Synthorx, Inc. announced company researchers will present preclinical data demonstrating the potential safety and anti-tumor effects of its lead product candidate, THOR-707, a “not alpha” Synthorin™ of interleukin-2 (IL-2) for the treatment of solid tumors at the 2019 American Society of Clinical Oncology (ASCO) Annual Meeting taking place May 31 – June 4 at McCormick Place, Chicago, IL. Marcos Milla, PhD., chief scientific officer of Synthorx, will present the company’s approach to utilizing its first-of-its-kind Expanded Genetic Alphabet platform technology to engineer IL-2 to improve its pharmacological profile. The presentation, titled “THOR-707: Using synthetic biology to reprogram the therapeutic activity of interleukin-2 (IL-2),” describes the use of the Synthorx Expanded Genetic Alphabet platform technology to design THOR-707, a recombinant IL-2 that is pegylated at one specific site, intended to block engagement of the alpha chain of the IL-2 receptor. In preclinical models, the “not alpha” feature of THOR-707 prevents proliferation of immunosuppressive CD4+ regulatory T cells as well as activation of non-lymphoid cells that trigger the serious complication of vascular leak syndrome (VLS) when IL-2 is used to treat cancer patients. The poster presentation will include data demonstrating expansion of CD8+ T cells without eosinophilia (a measurement of VLS) and durability of the CD8+ T cell expansion, regardless of whether THOR-707 is administered every 2, 3 or 4 weeks. The data also demonstrate that an anti-PD-1 antibody, when combined with THOR-707, increases interferon-gamma (IFN-?) release from T cell receptor-activated T cells, indicating the potential of this combination to enhance anti-tumor effects. The durability of these effects was demonstrated in a tumor model where re-challenged animals initially cured with THOR-707 + anti-PD-1 were found to reject additional challenges with tumor cells without subsequent drug administration. These data support the establishment of persistent anti-tumor memory T cell populations.