Singlomics Biopharmaceuticals to Present New Preclinical Data from IL1RAP mAb at the AACR 2024 Annual Meeting

On March 30, 2024 Singlomics Biopharmaceuticals, a company committed to the discovery and development of antibody therapeutics for cancer and immune diseases using single-cell sequencing technologies, reported a poster presentation of preclinical data from IL1RAP mAb at the upcoming American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2024 taking place April 5-10 in San Diego, California (Press release, Singlomics Biopharmaceuticals, MAR 30, 2024, View Source [SID1234643983]).

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AACR Poster Presentations Details:
Title:DX2206, a humanized monoclonal antibody that targets IL1RAP, exhibits potent inhibition of IL-1 pathways and activities against tumors in vitro and in vivo

Session Category: Experimental and Molecular Therapeutics
Session Title: Cancer Treatment: New Technologies
Session Date and Time: Tuesday Apr 9, 2024 1:30 PM – 5:00 PM
Location: Poster Section 22
Poster Board Number: 3
Published Abstract Number: 5794

About DX2206

The Interleukin-1 Receptor Accessory Protein (IL1RAP) is found on cancer cells, stromal cells, and infiltrating immune cells within the tumor microenvironment (TME) of various cancers. It plays an important role in tumor development at various stages by activating IL-1 superfamily pathway. High expression of members of the IL-1 superfamily such as IL1RAP, IL-1, IL-36, and IL36R are negatively correlated with pan-cancer overall survival. Epitope analysis indicated that DX2206 binds to a unique epitope within IL1RAP domain 2. In vitro assays demonstrated that DX2206 inhibited the activities IL-1, IL-33, and IL-36 pathways, with sub-nanomolar IC50s. Simultaneously, DX2206 induced a potent killing effect in the ADCC assay. In NCI-H358 CDX model, DX2206 significantly inhibited tumor growth. Taking together, DX2206 emerges as an outstanding preclinical candidate for cancer therapy. IND enabling study was ongoing to expedite the candidate into clinic.