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Hyperpigmentation is believed to be related to the enzyme tyrosinase which produces melanin. Among several chemicals known to inhibit tyrosinase production, such as hydroquinone, arbutin, and kojic acid, 4-butylresorcinol has been found to be the most powerful inhibitor by a wide margin.
Azelaic acid is used for treatment of skin pigmentation, including melasma and postinflammatory hyperpigmentation, particularly in those with darker skin types. It has been recommended as an alternative to hydroquinone. [25] As a tyrosinase inhibitor, [5] azelaic acid reduces synthesis of melanin. [26]
Crystal structure of the second generation Bcr-Abl tyrosine-kinase inhibitor nilotinib (red) in complex with an Abl kinase domain (blue). Nilotinib is used to treat chronic myelogenous leukemia (CML), a hematological malignancy. A tyrosine kinase inhibitor (TKI) is a pharmaceutical drug that inhibits tyrosine kinases.
Gefitinib is a tyrosine kinase inhibitor that targets the epidermal growth factor receptor, inducing favorable outcomes in patients with non-small cell lung cancers. A common, widespread cancer, non-small cell lung cancer is the cause of death in more people than breast, colorectal, and prostate cancer together. [15]
This toner takes skin-brightening to the next level by pairing kojic acid with vitamin C — yet another tyrosinase inhibitor — as well as bearberry extract, a plant-based alternative to ...
Decreasing tyrosinase activity has been targeted for the improvement or prevention of conditions related to the hyperpigmentation of the skin, such as melasma and age spots. [ 22 ] Several polyphenols, including flavonoids or stilbenoid , substrate analogues, free radical scavengers, and copper chelators, have been known to inhibit tyrosinase ...
“With Robbie, you can see the direct results of weight loss.” Dr. Sue Decotiis, a weight loss specialist, told The Mail: “He looks like a totally different person. “He has a longer face ...
Drug-induced pigmentation of the skin may occur as a consequence of drug administration, and the mechanism may be postinflammatory hyperpigmentation in some cases, but frequently is related to actual deposition of the offending drug in the skin. [2]: 125–6 The incidence of this change varies, and depends on the type of medication involved.