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Jonathan Alicea is an assistant editor for HCPLive. He graduated from Princeton University with a degree with English and minors in Linguistics and Theater. He spends his free time writing plays, playing PlayStation, enjoying the company of his 2 pugs, and navigating a right-handed world as a lefty. You can email him at email@example.com.
The Head of Immunology Medical Affairs at UCB discusses what bimekizumab is and how it works.
US Centers for Disease Control and Prevention (CDC) data places the prevalence of adult plaque psoriasis in 2013 around 7.4 million cases.
Several biologic treatments, such as adalimumab, etanercept, ixekizumab, and secukizumab, among others, have already been approved by the US Food and Drug Administration (FDA) for treatment in adults and/or pediatric populations—and the landscape continues to grow.
This year’s American Academy of Dermartology (AAD VMX) Virtual Meeting Experience saw the presentations of ongoing/emerging research focused on optimizing treatment for those living with the chronic autoimmune disease. One such novel agent is bimekizumab, a humanized monoclonal antibody that targets interleukin-17 (IL-17).
In an interview with HCPLive®, Jeffrey Stark, MD, Head of Immunology Medical Affairs, discussed the continued need for treatments in this patient population as well as what bimekizumab would offer to the therapeutic toolbox.
“Over the last couple of decades, a lot of progress—frankly—has been made in the area of plaque psoriasis,” Stark said. “There are multiple treatments available for these patients today that they did not have prior to that time. But, despite the availability of those treatments, there continue to be patients who do not respond.”
He mentioned that there remains a need to develop newer highly efficacious treatments that can especially help patients resistant to response—and that is the hope for bimekizumab.
Stark elaborated on the mechanism of the biologic, noting its ability to target both IL-17A and IL-17F.
“We believe that that novel mechanism of action is quite important,” stressed Stark. “IL-17A and IL-17F have overlapping biology, but we know that IL-17F can actually drive inflammation independently of IL-17A.”
And furthemore, he continued, targeting both may actually augment the effects of inflammation suppression.