Amunix turned heads back in March when it raised $73 million in a series A funding round that effectively transformed the company from a technology licenser to a biotech innovator. Amunix has been around since 2006, offering its half-life-extension technology to other biopharma developers. The funding allowed it to apply its tools to develop drugs that harness the immune system’s T cells to attack solid tumors.
Now it has preclinical evidence to back up its lead program, AMX-818 for HER2-positive solid tumors.
In mouse models of HER2-positive solid tumors, a single dose of AMX-818 caused large tumors to shrink, Amunix reported at the virtual meeting of the European Society of Medical Oncology (ESMO).
AMX-818 is a T-cell engager—a drug that’s designed to unleash an immune attack against tumors at the site of the cancer, with the goal of prompting tumor regression without touching off cytokine release syndrome (CRS), an immune over-reaction sometimes seen with CAR-T cell therapies. Amunix designed the drug to include sites that release proteases—enzymes in the tumor microenvironment that break down proteins.
In the mouse trial reported at ESMO, tumor shrinkage was dependent on that protease release, Amunix reported. A separate safety study in monkeys demonstrated no CRS, even at the maximum dose.
Amgen’s Blincyto, approved in 2018, is a bispecific T-cell engager. Several other companies have since jumped into this growing category, including Johnson & Johnson, which formed a collaboration with Lava Therapeutics in May develop gamma-delta T-cell engagers. Crescendo Biologics raised $70 million in 2018 to back the development of its bispecific T-cell engager.
Other companies that have tried to develop T-cell engagers have stumbled, however. Germany-based Affimed ended its T-cell engager program last year after safety issues in a phase 1 trial forced a clinical hold.
During ESMO, Amunix also reported data from a preclinical trial of another T-cell engager it is developing, this one targeting EGFR. In mouse models of BRAF-mutated cancer, the experimental drug caused tumors to shrink in a dose-dependent manner, the company reported.