Solid tumors represent the majority of adult cancers, however they are generally resistant to the promising area of immunotherapy due to their vast variability and ability to suppress the immune system.

Imvax’s platform is designed to circumvent both these challenges. Harnessing decades of research and multiple validated technologies, Imvax’s combination therapy captures the complete antigenic signature of a patient’s own tumor and converts it into a highly stimulatory ‘training program’ for the patient’s immune system. The comprehensive nature of this training is intended to result in both innate and adaptive immune stimulation to optimize long-term anti-tumor effects.

Here’s how we do it:

Step 1: Patient Cell Processing
After surgical removal, patient tumor samples undergo overnight tissue processing including radiation and treatment with an antisense therapy that stresses the cells toward an immunogenic cell death. This process promotes the release of the tumor’s entire antigenic signature along with immunostimulatory factors.

The tumor’s antigenic components and the antisense therapy are then temporarily implanted in the patient within small proprietary chambers. These provide a controlled interface with the immune system via micropores.

The intended result of this interface is immune absorption of the tumor’s full antigenic signature to induce innate and adaptive immune responses against remaining tumor tissue in the body.

Step 2: Multi-Layered Immune System Activation
A key part of the Imvax platform’s immune stimulation is delivered by an antisense therapy, IMV-001. This single-stranded nucleic acid is designed to act in multiple ways to enhance sensitization of the immune system to a tumor’s full, unique antigen signature.

Firstly, IMV-001 targets the IGF1R receptor, a cell growth controller common in tumors, but not most healthy cells. IMV-001 binds to IGF1R mRNA in tumor cells, from which the protein would be made, to promote a specific kind of tumor cell death which releases the tumor’s entire antigenic signature along with immunostimulatory factors.

IMV-001 also binds to IGF1R mRNA in local immunosuppressive M2 macrophages present at the implantation site. Inhibiting these macrophages further promotes a receptive environment for sensitization to the tumor antigens.

Finally, IMV-001’s sequence includes a short element called a CpG motif. As IMV-001 diffuses out of the chamber, this motif activates nearby antigen-presenting cells, now laden with tumor antigens. These cells consequently traffic to local lymph nodes to activate the adaptive immune system.