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Tamoxifen (20mg/capsule), 60 Capsules
Tamoxifen is a triphenylethylene-class selective estrogen receptor modulator (SERM) that exhibits ligand-dependent interactions with estrogen receptors ERα and ERβ.
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Voir les résultats d’analyse →Tamoxifen is a triphenylethylene-class selective estrogen receptor modulator (SERM) that exhibits ligand-dependent interactions with estrogen receptors ERα and ERβ. Experimental investigations have demonstrated that tamoxifen induces distinct receptor conformations that influence co-regulator recruitment, resulting in differential transcriptional activity across estrogen receptor signaling systems.
Its well-characterized pharmacology has made it a benchmark compound for studies of estrogen receptor modulation, ligand-receptor interactions, receptor conformational dynamics, nuclear receptor signaling, and transcriptional regulation.
Tamoxifen is also widely utilized in inducible CreERT2 systems, where ligand-dependent activation of modified estrogen receptor domains enables controlled recombination in genetic research models.
Research applications include ERα/ERβ pharmacology, SERM mechanism investigation, co-regulator recruitment studies, inducible recombination systems, and comparative analyses of selective estrogen receptor modulators.
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3D Molecular Structure
Drag to rotate · scroll to zoom| Chemical Formula | C26H29NO |
|---|---|
| Synonyms | Nolvadex (trade name), ICI-46474, TMX, (Z)-Tamoxifen |
| Molar Mass | 371.52 g/mol |
| CAS Number | 10540-29-1 |
| PubChem CID | 2733526 |
| Total Compound Content | 1,200 mg (20 mg per capsule) |
| Shelf Life | 36 months |
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What is tamoxifen's role in CreERT2 conditional recombination systems?
Tamoxifen is widely utilized in CreERT2-based inducible recombination systems, which employ a fusion protein consisting of Cre recombinase linked to a modified estrogen receptor ligand-binding domain. In the absence of ligand binding, the fusion protein remains functionally inactive.
Upon tamoxifen-mediated activation, CreERT2 undergoes conformational changes that permit recombinase activity at loxP recognition sites, enabling controlled genetic recombination. This mechanism has made tamoxifen an indispensable tool for studies requiring inducible and temporally regulated gene modification in experimental systems.
How do tamoxifen metabolites differ from the parent compound in estrogen receptor research?
Tamoxifen undergoes extensive metabolic conversion to several active metabolites, including endoxifen and 4-hydroxytamoxifen, which exhibit substantially greater affinity for estrogen receptors than the parent molecule.
These metabolites are frequently investigated in studies of estrogen receptor binding, ligand-receptor interactions, receptor conformational dynamics, and transcriptional regulation. Their enhanced receptor affinity makes them valuable tools for comparative analyses of estrogen receptor pharmacology and SERM-associated signaling mechanisms.
What distinguishes tamoxifen from other selective estrogen receptor modulators in research applications?
Tamoxifen is characterized by its extensively studied interactions with ERα and ERβ, its well-defined effects on receptor conformation and co-regulator recruitment, and its broad utility in both receptor pharmacology and inducible recombination systems. These properties make it a benchmark compound for investigations of selective estrogen receptor modulation, nuclear receptor signaling, transcriptional regulation, ligand-dependent receptor activity, and comparative studies of SERM pharmacology.
Customer Reviews (5)
I will reorder again soon. Thank you very much. The product is great.
Absolutely thrilled with the prompt communication, happy with the quality of this compound. Great value. My test results are great.
Cannot recommend enough how fast it shipped. it's an exceptionally pure batch. The research results have been great so far. Will purchase again soon.
Top-notch quality from the service. In addition, happy with the quality of this compound. Our lab's research outcomes exceeded what we expected. Will buy again.