(Synonyms: Z-Tamoxifen, trans-Tamoxifen, ICI47699) Copy Product Info
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Synonyms: Z-Tamoxifen, trans-Tamoxifen, ICI47699
Catalog No. T6906 Copy Product Info
Purity: 99.97%
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Tamoxifen is an orally active selective estrogen receptor modulator (SERM) that acts as an estrogen antagonist in breast cells and an agonist in bone, liver, and uterine cells. It can be used to induce gene knockout and liver injury models in mice, and also exhibits multiple biological activities, including activation of Hsp90, induction of autophagy and apoptosis, and inhibition of EBOV and MARV viral infections.
Cas No. 10540-29-1
Other Forms of Tamoxifen:
Tamoxifen-D5
Tamoxifen (Standard)
Tamoxifen citrate (Standard)
Tamoxifen-D3 hydrochloride
Tamoxifen Citrate
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Product Information
Bioactivity
Description
Tamoxifen is an orally active selective estrogen receptor modulator (SERM) that acts as an estrogen antagonist in breast cells and an agonist in bone, liver, and uterine cells. It can be used to induce gene knockout and liver injury models in mice, and also exhibits multiple biological activities, including activation of Hsp90, induction of autophagy and apoptosis, and inhibition of EBOV and MARV viral infections.
METHODS: Human breast cancer cells MCF-7 were treated with Tamoxifen (0.25-4 μM) for 24 h. Cell viability was measured using the CCK-8. RESULTS: Tamoxifen significantly inhibited the proliferation of MCF-7 cells in a dose-dependent manner. [1] METHODS: ER-negative breast cancer cells SK-BR3, MDA-MB-453, MDA-MB-468, MDA-MB-231, and HCC-1937 were treated with Tamoxifen (1-10 μM) for 24-36 h, and apoptosis was detected using Flow Cytometry. RESULTS: Tamoxifen induced apoptosis in MDA-MB-231, MDA-MB-468, MDA-MB-453 and SK-BR3 cells in a dose- and time-dependent manner, while no significant apoptotic effect was observed in HCC-1937 cells. [2]
In vivo
METHODS: To test the antitumor activity in vivo, Tamoxifen (100 mg/kg) was administered orally to NCr athymic nude mice bearing ER-negative breast cancer tumors MDA-MB-468 or HCC-1937 three times per week for four to five weeks. RESULTS: Tamoxifen significantly inhibited the growth of MDA-MB-468 tumors, whereas the growth of HCC-1937 tumors was not affected. [2] METHODS: To test the effect on mouse behavior, Tamoxifen (75 mg/kg in 10% ethanol+90% sunflower seed oil) was administered intraperitoneally to C57BL/6 mice once a day for seven days. RESULTS: Tamoxifen affects motor activity, socialization, and anxiety in mice. [3]
Synonyms
Z-Tamoxifen, trans-Tamoxifen, ICI47699
Disease Modeling Protocol
Conditional Genetic Engineering Disease Model
Modeling Mechanism：
Tamoxifen activates the AP-1 transcription factor (upregulating the expression of c-fos, c-jun, and ap1s1 by 3-7 times), driving the potent expression of MMP family genes (especially mmp9 and mmp13a) in skin epithelial cells (upregulated by 127-fold and 1145-fold, respectively). Excessive MMPs degrade the extracellular matrix, inducing skin epithelial cell cytotoxicity, apoptosis, and necrosis, ultimately leading to the tail necrosis phenotype.
1–15 μM tamoxifen (dissolved in 0.1% DMSO, final concentration) Static exposure in embryo medium Exposure by placing embryos/larvae individually in 96-well plates (containing 100 μL embryo medium); adult fish exposed directly to drug-containing medium
Dosing Frequency and Duration Model：
Embryonic stage: Continuous exposure from 6–120 hpf; Larval stage: Single 24-hour exposure at 48–72 hpf; Adult stage: Single 1.5-hour exposure
Validation：
Phenotypic validation: Specific necrosis appeared in the tail, which could extend to the pectoral fins and the entire skin of adult fish. Apoptotic signals (secA5-YFP) were spatiotemporally colocalized with the necrotic area. Molecular markers: qRT-PCR showed signi
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