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4-Hydroxyderricin

MCE China：4-Hydroxyderricin

Brand：MedChemExpress (MCE)

Cat. No.HY-N7204

CAS：55912-03-3

Purity：99.97%

Storage：4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：4-Hydroxyderricin, the major active ingredients of Angelica keiskei Koidzumi, is an orally active, potent selective MAO-B (Monoamine oxidase inhibitors) inhibitor with an IC50 of 3.43 μM. 4-Hydroxyderricin also mildly inhibits dopamine β (DBH)-hydroxylase activity. 4-Hydroxyderricin has antidepressant activity, anti-allergic, anti-diabetic, anti-oxidant, and antitumor effects. 4-Hydroxyderricin promotes apoptosis and cell cycle arrest through regulating PI3K/AKT/mTOR pathway in hepatocellular cells. 4-Hydroxyderricin inhibits osteoclast formation and accelerates osteoblast differentiation. 4-Hydroxyderricin is promising for research of inflammatory diseases.

In Vitro：4-Hydroxyderricin (0-10 μM, 48 h, 2, 7, 9 or 11 days) completely inhibits the formation of multinucleated osteoclastic cells, dose-dependently decreases RANKL mRNA expression in ST2 cells, increases the activity of alkaline phosphatase and the deposition of calcium in MC3T3-E1 cells and decreases H2O2 levels in osteoblasts[2]. 4-Hydroxyderricin (1-10 μM, 24 h) and Xanthoangelol (1-10 μM, 24 h) down-regulates LPS (HY-D1056)-mediated production of NO and TNF-α , reduces the DNA-binding activity of AP-1 and inhibis the phosphorylation of NF-κB in mouse macrophages[4]. 4-Hydroxyderricin (0-100 μM, 24 h and 48 h) inhibits the proliferation and metastasis, induces apoptosis by activating the mitochondrial apoptosis pathway and cell cycle arrest in HepG2 and Huh7 cells[5]. The IC50 values (micro mole) of 4-Hydroxyderricin from A. keiskei against MAO-A, MAO-B and DBH activities[1] Compounds MAO-A MAO-B DBH 4-hydroxyderricin 3520 3.43 12.0

In Vivo：4-Hydroxyderricin (25 or 50 mg/kg, p.o., twice daily for 14 days) inhibits tumor growth, prolongs the survival time and increases the survival rate in mice with subcutaneously implanted Lewis lung carcinoma (LLC)[3].

IC50 & Target：IC50: 3.43 μM (MAO-B)[1] In Vitro 4-Hydroxyderricin (0-10 μM, 48 h, 2, 7, 9 or 11 days) completely inhibits the formation of multinucleated osteoclastic cells, dose-dependently decreases RANKL mRNA expression in ST2 cells, increases the activity of alkaline phosphatase and the deposition of calcium in MC3T3-E1 cells and decreases H2O2 levels in osteoblasts[2]. 4-Hydroxyderricin (1-10 μM, 24 h) and Xanthoangelol (1-10 μM, 24 h) down-regulates LPS (HY-D1056)-mediated production of NO and TNF-α , reduces the DNA-binding activity of AP-1 and inhibis the phosphorylation of NF-κB in mouse macrophages[4]. 4-Hydroxyderricin (0-100 μM, 24 h and 48 h) inhibits the proliferation and metastasis, induces apoptosis by activating the mitochondrial apoptosis pathway and cell cycle arrest in HepG2 and Huh7 cells[5]. The IC50 values (micro mole) of 4-Hydroxyderricin from A. keiskei against MAO-A, MAO-B and DBH activities[1] Compounds MAO-A MAO-B DBH

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References：

[1]. Kim JH, et al. Xanthoangelol and 4-Hydroxyderricin Are the Major Active Principles of the Inhibitory Activities against Monoamine Oxidases on Angelica keiskei K. Biomol Ther (Seoul). 2013 May 30;21(3):234-40.  [Content Brief]

[2]. Hagiwara H, et al. 4-Hydroxyderricin inhibits osteoclast formation and accelerates osteoblast differentiation. Cytotechnology. 2019 Feb;71(1):15-22.  [Content Brief]

[3]. Kimura Y, et al. Antitumor and antimetastatic activities of 4-hydroxyderricin isolated from Angelica keiskei roots. Planta Med. 2004 Mar;70(3):211-9.  [Content Brief]

[4]. Yasuda M, et al. Inhibitory effects of 4-hydroxyderricin and xanthoangelol on lipopolysaccharide-induced inflammatory responses in RAW264 macrophages. J Agric Food Chem. 2014 Jan 15;62(2):462-7.  [Content Brief]

[5]. Gao X, et al. 4-Hydroxyderricin Promotes Apoptosis and Cell Cycle Arrest through Regulating PI3K/AKT/mTOR Pathway in Hepatocellular Cells. Foods. 2021 Aug 29;10(9):2036.  [Content Brief]