Every year, there are over 18 million cases of cancer detected and 10 million cancer related deaths. In fact, it is estimated that there are 1.6 million new cases of solid tumors in the U.S. alone – presenting one of the largest challenges to oncologists.
Certain cancers can bypass or hide from the immune system by engaging an immune checkpoint called PD-1, which represents an “off-switch” that cancers can exploit to escape from cancer-fighting T-cells. New treatments, called checkpoint inhibitors, block these “off-switches” and help keep cancer-fighting T-cells in attack mode to eliminate tumor cells.
However, anti-PD-1 checkpoint inhibitors that work to turn off the “off-switches” are only effective in an estimated 30% of the patients that receive these drugs. The other 70% of patients who receive anti-PD-1 checkpoint inhibitors don’t see their tumors go away. Those tumors lack essential immune elements that enable anti-PD-1 checkpoint therapy benefits. They are known as “cold” tumors – while “hot” tumors are likely to receive a benefit from checkpoint inhibitors. Our lead product candidate, TAVO™ (tavokinogene telseplasmid) is designed to help turn “cold” tumors “hot.”
The favorable safety profile we have observed to date supports ongoing clinical development of Intratumoral IL-12 with DNA-based IL-12. In clinical studies, TAVO has shown a favorable safety profile to date and has been generally well-tolerated across multiple treatment cycles with no treatment-related serious adverse events reported.
Data from our Phase II melanoma program provide preliminary evidence of anti-tumor activity with abscopal effect. These results paved the way for expansion of our immuno-oncology pipeline, including the design of a new study testing TAVO in triple negative breast cancer.
Data indicates that local delivery and expression of TAVO promotes tumor immunogenicity and increases tumor-infiltrating lymphocytes (TILs). As a pro-inflammatory cytokine, IL-12 can promote the recruitment of T-cells to the tumor. By driving T-cells or TILs into the tumor microenvironment, TAVO may enhance response to anti-PD-1 and convert anti-PD-1 non-responders to responders.