For a study, researchers sought to understand that the tumor microenvironment was rich in proteases that could cleave the linker, removing the mask and allowing CX-2009 to bind to CD166 locally. In phase I/II clinical trial, CX-2009 was tested in patients with advanced solid tumors. Eligible patients had advanced cancer and had received more than or equal to 2 prior treatments. Every 3 weeks (0.25–10 mg/kg) every 2 weeks (4–6 mg/kg), CX-2009 was given at escalating levels. The primary goal was to determine the phase II dose recommendation and safety profile (RP2D). Breast cancer (n=45) was the most common subtype among the 99 individuals recruited. The median number of previous therapy was 5 (1-19). At 8 mg/kg every 3 weeks and 6 mg/kg every 2 weeks, dose-limiting toxicities were reported. The RP2D was set at 7 mg/kg every 3 weeks based on tolerability. At doses of ≥4 mg/kg, tumor regression was observed. 2 patients (9%) showed confirmed partial responses, and 10 patients (45%) had stable disease in the hormone receptor-positive/HER2-nonamplified breast cancer category (n=22). Uptake in tumor lesions and protection of key organs were confirmed using zirconium-labeled CX-2009 imaging. In 18 of 22 posttreatment biopsies, activated, unmasked CX-2009 was detectable.CD166 was a newly discovered and widely expressed target. CX-2009 was the first conditionally activated CD166 antibody-drug combination to show clinical and translational activity in several tumor types.
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