Most established biologics for psoriasis — drugs like secukinumab (Cosentyx), adalimumab (Humira), and risankizumab (Skyrizi) — target a single inflammatory signal at a time, such as IL-17, IL-23, or TNF-alpha. Bimekizumab is the only approved biologic for psoriasis that blocks both IL-17A and IL-17F.
“IL-17A is considered the more potent inflammatory signal, while IL-17F is present in higher amounts in psoriatic skin,” says Garshick. “By targeting both, medications like bimekizumab may offer greater suppression of inflammation, which may translate to improved clinical outcomes for some patients, compared with blocking IL-17A alone.”
Research suggests that blocking IL-17A and IL-17F together may be more effective than solely neutralizing IL-17A in treating psoriasis.
“It’s about achieving a more complete blockage of the inflammatory signals behind psoriasis,” says Lawrence Green, MD, a clinical professor of dermatology at the George Washington University School of Medicine in Washington, DC.
Think of it as an inflammatory cascade — a chain reaction of immune signals that trigger inflammation in the skin. Some biologics work higher up in the cascade, such as IL-23 inhibitors, which act earlier in the disease process and may offer more gradual and potentially longer-lasting control. Others, like IL-17 inhibitors, act further downstream, closer to where inflammation is actively driving symptoms in the skin.
“Psoriasis isn’t driven by just one signal,” Dr. Green says. “So when you block more than one, like IL-17A and IL-17F, you’re casting a wider net on the inflammation.”
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