What is TECENTRIQ (atezolizumab)?
TECENTRIQ is a cancer immunotherapy.
TECENTRIQ is a monoclonal antibody designed to target and bind to a protein called PD-L1 (programmed death ligand-1), which is expressed on tumour cells and tumour-infiltrating immune cells.1 PD-L1 interacts with PD-1 and B7.1, both found on the surface of T cells, causing inhibition of T cells.1 By blocking this interaction, TECENTRIQ may enable the activation of T cells, restoring their ability to effectively detect and attack tumour cells.1
TECENTRIQ has led the way in cancer immunotherapy and was the first monoclonal antibody targeting PD-L1 to be approved by EMA as a treatment for a number of cancer types, receiving authorisation in September 2017.1,2
In Europe, TECENTRIQ has been licensed for locally advanced or metastatic urothelial carcinoma, non-small cell lung cancer, extensive-stage small cell lung cancer and triple-negative breast cancer.1
TECENTRIQ targets PD-L1 to restore antitumour T-cell activity
TECENTRIQ binds directly to PD-L1, increasing the ability of the immune system to attack the tumour and reduce disease progression.
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The first approved anti-PD-L1 cancer immunotherapy
Introducing the proposed mechanism of action for TECENTRIQ (atezolizumab). The first approved anti PD-L1 cancer immunotherapy. Cancer immunotherapies are designed to work with the immune system to combat cancer. The cancer immunity cycle characterises how a person’s own immune system can help protect the body against cancer. Through a series of complex interactions, the immune system can detect tumours and activate cytotoxic T-cells to infiltrate the tumour microenvironment and attack tumour cells. When functioning optimally the cancer immunity cycle is self-sustaining. However, in patients with cancer this immunity cycle can be disrupted allowing for unchecked tumour growth. Among other factors, this disruption can be caused by PD-1 or PD-L1, a negative immune regulator that can be expressed in the tumour microenvironment. Cytotoxic T cells that enter the tumour microenvironment may be deactivated by PD-L1 on tumour cells and tumour infiltrating immune cells. When PD-L1 binds to its receptors PD-1 or B7.1 on T cells, the T cells may be rendered inactive. As a result, anti-tumour immune activity may be suppressed in the tumour microenvironment causing disruption in the cancer immunity cycle.
TECENTRIQ is the first approved anti-PD-L1 cancer immunotherapy. TECENTRIQ targets PD-L1 in the tumour microenvironment, a key site of T cell deactivation. The proposed mechanism of action of TECENTRIQ has three distinct features:
DIRECT: TECENTRIQ is designed to bind directly to PD-L1 on tumour cells and tumour infiltrating immune cells in the tumour microenvironment.
COMPLETE: TECENTRIQ provides a dual blockade by preventing PD-L1 from binding to both the PD-1 and B7.1 receptor. Blocking interaction with PD-1 can reinvigorate suppressed T cells to kill cancer cells. Blocking interaction with B7.1 can enhance T-cell priming and activation in the lymph node.
SELECTIVE: In normal tissues TECENTRIQ may help minimise autoimmune reactions. TECENTRIQ spares interactions between PD-1 and PD-L2, potentially preserving immune homeostasis in normal tissue. In clinical trials blocking PD-L1 from binding to its receptors resulted in tumour shrinkage.
TECENTRIQ provides direct and complete blockade of PD-L1 interactions while selectively sparing PD-L2 interactions. This can restore antitumor T-cell activity and enhanced T-cell priming within the cancer immunity cycle.
For more information about TECENTRIQ the first approved anti PD-L1 cancer immunotherapy. Please contact your representative.
References & Notes
References & Notes
1 TECENTRIQ (atezolizumab), Summary of Product Characteristics. 27 March 2020. Available from: https://www.ema.europa.eu/en/medicines/human/EPAR/tecentriq (Accessed April 2020).
2 European Medicines Agency. Available from ema.europa.eu/en/medicines (Accessed May 2020).