Pharmacodynamics<unk> is an estrogen, or an agonist of the estrogen receptors (ERs), the and . It is also an agonist of membrane estrogen receptors (mERs), including the , , ER-X, and ERx.<unk> is highly selective for these ERs and mERs, and does not interact importantly with other steroid hormone receptors. It is far more potent as an estrogen than are other bioidentical estrogens like estrone and estriol. Given by subcutaneous injection in mice,<unk> is about 10-fold more potent than estrone and about 100-fold more potent than estriol. The ERs are expressed widely throughout the body, including in the breasts, uterus, vagina, fat, skin, bone, liver, pituitary gland, hypothalamus, and other parts of the brain. In accordance,<unk> has numerous effects throughout the body. Among other effects,<unk> produces breast development, feminization, changes in the female reproductive system, changes in liver protein synthesis, and changes in brain function. The effects of<unk> can influence health in both positive and negative ways. In addition to the aforementioned effects,<unk> has antigonadotropic effects due to its estrogenic activity, and can inhibit ovulation and suppress gonadal sex hormone production. At sufficiently high dosages,<unk> is a powerful antigonadotropin, capable of suppressing testosterone levels into the castrate/female range in men. There are differences between<unk> and other estrogens, such as non-bioidentical estrogens like natural conjugated estrogens and synthetic estrogens like ethinylestradiol and diethylstilbestrol, with implications for pharmacodynamics and pharmacokinetics as well as efficacy, tolerability, and safety. Pharmacokinetics<unk> can be taken by a variety of different routes of administration. These include oral, buccal, sublingual, intranasal, transdermal (gels, creams, patches), vaginal (tablets, creams, rings, suppositories), rectal, by intramuscular or subcutaneous injection (in oil or aqueous), and as a subcutaneous implant. The pharmacokinetics of<unk>  including its bioavailability, metabolism, biological half-life, and other parameters, differ by route of administration. Likewise, the potency of<unk>  and its local effects in certain tissues, most importantly the liver, differ by route of administration as well. In particular, the oral route is subject to a high first-pass effect, which results in high levels of<unk> and consequent estrogenic effects in the liver and low potency due to first-pass hepatic and intestinal metabolism into metabolites like estrone and estrogen conjugates. Conversely, this is not the case for parenteral (non-oral) routes, which bypass the intestines and liver. Different<unk> routes and dosages can achieve widely varying circulating<unk> levels. For purposes of comparison with normal physiological circumstances, menstrual cycle circulating levels of<unk> in premenopausal women are 40 pg/mL in the early follicular phase, 250 pg/mL at the middle of the cycle, and 100 pg/mL during the mid-luteal phase. Mean integrated levels of circulating<unk> in premenopausal women across the whole menstrual cycle have been reported to be in the range of 80 and 150 pg/mL, according to some sources.
Estradiol 
Estrogen
Estrogen 
Alfatradiol
Androgen
17α-Estradiol
Progesterone 
Progesterone