Orcinol glucoside


CAS No. : 21082-33-7

21082-33-7
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Cat. No. : HY-N0008
M.Wt: 286.28
Formula: C13H18O7
Purity: >98 %
Solubility: DMSO : 125 mg/mL (ultrasonic)
Introduction of 21082-33-7 :

Orcinol glucoside is an orally active, blood-brain barrier permeable osteoblast proliferation promoter that targets the Nrf2/Keap1, mTOR and p38 signaling pathways. Orcinol glucoside promotes Nrf2 nuclear translocation, upregulates antioxidant enzyme levels, enhances the phosphorylation of mTOR and p70S6K, and inhibits the enzymatic activity of HAS2 as well as the nuclear translocation of GR. Orcinol glucoside also alleviates oxidative stress, inhibits autophagic flux, osteoclastogenesis and TGF-β1-induced M2 polarization, while reducing collagen deposition and effectively promoting the proliferation, differentiation and mineralization of osteoblasts. Orcinol glucoside also exhibits anti-pulmonary fibrosis, anxiolytic and antidepressant activities. Orcinol glucoside can be used in the research of senile and glucocorticoid-induced osteoporosis, idiopathic pulmonary fibrosis (IPF), anxiety and other related diseases[1][2][3][4].
In Vitro:Orcinol glucoside (1-10 μM; 72 h) does not reduce the viability of H2O2-exposed RAW264.7 cells[1].
Orcinol glucoside (1-10 μM; 72 h) dose-dependently inhibits the differentiation and TRAP activity of RANKL- and H2O2-induced RAW264.7 osteoclasts[1].
Orcinol glucoside (5-10 μM; 48 h pre-incubation with RANKL before 4 h H2O2 exposure) activates the mTOR pathway in RANKL- and H2O2-induced RAW264.7 osteoclasts, increasing phosphorylation of mTOR and p70S6K[1].
Orcinol glucoside (10-100 nM; 72 h) promotes proliferation of primary mouse osteoblast cells in a dose-dependent manner at concentrations of 10, 50, and 100 nM over 72 h[2].
Orcinol glucoside (10-100 nM) upregulates p38 phosphorylation and the expression of osteogenic-related proteins (Collagen I, Runx2, Osx, Dlx5) in primary mouse osteoblast cells in vitro in a dose-dependent manner at concentrations of 10, 50, and 100 nM[2].
Orcinol glucoside (0-100 µM; 48 h) is non-toxic to NIH/3T3 mouse fibroblasts and HFL-1 human fibroblasts at concentrations ranging from 0 to 100 µM after 48 h incubation[3]. In Vivo:Orcinol glucoside (50-100 mg/kg, intragastric administration; daily dosing; for 10 consecutive weeks) alleviates senile osteoporosis in SAMP6 mice, significantly improves bone microstructure, reduces the levels of bone resorption biomarkers, and regulates oxidative stress and autophagy via the Nrf2/Keap1 and mTOR signaling pathways[1].
Orcinol glucoside (5-20 mg/kg, intragastric administration; daily dosing; for 8 consecutive weeks) dose-dependently increases BMD, BV/TV, Tb.Th and Tb.N in dexamethasone-induced osteoporotic mice by activating the p38 signaling pathway and upregulating downstream osteogenic proteins[2].
Orcinol glucoside (5 mg/kg, intragastric administration, once daily for 5 consecutive weeks) improves the bone microstructure and increases osteogenic biomarkers in dexamethasone-induced osteoporotic mice by activating p38, while p38 inhibitors block these effects[2].
Orcinol glucoside (25-100 mg/kg; p.o.; once daily; for 14 consecutive days) dose-dependently alleviates bleomycin-induced pulmonary fibrosis in male C57BL/6J mice by inhibiting the expression of fibrosis markers, HA accumulation, and TGF-β1 production, with an exposure-response relationship observed across different administration doses[3].
Orcinol glucoside (5-20 mg/kg; p.o.; single administration) exhibits anxiolytic activity in mice without inducing sedative effects[4].

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