Empowered Patient Podcast Focus on Resistance Pathways to Target Blood Cancers and Graft-Versus-Host Disease with Peter Ordentlich Syndax Pharmaceuticals
Peter Ordentlich, Chief Scientific Officer and Founder at Syndax Pharmaceuticals, a clinical oncology company, is focused on developing precision medicine approaches to treat cancer and chronic graft-versus-host disease. The menin protein plays a critical role in driving certain types of blood cancers, and the Synex therapy is a menin inhibitor that can disrupt this cancer-driving pathway. The platform is also developing an antibody addressing the unmet needs in cGVHD to reduce the disease-driving macrophages.
Peter explains, "Syndax is a clinical oncology company, which means we're focused primarily on cancer, and we're primarily doing clinical development. We started the company really looking at resistance pathways to developing cancer, and we've been focused on two main areas. One in the indication space of leukemia, which are certain types of blood cancers, and that's with a program we have around the small molecule drug called revumenib. We are also focused in another area of diseases called chronic graft-versus-host disease. These are diseases that happen post-stem cell transplant, and there we're developing an antibody called axatilimab. And so those two programs are really what we've been focusing on for the last five or six years and have led to each of those drugs."
"So menin is a very interesting protein, and basically what this is, it's called a scaffold protein. And you can imagine a scaffold, just something you build things upon. And so menin interacts with DNA through a variety of other factors, and you build on top of this a complex of other proteins that can turn genes on and off. And in the case of certain types of leukemias, the mutation that creates certain other cancer-causing proteins binds to menin. That's what drives certain genes that drive leukemia to always be turned on. And so what we've tried to do and others have tried to do is disrupt that interaction and essentially cause the scaffold to fall apart. And when that falls apart, you can no longer keep those genes on that drive leukemia, and instead, you have genes that essentially cause the cell to stop growing."
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