Tillkännagivande • May 22
Cellectis S.A., Annual General Meeting, Jun 25, 2026 Cellectis S.A., Annual General Meeting, Jun 25, 2026. Location: at the biopark auditorium, 11 rue watt, 4th floor, 75013., paris France Tillkännagivande • May 05
Cellectis S.A. to Report Q1, 2026 Results on May 11, 2026 Cellectis S.A. announced that they will report Q1, 2026 results After-Market on May 11, 2026 Tillkännagivande • Apr 29
Cellectis Presents Epigenetic Editing Platform To Turn Genes Off Without Altering DNA Cellectis presented new research on a TALE-based epigenetic editing approach, that does not cut or permanently modify the DNA sequence, making it a potentially safer alternative for genome editing, at the American Society of Gene and Cell Therapy annual meeting, that will be held on May 11-15, in Boston (MA). The data will be presented in a poster: Title: TALE-based epigenetic modulators show sustained knock-down of target genes in T-cells and HEPG2 via a high-throughput multiplex screening platform. Transcription activator-like effector-based epigenetic modulators (TALEM) are engineered fusion proteins consisting of a TALE DNA-binding domain with functional domains that mediate epigenetic modifications. These proteins can be precisely guided to a target location in the genome to switch genes on or off through a process known as epigenetic editing. Unlike traditional gene editing tools, this approach does not induce DNA breaks and DNA sequence modifications, making it a potentially safer alternative for genome editing. In this work, Cellectis developed a high-throughput screening system capable of rapidly assembling and testing hundreds of these TALEM, identifying which combinations are most effective at regulating a given gene. This strategy was used for two distinct genes: one highly expressed in hepatocytes (active in liver cells) and another implicated in T-cell dysfunction and exhaustion, a key challenge in cancer immunotherapy. In both cases, the approach achieved >90% reduction in gene activity, which remained stable throughout the study. Tillkännagivande • Mar 13
Cellectis S.A. to Report Q4, 2025 Results on Mar 19, 2026 Cellectis S.A. announced that they will report Q4, 2025 results at 5:40 PM, Central European Standard Time on Mar 19, 2026 Tillkännagivande • Nov 14
Cellectis S.A. Announces Board Appointments Cellectis S.A. announced in September 2025, appointed Kimberly A. Box to its Board of Directors, strengthening the Company’s governance and commercialization strategy leadership capabilities. Ms. Box brings extensive leadership experience in technology operations, strategic transformation, and scaling innovation into global markets, including three decades at Hewlett Packard in multiple executive roles. Her appointment reinforces Cibus’ readiness for upcoming product launches and supports the Board’s focus on long-term value creation and commercial execution. In November 2025, Cibus appointed Craig Wichner to its Board of Directors, strengthening the Company's agricultural sector expertise and strategic advisory capabilities. His extensive experience in sustainable agriculture, farmland investment management, and data-driven business models brings valuable perspective as Cibus advances its productivity and sustainability trait programs toward commercialization. Mr. Wichner is the Founder and Managing Partner of Farmland LP, a leading U.S. farmland investment management firm with more than $350 million in assets and over 19,000 acres under management. Mr. Wichner also serves on the Board's Strategy Committee and the special committee evaluating strategic alternatives to maximize shareholder value. Tillkännagivande • Nov 01
Cellectis S.A. to Report Q3, 2025 Results on Nov 07, 2025 Cellectis S.A. announced that they will report Q3, 2025 results After-Market on Nov 07, 2025 Tillkännagivande • Oct 31
Cibus, Inc. to Report Q3, 2025 Results on Nov 13, 2025 Cibus, Inc. announced that they will report Q3, 2025 results on Nov 13, 2025 Tillkännagivande • Sep 26
Factor Bioscience Files Complaint Against Cellectis, Inc. and Astrazeneca Alleging Infringement of Foundational Gene-Editing Patents Factor Bioscience Inc. (Factor) announced a complaint filed against Cellectis Inc., Cellectis SA, AstraZeneca PLC, AstraZeneca Ireland Limited, and AstraZeneca Holdings B.V. In the complaint, Factor alleges that Cellectis transformed its research program after learning about Factor's patented mRNA TALENs technology in 2013 and proceeded to illegally exploit that technology, including in its partnership with AstraZeneca, by infringing Factor's patents. The lawsuit focuses on the infringement of Factor's U.S. Patent Nos. 10,662,410, 10,829,738, and 10,982,229 – infringement that Cellectis has conducted itself and through a series of partnerships, including with AstraZeneca. For the past 14 years, Factor and its licensees have made tremendous strides towards making available breakthrough allogeneic cell therapies, including groundbreaking products for the treatment of cancer. Factor remains committed to increasing the accessibility of innovative therapeutic products through its internal development programs and in collaboration with its licensees and strategic partners. Tillkännagivande • Jul 29
Cellectis S.A. to Report Q2, 2025 Results on Aug 04, 2025 Cellectis S.A. announced that they will report Q2, 2025 results After-Market on Aug 04, 2025 Tillkännagivande • Jun 27
Cellectis S.A. Announces Board Changes During the Cellectis S.A.'s Combined General Meeting of Shareholders on June 26, 2025, André Muller was appointed as a Director of the Company’s Board of Directors, effective immediately. In addition, at the close of the Combined General Meeting of Shareholders, the term of Axel-Sven Malkomes expired and the previously announced resignation of Pierre Bastid became effective. In connection with the above-mentioned changes to the Board of Directors, the Board of Directors have appointed André Muller (Chair), Donald Bergstrom, and Rainer Boehm as the members of the Company’s Audit Committee. Each of Messrs. Muller, Bergstrom and Boehm is independent. Pharmaceuticals Ltd. a listed Swiss biotech company. Previously, Mr. Muller served as Chief Financial Officer of Idorsia Pharmaceuticals Ltd. and Actelion Pharmaceuticals Ltd. He held various financial positions at Pierre Fabre SA, an international pharmaceutical and dermo- cosmetics company. Mr. Muller holds a Master's degree in Business Administration from the EMLYON Business School in Lyon. Tillkännagivande • May 22
Cellectis S.A., Annual General Meeting, Jun 26, 2025 Cellectis S.A., Annual General Meeting, Jun 26, 2025. Location: 11 rue watt 4th floor, 75013, paris France Tillkännagivande • Apr 29
Cellectis Presents Non-Viral Gene Editing and Base Editing Innovation at the ASGCT Annual Meeting Cellectis unveils research data on TALEN®?-mediated non-viral transgene insertion for advancing cellular and gene therapies, and advancements in genetic editing using TALE base editors (TALEB), at the Society of Gene and Cell Therapy (ASGCT) annual meeting, that will be held on May 13-17, 2025 in New Orleans. The data are presented in two posters: TALEN®?- Mediated non-viral Transgene Insertion for the Advancement of Cellular and Gene Therapies. Cell and gene therapy approaches can use gene-editing tools and introduce transgenes to modify disease-associated genes, thus providing a potential therapeutic solution for a wide array of diseases. In this work, Cellectis combines TALEN®?- mediated gene editing with non-viral delivery of transgene for advancing cellular and gene therapies. and explores gene insertion-efficacy and cellular health using single-stranded DNA (ssDNA) for payload delivery in different cell types. This innovative approach has the potential to address the challenges associated with traditional lentiviral viral methods or AAV-mediated transgene insertion such as manufacturing constraints, potential genomic toxicities or limited payload size. Research data show: Non-viral methods for gene editing: TALEN®? mediated gene editing combined with non-viral templates (linear and circular bDNA) can be used for highly efficient gene insertion in T-cells as well as hematopoietic stem and progenitor cells (HSPCs) promoting viability and insertion specificity. Advantages of Circular bDNA over viral vectors: Transcriptomic analysis and in vivo data demonstrate that bssDNA-mediated cell engineering allows better maintenance of HSPC fitness as well as more stable gene editing, compared to traditional viral donor template-mediated transgene delivery. The implementation of these gene-editing techniques holds significant potential for the development of next-generation therapies, aiming to provide alternative efficient, and safe therapeutic options for patients with cancer, autoimmune diseases, monogenic disorders, and various other conditions. TALE base editors (TaleB) are fusions of a transcription activator-like effector domain (TALE), split-DddA deaminase halves, and a uracil glycosylase inhibitor (UGI). The C-to-T class of TALEB edits double-stranded DNA by converting a cytosine (C) to a thymine (T) and does not involve DNA strandNick. This method also takes advantage of a highly precise and efficient knock-in of bODN in primary T cells to develop an assay to assess how the composition and spacer variations of target sequences affect TALEB activity/efficiency. Research data show: Efficiency of C-to-T editing: TALEB enables efficient conversion of C to T. Variations in target sequences and surrounding bases affecting editing efficiency. An educated choice of the TALEB architecture further allows to control the editing outcome. Assessment of off-target editing risks: Studies have been conducted to evaluate off-target editing, showing no detectable editing in primary cells at previously described sites, highlighting the specificity of TALEB for potential therapeutic applications. Tillkännagivande • Apr 25
Cellectis S.A. to Report Q1, 2025 Results on May 08, 2025 Cellectis S.A. announced that they will report Q1, 2025 results on May 08, 2025 Tillkännagivande • Mar 08
Cellectis S.A. to Report Q4, 2024 Results on Mar 13, 2025 Cellectis S.A. announced that they will report Q4, 2024 results at 5:40 PM, Central European Standard Time on Mar 13, 2025 Tillkännagivande • Nov 06
Cellectis Presents Multiple Strategies to Enhance Car T-Cell Efficacy in Solid Tumors at the SITC Annual Meeting Cellectis announced that pre-clinical data to enhance CAR T cell activity against solid tumors while preventing potential toxicity, will be presented at the Society for Immunotherapy of Cancer’s 39th Annual Meeting (SITC), that will take place on November 6-10, 2024 in Houston, Texas. The data will be presented in a poster: Title: Breaking barriers in solid tumors with SMART allogeneic CAR T-cells. Date /Time: November 9th, 2024 from 9:00am to 8:30pm ET. Presenter: Beatriz Aranda-Orgilles, Associate Director, Immuno Oncology at Cellectis. Poster number: 254. Despite the success of CAR T-cell therapies treating blood cancers, these cutting-edge technologies continue to face obstacles in solid tumors. A main barrier is the hostile tumor microenvironment (TME), which forms an
immunosuppressive barrier and restricts T-cell infiltration into the tumor. Other contributing causes such as
tumor antigen diversity or low expression of CAR-targeted tumor-associated antigens (TAA) in normal tissues can
lead to antigen escape or on-target off-tumor toxicity, respectively. These factors can lead to relapse and
pose a challenge for therapeutic safety. Cellectis presents several strategies using TALEN®-mediated gene editing to generate allogeneic CAR T-cells while repurposing PD-1 function with tightly regulated functionalities, with the objective to increase efficacy and avoid potential toxicities in solid tumors. Using in vitro and in vivo techniques, it show that TME-induced FAP-dependent expression of CAR tethers cytotoxic activity to the tumor area and can minimize potential "on-target off-tumor" toxicities. In a parallel approach, it integrate IL-12 into PD-1 regulatory elements to confine IL-12 to the TME and inactivate TGFBR2 to overcome TGFB1-mediated resistance. This strategy enhances proliferation and infiltration of CAR T-cells, while reducing tumor burden and limiting side effects. Overall, its data show the potential of repurposing immune pathways to create armored allogeneic CAR T-cells with enhanced activity in immunosuppressive microenvironments while minimizing potential safety issues. These approaches have the potential to provide a therapeutic option for patients with solid malignancies. Tillkännagivande • Oct 31
Cellectis S.A. to Report Q3, 2024 Results on Nov 04, 2024 Cellectis S.A. announced that they will report Q3, 2024 results After-Market on Nov 04, 2024 Tillkännagivande • Aug 07
Cibus, Inc. Achieves Positive Initial Field Trial Results for Stacked Gene Editing Herbicide Tolerant Traits in Rice Cibus Inc. announced that it has positive initial field trial results of a novel weed management solution for rice farmers. Initial results have shown that using two herbicides provided an excellent weed management system in rice. If ultimately successful, stacking gene edited herbicide tolerant (HT) traits in a rice variety would enable the use of two herbicides with difference modes of action to control weeds. Rice containing stacked gene edited herbicide tolerant traits would allow farmers ultimately to use a comprehensive weed management solution. This stacked trait product would give farmers an excellent solution to manage weeds that impact yield and quality and would be applicable to many rice markets globally, providing a broader weed control solution to further reduce the risk of resistant weeds that often occur over time when using one mode of action herbicide. Cibus believes stacked traits are a key element of modernizing crop breeding. Gene editing provides the ability to develop complex traits more efficiently and to address major farming yield constraints such as weeds, disease and inefficient fertilizer use. Cibus is seeking to address each of these problems in its trait development pipeline. Importantly, Cibus is a leader in the development of gene edited traits in plants like herbicide tolerance in Rice. The Company's plant trait intellectual property is developed using its Rapid Trait Development System (RTDS®?) including Gene Repair Oligonucleotides (GRON) and molecular scissors including Transcription activator-like effector nucleases (TALENs). Tillkännagivande • Jun 14
Cellectis Announces the Publication of A Scientific Article in Nature Communications Cellectis S.A. announced the publication of a scientific article in Nature Communications, unveiling a non-viral gene therapy approach for sickle cell disease. Sickle cell disease (SCD) is one of the most common inherited diseases worldwide. SCD is caused by a single point mutation in the HBB gene, which encodes the subunit of hemoglobin (Hb). normally, red blood cells adopt a disc-like shape that allows them to move easily through the blood vessels and deliver oxygen throughout the body. In sickle cell disease, red blood cells become crescent or sickle"-shaped, a dysfunctional state that impacts blood flow, oxygen delivery and triggers multiple debilitating symptoms including intense pain crisis. Cellectis leverages TALEN technology and a non-viral gene repair template delivery to develop a clinically relevant gene editing process in hematopoietic stem and progenitor cells (HSPCs). This process enables efficient HBB gene correction with high precision, specificity and minimal genomic adverse events. Applying this HBB gene correction process to SCD patient-HSPCs results in over 50% expression of normal adult hemoglobin in mature red blood cells and in the correction of sickle phenotype, without inducing -thalassemic phenotype. Edited HSPCs engraft efficiently in an immunodeficient murine model and maintain clinically relevant levels of HBB gene correction events. This comprehensive preclinical data package sets the stage for the therapeutic application of autologous gene corrected HSPCs to address SCD. Tillkännagivande • May 29
Cellectis S.A. to Report Q1, 2024 Results on May 28, 2024 Cellectis S.A. announced that they will report Q1, 2024 results After-Market on May 28, 2024 Tillkännagivande • May 26
Cellectis S.A., Annual General Meeting, Jun 28, 2024 Cellectis S.A., Annual General Meeting, Jun 28, 2024. Location: 11 rue watt, paris France Tillkännagivande • May 03
Cellectis Announces Chief Financial Officer Changes Cellectis announced the resignation of Mr. Bing Wang from his position of the company with immediate effect, and the concomitant appointment of Mr. Arthur Stril as interim Chief Financial Officer, replacing Mr. Bing Wang. Mr. Stril joined the company in 2018 as Vice President, Corporate Development, and was appointed Chief Business Officer in 2020. He has been managing the company’s business development and portfolio management teams and most recently led the execution of the company’s strategic collaboration and investment agreements with AstraZeneca. As interim Chief Financial Officer, Mr. Stril will oversee the finance and investor relations functions, and continue to oversee the business development functions. He will remain based in the company’s New York office. Mr. Stril began his career at the European Commission’s Directorate-General for Competition, controlling global pharmaceutical mergers. He later became head of the Hospital Financing Unit at the French Ministry of Health. Since 2023, Mr. Stril serves on the board of directors of Primera Therapeutics as a director designated by the company. Mr. Stril graduated with a Master of Mathematics from Cambridge University and a Master of Physics from the École Normale Supérieure and holds immunotherapy and immuno-oncology diplomas from the University of Paris. Mr. Stril is also a member of the French Corps des Mines and is on the Board of Advisors of non-profit Life Science Cares. Tillkännagivande • Apr 23
Cellectis Presents Novel TALEN® Editing Processes Enabling Highly Efficient Gene Correction and Gene Insertion in HSPCs Cellectis will present first data exploring novel TALEN® editing processes in hematopoietic stem and progenitor cells (HSPCs) at the American Society of Gene and Cell Therapy (ASGCT) being held on May 7 to 11, 2024. Poster presentation: Intron Editing of HSPC Enables Lineage-Specific Expression of Therapeutics: Gene therapy using edited hematopoietic and progenitor stem cells (HSPCs) has the potential to provide a lifelong supply of genetically encoded therapeutics. The most therapies are impacted with the difficulty to cross the blood-brain barrier (BBB). The BBB is a continuous endothelial membrane that, along with pericytes and other components of the neurovascular unit, limits the entry of toxins, pathogens, protein and small molecules to the brain. Cellectis has developed a TALEN® mediated promoter-less intron editing technology that enables the expression of a therapeutic transgene exclusively by monocyte derived from edited HSPCs. The edited cells containing genetically encoded therapeutic proteins have the capacity to cross the blood-brain barrier and secrete the corresponding therapeutic within the brain. This novel editing approach is an important addition to the HSPC gene editing toolbox that might unlock new strategies for the treatment of metabolic and neurological diseases. Research data showed that: Intron editing can be performed within B-cell, T-cell, Monocyte-specific endogenous genes (CD20, CD4 and CD11b, respectively); Intron editing allows expression of transgenes in a lineage-specific manner without markedly impacting the expression of the endogenous gene targeted; Editing of CD11b intron using a therapeutic transgene encoding IDUA (the enzyme missing in Type-1 Mucopolysaccharidosis patients) enables to restrict the expression of IDUA to the myeloid lineage; Edited HSPCs efficiently engraft in the bone-marrow of immunodeficient mice and differentiate into edited myeloid cells that can cross the BBB and populate the brain; The intron editing strategy described in this work is versatile and could be potentially used to vectorize multiple genetically encoded-therapeutic proteins to the brain and thus address multiple metabolic and neurological disorders. Poster presentation: Circularization of Non-Viral Single-Strand DNA Template for Gene Correction and Gene Insertion Improves Editing Outcomes in HSPCs: The most of the gene insertion approaches used to edit HSPCs ex vivo are hampered by the low efficiency of DNA template delivery into their nucleus. Cellectis has developed and optimized a novel gene editing process, leveraging the TALEN® technology and circular single strand DNA template delivery, enabling highly efficient gene insertion in HSPCs. Research data showed that: Non-viral single strand DNA delivery associated to TALEN® technology allows gene insertion in long-term repopulating hematopoietic stem cells; Circularization of the single strand DNA further increases the rates of gene insertion without impacting cellular viability and fitness of HSPCs, facilitating the development of next generation of ex vivo cell therapies. Tillkännagivande • Dec 23
Cellectis S.A. Announces Board Appointments Cellectis S.A.'s shareholders also approved the appointments of Mr. Marc Dunoyer and Dr. Tyrell Rivers as directors of the Cellectis board of directors, which appointment remains subject to the completion of the Additional Investment. Mr. Marc Dunoyer is Chief Strategy Officer of AstraZeneca and Chief Executive Officer of Alexion, AstraZeneca Rare Disease. He had previously served as an Executive Director and AstraZeneca’s Chief Financial Officer from November 2013. Mr. Marc Dunoyer’s career in pharmaceuticals, which has included periods with Roussel Uclaf, Hoechst Marion Roussel and GSK, has given him extensive industry experience. He is a qualified accountant and joined AstraZeneca in 2013, serving as Executive Vice-President, Global Product and Portfolio Strategy from June to October 2013. Prior to that, he served as Global Head of Rare Diseases at GSK and (concurrently) Chairman, GSK Japan. Mr. Dunoyer is a member of the Boards of Orchard Therapeutics Plc and JCR Pharmaceuticals. He holds an MBA from HEC Paris and a Bachelor of Law degree from Paris University. Dr. Tyrell Rivers is Executive Director of Corporate Ventures at AstraZeneca, where he is responsible for creating and executing innovative, value-enhancing business strategies. Prior to assuming this role in 2014, he worked at MedImmune Ventures, specializing in life science investing. Earlier in his career, Dr. Rivers held various positions at Merck & Co., where he led technical support for commercial vaccines and directed global business initiatives for accessing key technologies for research and development. He currently serves as a Board member of ADC Therapeutics, Cerapedics, and Quell Therapeutics. Dr. Rivers holds his B.S. in Chemical Engineering from the Massachusetts Institute of Technology, a Ph.D. in Chemical Engineering from the University of Texas at Austin, and an M.B.A. from the New York University Stern School of Business. Tillkännagivande • Nov 02
Cellectis S.A. to Report Q3, 2023 Results on Nov 06, 2023 Cellectis S.A. announced that they will report Q3, 2023 results After-Market on Nov 06, 2023 Tillkännagivande • Oct 13
Cellectis and Imagine Institute Publish A Proof-Of-Concept Study of A Gene Surgery Candidate to Treat Activated Phosphoinositide 3-Kinase ? Syndrome Type 1 (APDS1) Cellectis announced the publication of a new research paper in Molecular Therapy -- Methods & Clinical Development, demonstrating the efficacy of its TALEN-mediated gene correction of mutated PIK3CD gene in APDS1 T-cells. The research work described in this article was jointly conducted by Imagine Institute and Cellectis teams. About APDS1: Activated phosphoinositide 3-kinase syndrome (also known as APDS type 1 or APDS1) is a rare but devastating disease caused by gain-of-function mutations in the PIK3CD gene and resulting in a combined immunodeficiency. Approved treatments for APDS1 consist in prophylactic measures including long term antibiotics and Ig (immunoglobulin) replacement therapy. Allogeneic hematopoietic stem/progenitor cell (HSPC) transplantation has been proposed as a definitive treatment for APDS1. However, the lack of compatible donor as well as graft failure, graft instability, and poor graft function are still major challenges that must be overcome to reach a positive therapeutic outcome. Thus, so far there are neither optimal nor long-term therapeutic solutions for APDS1 patients and new alternative treatments are highly regarded. The study published here aims at exploring an alternative therapeutic strategy by correcting the mutated PIK3CD gene associated to APDS1 by gene editing. This article describes a TALEN®-mediated gene insertion strategy that allows targeted correction of the dominant gain-of-function mutation of the PIK3CD gene by insertion of a functional sequence in a precise manner. Results show efficient gene insertion in APDS1 patients’ T-cells, normalization of PI3K signaling and rescue of T-cell cytotoxic functions. Preclinical results demonstrated that: The PIK3CD gene can be efficiently corrected by TALEN®-mediated gene insertion of the functional PIK3CD DNA sequence vectorized by AAV, in healthy donor and APDS1 patient T-cells. TALEN®-mediated PIK3CD gene correction rescues PI3K signaling in APDS1 patient T-cells. TALEN®-mediated PIK3CD gene correction normalizes the transcriptomic status of APDS1 patient CD8+ T-cells and rescues their cytolytic activity. In summary, demonstrate that the PIK3CD dominant gain of function mutation associated to APDS1 can be successfully corrected in APDS1 patient T-cells using TALEN® gene editing and AAV-based DNA repair matrix. This correction rescues the cytolytic function of APDS1 T-cells, normalizes their intracellular phospho-AKT levels found at basal and at activated states as well as the transcriptomic signature of certain genes involve in T-cells’ cytolytic function, activation, and fitness. Tillkännagivande • Jul 29
Cellectis S.A. to Report Q2, 2023 Results on Aug 03, 2023 Cellectis S.A. announced that they will report Q2, 2023 results at 5:40 PM, Central European Standard Time on Aug 03, 2023 Tillkännagivande • Jun 01
Cellectis Publishes an Article in Cancer Immunology Research Demonstrating Preclinical Evidence of UCART20x22 Product Candidate to Target a Broad Spectrum of Patients with B-Cell Malignancies Cellectis published an article in Cancer Immunology Research demonstrating pre-clinical proof-of-concept data of UCART20x22 product candidate, Cellectis’ first allogeneic dual CAR T-cell targeting the CD20 and CD22 antigens, to overcome current mechanisms of resistance to CAR T-cell therapies in B-cell Non-Hodgkin lymphoma (B-NHL), while providing a potential alternative to CD19 directed therapy. B-cell Non-Hodgkin lymphoma (B-NHL) remains one of the most common cancers worldwide, with reports an estimate of 544,000 new cases and 260,000 deaths worldwide in 2020. Despite the efficacy of current CAR T-cell therapies, studies on patients treated with autologous CAR T-cells are revealing several causes for relapses that includes: antigen loss, low antigen expression or insufficient CAR T-cell potency and persistence, among others. While several suitable targets to treat B-cells malignancies have been identified, CD19 has been the focus of attention leading to a crowded space with limited therapeutic alternatives for CD19 low or negative relapses. The limited amount of eligible treatment options after relapse from autologous CAR T-cell therapy or for patients not eligible for autologous therapies, underscores the urgent need to develop novel therapies with the potential to improve patient outcome. To address these challenges, Cellectis developed UCART20x22, its first allogeneic dual CAR T-cell product candidate targeting two validated antigens commonly expressed in B-cell malignancies, CD20 and CD22, and whose expression is preserved after CD19 CAR T-cell treatment. Cellectis provides pre-clinical proof of concept demonstrating potent and sustained activity of different designs of allogeneic CD20xCD22 CAR in vitro and in vivo against various antigen combinations and models recapitulating antigen escape, a current challenge in the field that can lead to treatment failure. Moreover, UCART20x22 is developed to be available off-the-shelf and to offer a solution for patients whose T-cells are not functional or for which autologous manufacturing fails. Preclinical data showed that: The use of a bicistronic vector favors the generation of dual CAR T-cells co- expressing both CD20 and CD22 CARs CAR T-cells efficiently and persistently eradicate double positive tumor cells over time. More importantly, compared to the single CAR, the dual CAR displayed similarly strong cytolytic activity over time against tumor cells expressing a single antigen, validating the benefit of using a dual CAR approach. Both CD20xCD22 CAR versions tested in this study potently targeted tumor cells in vivo in a dose dependent manner, with both doses of 3 and 10 million CAR T-cells achieving complete tumor clearance. Xenograft models mimicking antigen escape with an aggressive lymphoma model demonstrate that the dual CD20xCD22 CAR is capable to eliminate all tumors despite of losing one antigen, thus providing a potential solution for this challenge in the field. Bone marrow and spleen analysis of the surviving animals treated with the dual CAR at the end of the study, revealed that dual CAR T-cells efficiently eradicated the tumor and are capable to persist in the bone marrow for longer than one hundred days Primary NHL samples with variable levels of CD20 and CD22 can successfully be eradicated with the dual CD20xCD22 CAR suggesting that UCART20x22 has the potential to reach a large patient population. Full tumor elimination is achieved in a dose dependent manner in a Patient-Derived Xenograft (PDX) model recapitulating mantle cell lymphoma at day 20 with a dose of 3 million CAR T-cells or higher. UCART20x22 features TALEN®-mediated disruptions of the TRAC gene (to minimize the risk of graft-versus-host disease) and of the CD52 gene (to permit use of a CD52-directed monoclonal antibody in patients’ lymphodepletion regimen) to enhance CAR T engraftment, expansion and persistence. UCART20x22 is Cellectis’ first product candidate fully designed, developed and manufactured in-house at Cellectis. UCART20x22 is evaluated in the NATHALI-01 Phase 1/2a clinical study in patients with r/r B-NHL (NCT05607420). Tillkännagivande • May 23
Cellectis S.A., Annual General Meeting, Jun 27, 2023 Cellectis S.A., Annual General Meeting, Jun 27, 2023, at 14:30 Central Europe Standard Time. Location: Biopark auditorium, 11 rue Watt 4th floor, 75013 Paris France Agenda: To consider and approve the annual financial statements for the financial year ended December 31, 2022; to consider auditors’ report on the consolidated financial statements for the financial year ended December 31, 2022; to consider management report of the Group and presentation by the auditor of the annual financial statements for the financial year ended December 31, 2022; to consider and approve the consolidated financial statements for the financial year ended December 31, 2022; to consider appropriation of results for the financial year ended December 31, 2022; and to consider other business matters. Tillkännagivande • May 18
Cellectis S.A. Presents Clinical Data on AMELI-01 and Preclinical Data on Multiplex Engineering for Superior Generation of CAR T- Cells at ASGCT 2023 Cellectis S.A. presented clinical data on its Phase 1 AMELI-01 clinical trial (evaluating UCART123) that were unveiled in an oral presentation at the 64 American Society of Hematology (ASH) annual meeting, as well as preclinical data on multiplex engineering for superior generation of CAR T-cells, at the American Society of Gene and Cell Therapy (ASGCT) 2023 Annual Meeting. AMELI-01 is a Phase 1 open-label dose-escalation trial evaluating the safety, tolerability, expansion and preliminary activity of UCART123 given at escalating dose levels after lymphodepletion (LD) with either fludarabine and cyclophosphamide (FC) or FC with alemtuzumab (FCA) in patients with relapsed or refractory acute myeloid leukemia (r/r AML). The oral presentation reviewed preliminary data from patients who received UCART123 at one of the following dose levels: dose level 1 (DL1) 2.5x10 cells/kg; dose level 2 (DL2) 6.25x10 cells/kg; intermediate dose level 2 (DL2i) 1.5x10 cells/kg; or dose level 3 (DL3) 3.30x10 cells/kg after lymphodepletion with FC ([n=8, DL1 DL3) or FCA ([n=9, DL2 & DL2i). The FCA LD regimen resulted in robust lymphodepletion for greater than 28 days in all patients. Seven out of nine patients demonstrated UCART123 expansion, with maximum concentration (C) ranging from 13,177 to 330,530 cells/g DNA, an almost nine-fold increase compared with FC LD, and a significant increase in area under the curve (AUC) (0-28 days) (p=0.04; FC 10.2 versus FCA 34.9). Cytokine release syndrome (CRS) occurred in eight patients in the FC arm and nine patients in the FCA arm. In the FC arm, one patient experienced Grade 3 immune effector cell-associated neurotoxicity syndrome (ICANS) and two patients experienced Grade 4 protocol-defined dose limiting toxicities (DLTs) secondary to CRS. In the FCA arm, two patients experienced Grade 5 DLTs secondary to CRS. Evidence of UCART123 anti-tumor activity was observed in four patients out of fifteen at DL2 or above with best overall responses in the FCA arm. Two out of eight patients (25%) at DL2 in the FCA arm achieved meaningful response: A patient who failed five prior lines of therapy experienced a durable minimal residual disease (MRD) negative complete response (CR) with full count recovery at Day 56 that continues beyond one year. A patient with stable disease achieved greater than 90% bone marrow blast reduction (60% to 5%) at Day 28. The preliminary data show that adding alemtuzumab to the FC LD regimen was associated with sustained lymphodepletion and significantly higher UCART123 cell expansion, which correlated with improved anti-tumor activity. Overall, these preliminary data support the continued administration of UCART123 after FCA lymphodepletion in patients with r/r AML. Based on observed UCART123 expansion patterns and cytokine profiles, pursuant to an amended protocol, a second dose of UCART123 is given after 10-14 days to allow for additional UCART123 expansion and clinical activity without the use of additional lymphodepletion. The UCART123 cell expansion from thesecond dose of UCART123, in the setting of reduced disease burden, is expected to be safe and allow for clearance of residual disease. Tillkännagivande • May 13
Cellectis Publishes Article in Frontiers in Immunology Unveiling Pre-Clinical Data on A Novel Treatment Paradigm for Successful Car T Immunotherapy Against Stroma-Rich Solid Tumors Cellectis published an article in Frontiers Bioenginnering, demonstrating the efficacy of its TALEN® engineered FAP UCART-cells in cancer-associated fibroblast (CAF) depletion, reduction of desmoplasia and tumor infiltration. Adoptive cell therapy based on chimeric antigen receptor-engineered T (CAR-T) cells has proven to be lifesaving for many cancer patients. However, its therapeutic efficacy has so far been restricted to only a few malignancies, with solid tumors proving to be especially recalcitrant to efficient therapy. Poor intra-tumor infiltration by T cells and T cell dysfunction due to a desmoplastic, immunosuppressive microenvironment are key barriers for CAR T-cell success against solid tumors. Cancer-associated fibroblasts (CAFs) are critical components of the tumor stroma, evolving specifically within the tumor microenvironment (TME). The CAF secretome is a significant contributor to the extracellular matrix and a plethora of cytokines and growth factors that induce immune suppression. Together they form a physical and chemical barrier which induces a T cell-excluding ‘cold’ TME. CAF depletion in stroma rich solid tumors can thus provide an opportunity to convert immune evasive tumors susceptible to tumor-antigen CAR T-cell cytotoxicity. Cellectis used its TALEN®-based gene editing platform to engineer non-alloreactive, immune-evasive UCAR T-cells targeting the unique CAF marker Fibroblast Activation Protein, alpha (FAP) to test whether FAP UCAR T-cell pre-treatment can make ‘cold’ tumors susceptible to subsequent tumor-antigen targeting CAR T-cells. Cellectis also generated non-alloreactive CAR T-cells against the tumor associated antigen (TAA) Mesothelin which is overexpressed in most solid tumors including mesothelioma and large sub-sets of ovarian, breast, pancreatic and lung adenocarcinomas. The combination treatment strategy was tested in a pre-clinical mouse model of triple-negative breast cancer (TNBC), an aggressive, stroma-rich breast cancer sub-type with poor prognosis and very limited treatment options at present. Tillkännagivande • May 12
Cellectis Announces Poster Presentation on BALLI-01 at the European Hematology Association (EHA) 2023 Cellectis announced the release of an abstract, which was accepted for presentation at the European Hematology Association (EHA) Hybrid Congress, taking place on June 8-15, 2023 in Frankfurt, Germany. The company will present, in a poster session, updated clinical and translational data on its BALLI-01 clinical trial (evaluating UCART22) in patients with relapsed/refractory B-cell acute lymphoblastic Leukemia (r/r B-ALL). BALLI-01 investigation UCART22 product candidate in r/r B-ALL: The abstract includes preliminary clinical data from the Phase 1/2a, open label dose-escalation BALLI-01, in patients with r/r B-ALL having received UCART22 following lymphodepletion (LD) with either fludarabine, cyclophosphamide (FC) or FC with alemtuzumab (FCA). The data show that UCART22 was well tolerated and clinical responses were achieved. UCART22 continues to have a good safety profile, with no serious treatment emergent adverse events (TEAEs) or DLTs reported. Overall, these data support the safety and preliminary efficacy of UCART22 in a heavily pretreated r/r B-ALL population. UCART22 is a genetically modified allogeneic T-cell product manufactured from healthy donor cells. Donor-derived T-cells are transduced using a lentiviral vector to express the anti-CD22 chimeric antigen receptor (CAR) and are further modified using Cellectis’ TALEN® technology to disrupt the T-cell receptor alpha constant (TRAC) and CD52 genes to minimize risk of graft-vs-host disease (GvHD) and allow use of an anti-CD52 antibody for lymphodepletion (LD). Tillkännagivande • Feb 08
Cellectis S.A. has completed a Follow-on Equity Offering in the amount of $22 million. Cellectis S.A. has completed a Follow-on Equity Offering in the amount of $22 million.
Security Name: American Depositary Shares
Security Type: Depositary Receipt (Common Stock)
Securities Offered: 8,800,000
Price\Range: $2.5
Discount Per Security: $0.15 Tillkännagivande • Jan 22
Cellectis S.A. announced that it has received $20 million in funding from Cytovia Therapeutics, Inc. Cellectis S.A. announced a private placement and signed an agreement with Cytovia Therapeutics, Inc. for the gross proceeds of $20,000,000 (€18,458,698) on January 20, 2023. The company issued convertible notes in the transaction. Tillkännagivande • Jan 05
Cellectis S.A. Announces the Resignation of Alain Godard as a Member of the Board On December 31, 2022, Alain Godard informed the board of directors (the “Board”) of Cellectis S.A. (the “Company”) of his resignation as a member of the Board, effective immediately. 
