BOSTON--(BUSINESS WIRE)--Affini-T Therapeutics, Inc., a precision immunotherapy company unlocking the power of T cells against oncogenic driver mutations, today announced that data from its preclinical gene edited HLA-A*11:01 KRAS G12D (AFNT-212) and HLA-A*02:01 TP53 R175H T Cell Receptor (TCR) T cell therapy products for the treatment of solid cancers will be presented at the American Society of Gene & Cell Therapy (ASGCT) 27th Annual Meeting held in Baltimore, MD May 7-11.
“Our mission is to address the significant unmet needs of patients with hard-to-treat solid tumors by advancing precision immunotherapies that target oncogenic driver mutations,” said Loïc Vincent, Ph.D., Chief Scientific Officer, Affini-T Therapeutics. “We believe that our non-viral targeted knock-in platform, THRIVETM, will enable us to cost-effectively engineer safe and effective T cell therapy products. We look forward to presenting new data showing that THRIVETM-engineered A11 KRAS G12D-targeting TCR T cells (AFNT-212) and TP53 R175H-targeting TCR T cells demonstrated superior cytotoxicity against tumor cells relative to LVV-engineered cells both in vitro and in vivo, at ASGCT this year.”
Affini-T also announced that data from a genomic profiling dataset illustrating the low frequency of HLA loss of heterozygosity in cancer patients will be presented at ASGCT.
“TCR based therapies targeting cancer driver mutations recognize the human leukocyte antigen (HLA)/peptide complex on tumor cells,” said Dirk Nagorsen, M.D., Chief Medical Officer at Affini-T Therapeutics. “In this context, loss of heterozygosity (LOH) of HLA may be of interest but only in cases when the specific HLA allele that is presenting the targeted peptide is involved. Conversely, historical allele-agnostic HLA-LOH analyses, which assessed the loss of any MHC class I allele, would only be relevant in the setting of HLA-agnostic therapies, e.g., immune checkpoint inhibitors. We look forward to presenting data showing that the allele-specific HLA-LOH frequency is low, which suggests that allele-specific HLA-LOH frequency is unlikely to contribute significantly to clinical data readouts of TCR-based therapies.”
Poster presentation details are as follows:
Title: THRIVE TM Non-Viral Targeted Transgene Knock-In Platform Generates Specific and Potent TCR T Cell Products for the Treatment of Solid Cancers
Abstract #836, Session: G2 - Immune Targeting and Approaches with Genetically-Modified Cells and Cell Therapies
Session Date/Time: Wednesday, May 8, 2024, 12:00 PM – 7:00 PM
Presenting Author: Ankit Gupta, Ph.D., Senior Director, Gene Editing, Discovery, Affini-T Therapeutics
Title: Loss of Heterozygosity is Low for Specific HLA Alleles in Cancer Patients with Driver Mutations
Abstract #785, Session: F3 - Cancer – Targeted Gene and Cell Therapy
Session Date/Time: Wednesday, May 8, 2024, 12:00 PM – 7:00 PM
Presenting Author: Christian Roy, Ph.D., Associate Director, Precision and Translational Medicine, Affini-T Therapeutics
About Affini-T Therapeutics
Affini-T is a leading precision immunotherapy company targeting oncogenic driver mutations, beginning with KRAS, to develop potentially curative therapies for patients with solid tumors. We are advancing two distinct therapeutic modalities encompassing adoptive cellular therapies and bispecific T cell engagers, each designed to harness T cell immunity with unprecedented precision and potency against solid tumors. Our TCR-T cell therapy-enabling platforms utilize state-of-the-art engineering, synthetic biology, and gene editing capabilities to rewrite the rules of the tumor microenvironment and optimize T cell functions. Our bispecific T cell engager platform combines high throughput affinity maturation TCR discovery and biologics format constructions to target oncogenic driver mutations. Building on the world-class innovation inherent in our leadership team, founders, and technologies, we are powered to develop transformational medicines that last. For more information, visit affinittx.com and follow us on LinkedIn and X, formerly known as Twitter.
