Data To Be Presented on Gamida Cell Natural Killer (NK) Cell Therapy Candidate GDA-201 at the International Society for Cell & Gene Therapy 2023 Annual Meeting
New data for batch-to-batch variability and cytotoxicity of GDA-201 show long term stability and unique phenotype of allogeneic NAM-NK cell therapy
GDA-201 is in an ongoing Phase 1/2 clinical trial for non-Hodgkin lymphoma
Additionally, a poster will be presented with data from Gamida Cell’s pre-clinical NK cell therapy candidate GDA-501, an engineered intrinsic NK cell with a CAR modification targeting the HER2 protein.
“The data being presented at ISCT add to the body of evidence demonstrating the power of our nicotinamide (NAM) technology to enhance and expand cells,” said
Additional details about the presentations are as follows:
Title: GDA-201: Phenotypic and Functional Characterization of Cryopreserved Nicotinamide-Expanded Allogeneic Natural Killer Cells Demonstrate an Activated and Non-exhausted Phenotype
Abstract Number: 36
- Highlights: This study investigated the phenotype and function of GDA-201, NK cells expanded using Gamida Cell’s proprietary NAM technology. NAM-NK demonstrated increased expression of lymphoid homing marker CD62L and decreased levels of lineage exhaustion markers CD57 and CD161 compared with NK cells expanded in the absence of NAM. Batch-to-batch variability of 18 batches of cryopreserved formulation of GDA-201 from 18 donors demonstrated an overall variability of ≤25% in critical parameters including viability, phenotyping and cytotoxicity.
Title: GDA-501 HER2 Chimeric Antigen Receptor Natural Killer Cells: Dual Cytotoxicity in Solid Tumors Mediated via HER2 and TRAIL
Abstract Number: 1225
- Highlights: GDA-501, an expanded, enhanced and engineered NAM HER2-CAR NK cell, showed high levels of TNF-related apoptosis-inducing ligand (TRAIL) expression, suggesting possible meditation of target cell apoptosis. Compared with non-engineered NK cells cultured with NAM, GDA-501 cells displayed increased cytotoxicity against HER2+ tumor cells. When TRAIL was neutralized on GDA-501, a decrease in cytotoxicity was observed. These data suggest that the cytotoxic effect of GDA-501 may be mediated by dual mechanisms: HER2 binding by the HER2-CAR and apoptosis mediated by TRAIL.
Gamida Cellannounced it would discontinue the development of GDA-501 in March 2023.
GDA-201 is an intrinsic NK cell therapy candidate being investigated for the treatment of hematologic malignancies. Preclinical studies have shown that GDA-201 may address key limitations of cultured NK cells by increasing cytotoxicity and in vivo retention as well as proliferation in the bone marrow and lymphoid organs. Furthermore, these data suggest GDA-201 may improve antibody-dependent cellular cytotoxicity (ADCC) and tumor targeting of NK cells. A multicenter Phase 1/2 study of GDA-201 for the treatment of non-Hodgkin lymphoma is ongoing (NCT05296525).
GDA-201 is an investigational cell therapy candidate, and its safety and efficacy have not been established by the FDA or any other health authority.
Omisirge® is a registered trademark of
Forward Looking Statements
This press release contains forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995, including with respect to the potentially life-saving or curative therapeutic and commercial potential of GDA-201. Any statement describing Gamida Cell’s goals, expectations, financial or other projections, intentions or beliefs is a forward-looking statement and should be considered an at-risk statement. Such statements are subject to a number of risks, uncertainties and assumptions including those related to clinical, scientific, regulatory and technical developments and those inherent in the process of developing and commercializing product candidates that are safe and effective for use as human therapeutics. In light of these risks and uncertainties, and other risks and uncertainties that are described in the Risk Factors section and other sections of Gamida Cell’s Quarterly Report on Form 10-Q filed with the
Investor and Media Contact: