Targeting Macrophages Instead of T Cells to Overcome Treatment-Resistant Cancers with Dr. Petri Bono Faron Pharmaceuticals TRANSCRIPT
Download PDFDec 8, 2025
Dr. Petri Bono, Chief Medical Officer at Faron Pharmaceuticals, describes the development of bexmarilimad, a novel first-in-class immunotherapy that, unlike existing checkpoint inhibitors targeting T cells, targets the Clever 1 receptor on macrophages. This treatment is designed to reprogram the tumor microenvironment by switching marcophages from suppressive to active, enabling the patient's immune system to recognize and attack cancer cells. The primary disease target is higher-risk Myelodysplastic syndromes because the cancer cells in virtually all MDS patients express the Clever 1 target.
Petri explains, "We are developing a completely new type of treatment. Currently, cancer patients are treated with immunotherapies called checkpoint inhibitors that target immune checkpoints. But our approach is targeting completely different cells, not T cells, but rather macrophages. And that's why we are first in class with a novel mode of action. And that's why it's important that these macrophages are shown to, for example, contribute to treatment resistance in many tumors."
"Clever 1 actually is a receptor that was identified about 20 years ago. It found a certain macrophage as well as myeloid cells. And Clever 1 keeps the immune system in a tolerant and suppressive state. In cancer, for example, these Clever 1-positive macrophages essentially help the malignancy grow instead of helping to fight against it. And then our approach is that we want to block Clever 1 with our monoclonal antibody, bexmarilimab. So those macrophages switch the phenotype into an active antigen, preventing a pro-inflammatory state, and this reawakens immune surveillance. It allows T cells in the system to actually recognize the malignant cells themselves as dangerous and mount a proper antitumor response. So, a completely new mode of action by targeting Clever 1, we are not just adding another cytotoxic mechanism. We are removing the immune break and enabling the patient's own immune system to do the job that it was originally designed to do."
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