Alethia Biotherapeutics announced the U.S. Food and Drug Administration (FDA) has cleared its Phase 2 Investigational new drug (IND) application for AB-16B5, a potent inhibitor of the epithelial to mesenchymal transition (EMT). This allows the Company to initiate a multi-center trial of AB-16B5 in combination with docetaxel in previously treated subjects with metastatic non-small cell lung cancer (NSCLC) who have experienced disease progression following treatment with a platinum-containing doublet treatment and an anti-PD1 or PD-L1 immune checkpoint antibody.

“We are extremely pleased to have achieved this important milestone in the development of AB-16B5 and to continue to advance the clinical development of this promising antibody” said Yves Cornellier, President and CEO of Alethia.

“EMT is a central enabler for solid tumor progression because it triggers metastatic invasion, resistance to several classes of anti-cancer drugs and contributes to immune evasion. There is also increasing evidence that EMT contributes to resistance to immune checkpoint inhibitors. AB-16B5 may play an important role in overcoming these problems”, said Dr. Mario Filion, Chief Scientific Officer.

This multicenter, open-label, Phase 2 study of AB-16B5 in combination with docetaxel will enroll approximately 40 subjects with advanced NSCLC who have previously been treated with a platinum-containing doublet treatment and an anti-PD1 or PD-L1 immune checkpoint antibody, a patient population with very limited options. The primary objectives are to assess the anti-tumor efficacy of AB-16B5 in combination with docetaxel as measured by objective response rate and to determine the safety and tolerability of the combined drugs. Secondary objectives of the study include clinical benefit rate, percentage of subjects with complete response or partial response, duration of stable disease, progression-free survival and overall survival.

AB-16B5 is a humanized IgG2 monoclonal antibody that selectively binds and inhibits tumor-associated secreted clusterin, a protein expressed in many cancers. Tumor-associated secreted clusterin is induced early in the EMT cascade and its inhibition with AB-16B5 stops and reverts EMT in animal models. A Phase 1 study in subjects with advanced carcinomas demonstrated that AB-16B5 was safe and well tolerated and provided clinical benefit to several subjects. Stable disease was observed in several patients for up to one year. There was also evidence of EMT inhibition in tumor biopsies.