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, an 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 improved lives, they often fall short of delivering complete relief. Dr. Bunick argues that the future lies in bispecific and trispecific biologics, engineered to target multiple inflammatory pathways simultaneously. This approach promises deeper skin clearance, better itch and pain control, and life-changing improvements in quality of life.
Atopic dermatitis (AD), for instance, is a complex disease driven by a multitude of inflammatory pathways, not just a single culprit. As Dr. Bunick explains, “The underlying biology of AD is incredibly diverse, involving numerous cytokines that fuel the condition.” While existing mono-targeted biologics, primarily focusing on TH2 cytokines, have been game-changers, they don’t address the full spectrum of disease mechanisms in all patients. This is where bispecific and trispecific biologics come in, offering a more comprehensive attack on inflammation.
But here’s the part most people miss: beyond biologics, a new class of treatments called selective intracellular signaling inhibitors is gaining traction. Specifically, TYK2 inhibitors are generating buzz. While TYK2 is part of the Janus kinase (JAK) family, its inhibition works differently. “The key distinction lies in what TYK2 inhibitors target within the JAK enzyme family,” Dr. Bunick clarifies. Unlike traditional JAK inhibitors that bind to the kinase domain, TYK2 inhibitors act on the regulatory or allosteric domain, resulting in higher selectivity and fewer off-target effects.
First-generation TYK2 inhibitors like deucravacitinib have already shown impressive results in psoriasis, with over four years of data demonstrating sustained efficacy and a favorable safety profile. Dr. Bunick highlights that these treatments haven’t shown increased risks for malignancy, major cardiovascular events, or venous thromboembolism compared to baseline rates. Next-generation TYK2 inhibitors, such as zasocitinib and envudeucitinib, are designed for even greater precision, with phase 3 data for zasocitinib expected soon. While acne-like eruptions and folliculitis remain potential side effects, they are generally manageable.
Here’s where it gets even more intriguing: genetic studies support TYK2 as a safe target. Naturally occurring human variants with reduced TYK2 function are associated with lower rates of immune-mediated diseases, providing strong evidence for its therapeutic potential.
Looking ahead, Dr. Bunick is particularly excited about the role 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 raising the bar in clinical trials, challenging researchers to aim for transformative outcomes rather than modest response rates. “We need to push beyond incremental improvements and strive for truly game-changing therapies,” he asserts.
These advancements signal a paradigm shift in dermatology, moving toward treatments defined by pathway specificity, enhanced safety, and higher expectations for long-term disease control.
But what do you think? Are bispecific biologics and TYK2 inhibitors the future of inflammatory skin disease treatment? Or do you see other approaches holding more promise? Share your thoughts in the comments below and let’s spark a conversation about the future of dermatology!
