Proposed Mechanism of Action
Proposed mechanism of action for TECENTRIQ®
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 programmed death-ligand 1, or PD-L1, a negative immune regulator that can be expressed in the tumour microenvironment.2-4
TECENTRIQ provides direct and dual blockade of PD-L1 interactions while selectively sparing PD-L2 interactions. This can restore antitumour T cell activity and enhance T-cell priming within the cancer immunity cycle.2-4
TECENTRIQ® targets the Ligand PD-L1 to restore antitumour T-Cell activity
PD-L1 can contribute to immune deactivation in the tumour microenvironment.1-3
- PD-L1 is expressed on tumour cells and tumour infiltrating immune cells1
- Binding of PD-L1 to its receptors PD-1 and B7.1 can lead to the inhibition of anticancer T-cell activity in the tumour1
TECENTRIQ targets the ligand PD-L1 to restore antitumour T-cell activity.1,2,4
Features of TECENTRIQ® MoA
- Targets PD-L1 on tumour cells and tumour-infiltrating immune cells to reactivate T cells1
- Provides dual blockade of PD-1 and B7.1, which can reinvigorate suppressed T cells to kill cancer cells (via PD-1)5 and can enhance T-cell priming in the lymph node (via B7.1)1,4
- Spares PD-L2/PD-1 interactions1
- TECENTRIQ® Summary of Product Characteristics.
- Herbst RS, Soria JC, Kowanetz M, et al. Predictive correlates of response to the anti-PD-L1 antibody MPDL3280A in cancer patients. Nature. 2014;515:563-567.
- Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39:1-10.
- Chen DS, Irving BA, Hodi FS. Molecular pathways: next-generation immunotherapy--inhibiting programmed death-ligand 1 and programmed death-1. Clin Cancer Res. 2012;18:6580-6587.
- Keir ME et al. PD-1 and Its Ligands in Tolerance and Immunity Annu Rev Immunol 2008; 26: 677–704.
Date of preparation: October 2019