iTANK: A universal TCR/CAR T-cell enhancement technology platform, compatible with any TCR/CAR T-cell therapy for a multi-targeted attack on solid tumors

iTANK mode-of-action

CAR T-cell therapy

Treatment with TCR (T-cell receptors)-based therapies and CAR T-cells normally entails extracting and then genetically modifying and expanding the patient’s T-cells before they are returned to the patient intravenously to find and kill cancer cells.

CAR T: 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.

CAR T-cell finds and kills cancer cell
Hands using syringe in a lab environment

Challenges for TCR/CAR T-cells in solid tumors

The two main challenges that TCR/CAR T-cell therapies face in the treatment of solid tumors are the heterogenous expression of TCR/CAR target antigens and local immunosuppression that impedes their clinical implementation:

1. TCR/CAR target antigen heterogeneity

Heterogenous antigen expression on tumor cells increases the risk of antigen-escape and the formation of TCR/CAR T-cell resistant tumors.

2. Immunosuppressive tumor microenvironment

The microenvironment of solid tumors is highly immunosuppressive which both exhausts the TCR/CAR T-cells and makes it more difficult for them to infiltrate tumors, thus inhibiting their potential to kill cancer cells.

Combating TCR/CAR-target-antigen heterogeneity and reducing immunosuppression within solid tumors, with the help of the iTANK-platform, are of outmost importance for improving TCR/CAR-T therapy.


iTANK mode-of-action

iTANK TCR/CAR T-cells induce a pro-inflammatory microenvironment and activates the patient’s own killer T-cells against the whole repertoire of relevant tumor antigen targets.

Elicera has developed a technology platform called iTANK (immunotherapies Activated with NAP for efficient Killing) which directly counteracts the two major challenges TCR/CAR T-cell therapies face in treatment of solid tumors. The technology platform arms TCR/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:

  • be more successful in reducing tumor growth and enhancing survival of mice than conventional CAR-Ts.
  • be more effective in targeting tumors with heterogeneous antigen expression.
  • create an immunologically hot tumor microenvironment supporting dendritic cell maturation and bystander immunity observed as epitope spreading with infiltration of highly cytolytic proliferative killer T-cells that target tumor-associated antigens other than the CAR target antigen.
  • Create a pro-inflammatory microenvironment that directly counteracts immunosuppression and enhances the potency of the CAR T-cell.
  • Be effective in treatment of cancer regardless of the choice of CAR-molecule, tumor type, or mouse model, indicating the platform is universally compatible with other CAR-T technologies.
iTANK TCR/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.
Watch a presentation of preclinical PoC-data.

Scientific publications