Imagine a future where inflammatory skin diseases like eczema, psoriasis, and hidradenitis suppurativa are not just managed, but truly conquered. This is the bold vision driving groundbreaking research in dermatology, and Christopher Bunick, MD, PhD, is at the forefront of this revolution. In a recent interview with Dermatology Times at the South Beach Symposium 2026, Dr. Bunick, associate professor of dermatology at Yale School of Medicine and editor-in-chief of Dermatology Times, unveiled exciting developments that could transform how we treat these conditions. But here's where it gets controversial: while current treatments have made strides, they often fall short of addressing the full complexity of these diseases. Dr. Bunick argues that the future lies in bispecific and trispecific biologics, engineered to target multiple inflammatory pathways simultaneously. This approach promises not just symptom relief, but deeper skin clearance and a significant boost in quality of life. And this is the part most people miss: these therapies could potentially revolutionize treatment for patients who haven’t responded well to traditional mono-targeted biologics.
Atopic dermatitis (AD), for instance, is a prime example of a disease driven by multiple inflammatory pathways, not just the TH2 cytokines targeted by current treatments. Dr. Bunick explains, “AD’s underlying biology is incredibly diverse, involving a range of cytokines that contribute to the disease.” This complexity underscores the need for more sophisticated therapies. Bispecific and trispecific biologics aim to address this by tackling multiple pathways, offering hope for more comprehensive and lasting relief.
Beyond biologics, Dr. Bunick highlights the rise of selective intracellular signaling inhibitors, particularly those targeting tyrosine kinase 2 (TYK2). Here’s the twist: while TYK2 is part of the Janus kinase (JAK) family, its inhibitors work differently. “TYK2 inhibitors target the regulatory or allosteric domain of the enzyme, unlike traditional JAK inhibitors that bind to the kinase domain,” Dr. Bunick clarifies. This distinction results in higher selectivity and fewer off-target effects, potentially improving safety profiles.
First-generation TYK2 inhibitors like deucravacitinib have already shown impressive results in psoriasis, with over four years of data supporting their efficacy and safety. Dr. Bunick notes, “There’s no increased risk of malignancy, cardiovascular events, or venous thromboembolism compared to background rates.” Next-generation inhibitors, such as zasocitinib and envudeucitinib, are designed to be even more selective, with phase 3 data for zasocitinib expected soon. While acneiform eruptions and folliculitis remain potential side effects, they are generally manageable.
What’s truly fascinating is the genetic evidence supporting TYK2 as a safe target. Naturally occurring human variants with reduced TYK2 function are associated with lower rates of immune-mediated diseases, further validating this approach.
Looking ahead, Dr. Bunick is particularly excited about the potential of JAK and TYK2 inhibitors in treating conditions with unmet needs, such as vitiligo, alopecia areata, dermatomyositis, and hidradenitis suppurativa (HS). For HS, he calls for higher clinical trial standards, challenging the field to aim for transformative outcomes rather than modest response rates. “We need to raise the bar for what we consider success,” he asserts.
These advancements signal a paradigm shift in dermatology, moving toward therapies that are more precise, safer, and capable of delivering durable disease control. But here’s the question that lingers: Are we ready to embrace these innovative treatments, and what does this mean for the future of dermatological care? Share your thoughts in the comments—we’d love to hear your perspective!
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