It is still unclear why patients who should respond to anti–interleukin-5 therapies do not, noted Anne Reihman, MD, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado.
We’re trying to uncover why patients who should respond to anti–interleukin (IL)-5 therapies do not. Some patients just don’t have a good clinical response to these drugs, noted Anne Reihman, MD, third-year pulmonary and critical care fellow, University of Colorado, Division of Pulmonary Sciences and Critical Care Medicine, prior to this year's CHEST meeting.
How will you address the importance of anti–IL-5 therapy failure in patients with severe eosinophilic asthma?
The anti–IL-5 therapies we'll be discussing refer to the biologic therapies that are currently approved for management of severe eosinophilic asthma, and specifically, the drugs that we're talking about are mepolizumab, reslizumab, and benralizumab. These drugs work by blocking molecules along the IL-5 inflammatory pathway, which is involved in eosinophilic production and activation.
While these drugs have been shown to be very helpful in many patients with severe eosinophilic asthma, more recently, we've noticed that there's a group of patients that, though they look like they should be the correct phenotype to respond to these drugs, don't actually have a good clinical response and continue to have asthma exacerbations and symptoms despite initiation of these drugs.
And so it's this group of what we call nonresponders that were really interested in studying at the University of Colorado and kind of are the basis of what I'll be talking about [October 20 at CHEST]. So, I'll be discussing the current data around patients who don't respond to anti–IL-5 therapies.
And I'll preface this by saying that there's not a whole lot of data out there right now, but I will try and cover the current predictors of anti–IL-5 therapy response that we know about, as well as try and discuss some of the predictors that we're looking into, and then discuss possible mechanisms that may be driving anti–IL-5 therapy failure.