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.

Epinine or deoxyepinephrine is an active form of Ibopamine, which is used as a cardiovascular agent in congestive heart failure. Epinine is a stimulant of alpha-adrenoceptor activities: alpha-1 and alpha-2. Experiments on pig’s eyes have shown that epinine can be a promising candidate substance for intraoperative (e.g., cataract surgery) intracameral use in humans.

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.

AZD5672 was developed by AstraZeneca for the treatment of rheumatoid arthritis. It was found that the drug inhibits P-glycoprotein and is a CCR5 antagonist. Exists hypothesis that inhibition of CCR5 can bring benefits in the treatment of rheumatoid arthritis. In July 2009, Phase-II for Rheumatoid arthritis was discontinued.

AZD-1981, developed by AstraZeneca, is a potent (binding IC50 of 4nM), fully reversible, functionally non-competitive antagonist of human CRTh2. It blocks agonist-induced human eosinophil CD11b expression, shape change (including in whole blood), and chemotaxis as well as an basophil shape change and Th2-cell chemotaxis at IC50's of 8.5-50nM. Potency is similar across species as is plasma protein binding (~97%). AZD-1981 is a weak (10s of μM) inhibitor in vitro of CYP2C9, OATP1B1 and UGT1A1 as well as an inducer of CYP3A4. AZD-1981 was well tolerated and no safety concerns were identified.There was no beneficial clinical effect of AZD-1981, at a dose of 1000 mg twice daily for 4 weeks, in patients with moderate to severe COPD. AZD-1981 has being discontinued for asthma and chronic obstructive pulmonary disease. AstraZeneca is collaborating with Johns Hopkins University for the development of AZD-1981 in the treatment of chronic idiopathic urticaria. It is in phase II clinicals studies for the treatment of Urticaria.

Avelestat, also known as AZD9668, is a novel, oral inhibitor of neutrophil elastase (NE), an enzyme implicated in the signs, symptoms, and disease progression in NE-driven respiratory diseases such as bronchiectasis, Cystic Fibrosis and chronic obstructive pulmonary disease via its role in the inflammatory process, mucus overproduction, and lung tissue damage. Its development was discontinued due to unknown reasons. Nevertheless, this drug in the phase II of clinical trial as adjunctive therapy in improving insulin sensitivity of insulin-resistant type 2 diabetic subjects. The drug's clinical profile suggests that it will be well tolerated with few, if any, side effects, and the existence of simple methods that can indirectly measure its activity in vivo.

AstraZeneca was developing AZD-8055, an orally active mTORC1/mTORC2 inhibitor, for the treatment of advanced solid tumours. AZD-8055 is an ATP-competitive mTORC1/2 inhibitor that exhibits immunosuppressive and anticancer chemotherapeutic activities. AZD-8055 promotes antibody class switching in B cells at low doses and decreases B cell proliferation and differentiation at high doses. In vivo, this compound suppresses CC4 and CD8 T cell proliferation, increasing survival among MHC-mismatched heart transplant recipients. In vitro, AZD-8055 decreases viability of brain tumor cells; in vivo, it inhibits tumor growth. AZD-8055 had been in phase I trials by AstraZeneca for the treatment of malignant gliomas and solid tumours. However, this research has been discontinued.

Barasertib (AZD1152) is a dihydrogen phosphate prodrug of a pyrazoloquinazoline Aurora kinase inhibitor [AZD1152–hydroxyquinazoline pyrazol anilide (HQPA)] and is converted rapidly to the active AZD1152-HQPA in plasma. AstraZeneca was developing the aurora kinase inhibitor, barasertib (AZD 1152) as a therapeutic for cancer. AZD1152-HQPA is a highly potent and selective inhibitor of Aurora B (Ki, 0.36nmol/L) compared with Aurora A (Ki, 1,369nmol/L) and has a high specificity versus a panel of 50 other kinases. Consistent with inhibition of Aurora B kinase, addition of AZD1152-HQPA to tumour cells in vitro induces chromosome misalignment, prevents cell division, and consequently reduces cell viability and induces apoptosis. Barasertib (AZD1152) potently inhibited the growth of human colon, lung, and haematologic tumour xenografts (mean tumour growth inhibition range, 55% to ≥100%; P < 0.05) in immunodeficient mice. Detailed pharmacodynamic analysis in colorectal SW620 tumour-bearing athymic rats treated i.v. with Barasertib (AZD1152) revealed a temporal sequence of phenotypic events in tumours: transient suppression of histone H3 phosphorylation followed by accumulation of 4N DNA in cells (2.4-fold higher compared with controls) and then an increased proportion of polyploid cells (>4N DNA, 2.3-fold higher compared with controls). Histologic analysis showed aberrant cell division that was concurrent with an increase in apoptosis in AZD1152-treated tumours. Bone marrow analyses revealed transient myelosuppression with the drug that was fully reversible following cessation of Barasertib (AZD1152) treatment. Barasertib (AZD1152) was in phase III for the treatment of Acute myeloid leukaemia, but later these studies were discontinued.

AstraZeneca was developing AZD-7762 for the treatment of solid tumours. AZD-7762 is a potent inhibitor of Chk1 that binds in the ATP binding pocket (IC50 of 5nM; Ki of 3.6nM). AZD-7762 has activity on a range of other kinases {examples with a < 5 fold selectivity included Rous sarcoma oncogene cellular homolog (SRC) family members (e.g., Fgr, Fyn, lymphocyte-specific protein-tyrosine kinase [Lck], and Lyn, but not SRC), Flt1/3, colony stimulating factor receptor (CSF1R), RET, Abelson tyrosine kinase (Abl), and checkpoint kinase 2 (Chk2)}. It is not known if these in vitro kinase inhibitions translate into an effect in vivo. In combination with DNA-damaging agents (gemcitabine, topotecan, doxorubicin, and cisplatin), AZD-7762 inhibits tumour cell growth in vitro with a mode of action that correlates with Chk1 inhibition and abrogation of the Gap 2 (G2) and S phase checkpoints. Rightward shifts in 50% growth inhibition (GI50) values over DNA-damaging agents alone ranged from 5- to 20-fold with gemcitabine demonstrating the largest shifts followed by topotecan. In combination with radiation, AZD-7762 enhances tumour cell growth inhibition and death with survival enhancement ratios ranging from 1.7 to 1.9. Triple combinations with AZD-7762, gemcitabine, and radiation yield the largest survival enhancement ratios. AZD-7762 had been in phase I clinical trials by AstraZeneca for the treatment of solid tumors. However, this study was terminated for the safety reason in 2011.

Sameridine was developed as a compound with both local anesthetic and opioid properties (partial micro-opioid receptor agonist). This drug participated in clinical trials when administered intrathecally to provide anesthesia for surgery and extended postoperative analgesia. However, further development of this drug was discontinued.