Alpha ArbutinvsMandelic Acid

Alpha arbutin (4-hydroxyphenyl-alpha-D-glucopyranoside) is a glycosylated hydroquinone with glucose bound to the para position. Alpha-glucosidase and other glycosidases slowly hydrolyze the bond, releasing hydroquinone in controlled low concentrations—avoiding peak levels that cause irritation and ochronosis. Released hydroquinone inhibits tyrosinase by competing with tyrosine and through copper chelation at the catalytic center, reducing L-DOPA to dopaquinone conversion. The alpha anomer provides greater stability and skin penetration than beta arbutin. May also inhibit melanosome maturation. Gradual release creates sustained low-dose tyrosinase inhibition that brightens over 8-12 weeks with minimal side effects.

Mandelic acid (152 Da, the largest common AHA) exfoliates through calcium chelation and corneodesmosome disruption like other AHAs, but its large molecular size results in slower, more even epidermal penetration with reduced risk of hot-spot irritation and stratum corneum over-exfoliation. Its phenyl ring confers partial lipophilicity, enabling penetration into the pilosebaceous unit and follicular infundibulum—unlike purely hydrophilic glycolic and lactic acids. Within pores, mandelic acid exerts mild comedolytic effects by disrupting keratinocyte cohesion in the follicular epithelium, similar to salicylic acid. It demonstrates antibacterial activity against Cutibacterium acnes (Propionibacterium acnes) through membrane disruption. Mandelic acid also inhibits tyrosinase and reduces melanosome transfer to keratinocytes, providing brightening benefits. This profile makes it particularly suitable for acne-prone skin, hyperpigmentation, and darker skin tones (Fitzpatrick IV–VI) where gentler exfoliation minimizes post-inflammatory hyperpigmentation risk.