Cantargia presents anti-metastatic effect of IL1RAP blocking antibody at AACR

Today, Cantargia AB presents novel data using antibody therapy against interleukin 1 receptor accessory protein (IL1RAP) at the American Association of Cancer Research (AACR) Annual Meeting 2018 in Chicago. The antibody is a novel mouse-specific surrogate of Cantargia’s proprietary antibody CAN04 currently investigated in clinical trials. The surrogate antibody counteracted metastases in an in vivo model of triple negative breast cancer. Mechanistically the antibody binds and blocks signalling through mouse IL1RAP, accumulates in the tumor tissue and recognizes IL1RAP expressing tumor infiltrating myeloid immune cells.

Tumor progression, including metastasis, involves complex biological events in the tumor microenvironment and the IL-1 system has been implicated to have a role in this process. Cantargia’s antibodies against IL1RAP can block this system and have previously shown to have antitumor activities against human tumors in mice with a defective immune system.

In this novel study, a newly designed antibody against mouse IL1RAP significantly circumvented metastases in an in vivo model of breast cancer in mice with a fully functional immune system. The antibody is designed for studies in immunocompetent mice and is a surrogate antibody of Cantargia’s lead candidate CAN04. The study was designed to evaluate effects on tumor development and metastasis by targeting IL1RAP on non-tumor cells. One type of immune cells involved in tumor metastasis is myeloid cells, that create a metastasis-promoting, tumor-supportive and immune-suppressive microenvironment. The surrogate antibody binds these cells through IL1RAP and accumulates in the tumor. The data from this new study are consistent with an antitumor effect mediated by an modulation of these immune-suppressive cells.

The poster can be viewed at Cantargia’s webpage

“These preclinical findings are truly exciting. Cantargia’s lead project is a fully humanized antibody, CAN04, against IL1RAP. CAN04 is currently in a phase I/IIa clinical study focused on the treatment of non-small cell lung cancer and pancreatic cancer, i.e. solid tumors with an inflammatory tumor microenvironment. This new preclinically documented anti-metastatic effect provides a novel mechanism as an ‘add-on’ that could significantly increase the clinical relevance of CAN04 in future treatment of cancer”, says Göran Forsberg, CEO Cantargia. 

For further information, please contact
Göran Forsberg, CEO
Telephone: +46 (0)46-275 62 60

This constitutes information which Cantargia is required to publish under the EU’s Market Abuse Regulation and the Swedish Securities Market Act. The information was submitted for publication through the above contact person on 16 April 2018, at 15:00.

About Cantargia

Cantargia AB (publ), 556791-6019, is a biotech company that is developing antibody-based treatments for life-threatening diseases. The original discovery by the research team behind Cantargia was the overexpression of a specific target molecule, interleukin 1 receptor accessory protein (IL1RAP) in leukemic stem cells. Subsequent research has also identified IL1RAP in many other forms of cancer. The company’s main project, the CAN04 antibody targeted at IL1RAP, is being studied in the CANFOUR clinical phase I/IIa study, where the primary focus is on non-small cell lung cancer and pancreatic cancer. CAN04 has two modes of action: it blocks the function of IL1RAP and stimulates the immune system to destroy tumour cells. Cantargia’s second project, currently in the research phase, is aimed at developing an IL1RAP-binding antibody that is optimised for treatment of autoimmune and inflammatory diseases.

Cantargia is listed on Nasdaq Stockholm First North (ticker: CANTA). Sedermera Fondkommission is the company’s Certified Adviser. More information about Cantargia is available at 

About Us

Cantargia AB (publ), 556791-6019, is a biotech company which is listed on Nasdaq Stockholm (ticker: CANTA). More information about Cantargia is available at


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