Model ACB1801 - Beta-Carboline Derivative
Our patented Beta-carboline derivative (ACB1801) is an actin dynamic modulator which induces cellular F-actin network remodeling (tumor reversal); this in turn translates into immuno-competency that allows the immune system to recognize tumor cells and thereby enhances the efficacy of checkpoint-inhibitor immune therapy. Immune checkpoint-inhibitors directly target the immune system of the body and do not harm healthy cells in the process.
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The science behind ACB1801
Cancer cells are known to co-opt the checkpoints – in effect “hacking” the immune system – by sending out false signals indicating that the cells are healthy; this with the result that the T-cells are shut down, thus preventing the immune system from attacking the tumor cells. Checkpoint-inhibitors deactivate the “brakes” and allow the T-cells to get moving again.
Preventing tumors to evade the immune surveillance requires a high expression in cells of TAP and a high level of MHC-1, with an appropriated MHC-1 mediated antigen presentation pathway.
To restore both TAP1 and MHC-1 presentation after loss of tumor phenotype characters, ACB1801 induces genetic and epigenetic modifications. ACB1801, thanks to the restoration of the actin cytoskeleton network in tumor cells, favors the trafficking of antigenic peptides and increases the MHC-1 expression at the tumor cell membrane.
ACB1801 has shown very promising results in the melanoma B16-F10 mouse model, where it displays non cytotoxic, immune-mediated antitumor effect and a strong potentiation of an anti PD-1 antibody (see chart).
Colorectal cancer is the lead target for the first clinical trial program followed by ovarian and melanoma. ACB1801 converts non-responder patients (MSI-L/pMMR) with colorectal and other cancers into candidates for anti-PD-1 therapy.
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