What are the benefits of bakuchiol for the skin?

• Bakuchiol has an antibacterial effect.

  Another benefit of bakuchiol for acne-prone skin: its ability to inhibit the growth of C. acnes. According to studies conducted in vitro, this ingredient has an IC50 (50% inhibitory concentration) of 0.6 µg/mL, below that of salicylic acid (27 µg/mL), highlighting its ability to limit bacterial proliferation responsible for acne-related inflammation. IC50 refers to the minimal concentration that inhibits 50% of a bacterial population. Diffusion tests were performed and the inhibition zone measured 37 mm for bakuchiol versus 12 mm for salicylic acid.

• Bakuchiol has anti-inflammatory activity.

  Bakuchiol has anti-inflammatory activity and can inhibit cyclo-oxygenases (COX), pro-inflammatory prostaglandins. A study showed this compound has strong activity against COX-1 (CI50 = 14.7 µg/mL) and moderate activity against COX-2 (CI50 = 514 µg/mL). It reduces nitric oxide production, a pro-inflammatory mediator involved in worsening acne lesions. These anti-inflammatory effects reduce redness associated with imperfections.

What do clinical studies show about bakuchiol’s effect on acne?

Bakuchiol’s effects on skin imperfections have been confirmed in several clinical studies. One compared four formulations: 1% bakuchiol, 2% salicylic acid, a combination of 1% bakuchiol and 2% salicylic acid, and a placebo. Sixty participants with acne applied one of these creams to the face twice daily for six weeks. Efficacy was assessed using the Global Acne Grading System, a common clinical trial tool. Results, shown in the table below, demonstrate a significant reduction in acne lesion counts, both inflammatory lesion types (papules, pustules, nodules) and non-inflammatory lesions (open and closed comedones).

Bakuchiol’s efficacy in reducing wrinkles has been demonstrated in several clinical studies. One study involved 44 participants who applied either a 0.5% retinol cream or a 0.5% bakuchiol cream daily for 12 weeks. After 12 weeks, a significant reduction in wrinkles was observed in both groups and was more pronounced in the retinol group. However, retinol was linked to more adverse effects: 20% of that group reported skin peeling, compared with 10% in the bakuchiol group.

Bakuchiol targets hyperpigmentation by acting on melanogenesis, the process of melanin synthesis. Bakuchiol first inhibits the tyrosinase enzyme, which converts tyrosine into melanin. It reduces expression of proteins involved in melanogenesis, including TRP-1 (tyrosinase-related protein 1) and TRP-2. These proteins function in later steps of melanin maturation and support pigment stability in melanosomes, the organelles where melanin is synthesized.

In addition to modulating melanin production, bakuchiol modulates its transport. It inhibits dendrite formation, the cellular extensions that allow melanocytes to transfer melanin to surrounding keratinocytes, contributing to its dispersion on the skin surface. This inhibition occurs through the modulation of several cellular signaling pathways, including Rac/Cdc42/α-PAK, which is involved in cytoskeletal dynamics. Bakuchiol can interfere with primary cilium formation in melanocytes—a cellular structure involved in pigmentation regulation. These different effects allow bakuchiol to act on brown spots.

The study mentioned earlier, in which 44 participants applied daily for twelve weeks a cream containing either 0.5% retinol or 0.5% bakuchiol, also examined the impact of these treatments on pigmentation. The results showed a significant improvement in skin tone uniformity among users of both products.

Bakuchiol is also known for its antioxidant action, due to its chemical structure rich in phenolic groups. These groups give it the ability to neutralize reactive oxygen species (ROS), unstable molecules generated by UV exposure or pollution. When produced in excess, free radicals trigger an oxidation cascade that damages membrane lipids, structural skin proteins such as collagen and elastin, and cellular DNA. Bakuchiol traps these free radicals before they attack skin molecules and regulates signaling pathways involved in ROS production, such as NF-κB and MAPK.

A study examined bakuchiol's antioxidant activity and compared it to that of the vitamin E, a recognized antioxidant. The ability of these molecules to inhibit several free radical types was tested and their IC50 values were measured. The results are shown in the table below and indicate that bakuchiol has broad antioxidant activity against different free radical species.

Bakuchiol may support skin healing by exerting a positive effect on the extracellular matrix. This structure, which serves as a scaffold for the dermis, consists of collagen, elastin, laminin, and fibronectin. During the healing process, a remodeling of this matrix is necessary : new fibers are produced, while metalloproteinases such as collagenase and elastase break down existing structures. However, excessive activity of these enzymes can weaken forming tissue and impair skin healing. One study showed that bakuchiol inhibited collagenase (CI50 0.1% w/w) and elastase (CI50 between 1 and 5 µg/mL). By limiting collagen and elastin breakdown, it promotes a stable environment conducive to dermal fiber regeneration.

Bakuchiol may protect dermal structure during healing, but these promising in vitro effects require clinical validation.

Bakuchiol may soothe mild skin irritation because it can modulate the production of certain pro-inflammatory mediators. Studies on mouse macrophages activated by interferon-γ (IFN-γ) or bacterial lipopolysaccharide (LPS) showed that bakuchiol reduces the expression of inducible nitric oxide synthase (iNOS), a key enzyme in macrophage activation during inflammation. This reduction in iNOS results from bakuchiol’s inhibition of nuclear factor κB (NF-κB). NF-κB plays a central role in the inflammatory cascade: when activated, it stimulates the production of pro-inflammatory cytokines such as IL-6.

Moreover, experiments conducted in vivo in rats showed that bakuchiol application could reduce induced edema formation, confirming its anti-inflammatory potential in a living organism. However, despite these encouraging results, no clinical study in humans has validated these skin anti-inflammatory effects. These findings call for caution and further clinical research.