Cellectis Presents First Preclinical Data on UCARTMESO, an Allogeneic CAR-T Cell Product Candidate Targeting Mesothelin to Treat Solid Tumors at the Annual Meeting of the Society for Immunotherapy of Cancer

November 12, 2021 – New York – Cellectis S.A. (NASDAQ: CLLS – EURONEXT GROWTH: ALCLS) (the “Company”), a clinical-stage gene-editing company employing its core technology to develop products based on gene-editing with a portfolio of allogeneic chimeric antigen receptor (CAR-)T cells in the field of immuno-oncology and gene-edited hematopoietic stem cells in other indications, announced the first preclinical data on UCARTMESO, its allogeneic CAR-T cell product candidate targeting mesothelin, being developed for patients with mesothelin-expressing solid tumors.

The data were presented today in a poster session at the Society for Immunotherapy of Cancer (SITC) 36th Annual Meeting titled “Mesothelin (MSLN) targeting allogeneic CAR-T cells engineered to overcome tumor immunosuppressive microenvironment”. Poster # 143.

The poster presentation highlighted the following preclinical data:

• Mesothelin is an interesting target for CAR-T cell therapy for solid tumors because it is highly and consistently expressed in mesothelioma and pancreatic cancers. It is also over-expressed in subsets of other solid tumors (ovarian cancer, non-small cell lung cancer, gastric cancer, triple-negative breast cancer) while modestly expressed in healthy cells, indicating that targeting mesothelin may result in a safe and effective therapy.
• UCARTMESO product candidate is composed of allogeneic non-alloreactive T cells edited with TALEN®-encoding mRNAs to disrupt TRAC, CD52 and TGFBR2 genes, and transduced ex vivo with a recombinant lentiviral vector (rLV) to express a second-generation CAR targeting MSLN. It is the first TALEN®-induced triple knock out (KO) product candidate in the allogeneic CAR-T space.
• The preclinical data demonstrated potent activity of UCARTMESO in vitro and in vivo against MSLN expressing cell lines, and in vivo activity in pancreatic and pleural mesothelioma mouse models.
• Due to TGFBR2 KO, UCARTMESO was shown to restore IL2RA upregulation upon in vitro activation, even in media rich in TGFB1, which contributes to the immune suppressive microenvironment in tumors.

Laurent Poirot, PhD, Senior Vice President Immunology, noted: “Overall, the data demonstrated that the TGFBR2 gene knock out provides valuable additional properties to UCARTMESO, which may result in a very effective therapy despite an immune suppressive tumor microenvironment, and supports its clinical development for the treatment of solid tumors.”

A copy of the presentation will be available on Cellectis’ website here, shortly after the event.