1. Oxyresveratro can inhibit tyrosinase activity. 2. Oxyresveratro is useful to trauma models, as toxicity to glia could be beneficial by inhibiting reactive gliosis. 3. Oxyresveratrol (trans-Oxyresveratrol) has antioxidant activity, can reduce neuronal oxidative damage and protect hepatocytes against oxidative stress and mitochondrial dysfunction, which may be associated with activation of Nrf2.

Oxyresveratrol 4-O-β-D-glucopyranoside (Compound 3) is a natural product extracted from the root bark of Morus atropurpurea, with potential applications in the research of diabetes, arthritis, rheumatism, cough, and headache [1].

Oxyresveratrol-2-O-beta-D-glucopyranoside shows better tyrosinase inhibitory activities than kojic acid.

Oxyresveratrol-3'-O-beta-D-glucopyranoside shows tyrosinase inhibitory activity, it may be a potential candidate as skin-whitening agents without posing any serious side effects.

4'-Prenyloxyresveratrol is a natural product from Morus wittiorum.

trans-Trimethoxyresveratrol (MR-3), a natural methoxylated analog of resveratrol, inhibits breast Y cell invasiveness by downregulation of PI3K/Akt and Wnt/β-catenin signaling cascades and reversal of epithelial-mesenchymal transition.

4'-Methoxyresveratrol (4'-O-Methylresveratrol) is a natural product form the roots of Rheum palmatum L,has significant hypoglycemic, anti-inflammatory, and antioxidant effects.4'-Methoxyresveratrol alleviates AGE-induced inflammation through suppressing RAGE-mediated MAPK/NF-κB signaling pathway and NLRP3 inflammasome activation.

1. Mulberroside has nephroprotective, hypoglycemic, and antidiabetic effects. 2. Mulberroside A is a glycosylated stilbene of oxyresveratrol; thus, the deglycosylation of Mulberroside A resulted in enhanced inhibition of melanogenesis. 3. Mulberroside A has anti-inflammatory antiapoptotic effects. by decreasing the expressions of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 and inhibiting the activation of NALP3, caspase-1, and nuclear factor-κB and the phosphorylation of extracellular signal-regulated protein kinases, the c-Jun N-terminal kinase, and p38.