Conventional cancer therapies such as chemotherapy and radiation have a significant downfall: while targeting cancerous tumors, they also damage healthy cells which can lead to undesirable patient side-effects.

Despite high expectations at the onset, treatments using monoclonal antibodies have historically faced limitations.

While attempting to discover why monoclonal antibodies were not performing as expected, researchers at Stanford and Yale discovered that the signal regulatory protein α (SIRPα) was triggering the CD47 alarm. When triggered, the CD47 protein acts as a shield, hiding tumors from the impact of antibodies.

To overcome this challenge, researchers developed an anti-SIRPα antibody, KWAR23, which disables the CD47 shield, revealing tumors to the patient’s immune system.

When combined with an existing anti-tumor antibody, KWAR23 was shown to eliminate certain tumor cell lines. These anti-SIRPα antibodies may open up a promising new avenue for cancer treatment.

Read more about this research in the full paper published in PNAS.

Our mouse macrophages have been shown to express SIRPα and to phagocytose antibody coated tumor cells.

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