Tamoxifen - CAS 10540-29-1
Catalog number: B0084-358326
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C26H29NO
Molecular Weight:
371.51
COA:
Inquire
Targets:
Estrogen Receptor/ERR
Description:
Tamoxifen, a selective estrogen response modifier, is used in the advanced treatment of breast and ovarian cancer for it could be metabolized to two active ingredients, 4-hydroxytamoxifen and endoxifen.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-358326 50 g $250 In stock
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Brife Description:
estrogen response modifier, breast and ovarian cancer
Purity:
95%
Appearance:
fine off-white crystalline powder
Synonyms:
(Z)-1-(p-Dimethylaminoethoxyphenyl)-1,2-diphenyl-1-butene, trans-2-[4-(1,2-Diphenyl-1-butenyl)phenoxy]-N,N-dimethylethylamine
Solubility:
DMSO 100 mg/mL; Water <1 mg/mL
Storage:
2-8ºC
MSDS:
Inquire
Application:
Tamoxifen is used in the advanced treatment of breast and ovarian cancer.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Quantity:
Grams-Kilos
Melting Point:
97-98ºC
Density:
1.042 g/cm3
InChIKey:
NKANXQFJJICGDU-QPLCGJKRSA-N
InChI:
InChI=1S/C26H29NO/c1-4-25(21-11-7-5-8-12-21)26(22-13-9-6-10-14-22)23-15-17-24(18-16-23)28-20-19-27(2)3/h5-18H,4,19-20H2,1-3H3/b26-25-
Canonical SMILES:
CCC(=C(C1=CC=CC=C1)C2=CC=C(C=C2)OCCN(C)C)C3=CC=CC=C3
1.SiO2 nanoparticles modified CPE as a biosensor for determination of i-motif DNA/Tamoxifen interaction.
Heydari E1, Raoof JB2, Ojani R1, Bagheryan Z1. Int J Biol Macromol. 2016 May 2. pii: S0141-8130(16)30406-8. doi: 10.1016/j.ijbiomac.2016.05.001. [Epub ahead of print]
Cytosine-rich DNA sequences can form a highly ordered structure known as i-motif in slightly acidic solutions. The stability of the folded i-motif structure is a good strategy to inhibit the telomerase reaction in cancer cells. The electrochemical biosensor was prepared by modifying carbon paste electrode with SiO2 nanoparticles to investigate drugs which can stabilize this structure. Tamoxifen (Tam), an antiestrogen hormonal agent for treatment of breast cancer, was chosen as the model ligand and its interaction with i-motif structure was examined. The interaction between i-motif DNA and Tam was studied in PBS buffer and [Fe(CN)6]3- through the cyclic voltammetry and square wave voltammetry methods. The oxidation peak of Tam, due to the i-motif DNA/Tam interaction, was observed after i-motif immobilized on the surface of the electrode. The i-motif formation was investigated by circular dichroism spectroscopy and the results showed that this structure can certainly be made with pH around 4.
2.Sustained release of melatonin: A novel approach in elevating efficacy of tamoxifen in breast cancer treatment.
Sabzichi M1, Samadi N2, Mohammadian J3, Hamishehkar H4, Akbarzadeh M5, Molavi O6. Colloids Surf B Biointerfaces. 2016 Apr 22;145:64-71. doi: 10.1016/j.colsurfb.2016.04.042. [Epub ahead of print]
BACKGROUND: Finding advanced anti-cancer agents with selective toxicity in tumor tissues is the goal of anticancer delivery systems. This study investigated potential application of nanostructured lipid carriers (NLCs) in increasing melatonin induced cytotoxicity and apoptosis in MCF-7 breast cancer cells.
3.Ceramide-tamoxifen regimen targets bioenergetic elements in acute myelogenous leukemia.
Morad SA1, Ryan TE2, Neufer PD2, Zeczycki TN1, Davis TS1, MacDougall MR1, Fox TE3, Tan SF4, Feith DJ4, Loughran TP Jr4, Kester M3, Claxton DF5, Barth BM6, Deering TG4, Cabot MC7. J Lipid Res. 2016 May 2. pii: jlr.M067389. [Epub ahead of print]
The objective of our study was to determine the mechanism of action of the short-chain ceramide analog, C6-ceramide, and the breast cancer drug, tamoxifen, which we show co-actively depress viability and induce apoptosis in human acute myelogenous leukemia (AML) cells. Exposure to the C6-ceramide-tamoxifen combination elicited decreases in mitochondrial membrane potential and Complex I respiration, increases in reactive oxygen species (ROS), and release of mitochondrial pro-apoptotic proteins. Decreases in ATP levels, reduced glycolytic capacity, and reduced expression of inhibitors of apoptosis proteins (IAP) also resulted. Cytotoxicity of the drug combination was mitigated by exposure to antioxidant. Cells metabolized C6-ceramide by glycosylation and hydrolysis, the latter leading to increases in long-chain ceramides. Tamoxifen potently blocked glycosylation of C6-ceramide and long-chain ceramides. N-Desmethyltamoxifen, a poor antiestrogen and the major tamoxifen metabolite in humans, was also effective with C6-ceramide, indicating that traditional antiestrogen pathways are not involved in cellular responses.
4.Tamoxifen in men: a review of adverse events.
Wibowo E1, Pollock PA1, Hollis N2, Wassersug RJ3. Andrology. 2016 May 6. doi: 10.1111/andr.12197. [Epub ahead of print]
Tamoxifen is an off-label option to treat men for breast cancer, infertility, and idiopathic gynecomastia. Lately, tamoxifen has been proposed as a treatment to prevent gynecomastia in prostate cancer patients receiving antiandrogen therapy. We reviewed the adverse events (AEs) reported in studies of men prescribed tamoxifen for these conditions to better understand its side-effect profile. We searched PubMed for randomized controlled trials (RCTs) that included safety data of tamoxifen treatment in men with prostate cancer, breast cancer, infertility, and idiopathic gynecomastia. Non-RCTs were also reviewed. The results demonstrate that the AE profile in tamoxifen-treated male populations varied. Excluding breast events, gastrointestinal, and cardiovascular problems were the most commonly reported AEs in prostate cancer patients, whereas more psychiatric disorders were reported in male breast cancer patients. Few AEs have been documented in men receiving tamoxifen for infertility and idiopathic gynecomastia.
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CAS 10540-29-1 Tamoxifen

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