SMB00388
2,4,3′,5′-四甲氧基二苯乙烯
≥98% (HPLC)
别名:
2,4,3′,5′-tetramethoxystilbene, 1-[(1E)-2-(3,5-dimethoxyphenyl)ethenyl]-2,4-dimethoxy-benzene, 2,3′,4,5′-Tetramethoxystilbene
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关于此项目
经验公式（希尔记法）:
C18H20O4
化学文摘社编号:
分子量:
300.35
NACRES:
NA.79
PubChem Substance ID:
UNSPSC Code:
85151701
MDL number:
产品名称
2,4,3′,5′-四甲氧基二苯乙烯, ≥98% (HPLC)
Quality Level
InChI
1S/C18H20O4/c1-19-15-8-7-14(18(12-15)22-4)6-5-13-9-16(20-2)11-17(10-13)21-3/h5-12H,1-4H3/b6-5+
SMILES string
COC1=CC(OC)=CC=C1/C=C/C2=CC(OC)=CC(OC)=C2
InChI key
JDBCWSHYEQUBLW-AATRIKPKSA-N
assay
≥98% (HPLC)
form
powder
technique(s)
HPLC: suitable
color
white to yellow
storage temp.
−20°C
Biochem/physiol Actions
2,3′,4,5′-Tetramethoxystilbene, also known as TMS, is a selective and competitive inhibitor of cytochrome P450 1B. It is a synthetic trans-stilbene analog. TMS is an analog of resveratrol and is an anti-cancer agent. TMS is cytotoxic to gefitinib-resistant (G-R) non-small-cell lung cancer (NSCLC) cells. It binds to sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) and promotes apoptosis and autophagy. TMS is also a selective inhibitor of CYP1B1.
A new selective and potent inhibitor of human cytochrome P450 1B1 and its application to antimutagenesis
Chun YJ, et al.
Cancer Research, 61(22), 8164-8170 (2001)
The resveratrol analogue, 2, 3?, 4, 5?-tetramethoxystilbene, does not inhibit CYP gene expression, enzyme activity and benzo [a] pyrene-DNA adduct formation in MCF-7 cells exposed to benzo [a] pyrene
Einem Lindeman T, et al.
Mutagenesis, 26(5), 629-635 (2011)
(Z) 3, 4, 5, 4?-trans-tetramethoxystilbene, a new analogue of resveratrol, inhibits gefitinb-resistant non-small cell lung cancer via selectively elevating intracellular calcium level
Fan XX, et al.
Scientific Reports, 5, 16348-16348 (2015)
Modulation of human cytochrome P450 1B1 expression by 2, 4, 3?, 5?-tetramethoxystilbene
Chun YJ, et al.
Drug Metabolism and Disposition, 33(12), 1771-1776 (2005)
Maria Tsachaki et al.
Cellular and molecular life sciences : CMLS, 77(6), 1153-1175 (2019-07-16)
Metabolic reprogramming of tumor cells involves upregulation of fatty acid (FA) synthesis to support high bioenergetic demands and membrane synthesis. This has been shown for cytosolic synthesis of FAs with up to 16 carbon atoms. Synthesis of long-chain fatty acids
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