Acute myeloid leukaemia (AML) is the most common aggressive leukaemia. Over the last three decades, there have been improvements in survival and quality of life for AML patients, mainly thanks to advances in supportive care. Unfortunately, however, in many cases the disease is still difficult to treat, especially for elderly, frail patients who the disease predominantly affects. So there’s an urgent need for new therapies that are more effective and kinder than current chemotherapies.
In collaboration with researchers at Stanford University, we’ve found that the leukaemic stem cells that drive the growth of AML, as well as other AML cells, protect themselves from being eaten by immune cells by expressing a “don’t eat me” signal, a protein called CD47.
We’ve developed a novel therapy that enables the body’s own immune cells to eliminate AML cells. The drug is an immune protein – an antibody – that sticks to CD47, so that the “don’t eat me” signal is blocked. The hope is that this will unleash killer immune cells to attack the rogue AML cells.
What we’re doing
We’re now running the first clinical trial of this anti-CD47 antibody in AML in collaboration with Stanford and the Medical Research Council, to understand how the drug works in humans, and to ensure that it’s safe before it’s given to lots of patients.
The UK is running the blood cancer part of the trial for AML patients across 7 treatment centres in the UK, while Stanford is testing the drug on solid tumours.