The treatment is based on using a chimeric antigen receptor (CAR) that is placed on the surface of the T-cell so that it recognizes a specific target (an antigen) on the tumor cells and can then attack and kill the tumor cells.
The success of CAR T-cell therapies has been remarkable in treatment of hematological cancers and has to date resulted in five market approved products for treating B-cell and plasma cell malignancies. However, no CAR T-cell therapy has yet been approved for treatment of solid tumors.
The two main challenges that CAR T-cell therapies face in the treatment of solid tumors are the heterogenous expression of CAR target antigens and local immunosuppression that impedes their clinical implementation:
Heterogenous antigen expression on tumor cells increases the risk of antigen-escape and the formation of CAR T-cell resistant tumors.
The microenvironment of solid tumors is highly immunosuppressive which both exhausts the CAR T-cells and makes it more difficult for them to infiltrate tumors, thus inhibiting their potential to kill cancer cells.
Combating CAR-target-antigen heterogeneity and reducing immunosuppression within solid tumors, with the help of the iTANK-platform, are of outmost importance for improving CAR-T therapy.
Elicera has developed a technology platform called iTANK (immunotherapies Activated with NAP for efficient Killing) which directly counteracts the two major challenges CAR T-cell therapies face in treatment of solid tumors. The technology platform arms CAR T-cells with a pluripotent proinflammatory neutrophil-activating protein (NAP) from Helicobacter pylori which induces bystander immunity via epitope spreading. The system is independent of tumor types and target antigens.
The NAP is a multifaceted immune activator, able to stimulate other cells to secrete cytokines and chemokines. Using a bacterial derived factor is also more immunogenic and believed to turn the suppressive “cold” environment to “hot”.
iTANK-enhanced CAR(NAP)-Ts have been shown to:
iTANK CAR T-cells induce a pro-inflammatory microenvironment and activates the patient’s own CD8+ killer T-cells against the whole repertoire of relevant tumor antigen targets.