Canakinumab & Darbepoetin Alfa in Lower-Risk MDS | David Sallman, MD | ASH 2023

Hi, I'm David Salman from Moffitt Cancer Center in Tampa, Florida. It's really a pleasure to be speaking with you at the ASH 2023 Congress. So I'd like to highlight one abstract that we're presenting, which is a drug called Canikiniumab, which is a really novel and really first in class drug that targets what's called interleukin 1 beta. So just a very brief background, in patients that have lower risk myelodysplastic syndrome, it's a very inflammatory disease. We know that patients can have very high symptom burdens such as fatigue, and this is really often the major kind of morbidity of the disease and something that we are often trying to improve. And that's really targeting this may give us really the best promise to improve the quality of life of patients while at the same time can we change the actual natural history of the disease. Again, interleukin 1 beta is an inflammatory cytokine that is sort of the end product of the inflammatory cell death called pyruptosis. And again, all this does is deplete that cytokine. So this is one of the first trials looking at this, and we actually did it in combination with another drug called darbapuetin, which ideally tells your body to make more red blood cells, and we've done this in lower risk MDS patients. I think the data that we see to date is it has been very, very safe, really almost no toxicity from the agent. And what we are able to see is that we can block these inflammatory pathways in the cells from patients. I think unfortunately, at least with just this agent that only targets interleukin 1 beta, we're not able or we've not seen yet to date significant improvement of blood counts. But I think, again, this is one of the first looks into targeting the inflammatory pathway in MDS patients, and potentially this in combinations with other novel agents that target the inflammatory pathway may again give us the best hope to really dramatically improve quality of life of some of our patients, as well as ideally change the natural history of the disease.