How does AA work? It inhibits tyrosinase activity, the key enzyme in melanin production. This is done by blocking the interaction of this enzyme with its substrate (in the same way that HQ does it). Under alkaline conditions (high pHs) AA is transformed into HQ. This process does not occur in the human skin (which is acidic or neutral). Interestingly, two skin resident bacteria (Staphylococcus epidermidis and Staphylococcus aureus) can hydrolyze AA limiting its efficacy. Few clinical studies evaluated the effect of AA alone on pigmented skin. Thus, most of the time companies pair this active molecule with niacinamide, licorice extract, retinoid, glabridin, kojic acid, azelaic acid, vitamin C, soya bean extracts, niacinamide and/or chamomile extracts. One clinical study showed that a formulation containing 3% AA improved skin pigmentation in almost 72% of the subjects after 12 weeks of treatment.
Deoxyarbutin (4-[(tetrahydro-2H-pyran-2-yl)oxy] phenol, D-Arb) is a glucoside derivative of HQ more potent than AA and less toxic than HQ. This molecule has a greater potential for skin depigmentation than AA or beta-arbutin.
FINAL THOUGHTS: I am not a big fan of arbutins to be honest. Although there is a lot of in vitro data supporting their activity and tolerability, the lack of clinical proof makes me a little bit uneasy. In most of the published clinical trials, arbutins are used in combination with other whitening ingredients and therefore it is hard to decide if they actually contribute to the final result. In addition, the potential conversion of arbutins into HQ once absorbed by the skin (which is still under scientific debate) did not help these molecules to enter into my “good chemicals” book.
#skincarescience #theskinbiologist #Flawlesscanvas_skincare #antiaging #hyperpigmentation #skincareingredients #skincareproducts #evenskintone