Unlocking Cell Therapy
Cell-based therapies, particularly those based on chimeric antigen receptor T-cells (CAR-T), have proven to be highly effective for patients with hematological cancers. However, there are numerous obstacles to the use of CAR-T cell therapy for the treatment of solid tumors, including:
Poor immune cell infiltration of and survival within tumors
Immunosuppressive properties of the tumor microenvironment
Systemic toxicity issues linked to off-target CAR-T cell reactivity
T-SIGn® therapeutics have the potential to be used in combination with CAR-T and other cell therapies to overcome these limitations via expression of target antigens to enhance the activation, survival and efficacy of cell therapies in the solid tumor setting.
Akamis Bio has generated promising preclinical data supporting the use of T-SIGn® therapeutics to enhance the efficacy of CAR-T cell therapy in a human tumor xenograft model; key supportive evidence from studies with that model include:
Gene expression profile demonstrating T-SIGn®-mediated tumor microenvironment remodeling
Enhanced T-cell activation and recruitment of innate immune cells into the tumor
T-SIGn® transgene payload-driven enhancement of efficacy vs. CAR-T monotherapy
Clearance of both primary and metastatic tumors
Learn more about the use of T-SIGn® therapeutics in combination with CAR-T cell therapy in the following publication:
T-SIGn® therapeutics are viral vector based, tumor gene therapies which are capable of homing specifically to primary and metastatic solid tumors following intravenous delivery.
We have a growing pipeline of T-SIGn® therapeutics capable of driving the intratumoral expression of a broad range of therapeutic proteins, as well as immunologically active biomolecules which aim to enable a patient’s immune system to recognize, attack, and clear solid tumors.
Our clinical studies are investigating the use of T-SIGn® therapeutics in the monotherapy setting, as well as in combination with other immuno-oncology agents to target specific solid tumor immune resistance mechanisms.