Verdiperstat (formerly known as AZD 3241) was developed as a selective inhibitor of myeloperoxidase, an enzyme that acts as a key driver of pathological oxidative stress and inflammation in the brain. Verdiperstat was studied in patients with a number of neurodegenerative disorders, including multiple system atrophy and Parkinson's disease. Verdiperstat participated in phase II clinical trials for both diseases. As a result, studies for Parkinson disease were discontinued. In the case of multiple system atrophy, the drug has received the orphan drug status.

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.

Sapitinib is an oral, reversible and equipotent inhibitor of EGFR, HER2 and HER3 signalling. The drug was tested in phase II of clinical trials in patients with breast cancer, colorectal cancer, gastric cancer and NSCL carcinoma, however its development for breast cancer therapy seems to be terminated. Sapitinib absorption is rapid and the drug is totally cleared by metabolism with the major routes being oxidation and amine or ether cleavage around the piperidine ring with subsequent glucuronide or sulphate conjugation.

Flutafuranol F-18 (also known as NAV4694), a fluorine-18 labeled positron emission tomography (PET) imaging agent that was developed for diagnostic use. Flutafuranol F-18 binds to beta-amyloid deposits in the brain that could then be imaged in PET scans. It is known that amyloid plaque pathology is a required feature of Alzheimer’s disease (AD) and the presence of amyloid pathology is a supportive feature for the diagnosis of probable AD. Patients who are negative for amyloid pathology do not have AD. Thus, flutafuranol F-18 was studied in phase III clinical trial as an aid in the imaging for patients with Alzheimer’s disease and in phase II clinical trial for patients with mild cognitive impairment.

AZD-1480 was being developed by AstraZeneca for the treatment of myeloproliferative disorders and solid tumours. AZD-1480 is a novel ATP-competitive JAK2 inhibitor with IC50 of 0.26 nM in a cell-free assay, selectivity against JAK3 and Tyk2, and to a smaller extent against JAK1. AZD-1480 had been in phase I clinical trials by AstraZeneca for the treatment of hepatocellular carcinoma and myelofibrosis. However, this study has been terminated for the safety and efficacy reasons in 2012.

AZD0328, a spirofuropyridine, is a selective alpha7 nicotinic receptor agonist. This drug participated in clinical trials phase II in patients with schizophrenia. However, studies were terminated because the drug didn’t meet the current target product profile. Besides AZD0328 has been studied in phase I for the treatment of Alzheimer's disease.

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.

AZD4818 was developed by AstraZeneca as CCR1 receptor antagonist for the treatment of patients with chronic obstructive pulmonary disease. The study was discontinued, because of a lack of clinical efficacy.

Atecegetran metoxil (more widely known as AZD0837), an anticoagulant and a prodrug, converted to a selective and reversible direct thrombin inhibitor (AR-H067637). Atecegetran metoxil participated in phase II clinical trials to prevent the stroke and systemic embolism in patients with non-valvular atrial fibrillation. The development of atecegetran metoxil was discontinued, due to a limitation identified in the long-term stability of the extended-release drug product.

AZD1305, an antiarrhythmic agent, blocks the hERG potassium channel, the L-type calcium, and the Sodium channel protein Nav1.5. AZD1305 participated in clinical trials for the management of atrial fibrillation and Left ventricular dysfunction. The benefit-risk profile was judged as unfavorable and the AZD1305 development programme was discontinued.