We’re targeting the underlying biological drivers of cancer by focusing on four different scientific platforms: Immuno-Oncology, Tumour Drivers and Resistance, DNA Damage Response, and Antibody Drug Conjugates.
We’re concentrating on biomarker-driven indications to dramatically improve five-year survival in five tumour types, including ovarian cancer and non-small cell lung cancer (NSCLC).
Our patient-centric approach focuses on 1) identifying and treating patients earlier in the course of their disease with curative intent; and 2) supporting relapsed and refractory patients by tackling primary or acquired resistance.
We’re expanding our presence across geographies to deliver timely treatments to patients in the US, UK, Italy, France, Germany, Spain, Japan, and China.
Among the many different types of cancer that our scientists explore, we are developing new treatment approaches for the following types of cancer:
We’re concentrating on four scientific platforms that we believe show the greatest potential for yielding effective medicines for cancer patients.
Activating the body’s own immune system to help fight cancer
Targeting the genetic mutations and resistance mechanisms that enable cancer cells to evade treatment, survive, and proliferate
Targeting the DNA repair process to block cancer cells’ ability to reproduce
Delivering highly potent cancer-killing agents directly to cancer cells via a linker attached to a targeted antibody
Adenosine signaling is part of the normal immune response: it helps shut off the immune system to avoid a response that is too strong, which could lead to a harmful autoimmune reaction and potential tissue injury. Tumours can hijack the adenosine pathway to signal to immune cells that a response is not needed, allowing the cancer to evade an immune response.1 AstraZeneca is evaluating various ways of interrupting the immunosuppressive process of the adenosine pathway to allow a robust immune response against cancer to successfully take place.
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Irregular activity of the WEE1 kinase, a kinase regulator of cell cycle checkpoints in healthy cells,2,3 has been linked to cancers such as ovarian and non-small cell lung cancer.4,5 Inhibiting this activity has demonstrated interference with DNA damage response within tumour cells and can eventually lead to their death.6 AstraZeneca is currently evaluating an investigational, highly selective WEE1 inhibitor designed to leverage this mechanism for a variety of solid tumours.
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Many cellular processes are regulated by a signaling network composed of three key enzymes, but this network is often disrupted in a number of cancers.7,8,9 Gene amplification of AKT (protein kinase B) has been identified as a tumour driver, and its mutations are thought to mediate resistance to conventional chemotherapies.10 AstraZeneca is currently exploring an investigational pan AKT-kinase inhibitor as a potential treatment for advanced solid tumours and metastatic malignancies.
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In about 70% of breast cancers, specific oestrogen receptors are over-expressed, and even when patients are treated with current therapies targeting this driver, many still progress.11,12 To address this need for effective treatment alternatives, AstraZeneca is currently developing a selective oestrogen receptor downregulator, an innovative investigational molecule being explored in clinical trials as a potential oral treatment for types of advanced breast cancers with certain receptor mutations.
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HER2 is a tyrosine kinase receptor growth-promoting protein found on the surface of some cancer cells that is associated with aggressive disease and poorer prognosis in breast cancer patients.13 To be considered HER2-positive, tumour cancer cells are usually tested by one of two methods: immunohistochemistry (IHC) or fluorescent in situ hybridization (FISH).14 AstraZeneca has entered into a collaboration with Daiichi Sankyo to jointly develop and commercialise an antibody drug conjugate (ADC) designed to delivery cytotoxic chemotherapy via a human epidermal receptor 2 (HER2) antibody for breast and gastric cancer.
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Breast cancer susceptibility genes 1/2 (BRCA1 and BRCA2) produce proteins responsible for repairing damaged DNA and play an important role maintaining the genetic stability of cells.15 When either of these genes is mutated, or altered, DNA damage may not be repaired properly, increasing the chance of additional genetic alterations that can lead to cancer.15 AstraZeneca is developing treatments that block DNA damage response in cells across a broad range of cancers.
Lung cancer is at the forefront of AstraZeneca’s research and development focus. Our expanding portfolio aims to provide medicines that can improve outcomes at every stage of the disease. But we know if we are to make meaningful progress for lung cancer patients, we cannot work alone. We have partnered with the International Association for the Study of Lung Cancer (IASLC), the Global Lung Cancer Coalition (GLCC), and Guardant Health to form the Lung Ambition Alliance. Together we are taking urgent action to double five-year survival in lung cancer globally by 2025 – prioritising research and projects that increase screening, deliver innovative medicine and improve quality care.
The great advance of personalised healthcare, in oncology, has been the realisation that some tumours are driven by individual genes. So if you can find out which genes these are, you can develop a medicine that's best for that tumour, and then select patients that are best for that medicine.
Genomics is the foundation of what science can do to understand the causes of disease and develop new medicines.
and help us deliver life-changing medicines
Be among our employees who continue to make us an innovation-driven company that stands firmly among the world’s leaders in biopharmaceuticals.
Phase III/LCM Projects: refers to assets that are pivotal in Phase II/III or have been submitted for regulatory approval, and may include assets that are launched in one or more major markets (removed when launched in all applicable major markets).
Phase I
Phase II
Phase III
LCM Projects
We cannot provide detailed information about our prescription medicines on this website, in compliance with regulations. Our medicines are approved in individual countries for specific uses and the information we provide for patients is governed by local regulations. In some cases, health care professionals and patients can visit local AstraZeneca websites to find out more about our medicines. Please note that in some countries we are not allowed to provide very much, or sometimes any, information on our prescription medicines so you should seek alternative trustworthy sources. Always ask a healthcare professional for advice about medicines.
anastrozole
acalabrutinib
bicalutamide
trastuzumab deruxtecan
fulvestrant
durvalumab
gefitinib
olaparib
osimertinib
goserelin acetate implant
We publish information about the registration and results of all new and ongoing clinical trials for all products in all phases on our dedicated website.
Our medicines are approved in individual countries for specific uses. Visit your local AstraZeneca site to find out more.
References
1. Leone RD, Emens LA. Targeting adenosine for cancer immunotherapy. J Immunother Cancer. 2018;6:57. https://doi.org/10.1186/s40425-018-0360-8.
2. McGowan CH, Russell P. Human Wee 1 kinase inhibits cell division by phosphorylating p34cdc2 exclusively on Tyr15. EMBO J. 1993 Jan; 12(1):75-85.
3. Tominaga Y, Li C, Wang RH, Deng CX. Murine Wee1 plays a critical role in cell cycle regulation and preimplantation stages of embryonic development. J Biol Sci. 2006; 2(4):161-170.
4. Guertin AD, Li J, Liu Y, et al. Preclinical evaluation of the Wee-1 inhibitor MK-1775 as a single-agent anticancer therapy. Mol Cancer Ther. 2013 Aug;12(8):1442-1452.
5. Do K, Doroshow JH, Kummar S. Wee1 kinase as a target for cancer therapy. Cell Cycle. 2013 Oct 1; 12(19), 3159-3164.
6. Hirai H, Iwasawa Y, Okada M, et al. Small-molecule inhibition of Wee-1 kinase by MK-1775 selectively sensitizes p53-edficient tumor cells to DNA-damaging agents. Mol Cancer Ther. 2009 Nov; 8(11):2992-3000.
7. Altomare DA, Testa JR. Perturbations of the AKT signaling pathway in human cancer. Oncogene. 2005 Nov 14;24(50):7455-7464.
8. Liu P, Cheng H, Roberts TM, Zhao JJ. Targeting the phosphoinositide 3-kinase pathway in cancer. Nat Rev Drug Discov. 2009 Aug;8(8):627-644.
9. Clark AS, West K Streicher S, Dennis PA. Constitutive and inducible AKT activity promotes resistance to chemotherapy, trastuzumab, or tamoxifen in breast cancer cells. Mol Cancer Ther. 2002 Jul;1(9):707-717.
10. Huang W-C, Hung M-C. Induction of AKT activity by chemotherapy confers acquired resistance. J Formos Med Assoc. 2009 Mar;108(3):180-194.
11. Selli, C., et al. Accurate prediction of response to endocrine therapy in breast cancer patients: current and future biomarkers. Breast Cancer Res. 2016; 18: 118 .
12. Basaran GA, et al. Ongoing unmet needs in treating estrogen receptor-positive/HER2-negative metastatic breast cancer. Cancer Treat Rev. 2018;63:144-155..
13. Mitri, Z. et al. The HER2 Receptor in Breast Cancer: Pathophysiology, Clinical Use, and New Advances in Therapy. Chemother Res Pract. 2012; 2012: 743193. doi: 10.1155/2012/743193. Accessed April 2019.
14. Carlson B. HER2 TESTS: How Do We Choose? Biotechnol Healthc. 2008; 5(3): 23–27.
15. The Royal Marsden NHS Foundation Trust. A beginner’s guide to BRCA1 and BRCA2. Available at: https://www.royalmarsden.nhs.uk/sites/default/files/files_trust/beginners-guide-to-brca1-andbrca2.PDF. Accessed May 2019.
Veeva ID: Z4-22142
Date of Prep: March 2020
Date of Expiry: March 2022
