CAS No.: 50-28-2
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Beta-Estradiol; 17beta-Estradiol; 50-28-2; Oestradiol; Dihydrofolliculin
|Description:||Therapeutic Estradiol(CAS: 50-28-2) is a synthetic form of estradiol, a steroid sex hormone vital to the maintenance of fertility and secondary sexual characteristics in females, that may be used as hormone replacement therapy. Typically esterified, estradiol derivatives are formulated for oral, intravaginal, transdermal, or parenteral administration. As the primary, most potent estrogen hormone produced by the ovaries, estradiol binds to and activates specific nuclear receptors.|
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Therapeutic Estradiol(CAS: 50-28-2) is a synthetic form of estradiol, a steroid sex hormone vital to the maintenance of fertility and secondary sexual characteristics in females, that may be used as hormone replacement therapy. Typically esterified, estradiol derivatives are formulated for oral, intravaginal, transdermal, or parenteral administration. As the primary, most potent estrogen hormone produced by the ovaries, estradiol binds to and activates specific nuclear receptors. Estradiol exhibits mild anabolic and metabolic properties, and increases blood coagulability. It may play a role in immune and inflammatory processes.
Estradiol is a naturally occurring hormone circulating endogenously in females. It is commercially available in several hormone therapy products for managing conditions associated with reduced estrogen, such as vulvovaginal atrophy and hot flashes. Some available forms of estradiol include oral tablets, injections, vaginal rings, transdermal patches, sprays, gels, and creams. When used for oral or IM administration, estradiol is commonly synthesized as a pro-drug ester (such as [DB13952], [DB13953], [DB13954], [DB13955], and [DB13956]). Because it has a low oral bioavailability on its own, estradiol is commonly formulated with an ester side-chain. [DB00977] (EE) is a synthetic form of estradiol commonly used as the estrogenic component of most combination oral contraceptive pills (OCPs). Ethinyl estradiol is different from estradiol due to its higher biovailability and increased resistance to metabolism, rendering it more suitable for oral administration.
17beta-estradiol is the 17beta-isomer of estradiol. It has a role as an estrogen, a human metabolite, an EC 18.104.22.168 (aldehyde oxidase) inhibitor, a Daphnia magna metabolite and a mouse metabolite. It is a 17beta-hydroxy steroid and an estradiol.
. Horm Behav. 2014 Sep;66(4):602-18. doi: 10.1016/j.yhbeh.2014.08.011. Epub 2014 Sep 7.
Estradiol and cognitive function: past, present and future.
Author information: (1)Department of Psychology, Hunter College of CUNY, New York, NY, USA. Electronic address: [email protected]
A historical perspective on estradiol's enhancement of cognitive function is presented, and research, primarily in animals, but also in humans, is reviewed. Data regarding the mechanisms underlying the enhancements are discussed. Newer studies showing rapid effects of estradiol on consolidation of memory through membrane interactions and activation of inter-cellular signaling pathways are reviewed as well as studies focused on traditional genomic mechanisms. Recent demonstrations of intra-neuronal estradiol synthesis and possible actions as a neurosteroid to promote memory are discussed. This information is applied to the critical issue of the current lack of effective hormonal (or other) treatments for cognitive decline associated with menopause and aging. Finally, the critical period hypothesis for estradiol effects is discussed along with novel strategies for hormone/drug development. Overall, the historical record documents that estradiol positively impacts some aspects of cognitive function, but effective therapeutic interventions using this hormone have yet to be realized.
DOI: 10.1016/j.yhbeh.2014.08.011 PMCID: PMC4318702 PMID: 25205317 [Indexed for MEDLINE]
. Peptides. 2001 Aug;22(8):1251-63. doi: 10.1016/s0196-9781(01)00449-1.
Estradiol, CCK and satiation.
Author information: (1)Weill Medical College of Cornell University, E. W. Bourne Laboratory, Department of Psychiatry, 21 Bloomingdale Road, White Plains, NY 10605, USA. [email protected]
Estradiol has long been known to inhibit feeding in animals, but the mechanism(s) mediating its effects have not been clear. Demonstrations that estradiol's feeding effects are expressed as decreases in meal size coupled with the emerging consensus that cholecystokinin (CCK) released from the small intestines during meals is a physiological negative-feedback signal controlling meal size (i.e. satiation) suggested a new approach to the problem of the mechanisms of estradiol's inhibitory effect on feeding. Progress on this approach is reviewed here. Experimental manipulations of exogenous and endogenous CCK and estradiol have produced converging evidence that estradiol cyclically increases the activity of the CCK satiation-signaling pathway so that meal size and food intake decrease during the ovulatory or estrus phase of the ovarian cycle. This is a striking example of the modulation of the operation of a control of meal size by the physiological context in which the meal occurs. Estradiol also produces a tonic decrease in meal size, but this apparently does not involve the CCK satiation-signaling pathway. Where and how estradiol acts to increase the potency of the CCK satiating-signaling pathway are not known. Several possible sites are suggested by the observations that estradiol treatment increases feeding- and CCK-induced expression of c-Fos in ovariectomized animals in brain areas including the nucleus tractus solitarius, paraventricular nucleus of the hypothalamus, and central nucleus of the amygdala. Tests with null mutation mice indicate that estrogen receptor-alpha is necessary for estradiol's feeding effects. Finally, the possibilities that estradiol exerts important influences on normal or disordered eating in women are discussed. It is concluded that estradiol exerts a biologically significant action on CCK satiation in animals. Further research to determine whether this action of estradiol has a role in the pathogenesis, course, or treatment of disordered eating in women is indicated.
DOI: 10.1016/s0196-9781(01)00449-1 PMID: 11457518 [Indexed for MEDLINE]
. Physiol Behav. 2011 Sep 26;104(4):517-24. doi: 10.1016/j.physbeh.2011.04.014. Epub 2011 Apr 20.
The ovarian hormone estradiol plays a crucial role in the control of food intake in females.
Author information: (1)Program in Neuroscience, Florida State University, 1107 West Call Street,Tallahassee, FL 32306-4301, USA. [email protected]
Despite a strong male bias in both basic and clinical research, it is becoming increasingly accepted that the ovarian hormone estradiol plays an important role in the control of food intake in females. Estradiol's feeding inhibitory effect occurs in a variety of species, including women, but the underlying mechanism has been studied most extensively in rats and mice. Accordingly, much of the data reviewed here is derived from the rodent literature. Adult female rats display a robust decrease in food intake during estrus and ovariectomy promotes hyperphagia and weight gain, both of which can be prevented by a physiological regimen of estradiol treatment. Behavioral analyses have demonstrated that the feeding inhibitory effect of estradiol is mediated entirely by a decrease in meal size. In rats, estradiol appears to exert this action indirectly via interactions with peptide and neurotransmitter systems implicated in the direct control of meal size. Here, I summarize research examining the neurobiological mechanism underlying estradiol's anorexigenic effect. Central estrogen receptors (ERs) have been implicated and activation of one ER subtype in particular, ERα, appears both sufficient and necessary for the estrogenic control of food intake. Future studies are necessary to identify the critical brain areas and intracellular signaling pathways responsible for estradiol's anorexigenic effect. A clearer understanding of the estrogenic control of food intake is prerequisite to elucidating the biological factors that contribute to obesity and eating disorders, both of which are more prevalent in women, compared to men.
DOI: 10.1016/j.physbeh.2011.04.014 PMCID: PMC3139826 PMID: 21530561 [Indexed for MEDLINE]
. Neuropsychopharmacology. 2016 Feb;41(3):774-80. doi: 10.1038/npp.2015.202. Epub 2015 Jul 9.
Estradiol and Progesterone have Opposing Roles in the Regulation of Fear Extinction in Female Rats.
Graham BM(1), Daher M(1).
Author information: (1)School of Psychology, The University of New South Wales Australia, Sydney, NSW, Australia.
Fear extinction, the laboratory basis of exposure therapy for anxiety disorders, fluctuates across the female rat estrous cycle, where extinction is enhanced during proestrus (high estradiol and progesterone), and impaired during metestrus (low estradiol and progesterone). During the estrous cycle increasing levels of estradiol precede and then overlap with increased levels of progesterone. We sought to isolate the impact of these hormonal changes on fear extinction by systematically treating ovariectomized female rats with estradiol alone, or in combination with progesterone. We found that estradiol alone facilitated extinction recall, whereas the effects of progesterone on estradiol-treated rats were biphasic and dependent on the time interval between progesterone administration and extinction training. Progesterone potentiated estradiol's facilitation of extinction recall when extinction training occurred 6 h after progesterone administration. However, progesterone abolished estradiol's facilitation of extinction recall when extinction training occurred 24 h after progesterone administration. Furthermore, in naturally cycling rats, blocking progesterone receptor activation during proestrus (when progesterone levels peak) prevented the impairment in extinction recall in rats extinguished during metestrus. These results suggest that in naturally cycling females whereas cyclical increases in estradiol facilitate fear extinction, cyclical increases in progesterone may lead to fear extinction impairments. As extinction training took place after the hormonal treatments had been metabolized, we propose that genomic mechanisms may at least partly mediate the impact of cyclic fluctuations in sex hormones on fear extinction.
DOI: 10.1038/npp.2015.202 PMCID: PMC4707823 PMID: 26156559 [Indexed for MEDLINE]
. Horm Behav. 2020 Apr;120:104694. doi: 10.1016/j.yhbeh.2020.104694. Epub 2020 Jan 27.
Temporal and bidirectional influences of estradiol on voluntary wheel running in adult female and male rats.
Krentzel AA(1), Proaño S(2), Patisaul HB(3), Meitzen J(4).
Author information: (1)Department of Biological Sciences, North Carolina State University, Raleigh, NC, United States of America; W.M. Keck Center for Behavioral Biology, North Carolina State University, Raleigh, NC, United States of America. Electronic address: [email protected] (2)Department of Biological Sciences, North Carolina State University, Raleigh, NC, United States of America; W.M. Keck Center for Behavioral Biology, North Carolina State University, Raleigh, NC, United States of America. (3)Department of Biological Sciences, North Carolina State University, Raleigh, NC, United States of America; W.M. Keck Center for Behavioral Biology, North Carolina State University, Raleigh, NC, United States of America; Center for Human Health and the Environment, North Carolina State University, Raleigh, NC, United States of America. (4)Department of Biological Sciences, North Carolina State University, Raleigh, NC, United States of America; W.M. Keck Center for Behavioral Biology, North Carolina State University, Raleigh, NC, United States of America; Center for Human Health and the Environment, North Carolina State University, Raleigh, NC, United States of America; Comparative Medicine Institute, North Carolina State University, Raleigh, NC, United States of America.
The sex steroid hormone 17β-estradiol (estradiol) regulates animal behavior as both a non-rapid hormone signal and as a rapid-acting neuromodulator. By practical necessity, estradiol's divergent temporal actions on rodent behavior are typically studied singularly and in one sex. We hypothesized that estradiol simultaneously acts through both temporal mechanisms to sex-specifically modulate a single behavior; and furthermore, that estradiol action in one temporal domain may regulate action in another. To test this hypothesis, we utilized one of the most robust rat behaviors exhibiting sex differences and estradiol-responsiveness, voluntary wheel running. Adult female and male rats were gonadectomized and exposed to daily repeated estradiol benzoate (EB) injections. Estradiol-sensitive running behavior was continually assessed in both the rapid and non-rapid temporal domains. We found that in female rats, estradiol rapidly decreased voluntary wheel running, but only after prior daily EB injections, supporting the hypothesis that non-rapid estradiol action influences rapid estradiol actions. Males exhibited a similar but less robust response, demonstrating sex-responsiveness. This rapid estradiol-induced decrease in running contrasted to non-rapid estradiol action which overall increased running in both sexes, revealing a bidirectional nature of estradiol's temporal influence. Non-rapid estradiol action also demonstrated sex-responsiveness, as a higher dose of EB was required to induce increased running in males compared to females. These findings indicate that estradiol rapidly, non-rapidly, and bidirectionally modulates wheel running in a sex-responsive manner, and that rapid estradiol action is modulated by non-rapid estradiol action. Overall, these data illustrate estradiol as a pleiotropic sex-responsive neuromodulator of a single behavior across temporal domains.
DOI: 10.1016/j.yhbeh.2020.104694 PMCID: PMC7117976 PMID: 31978389 [Indexed for MEDLINE]
Originator: CAPA Vision
Developer: CAPA Vision; Redwood Pharma
Class: Antineoplastics; Estradiol congeners; Estrenes; Hormonal replacements; Small molecules
Mechanism of Action: Estrogen receptor agonists
Orphan Drug Status: No
New Molecular Entity: No