MCLA-128 is an ADCC-enhanced Biclonics® that bind to HER2 and HER3- expressing solid tumor cells. MCLA-128 is designed to overcome the inherent and acquired resistance of tumor cells to HER2-targeted therapies using two mechanisms: 1) blocking growth and survival pathways to stop tumor expansion while preventing tumor cells escaping through activation of the HER3/heregulin pathway and 2) recruitment and enhancement of immune effector cells to directly kill the tumor.
MCLA-117 is a Biclonics® that binds to CD3, a cell-surface molecule present on all T cells, and CLEC12A, a cell surface molecule present on Acute Myleoid Leukemia (AML) cells and stem cells. MCLA-117 is designed to recruit and activate T-cells to kill CLEC12A-expressing AML tumor cells and stem cells, which may prevent recurrence of tumors.
MCLA-158 is an ADCC-enhanced Biclonics® for the treatment of solid tumors, including the potential treatment of colorectal cancer, that binds to cancer stem cells expressing leucine-rich repeat-containing G protein-coupled receptor 5 and epidermal growth factor receptors. MCLA-158 is designed to use two different mechanisms of action. The first blocks growth and survival pathways in cancer stem cells. The second involves the recruitment and enhancement of immune effector cells to directly kill cancer stem cells that persist in solid tumors and cause relapse and metastasis.
MCLA-134 is a Biclonics® that is designed to bind to a combination of two immunomodulatory targets expressed by T cells. MCLA-134 is designed to activate unresponsive tumor infiltrating T cells to kill cancer cells.
MCLA-145 is a Biclonics® that is designed to bind to a tumor-associated target with an immunomodulatory target involved in checkpoint inhibition. MCLA-145 is designed to simultaneously reverse immune system suppression at the tumor site while attracting immune effector cells to directly kill the targeted tumor.
We intend to leverage our Biclonics® technology platform to identify multiple additional bispecific antibody candidates and advance them to clinical development.
Our current focus is on a number of immunotherapeutic targets and pathways that have demonstrated promising tumor killing ability in early-stage clinical trials and scientific literature.