IL-23 Inhibitors in the Treatment of Plaque Psoriasis


Mechanism of action and dosing of IL-23 inhibitors use to treat plaque psoriasis as explained by advanced practice providers.


Matthew Brunner, MHS, PA-C, DFAAPA: Tell us a little about the mechanism of action for the IL-23 inhibitors. I want to talk about that a little before we talk about some of these newer agents.

Lakshi Aldredge, MSN, ANP-BC, DCNP: The IL-23s have changed the way we’ve looked at psoriasis in the last 10 years. They are the new kids on the block, but when I say new kids, we have more than 5 years’ worth of safety data in several of these molecules. If you think about a target or a bull’s-eye, that’s the way that I explain how our understanding of psoriasis treatment options have changed. If you look at the center of the bull’s-eye as the target of curing psoriasis, the TNF-α [tumor necrosis factor-alpha] is hitting the outside of the outer rings of the target. Highly effective, and they do clear the skin, but they can be less effective than the next ring, which is the IL-17 inhibitors. They get a little closer to that bull’s-eye. They’re targeting IL-17, which we know psoriasis is a Th-17–mediated disease, and IL-17 is definitely a driver of inflammation and psoriasis. IL-17 inhibitors are getting closer on that bull’s-eye. Then IL-23 is even closer. We’re getting really close to the bull’s-eye with the IL-23–specific inhibitors. Why is that? What we know is that IL-23 is further downstream. And when we target IL-23, we’re being more specific in targeting the agents that are causing more of the inflammation. It’s much more specific in its targeting. It does target a little of IL-17 as well and a little of TNF-α, but its main mechanism of action is focusing on that IL-23 molecule.

Our understanding of psoriasis shows that this is also 1 of the key drivers of psoriasis, if not the major driver. The other important factor in targeting IL-23 is that we see that it’s a safer option. We don’t see some of those risks or signals for adverse effects that we saw with the TNF-α inhibitors. We don’t see an increased risk of infections. We don’t see an increased risk of heart failure or nuance at heart failure. We don’t see an increased risk of irritable bowel disease or Crohn disease. And we don’t see an increased risk of malignancies or any other bad things that may have been associated with some of those other targeted mechanisms.

The IL-23s are specific in their target. They’re more downstream, so they’re more specific and getting to that bull’s-eye. They have a very high efficacy rate with a very excellent safety profile. They fit all the things that patients want. They want something that works very effectively, so we see very high levels of skin clearance in the IL-23 inhibitors. They want something that’s very safe, and we’ve seen that with the IL-23 inhibitors. Even 5 years’ safety data show that we aren’t seeing any long-term risks of infection malignancies, heart issues, or cancers. And it works very quickly. The other important factor is the dosing is convenient, with sometimes every 3 months dosing, if not every 2 months. It’s convenient in that way. It’s a targeted therapy that looks very efficacious and very safe.

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Transcript edited for clarity.

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