By integrating clinical insights into each aspect of the drug discovery and development process, we are creating a novel paradigm in cancer treatment with the goal of providing better therapies for patients in need.
In July 2019, we updated our strategic collaboration with Celgene, originally established in July 2016. Under the terms of a new license agreement, Celgene has licensed worldwide rights to JTX-8064, a, highly-selective, potential first-in-class antibody that targets the LILRB2 receptor on macrophages. Jounce retains full worldwide rights to its pipeline beyond JTX-8064, including vopratelimab, JTX-4014 and all discovery programs, as Jounce and Celgene have also entered into a mutual agreement to terminate their original strategic collaboration agreement.
Our lead product candidate, vopratelimab, is a monoclonal antibody that binds to and activates the Inducible T cell CO–Stimulator (ICOS), a protein on the surface of certain T cells that we believe will stimulate an immune response against a patient’s cancer. Vopratelimab is intended to treat solid tumors as a single agent and in combination with other therapies, and is currently being evaluated in a Phase 1/2 clinical trial, the ICONIC trial. Vopratelimab is based on insights generated by our founders, Drs. Jim Allison and Padmanee (Pam) Sharma, which showed that elevated expression of ICOS correlated with positive clinical outcomes and, subsequently, that providing an agonist signal through ICOS leads to anti-tumor activity in vivo. Their experience paved the way for our translational approach. Based on these insights and additional preclinical evidence, we initiated our ICOS program and:
Most first-wave immunotherapy treatments have focused on activating T cells within tumors, an approach that has successfully led to medicines that are making a difference in patients’ lives. However, many patients still do not achieve long-lasting responses on these treatments. This may occur for two reasons: (1) insufficient numbers of T cells within a certain tumor or tumor type; or (2) the presence of suppressive mechanisms that inhibit or reduce the activity of the immune system. In both of these scenarios, therapies targeting T cells are less likely to be successful.
We believe that the ability to target different immune cell types, such as innate immune cells, may allow us to (1) pursue tumor types not currently served by therapies which target adaptive immune cells; as well as (2) potentially convert the TME from an immunosuppressive environment to an immune-activating environment. We believe our differentiated approach to understanding and interrogating these other immune cell types competitively positions us to exploit the promise of immunotherapy in cancer.
Our translational approach led us to characterize large numbers of human tumors in which the innate immune or stromal mechanisms may be suppressing or repelling the immune system within the TME. We have strived to create a balanced pipeline with both T cell and Beyond T cell programs in order to optimize the use of the immune system, and to couple this pipeline with novel patient selection strategies.
The tumor microenvironment (TME) refers to the cellular environment that makes up a tumor. This environment includes blood vessels, immune cells, fibroblasts, myeloid cells, lymphocytes, signaling molecules and the extracellular matrix.
Our approach to identifying novel targets and mechanisms, while initially focused on tumor-associated macrophages (TAMs), is a repeatable approach that we believe can be applied to other cell types in the tumor microenvironment.