o AVS100 is a highly specific HDAC6 inhibitor targeted for the treatment locally advanced or metastatic solid tumors, in clinical combination with existing PD-1 inhibitors. In metastatic melanoma for instance, only 20-30% of current patients are responsive to existing anti-PD-1 immunotherapies, highlighting a significant unmet need. AVS100 has been proven in preclinical in-vivo models to downregulate PD-L1 expression, reduce tumor growth, and provide an increase in the overall M1/M2 macrophages in the tumor microenvironment. It has been shown to have mechanistic impact on the polarization of macrophages towards the anti-tumoral M1 phenotype. Through this novel approach, we believe AVS100 can help increase the overall response rate for patients on existing immunotherapies, as well as open a window for additional patients to respond. Our collaboration is with Alejandro Villagra PhD’s lab out of Georgetown University.
AVS200 is a next generation autologous HDAC6i-activated macrophage-based cell therapy. AVS200 utilizes HDAC6i to protect the M1 phenotype of macrophages ex-vivo prior to administration and has been proven in numerous humanized mouse models to cause a significant decrease in tumor size as well as the ability to sustain conformance of the M1 phenotype with these introduced macrophages. Our belief is that AVS200 can also act as a platform therapy, regardless of macrophage therapy, in order to ensure ‘locking’ of the anti-tumoral M1 phenotype. Our collaboration of this program is also with Georgetown researchers.
AVS300 is a mRNA based TEM1 cancer vaccine and utilizes a differentiated approach to directly attack tumor vasculature. Tumor Endothelial Market 1 (TEM1) is abundantly expressed in endothelium and/or stroma of numerous cancers. Cross-priming can work in concert with anti-TEM1 immune response to eradicate a large number of tumor and endothelial cells. AVS300 is a joint-development collaboration with researchers at the University of Pennsylvania.