Recombinant EphB4-HSA Fusion Protein and Azacitidine or Decitabine for Relapsed or Refractory Myelodysplastic Syndrome, Chronic Myelomonocytic Leukemia, or Acute Myeloid Leukemia Patients Previously Treated With a Hypomethylating Agent
Key claim: A recombinant EphB4-HSA fusion protein combined with azacitidine or decitabine is being evaluated for safety and efficacy in patients with HMA-refractory MDS, CMML, or AML.
Abstract
This trial studies the side effects of recombinant EphB4-HSA fusion protein when given together with azacitidine or decitabine in treating patients with myelodysplastic syndrome, chronic myelomonocytic leukemia, or acute myeloid leukemia that has come back or has not responded to previous treatment with a hypomethylating agent. Recombinant EphB4-HSA fusion protein may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Hypomethylating agents, such as azacitidine and decitabine, slow down genes that promote cell growth and can kill cells that are dividing rapidly. Giving recombinant EphB4-HSA fusion protein together with azacitidine or decitabine may work better in treating patients with myelodysplastic syndrome, chronic myelomonocytic leukemia, or acute myeloid leukemia.
Why this matters
HMA failure marks a transition point where CMML and MDS/MPN overlap patients face dismal outcomes and frequently progress toward leukemic transformation, yet prospective salvage options remain extremely limited. Testing a first-in-class EphB4-HSA fusion protein on top of azacitidine or decitabine introduces receptor tyrosine kinase blockade as a mechanistically novel axis distinct from the BCL-2, IDH1, FLT3, CSF-1R, and epigenetic strategies currently dominating the CMML and MDS/MPN salvage pipeline. If active, it would broaden the post-HMA armamentarium across CMML, MDS/MPN overlap, and the blast-phase transformation continuum.