Elicera Therapeutics presents preclinical proof-of-concept data for its iTANK-platform at the European Society of Cell & Gene Therapy Congress

Gothenburg, October 20, 2021 - Elicera Therapeutics AB (publ), a clinical stage cell and gene therapy company that develops immunooncological treatments focusing on CAR T-cells and oncolytic viruses, presented preclinical proof-of-concept data for the company's iTANK-platform at the ESGCT (European Society of Gene & Cell Therapy) Virtual Congress 2021.

Elicera's technology platform - iTANK (immunoTherapies Activated with NAP for efficient Killing) - has been developed to optimize the effect of CAR T-cell therapies by generating a dual mechanism-of-action. In addition to the effect of the CAR T-cells, CD8 + killer T-cells are activated, which gives a double attack on the tumor cells and creates a systemic and long-term immune response against cancer.

CAR T-cell therapies have a proven ability to cure previously difficult-to-treat patients with various forms of blood cancer. However, two main challenges remain in the treatment of solid tumors that, due to a highly hostile tumor microenvironment, exhaust and inhibit the effect of CAR T-cells. In addition, it is difficult to identify a target antigen on solid tumors that is expressed on all tumor cells. This means that some tumor cells can escape being attacked by CAR T-cells and that resistant tumors form. With the iTANK-technology, Elicera hopes to meet these challenges.

"The data presented at the ESGCT Congress provides preclinical proof-of-concept for the iTANK-platform and its ability to enhance the efficacy of CAR T-cells and addresses the problem of antigen heterogeneity. This is very exciting as our technology platform can be used to amplify the effect of all CAR T-cell therapies under development, not just our own", says Jamal El-Mosleh, CEO of Elicera Therapeutics.

The iTANK-platform's mechanism-of-action:

The iTANK technology platform arms CAR T-cells with a transgene that codes for a Helicobacter Pylori neutrophil-activating protein (NAP). When the CAR T-cell binds to tumor cells, NAP is released which will activate surrounding cells that further releases cytokines and chemokines. This in turn creates a proinflammatory environment which directly combats the hostile tumor microenvironment in solid tumors and strengthens the function of the CAR T-cells. The proinflammatory environment will also induce a so called "bystander" immune activation, meaning that antigen-presenting-cells will be recruited to the tumor site, where they will pick up the whole set of relevant tumor target antigens that have been released from the CAR T-cell tumor attack. These target antigens will then be presented to CD8+ killer T-cells in the lymph nodes that will subsequently seek out and destroy tumor cells that carry these target antigens.

Summary of proof-of-concept data presented at the ESGCT Congress:

Associate professor and co-founder of Elicera Therapeutics, Di Yu, presented preclinical data at the ESGCT Virtual Congress 2021 showing that:
  • NAP is secreted only when CAR T-cells bind to tumor cells.

  • NAP induces a bystander immune response to counteract the antigen heterogeneity problem. Several in vivo studies in different mouse models showed that only mice treated with iTANK enforced CAR T-cells showed a reactivity against tumors that lacked the CAR T-cells target antigen resulting in increased tumor response and increased survival in mice compared to treatment with conventional CAR T-cells, not armed with iTANK.

  • CAR T-cells armed with the iTANK-platform showed less exhaustion and improved activity in comparison to conventional CAR T-cells.

  • Arming CAR-T cells with the iTANK-platform is effective against cancer regardless of the choice of CAR-molecule, tumor type, or mouse model, indicating the platform is universally compatible with other CAR-T technologies.

The preclinical data will also be presented publicly at an HC Andersen Online event

October 20th, 2021 11:00 - 11:20 Europe / Copenhagen.

Read more or register for free here:


Source: Cision

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