iOmx Therapeutics to present new data on lead programs and I/O target screening platform at AACR 2024

  • OMX-0407: clinical-stage, spectrum selective SIK kinase inhibitor with dual effect on tumor growth and immune evasion
  • IOMX-0675: best-in-class antibody targeting immunosuppressive receptors LILRB1 & LILRB2 on immune cells
  • iOTarg screening platform: uncovering novel mechanisms of immune evasion in colorectal cancer

MARTINSRIED, Germany and MUNICH, Germany, April 03, 2024 (GLOBE NEWSWIRE) -- iOmx Therapeutics AG (iOmx), a clinical-stage biopharmaceutical company translating unexplored immune evasion biology into a growing pipeline of biomarker-enabled drug programs, today announces that it will present new data on its lead I/O drug candidates OMX-0407 and IOMX-0675, plus its proprietary iOTarg™ screening platform at the upcoming American Association for Cancer Research (AACR) Annual Meeting 2024 taking place from April 5-10, 2024, in San Diego, California.

"We are excited to share updates on our two lead I/O programs targeting a broad range of solid tumor indications and our high-throughput target screening platform – iOTarg. The data presented will provide insights into the mode of action of our clinical-stage candidate OMX-0407 and for the first time publicly introduce our second lead candidate IOMX-0675, a highly differentiated, best-in-class antibody that impressively re-activates adaptive and innate immunity in the tumor microenvironment,” said Dr. Apollon Papadimitriou, CEO of iOmx Therapeutics. ”Together with the new targets identified by our screening platform, this marks a step forward in our mission to uncover novel immune evasion mechanisms and develop targeted therapies that significantly improve patient outcomes in cancer treatment.”

Details of the abstracts and the poster presentations:

OMX-0407: spectrum-selective SIK kinase inhibitor with dual effect on tumor growth and immune evasion
An in-depth mode of action analysis demonstrated that spectrum selective kinase inhibitor OMX-0407 drives cell-cycle arrest in vitro and in vivo. Through tyrosine kinase signaling, OMX-0407 interferes with cell cycle regulation and cancer cell proliferation. Complementary to this direct mode of action, OMX-0407 also potentiates tumor cell apoptosis in response to death receptor ligands including tumor necrosis factor through salt inducible kinase signaling. With this dual mode of action, OMX-0407 has shown striking single-agent efficacy in multiple pre-clinical tumor models. The spectrum selective SIK kinase inhibitor is currently in Phase I clinical trial.

Title: Salt-inducible kinase inhibitor OMX-0407 drives cell-cycle arrest in vitro and in vivo: An in-depth MoA analysis by phospho-proteomics
Abstract number: 514/11
Session title: Cell cycle, transcription regulation, and anticancer drug action, Section 21
Date and time: April 7, 2024; 1:30 PM – 5:00 PM PDT

IOMX-0675: a best-in-class cross-specific antibody repolarizing the tumor microenvironment
IOMX-0675 addresses a key immunoregulatory receptor family expressed on myeloid cells and other immune cells. This receptor superfamily, the leukocyte immunoglobulin-like receptor (LILRs), contains both immune-suppressive and immune-activating receptors, displaying very high structural homology. The antibody IOMX-0675 targets the two most potent immunosuppressive members of this family, namely LILRB1/2. In a dual targeting approach, iOmx has generated a fully human, cross-specific, high-affinity ligand-blocking antibody that simultaneously neutralizes these two key immune-suppressive receptors, while sparing the closely related immune-activating LILR family members, LILRA1 and LILRA3. Dual targeting of these receptors on myeloid cells results in a pronounced anti-tumor immune response, retuning the tumor microenvironment and activating T cells against cancer cells. The specificity and dual approach of IOMX-0675 indicate its potential as a promising candidate to provide a new treatment avenue for patients with limited options due to resistance to current therapies.

Title: IOMX-0675, a LILRB1 and LILRB2 cross-specific anybody, effectively repolarizes immunosuppressive myeloid cells and activates T cells leading to potent tumor cell killing
Abstract number: 1362 / 13
Session title: Immune Checkpoints and Inhibitory Molecules 1, Section 3
Date and time: April 8, 2024; 9:00 AM – 12:30 PDT

iOTarg™ Screening Platform: Uncovering Colorectal Cancer Evasion Mechanisms
iOmx's high-throughput iOTarg™ platform reveals novel mechanisms of colorectal cancer evasion of antigen-specific T cell killing. This pioneering research identifies new therapeutic targets, offering prospects for expanding treatment options in immune oncology.

Title: iOTarg™ screening platform reveals novel mechanisms of colorectal cancer evasion from antigen-specific tumor cell killing by T cells
Abstract number: LB080 / 16
Session title: Immunology 1, Section 54
Date and time: April 7, 2024; 1:30 PM – 5:00 PM PDT

About iOmx Therapeutics
iOmx Therapeutics ( is a clinical-stage company that harnesses deep tumor and myeloid biology insights, along with its proprietary iOTarg™ target screening platform, to generate novel treatments for the most prevalent solid tumor indications. The company is translating unexplored immune evasion biology into a growing pipeline of biomarker-enabled drug programs. Focused on developing drugs with single agent activity, iOmx is creating potential new backbone therapies in a modality-open fashion. By applying its comprehensive drug discovery & development expertise, iOmx is committed to shaping the future of cancer therapy. The company’s lead program OMX-0407, is a proprietary first-in-class spectrum-selective SIK kinase inhibitor, currently being investigated in Phase I clinical trials to treat multiple solid tumors. iOmx is backed by international venture capital investors, such as Athos Biopharma, Sofinnova Partners, Wellington Partners, MIG Capital and M Ventures. iOmx is based in Martinsried/Munich, Germany.

Media contact
MC Services AG
Katja Arnold, Julia von Hummel, Shaun Brown
T: +49(0)89 2102280