In medicine, the most interesting discoveries are often the ones nobody was looking for. Verteporfin, a photosensitising agent used in photodynamic therapy for wet age-related macular degeneration since the late 1990s, has no obvious connection to hair loss. But a 2021 paper in Science Translational Medicine by researchers at Stanford changed that, and the field hasn't been quite the same since.

YAP, the mechanotransduction effector that verteporfin inhibits.
Figure 1. YAP, the mechanotransduction effector that verteporfin inhibits. · Wikimedia Commons / YAP1

The discovery came from a different wound healing context entirely. George Gurtner's lab at Stanford was investigating scar formation in general, not hair specifically. Verteporfin inhibits YAP, yes-associated protein, a mechanotransduction effector that responds to the mechanical stiffness of wound tissue. When a wound closes under tension, YAP activity drives fibroblasts toward a pro-fibrotic, scar-forming phenotype. When YAP is inhibited by verteporfin, wound healing shifts toward a more regenerative, fetal-like pattern. And fetal wounds, unlike adult wounds, heal without scars and with follicle regeneration.

Stages of wound healing relevant to verteporfin's anti-scar mechanism.
Figure 2. Stages of wound healing relevant to verteporfin's anti-scar mechanism. · Wikimedia Commons / Wound healing

The connection to hair transplant surgery is direct. Current hair transplant techniques, both follicular unit transplantation (FUT) and follicular unit extraction (FUE), leave behind wounds that heal as scars. The scarred tissue doesn't support follicle regeneration. You can transplant existing follicles from a donor area, but you can't grow new ones in wound tissue. This limits the ceiling for transplant outcomes and contributes to the visible plugginess and unnatural patterns in some earlier generation results.

Fibroblasts drive scar formation; YAP/verteporfin inhibition redirects them toward regeneration.
Figure 3. Fibroblasts drive scar formation; YAP/verteporfin inhibition redirects them toward regeneration. · Wikimedia Commons / Fibroblast

If verteporfin can suppress YAP-mediated scar formation in hair transplant wounds, it potentially opens two possibilities. First, it could improve the quality of healing at the recipient site, allowing denser packing of transplanted follicles without the tension-mediated scarring that constrains conventional technique. Second, and this is the more speculative but more exciting application, it might enable some degree of follicle neogenesis at the wound site: genuinely new follicles forming from wound-associated progenitor cells rather than transplanted ones.

A 2023 case series from researchers at University of Southern California published in Plastic and Reconstructive Surgery reported on ten patients who received verteporfin injected intradermally into hair transplant recipient sites at the time of surgery. After 12 months, those patients showed improved hair density in treated versus untreated zones, with some evidence of follicle structures forming at sites that hadn't received transplanted grafts. The case series design means confounding is possible, but the follicle morphology on histology was consistent with neogenesis rather than transplant growth.

Formal Phase 2 trials are now underway at three US academic centres. The mechanistic case for verteporfin in this application is unusually solid, the YAP pathway is well characterised, the drug is already approved (which reduces regulatory uncertainty for off-label investigational use), and the wound healing biology is coherent. The unknowns are whether the effect size in a large randomised trial will match the early case series enthusiasm, and what the optimal dosing and timing relative to surgery actually is. Those answers should come from the current trials by late 2026 or early 2027.