SAN DIEGO, November 10, 2017 – eFFECTOR Therapeutics, Inc., a leader in the development of selective translation regulators (STRs) for the treatment of cancer, today announced a poster presentation of preclinical data for its lead product candidate, eFT508, that defines its immunological mechanism of action and activation of anti-tumor immune response. In vitro and in vivo preclinical models demonstrate eFT508 selectively downregulates key immune checkpoint proteins without compromising T cell activation or viability. These data are being presented at the Society for Immunotherapy of Cancer (SITC) 32nd annual meeting being held in National Harbor, Maryland on November 10-12, 2017. The poster (#368) is titled “eFT508, a potent and highly selective inhibitor of MNK1 and MNK2, is an activator of anti-tumor immune response”.
“These data highlight the potential of eFT508 to induce an anti-tumor immune response and enhance response to immune checkpoint inhibitors,” said Kevin Webster, Ph.D., senior vice president, cancer biology, eFFECTOR Therapeutics. “We are currently conducting a Phase 2 clinical trial of eFT508 as a single agent and in combination with avelumab in patients with microsatellite stable colorectal cancer, under a clinical collaboration and supply agreement between eFFECTOR and a global strategic alliance of Pfizer and Merck KGaA, Darmstadt, Germany. We are also completing our initial Phase 1 clinical development activities targeting solid tumors, and lymphoma and anticipate initiating additional Phase 2 development activity in 2018.”
In addition, the presentation will highlight that eFT508 has a favorable impact on multiple steps in the cancer immune response including activating antigen presenting cells, expanding memory T cells and enhancing cytotoxic T cell function. eFT508 additionally showed substantial anti-tumor activity mediated through tumor infiltrating lymphocytes in multiple tumor models including genetically engineered mouse models of non-small cell lung cancer and hepatocellular carcinoma.
eFT508 is a selective translation regulator and is part of a new class of cancer treatments known as immunotherapies that are designed to harness the body’s own immune system in fighting cancer. eFT508 is a highly potent and selective, oral inhibitor of MNK1 and MNK2. MNK1/2 are terminal kinases in key oncogenic signaling pathways, including KRAS-BRAF-MEK-ERK, and are activated by the mitogen-activated protein kinases (MAPK) in multiple immune cell types. MNK1 and MNK2 integrate MAPK pathway signaling at the level of mRNA translation, resulting in decreased anti-tumor immune activity due to selective upregulation of several immune checkpoint receptors and specific immunosuppressive cytokines. eFT508 selectively blocks MNK1/2 driven mRNA translation, thereby promoting anti-tumor immune response. eFT508 is currently being evaluated in a Phase 2 clinical trial in patients with microsatellite stable colorectal cancer (NCT03258398), in a dose escalation study in patients with advanced solid tumors (NCT02605083) and dose escalation and cohort expansion study in patients with advanced lymphomas (NCT02937675).