Chimeric antigen receptor (CAR)-T cell therapies involve genetically modifying a patient’s T cells to recognize and attack cancer cells. These CARs provide immune effector cells with the tumor targeting specificity of a monoclonal antibody. By redirecting the immune system to eliminate malignant cells, CAR-T cells act as a living drug, expanding in the patient and enabling long-term antitumor activity. CAR-T cells can be classified as either autologous (derived from the T cells of the cancer patient) or allogeneic (derived from the T cells of a healthy donor).
Despite the vast potential of CAR-T cell therapies, major challenges persist for both autologous and allogeneic approaches:
We believe we can disrupt the conventional approaches to both autologous and allogeneic CAR-T cell therapies by leveraging our highly innovative technology platforms, proprietary techniques, in-house expertise, clinical development strategy, and scalable manufacturing processes.
Our autologous platform producing CAR-T cell therapies that utilize next-day manufacturing to deliver younger, less exhausted T cells with enhanced activities.
We have a suite of proprietary genetic engineering techniques, Dual CAR and Enhanced CAR, that can be leveraged with our FasTCAR and TruUCAR technology platforms to further enhance the therapeutic effects of our CAR-T product candidates.
Dual CAR is designed to control relapse in patients in FasTCAR by reducing the likelihood of antigen escape and to reduce rejection of the CAR-T cells by patients treated with TruUCAR-enabled allogeneic CAR-T cell therapies. Stimulated by two CARs, dual antigen targeting CAR-T cells have the potential to maintain in vivo longer than single antigen targeting CAR-T cells. The second CAR can be designed to target early lineage cells or progenitors that will ultimately develop into cancer cells.
Enhanced CAR further strengthens CAR-T cells’ functionality, for example by overcoming the immunosuppressive tumor microenvironment (TME) and/or increasing cytokine signaling. Working on the hypothesis that PD-1 mediated immunosuppression causes CAR-T cell hypofunction, we utilize CRISPR/Cas9 to knock out PD-1 expressed on CAR-T cells to release potential suppression from programmed death-ligand 1 (PD-L1) expressed on tumor cells and other suppressive immune cells in tumor tissue. With Enhanced CAR, we can also enable CAR-T cells to achieve intended functions by regulating the expression of one or a combination of cytokine, cytokine receptors or checkpoint ligands.