Science's New Self-Tanner Darkens Skin from the Inside Out

The onset of summer means it’s time for beach trips, baseball games, outdoor concerts, pig pickin’s, and all those lovely outdoor activities that require smearing yourself with sunblock. Whether you hate the endless task of protecting your skin from sunburns and their accompanying DNA damage or you welcome the opportunity to build that base tan (PSA: don’t do that), take comfort in the fact that scientists have found a way to make getting a golden glow a little safer for everyone.

In a study published Tuesday in the open-access journal Cell Reports, researchers at Mass General-Harvard Medical School and Boston University School of Medicine say they’ve developed a topical drug that helps tan skin without exposing it to UV damage. This isn’t your drugstore self-tanner or the sickly orange tint spray-painted onto aging celebs; this is a medical drug that helps skin cells produce melanin, the pigment that naturally makes skin dark. When people lie out in the sun to get some color, they’re actually just boosting their cells’ melanin production.

While melanin naturally helps protect the skin against sun damage, tanning to produce more melanin results in skin damage. Therefore, a product that could help people produce protective melanin without tanning represents a significant advance in sun protection, senior author David Fisher, a dermatology researcher at Mass General, tells Inverse.

“Sun-tanning or tanning at an indoor tanning bed are not healthy activities, from a medical perspective, because they are both clearly associated with formation of skin cancers, some of which may be lethal,” Fisher says. “They are also associated with acceleration of ‘photo-aging’ which is skin injury that hastens the appearance of wrinkles, and other indications of UV damage. It is possible that this approach may minimize the need for people to seek UV as a trigger of tanning.”

To test this topical drug, Fisher, along with co-lead authors Nisma Mujahid and Yanke Liang, applied it to human skin samples in the lab. When the team applied the experimental compound, developed in conjunction with Dana-Farber Cancer Institute chemist Nathanael Gray, Ph.D., it induced melanin development along the same pathway that UV radiation produces melanin, making the skin darker — but it didn’t cause the same kind of damage that radiation would cause.

This builds on Fisher’s team’s research from about ten years ago, in which they found that forskolin, a compound derived from a tropical palm, could darken the skin of red-haired fair-skinned mice, which share the same solar shortcomings as Ed Sheeran. It doesn’t really work on humans’ skin, though, so this new development is a promising step forward.

“We are excited by these observations,” says Fisher. “The process of deriving skin-penetrating agents with this property was not easy. It required a close collaboration with chemist Dr. Nathanael Gray, together with numerous tests of the compounds in the laboratory.”

Does this mean that sunblock might soon become a thing of the past? Not likely. Fisher says that even if a product reaches the market, it would mostly work as a supplement to conventional sunblocks and sunscreens. Fortunately, this could happen soon: Fisher is already in conversation with commercial partners, and he hopes to begin clinical trials in the near future.

“We are eager to see this enter into the clinic as soon as possible,” he says. “Safety/toxicity testing will be very important as a first step. The timing is uncertain but hopefully within the coming few years.”

Abstract: The presence of dark melanin (eumelanin) within human epidermis represents one of the strongest predictors of low skin cancer risk. Topical rescue of eumelanin synthesis, previously achieved in “redhaired” Mc1r-deficient mice, demonstrated significant protection against UV damage. However, application of a topical strategy for human skin pigmentation has not been achieved, largely due to the greater barrier function of human epidermis. Salt-inducible kinase (SIK) has been demonstrated to regulate MITF, the master regulator of pigment gene expression, through its effects on CRTC and CREB activity. Here, we describe the development of small-molecule SIK inhibitors that were optimized for human skin penetration, resulting in MITF upregulation and induction of melanogenesis. When topically applied, pigment production was induced in Mc1r-deficient mice and normal human skin. These findings demonstrate a realistic pathway toward UV-independent topical modulation of human skin pigmentation, potentially impacting UV protection and skin cancer risk.