AZD-8186 is a potent and selective inhibitor of PI3Kβ and PI3Kδ with IC50 of 4 nM and 12 nM, respectively. AZD-8186 is currently in phase 1 clinical trials. Combination therapy using AZD-8186 with androgen deprivation results in long-lasting tumor regression, which persisted after treatment cessation.

AZD-7687 is a potent inhibitor of Diacylglycerol O-acyltransferase 1 (DGAT1) which was developed by AstraZeneca for the treatment obesity and type 2 diabetes mellitus. AZD-7687 reached phase I of clinical trials, but was discontinued by unknown reasons.

AZD4017, a 11β-hydroxysteroid dehydrogenase type 1 inhibitor, has been developed by AstraZeneca for the treatment of obesity, raised intraocular pressure (IOP) and type 2 diabetes. Inhibition of 11β-HSD1 is an attractive mechanism for the treatment of obesity and other elements of the metabolic syndrome. However, studies were discontinued due to safety and efficacy reasons. Besides, specific inhibition of 11β-HSD1 can decrease intracranial pressure and consequently treat patients with Idiopathic Intracranial Hypertension (IIH), thus AZD4017 participated in phase II clinical trials to treat this disease. IIH, also known as benign intracranial hypertension or pseudotumor cerebri, is a condition of unknown etiology characterized by elevated intracranial pressure (ICP) and papilledema. In addition, AZD4017 in combination with prednisolone participated in phase II clinical trials for patients with Iatrogenic Cushing's Disease. It was postulated that the adverse metabolic effects of prednisolone could be reduced by co-administration of AZD4017.

AZD5423, a non-steroidal glucocorticoid receptor agonist, was participated in clinical trials phase II for treatment of Asthma, and Chronic Obstructive Pulmonary Disease. However, the development of the product was discontinued.

AZD-8835 is a potent inhibitor of PI3Kα and PI3Kδ with selectivity versus PI3Kβ, PI3Kγ, and other kinases that preferentially inhibited growth in cells with mutant PIK3CA status, such as in estrogen receptor-positive (ER(+)) breast cancer cell lines BT474, MCF7, and T47D (sub-umol/L GI50s). Consistent with this, AZD-8835 demonstrated antitumor efficacy in corresponding breast cancer xenograft models when dosed continuously. AZD-8835 is a selective, oral inhibitor of PI3K isoforms α and δ with the following activity in enzymatic assays: PI3K α – IC50 = 6nM (equipotent vs wt and E545K / H1047R mutants); PI3K δ – IC50 = 6nM; PI3K γ – IC50 = 90nM; PI3K β – IC50 = 431nM. Inhibition of signalling in cells (pAKT endpoint): PI3K α – IC50 = 57nM; PI3K δ – IC50 = 49nM; PI3K β – IC50 = 3.6uM; PI3K γ - IC50 = 532nM. AZD-8835 is in phase I clinical studies by AstraZeneca for the treatment of advanced solid tumors and ER+ and HER-2 negative breast cancer.

AstraZeneca was developing AZD-2066, a metabotropic glutamate receptor 5 (mGLUR5) antagonist, for the oral treatment of pain indications (e.g. chronic neuropathic pain and painful diabetic neuropathies), depressive disorders and gastro-oesophageal reflux disease. AZD-2066 had been in phase II clinical trials by AstraZeneca for the treatment of diabetic neuropathic pain and phase I for the treatment of gastrooesophageal reflux disease (GERD). However, this reasearch had being discontinued.

AZD-1208 is an orally available, potent and highly selective Pim inhibitor that effectively inhibits all three isoforms. AZD-1208 inhibits the growth of several AML cell lines and sensitivity correlates with the level of Pim-1 expression, STAT5 activation and presence of protein tyrosine kinase mutation. AZD-1208 causes cell cycle arrest and apoptosis in MOLM-16 cells in culture. This is accompanied by a dose-dependent reduction in phosphorylation of BAD, 4EBP1 and p70S6K. In addition, AZD-1208 leads to potent inhibition of colony growth of primary AML cells from bone marrow aspirates and downregulates phosphorylation of Pim targets. AZD-1208 was in Phase 1 trials to evaluate the safety and tolerability profile and to determine the maximum tolerated dose (MTD). There were two trials where AZD-1208 had been administered orally in AML and solid tumour (of all types) patients. The studies had being discontinued due to safety reasons.

AZD-4547 is an orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) with potential antineoplastic activity. FGFR inhibitor AZD4547 binds to and inhibits FGFR, which may result in the inhibition of FGFR-related signal transduction pathways, and, so, the inhibition of tumor cell proliferation and tumor cell death. FGFR, up-regulated in many tumor cell types, is a receptor tyrosine kinase essential to tumor cellular proliferation, differentiation and survival. AZD-4547 is a selective FGFR inhibitor targeting FGFR1/2/3 with IC50 of 0.2 nM/2.5 nM/1.8 nM in cell-free assays, weaker activity against FGFR4, VEGFR2 (KDR), and little activity observed against IGFR, CDK2, and p38. Compared to FGFR1-3, AZD-4547 displays weaker activity against FGFR4 with IC50 of 165 nM. AZD-4547 only inhibits recombinant VEGFR2 (KDR) kinase activity with IC50 of 24 nM, in the in vitro selectivity test against a diverse panel of representative human kinases. AZD-4547 is under clinical investigation for the treatment of FGFR-dependent tumors. It is in phase II clinical studies for the treatment of breast cancer; gastric cancer; lung cancer; oesophageal cancer and in phase II/III clinical studies for the treatment of non-small cell lung cancer.

Pavinetant, also known as MLE-4901, AZD-4901, AZD-2624, is a small molecule, orally active, selective neurokinin-3 (NK3) receptor antagonist developed for schizophrenia, hot flashes, and Polycystic ovary syndrome. The development for schizophrenia was discontinued due to lack of effectiveness. Phase II trials for polycystic ovary syndrome and for hot flashes showed the clinical risks exceeded benefits, in addition, abnormal liver function was observed, and that is why these studies were also discontinued.

AZD-3514 is a down-regulator of androgen receptors. The drug was synthesized by AstraZeneca for the treatment of castrate-resistant prostate cancer and even reached phase I, however, its development was terminated.