Tori Strong has completed his PhD from the University of Texas Medical Branch at Galveston. He is the director of Intellectual Property and Technology at Vyripharm Biopharmaceuticals, a premier biotech organization. He has served as a Patent Examiner for the USPTO and is now directly involved in the technology development to commercialization which includes strategies of building intellectual propery.
Novel Formulation of Cannabinoid Analogues Treating DLBCL and MCL: Diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL) represent the most common and most aggressive forms of Non-Hodgkin lymphoma (NHL) respectively. With CB1 antagonists as potential therapeutics for both DLBCL and MCL, we formulated VYR-206, developed from existing obesity treatment Rimonabant by the addition of our tetraazacyclic (N4) conjugate derivative. This allows the potential for image guided theranostic application for diagnosis, precision and assessment of therapeutic response through radiotracer chelation. Our study is aimed at demonstrating VYR-206 activity in DLBCL and MCL for sensitivity or resistance. Cells from representative DLBCL and MCL cell lines were plated at 5,000 cells per well. The cells were incubated for 72 hours in 20 µL medium with 10% FBS and varied concentrations of experimental cannabinoid antagonist VYR-206, Rimonabant, or dimethylsulfoxide (DMSO). Viability assays were conducted using Celltiter-Glo Luminescent Cell Viability Assay. Experiments were performed 2-3 times independently, with concentration tested in triplicate. Most DLBCL cell lines treated with VYR-206 had a reduction in viability at concentrations of 50μM or greater with few cells line displaying limited response even at concentrations of 100μM. Increased variability is seen among MCL cell lines treated with VYR-206, most having a reduction of viability at concentrations of 25μM or greater, with few cell lines at concentrations of 50μM and 2 cell lines showing no response even at concentrations of 100μM. The discrepancy in response in both DLBCL and MCL may be due to genetic variability among cell lines.