The Promising Future of Vitiligo Treatment

John E. Harris, MD, PhD, explains how JAK inhibitors and biologic therapy may advance the field from "Iron Age" era treatment strategy.

Advancement in vitiligo care has practically been stalled for thousands of years. But now, a swath of innovations may push treatment capability to long sought-after heights.

In an interview with HCPLive during the American Academy of Dermatology (AAD) 2022 Annual Meeting in Boston this weekend, John E. Harris, MD, PhD, professor and chair of the Department of Dermatology at UMass Chan Medical School, discussed the history of stagnancy that has plagued patients with chronic skin condition.

“During the Iron Age, there are documents that tell us how to treat vitiligo, including eating black seeds with sorlands in them and then sitting out in the sun—which is essentially PUVASOL that we’ve used as recently as this last decade,” Harris explained. “We’ve now evolved slightly beyond that to use narrow-band UV—very effective for vitiligo, but really cumbersome—and it’s only a slight advance over what we were using in the Iron Age.”

Even monobenzone cream, the lone vitiligo treatment currently approved by the US Food and Drug Administration (FDA), was deemed a failed therapy by Harris; famously the treatment of pop star Michael Jackson, the topical therapy is associated with removing patient’s skin pigmentation altogether.

But now with new JAK inhibitors in development—including ruxolitinib cream, which is seeking FDA approval later this year—patients may have more options to address vitiligo. Harris additionally discussed oral therapy candidates, and pathway-inhibiting agents such as memory cell-targeting biologics.

“Resonant memory T-cells form in the skin with vitiligo,” Harris said. “These T-cells crawl into the skin, they find melanocytes and they kill them—that’s what gives you white spots. And a proportion of those cells convert into a memory state called resonant memory.”

“We found those cells require interleukin 15 (IL-15) signaling to be maintained in the skin, and when you block IL-15, they actually exit the skin and are erased from the epidermis,” Harris explained.