New research from Emma Guttman-Yassky and colleagues at the Icahn School of Medicine at Mount Sinai, in collaboration with Pfizer, has revealed links between inflammation and alopecia-related hair loss, as well as the potentials of ritlecitinib to stimulate hair regrowth.

Ritlecitinib – produced by Pfizer under the brand name Litfulo – targets and inhibits both Janus kinase 3 (JAK3) and TEC family kinases (IL-2–inducible T-cell kinase (ITK) and Bruton tyrosine kinase (BTK)), reducing JAK3-mediated immune signalling and driving hair regrowth.

The researchers noted that the role of JAK3 in alopecia uncovered the role of inflammation, and not just fibrosis, in disease activity. Guttman-Yassky commented: “We’ve done a study in scarring alopecia that showed for the first time that they are not all about fibrosis. There is actually an inflammatory component. And particularly, it involves elevation of JAK3.”

Scarring alopecia has long been thought to be irreversible due to fibrosis, but the researchers considered the possibility that targetable immune mechanisms might be the underlying cause of scarring alopecia. Molecular work carried out by the researchers identified JAK3 activity in follicles affected by scarring alopecia, suggesting that targeted intervention may be possible.

Guttman-Yassky said: “When you dampen the inflammation, you will be able to also change the fibrosis component and allow hair growth.”

The researchers also noted that early intervention is vital: receiving treatment within three and a half years of developing scarring alopecia makes potential hair regrowth far more likely.

While ritlecitinib has been approved for the treatment of severe alopecia areata (AA) in various regions, treatment for scarring alopecia still offers inconsistent disease control. 

The new research could uncover a future JAK3-inhibiting treatment pathway, tackling inflammation before fibrosis has a chance to develop.