AstraZeneca was developing the thiazole AR-AO-14418, a selective inhibitor of glycogen synthase kinase 3β (GSK-3β), for the treatment of Alzheimer's disease and major depressive disorder. AR-AO-14418 is an important research tool in as much as, at concentrations that AR-AO-14418 is able to inhibit GSK3 activity, this compound did not affect the activity of other 26 protein kinases tested, and especially does not inhibit cdc2 and cdk5, two GSK3-related kinases that are inhibited by published GSK3 inhibitors. Furthermore, AR-AO-14418 constitutes a lead compound with therapeutic potential for the treatment of AD, as well as other neurodegenerative disorders. Later preclinical studies of AR-AO-14418 were discontinued.

AZD-5597 is potent imidazole pyrimidine amide CDK inhibitor with in vitro anti-proliferative effects against a range of cancer cell lines. AZD-5597 exhibited excellent aqueous solubility, photostability, hydrolytic stability, plasma stability and the lack of CYP inhibition. In nude mice implanted subcutaneously with SW620 human colon adenocarcinoma cells, AZD-5597 (15 mg/kg, dosed intermittently for 3 weeks, ip) inhibited tumor volume by 55%. The overall profile of AZD-5597 indicated that it was suitable for further development as an iv agent.

AZ-628 is a new pan-Raf inhibitor for BRAF, BRAFV600E, and c-Raf-1 with IC50 of 105 nM, 34 nM and 29 nM in cell-free assays. Specificity profliling indicates that AZ-628 also inhibits activation of number of tyrosine protein kinases including VEGFR2, DDR2, Lyn, Flt1, FMS and others. AZ-628 inhibits anchorage-dependent and -independent growth, causes cell cycle arrest, and induces apoptosis in colon and melanoma cell lines harboring B-RafV600E mutation. The profile of AZ-628 cross-reactivity suggests that similar to sorafenib, AZ-628 may be antiangiogenic based on inhibition of VEGFR2. AZ-628 is remarkably effective at inhibiting the growth of a specific subset of human cancer cell lines derived from melanomas, thyroid cancers, and colorectal cancers that harbor the BRAF V600E mutation. Preclinical evaluation is in progress.

AZ-23 is an ATP-competitive, tight-binding kinase inhibitor of TrkA, which was investigated by AstraZeneca as an orally bioavailable compound for cancer treatment.

M-475271 (AZM475271) is an investigational drug targeting cancer invasion and metastasis. It is an aminoquinoline class inhibitor with high affinity and specificity for the nonreceptor tyrosine kinase (Src). In vitro AZM475271 demonstrated strong dose-dependent inhibition of Src tyrosine kinase activity in the L3.6pl human pancreatic carcinoma cell line. The IC50 concentration of AZM475271 to inhibit the phosphorylation of c-Src, lck, and c-yes was 0.01, 0.03, and 0.08 uM, respectively, in comparison with an IC50 of 0.7 uM AZM475271 to inhibit KDR. AZM475271 reduced tumor size, vascularity and metastasis, and increased apoptosis in human pancreatic cells grown orthotopically in nude mice. It also exhibited antiangiogenic activity in vitro and in vivo, and sensitized tumor cells to the cytotoxic effects of gemcitabine. The effect of daily oral treatment with M475271 on subcutaneous tumors and lung metastasis caused by human lung adenocarcinoma cells in NK-cell depleted SCID mice demonstrated inhibition of the growth of subcutaneous tumors via inhibition of tumor cells proliferation, VEGF production and/or vascularization in the mice in a dose-dependent manner. In the metastasis model with A549 cells, the lung weight in the M475271 (50 mg/kg)-treated group was less than that of the control group, despite no difference in the number of metastatic nodules. These findings suggest that M475271 may be efficacious in treating pancreatic adenocarcinomas and might be helpful for controlling the progression of human lung adenocarcinomas.

AZD-9272 is an orally bioavailable and brain-penetrant potent and selective mGluR5 negative allosteric modulator. It exhibits high selectivity for mGluR5 over other mGlu receptors. It had been in phase I clinical trials for the treatment of gastroesophageal reflux disease and neuropathic pain. Single doses of the centrally acting mGluR5-antagonist AZD-9272 did not reduce C-fibre evoked pain, central sensitization or flare reaction in the study aimed to investigate its effect on electrically induced pain, central sensitization and axon reflex flare.

Etidocaine, marketed under the trade name Duranest, is a local anesthetic given by injection during surgical procedures and labor and delivery. Etidocaine has a long duration of activity, and the main disadvantage of using during dentistry is increased bleeding during surgery. Etidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action.

Elobixibat is the first in class ileal bile acid transporter (IBAT) inhibitor. IBAT inhibitors block ileal absorption of bile acids by: (1) interrupting the enterohepatic circulation of bile resulting in a fall in serum cholesterol and (2) increasing the delivery of bile acids into the colon. Elobixibat stimulates both motor and secretory functions in the colon. Elobixibat is approved in Japan for the treatment of chronic constipation. Elobixibat has potential benefit in the treatment of non-alcoholic steatohepatitis.

Bambuterol is an active precursor of the selective beta2-adrenergic agonist terbutaline. Bambuterol is the bis-N,N-dimethyl-carbamate of terbutaline. Bambuterol is a remarkably selective and potent inhibitor of cholinesterase. BAMBEC (Bambuterol hydrochloride) oral solution or tablets are indicated for the management of asthma, bronchospasm and/or reversible airways obstruction.

Cediranib (AZD-2171) is a VEGFR-2 kinase inhibitor which was developed by AstraZeneca for the treatment of cancer. The drug reached the final stage of approval by European Medicines Agency in 2008 under the name Zemfirza (it was recommended to be taken in combination with platinum-based chemotherapy), however on 19 September 2016 AstraZeneca decided to withdraw the Marketing Authorisation Application.