Targeting the Biology that Drives Myelodysplastic Syndromes


Why Relapsed / Refractory High-Risk MDS

This intersection of compelling biology and significant need has shaped our commitment to relapsed/refractory high-risk myelodysplastic syndromes (MDS).

Hypomethylating agents are the standard of care for high-risk MDS, yet the vast majority of patients are refractory to or relapse after treatment. In relapsed/refractory high-risk MDS, only one treatment has been approved in the past two decades, and it targets a mutation found in ~3% of patients.

Our first-in-class antibody, LYT-200, engages a foundational driver of MDS. This approach has the potential to introduce a mutation-agnostic treatment option into the whitespace of the relapsed/refractory treatment setting.

A Foundational Target

Galectin-9 is an important oncogenic driver and potent immunosuppressor that plays a central role in some of the most difficult-to-treat cancers. It has been shown to support malignant stem cell and blast cell survival while also suppressing anti-tumor immune activity. This convergence of tumor and immune biology provides a differentiated opportunity to intervene in the foundational mechanisms that drive disease.

In myelodysplastic syndromes (MDS), galectin-9 is produced by malignant blast cells. Galectin-9 levels increase with disease progression and leukemic transformation, and elevated levels are associated with shorter survival. Together, these findings suggest that galectin-9 is not simply a marker of disease, but may contribute to the underlying biology of MDS.

A Mutation-Agnostic, Dual Mechanism of Action

LYT-200 is a fully human IgG4 monoclonal antibody against galectin-9. It is designed to address the bone marrow and systemic ecosystem associated with MDS disease progression. Importantly, targeting galectin-9 is a mutation-agnostic approach aimed at disease biology rather than a specific genetic alteration.

Phase 1b Results

Phase 2 Design