of icopezil were underway in Japan and in the USA for the treatment of patients with Alzheimer's disease. However, Pfizer has discontinued these studies.

Nebracetam (WEB1881FU) is a pyrrolidinone nootropic. Like other racetams, it is an aminomethyl pyrrolidinone derivative of piracetam. It was first synthesized in Germany in the late 1980s, where it was manufactured by Boehringer Ingelheim. Nebracetam is a M1-muscarinic agonist. In Jurkat cells Nebracetam induced a rise of [Ca2+]i in the medium with 1 mM Ca2+ and without Ca2+ (plus 1 mM EGTA). The nebracetam-induced [Ca2+]i rise was blocked by atropine greater than pirenzepine greater than AF-DX 116. Nebracetam facilitates the ganglionic muscarinic transmission through acting on presynaptic sites. Nebracetam has been investigated as a cognition-enhancing drug, but most of the studies have taken place in animal models. It has been shown to protect neurons in animals exposed to low levels of oxygen and low blood sugar. Nebracetam is also protective against glutamate toxicity, presumably via its modulation of calcium entry. In animal models of Alzheimer’s disease, nebracetam improved memory in a dose-dependent manner. It also protected against ischemia- (lack of oxygen) induced neuronal death in a rat model of stroke. The compound has also been tested as a possible antidepressant, presumably because its mechanism of action (reducing dopaminergic and serotonergic uptake) is similar to other commonly used antidepressants. Some studies have taken place in humans. A single dose was shown to alter brain waves in healthy volunteers, who showed increased alpha activity and an associated decrease of slow activity and of fast activity in the frontal cortex. These results imply that nebracetam might improve linguistic learning and memory processing. A trial in dementia patients reported that significant clinical improvement occurred after 8 weeks. However, other studies did not replicate this finding.

Oxadimedine, an antihistamine that was developed as a local anesthetic. Information about the current use of this compound is not available.

Giripladib (PLA 695) is a Cytosolic phospholipase A2 (cPLA2) inhibitor. cPLA2 is associated with tumor progression and radioresistance in mouse tumor models. In these models, treatment with giripladib attenuates radiation induced increases of phospho-ERK and phospho-Akt in endothelial cells. Combined with irradiation, giripladib reduces migration and proliferation in endothelial cells (HUVEC & bEND3) and induces cell death and attenuated invasion by tumor cells (LLC &A549). The combination treatment of giripladib and irradiation also delayes growth in both LLC and A549 tumors and results in reduced tumor vasculature. Phase I studies have been conducted to test the gastrointestinal safety of giripladib, and potential pharmacokinetic interaction with other compounds. A phase II study was terminated.