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DMU-212(resveratrol analog)

  Cat. No.:  DC22291   Featured
Chemical Structure
134029-62-2
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More than 5000 active chemicals with high quality for research!
Field of application
DMU-212, a methoxylated resveratrol analog, has significant anticancer activity, and selectively targets tumor cells.
Cas No.: 134029-62-2
Chemical Name: Benzene,1,2,3-trimethoxy-5-[(1E)-2-(4-methoxyphenyl)ethenyl]-
Synonyms: Benzene,1,2,3-trimethoxy-5-[(1E)-2-(4-methoxyphenyl)ethenyl]-;1-(4-methoxyphenyl)-2-(3,4,5-trimethoxyphenyl)ethene;1,2,3-trimethoxy-5-[(1E)-2-(4-methoxyphenyl)ethenyl]Benzene;3,4,5,4'-TETRAMETHOXYSTILBENE;1,2,3-trimethoxy-5-[(E)-2-(4-methoxyphenyl)ethenyl]benzene;1,2,3-Trimethoxy-5-[(E)-2-(4-methoxyphenyl)vinyl]benzene;benzene, 1,2,3-trimethoxy-5-[(E)-2-(4-methoxyphenyl)ethenyl]-;1,2,3-Trimethoxy-5-[(1E)-2-(4-methoxyphenyl)ethenyl]-benzene;DMU 212;MR-4;(E)-1,2,3-Trimethoxy-5-[2-(4-methoxyphenyl)ethenyl]benzene;DMU-212
SMILES: COC1C=C(/C=C/C2C=CC(OC)=CC=2)C=C(OC)C=1OC
Formula: C18H20O4
M.Wt: 300.349
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: DMU-212 is a methylated derivative of Resveratrol (HY-16561), with antimitotic, anti-proliferative, antioxidant and apoptosis promoting activities. DMU-212 induces mitotic arrest via induction of apoptosis and activation of ERK1/2 protein. DMU-212 has oral bioavailability[1][2].
In Vivo: DMU-212 (50 mg/kg; i.g.; three times a week; for 14 days) inhibits tumor growth in xenograft model of human ovarian cancer[2]. Animal Model: 6-weeks-old SCID female mice (20-24 g), with ovarian cancer xenografts[2] Dosage: 50 mg/kg Administration: Oral gavage, three times a week, for 14 days Result: Lower tumor burden.
In Vitro: DMU-212 (0.3125-40 μM) inhibits growth of A375, MeWo, Bro and M5 cells human melanoma cells[1]. DMU-212 (30-50 μM; 24 hours) induces upregulation of cell cycle inhibitors, apoptosis and ERK activation in A375 cells[1]. DMU-212 induces upregulation of cell cycle inhibitors, apoptosis and ERK activation in A375 cells[1]. DMU-212 induces G2/M arrest and apoptosis in cancer cells[1]. DMU-212 induces mitotic arrest, apoptosis and activation of ERK1/2 protein[1]. Cell Proliferation Assay[1] Cell Line: A375 cells, MeWo cells, M5 cells, Bro cells Concentration: 0.3125 μM, 0,625 μM, 1.25 μM, 2.5 μM, 5 μM, 10 μM, 20 μM, 40 μM Incubation Time: 96 hours Result: Inhibited the cellular proliferation of human melanoma cells at submicromolar or micromolar concentrations (IC50=0.5 μM for A375 and Bro and IC50= 1.25 μM for MeWo and M5 cells). Cell Cycle Analysis[1] Cell Line: A375 cells Concentration: 20 μM, 30 μM, 50 μM Incubation Time: 24 hours Result: Caused a marked increase in the levels of p21, p53 and cyclin B1 proteins with a concomitant decrease in the levels of cyclin A2. Western Blot Analysis[1] Cell Line: A375 cells Concentration: 20 μM, 30 μM, 50 μM Incubation Time: 24 hours Result: Significant upregulation of Bax, caspase 3 and caspase 9 protein levels, while the levels of the anti-apoptotic protein Bcl-2 were decreased.
References: [1]. Vasilis Pericles Androutsopoulos, et al. Activation of ERK1/2 is required for the antimitotic activity of the resveratrol analogue 3,4,5,4'-tetramethoxystilbene (DMU-212) in human melanoma cells. Exp Dermatol. 2015 Aug;24(8):632-4. [2]. Hanna Piotrowska, et al. DMU-212 inhibits tumor growth in xenograft model of human ovarian cancer. Biomed Pharmacother. 2014 May;68(4):397-400.
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