Browse and review clinical resources related to oncology below.
Cytokine Release Syndrome (CRS) Overview
Learn more about CRS
To view a PDF of the above document, please click here.
The PD-L1 Pathway
We are continuing to advance the understanding of cancer immunotherapy by researching pathways that can be targeted simultaneously with the PD-L1/PD-1 pathway to address various immune escape mechanisms in cancer.
PD-L1 pathway inhibition has taken an important role in helping to restore a key part of the cancer immunity cycle.1
Immune Escape
Tumor cells can escape the antitumor immune response in several ways
Tumor cells can evade the immune system by disrupting any of the key T-cell activities necessary to initiate and perpetuate an antitumor immune response: T-cell generation, T-cell infiltration, or tumor cell killing.1-3
Disruption of any steps of the cancer immunity cycle can ultimately result in tumor growth.2
*Tumor cell killing by CD8+ T cells.
Targeting PD-L1 simultaneously with other pathways may help restore the cancer immunity cycle
As a key immunosuppressive driver, the PD-L1 pathway is an important target that may help invigorate antitumor T-cell activity in the tumor microenvironment.1,4
PD-L1 inhibition may help restore tumor cell killing.4*
*Tumor cell killing by CD8+ T cells.
In cancer, the PD-L1 ligand is expressed on tumor cells and immune cells. When bound to its receptors, PD-1 and B7.1 on T cells, PD-L1 deactivates cytotoxic T cells.
PD-L1 inhibition may prevent T-cell deactivation.
Reinvigorated T cells can then attack and kill tumor cells.
However, cancers may use multiple immune escape mechanisms. Targeting PD-L1 simultaneously with other pathways may be necessary to restore a fully functional cancer immunity cycle.1
We are actively researching pathway combinations with PD-L1.5