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Chroma Medicine Highlights Data Demonstrating Durable Multiplex Epigenetic Editing to Enhance Allogeneic CAR T at 65th ASH Annual Meeting

Multiplex allogeneic epigenetic edits demonstrate elimination of graft-versus-host disease and resistance of CD8+T, CD4+T, and NK cell responses, while preserving genomic integrity

Chroma’s allogeneic approach has the potential to drive greater persistence of a CAR T relative to current allogeneic approaches in the clinic

Boston, December 10, 2023 – Chroma Medicine, Inc., (Chroma) a genomic medicine company pioneering single-dose epigenetic editing therapeutics, today presented data demonstrating the potential of its multiplex epigenetic editing platform to enhance functional allogeneic chimeric antigen receptor (CAR) T cells at the American Society of Hematology (ASH) 65th Annual Meeting in San Diego.

Allogeneic CAR T cell products offer advantages over autologous CAR T cells and have the potential to broaden access to cancer immunotherapy; however, their clinical effect remains limited by lack of durable response and challenges related to immunogenicity and graft-versus-host disease. Incorporating additional edits may help produce cells resistant to rejection—potentially improving allogeneic T cell persistence—but using editing technologies that rely on double- or single-stranded DNA breaks can result in unintended genomic changes. Chroma’s epigenetic editing technology has the potential to provide durable modulation of gene expression without cutting or nicking the DNA, making it well-suited for simultaneous targeting of multiple genes to enhance generation of persistent allogeneic CAR T cells.

“The data presented at ASH illustrate the tremendous potential of epigenetic editing to accelerate allogeneic CAR T approaches by enhancing functional allogeneic cells to avoid common genotoxic challenges observed in nuclease-based gene editing and base editing,” said Vic Myer, Ph.D., Chroma’s President and CSO. “We believe harnessing nature’s innate mechanism for gene regulation unlocks vast opportunity to efficiently, effectively, and simultaneously silence many target genes, and the data presented underscore the strength of this approach in ex vivo cell therapies.”

The poster presentation shows Chroma’s epigenetic editor in primary T cells induces durable silencing of T cell receptor and MHC class I and MHC class II expression, maintained through restimulation. The data also demonstrate that multiplex epigenetic editing of CAR T cells does not interfere with cytotoxic anti-tumor function, further highlighting the potential to create CAR T cell therapies with greater accessibility, durability, and efficacy for patients.

Details for Chroma’s poster presentation at the 2023 ASH Annual Meeting are as follows:

Title: Durable Multiplex Epigenetic Editing for Generation of Allogeneic CAR T Without Chromosomal Rearrangements
Presenter: Jamie Schafer, Ph.D., Associate Director, Ex Vivo Program Sciences, Chroma Medicine
Session: 703. Cellular Immunotherapies: Basic and Translational: Poster II
Session Date and Time: Sunday, December 10, 2023, 6:00 - 8:00p PT

The poster presentation is available on Chroma’s website.

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About Chroma Medicine

Chroma Medicine is a biotechnology company pioneering a new class of genomic medicines that harnesses epigenetics, nature’s innate mechanism for gene regulation, to deliver precise, programmable single-dose therapeutics while preserving genomic integrity. The company’s modular platform enables development of medicines that can address a wide range of complex diseases, whether they require silencing, activation, or targeting multiple genes at once. Chroma was founded by the world’s foremost experts in genomic research and is led by a veteran team of industry leaders and scientists with deep experience in genomic medicine, drug discovery, and development. For more information, please visit chromamedicine.com or follow the company on LinkedIn and X (formerly known as Twitter).

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2024 Chroma Medicine. All rights reserved.
2024 Chroma Medicine. All rights reserved.