6936-94-3

Usage

Uses

Used in Hormone Replacement Therapy:
4-nitroestradiol is used as a hormone replacement therapy agent for managing symptoms associated with menopause and other conditions related to estrogen deficiency. Its ability to selectively bind to estrogen receptors and regulate gene expression makes it a potential candidate for hormone replacement therapy.
Used in Cancer Treatment:
4-nitroestradiol is used as a cancer treatment agent, particularly against hormone-dependent cancers such as breast and endometrial cancers. It modulates estrogen receptor function and has shown potential in inhibiting tumor growth and progression.
Used in Research:
4-nitroestradiol is used as a research tool for studying estrogen receptor function and the role of estrogen in various physiological processes. Its unique properties make it valuable for understanding the mechanisms of estrogen action and for developing new therapeutic interventions.
Used in Pharmaceutical Industry:
4-nitroestradiol is used as a pharmaceutical compound for developing new drugs and therapies targeting estrogen receptors. Its potential applications in hormone replacement therapy, cancer treatment, and research make it a promising candidate for further development and commercialization.
Note: The use of 4-nitroestradiol also raises some concerns due to its potential toxic effects, and further research is needed to fully understand its mechanisms of action and potential applications.

Upstream product

• 50-28-2 estradiol 
• 5976-74-9 4-nitroestrone 
• 64-19-7 acetic acid 

Downstream Products

• 20823-11-4 2,4-dinitro-17β-estradiol 
• 6301-88-8 4-aminoestra-1,3,5(10)-triene-3,17β-diol 

Relevant academic research and scientific papers

Bismuth nitrate-induced novel nitration of estradiol: An entry to new anticancer agents

Direct nitration of estradiol was carried out using metal nitrates on solid surfaces under mild condition, and a combination of bismuth nitrate pentahydrate impregnated KSF clay was found to be the best reagent to synthesize 2- and 4-nitroestradiol effectively. Furthermore, various basic side chains were introduced, through O-linker at C-3, to these nitroestradiols. The ability of these derivatives to cause cytotoxicity in Estrogen Receptor (ER)-positive and ER-negative breast cancer cell lines, as well as cancer cell lines of other origins, was examined. Qualitative structure activity relationship (SAR) has also been studied. We found that a basic side chain containing either a piperidine or morpholine ring, when conjugated to 2-nitroestradiol, was particularly effective at causing cytotoxicity in each of the cancer cell lines examined. Surprisingly, this effective cytotoxicity was even seen in ER-negative breast cancer cells.

17beta-Estradiol nitration by peroxidase/H2O2/NO2-: a chemical assessment.

Nitration of 17beta-estradiol by H(2)O(2) and nitrite in the presence of various peroxidases, viz. horseradish peroxidase, lactoperoxidase, and peroxidase-containing homogenates from bovine uteri, was systematically investigated to assess on a chemical basis its potential relevance to the mechanisms of impairment of estrogen functions under oxidative/nitrosative stress conditions. In the presence of excess nitrite 17beta-estradiol reacted smoothly to give 2-nitroestradiol (1), 4-nitroestradiol (2), and 2,4-dinitroestradiol (3). With 10-300 microM estradiol, formation yields of 1-3 were 12-55%, but dropped to 1% or less at lower estrogen concentration, for example, 1 microM, or in plasma as the reaction medium. Time course analysis showed that 2 is the prevalent nitration product under conditions of slow generation of nitrating species, suggesting some regioselectivity for estradiol nitration at C-4, whereas 1 prevails with bolus addition of reagents, due to faster degradation of 2. Competition experiments carried out with (15)NO(2)- showed that 2 is about twice more susceptible to nitration than 1 as determined by (15)N NMR analysis of the resulting 3. The biological effects of 1 and 2 were preliminarily tested on in vitro bovine embryo cultures. When 1 and 2 were substituted to the standard 17beta-estradiol in the oocyte maturation, a significant decrease in both cleavage and blastocyst efficiency was observed in the case of 1 but not 2. Overall, these results suggest that estradiol nitration is a potential pathway of hormonal dysfunction and toxicity but would require elevated estrogen levels of questionable physiological relevance.