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.
TECENTRIQ provides direct and complete 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.
TECENTRIQ® TARGETS THE LIGAND PD-L1 TO RESTORE ANTITUMOUR T-CELL ACTIVITY
PD-L1 is a key source of immune deactivation in the tumour microenvironment1–3
- PD-L1 is expressed on tumour cells and tumour infiltrating immune cells
- Binding of PD-L1 to its receptors PD-1 and B7.1 can lead to the inhibition of anticancer T-cell activity in the tumour
TECENTRIQ targets the ligand PD-L1 to restore antitumour T-cell activity1,2,4
Distinct features of TECENTRIQ
- Targets PD-L1 on tumour cells and tumour-infiltrating immune cells to reactivate T cells
- Provides dual blockade of PD-1 and B7.1, which can reinvigorate suppressed T cells to kill cancer cells (via PD-1) and can enhance T-cell priming in the lymph node (via B7.1)
- Spares PD-L2/PD-1 interactions, helping to minimise autoimmune reactions in healthy tissue
1. TECENTRIQ prescribing information.
2. 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.
3. Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39:1-10.
4. 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.
MatCode Approval No.: -1905-V2-3253