<unk>  (E2S), or 17β-estradiol 3-sulfate, is a natural, endogenous steroid and an estrogen ester. E2S itself is biologically inactive, but it can be converted by steroid<unk> se (also called estrogen<unk> se) into<unk> , which is a potent estrogen. Simultaneously, estrogen sulfotransferases convert<unk>  to E2S, resulting in an equilibrium between the two steroids in various tissues. Estrone and E2S are the two immediate metabolic sources of<unk> . E2S can also be metabolized into estrone<unk>  (E1S), which in turn can be converted into estrone and<unk> . Circulating concentrations of E2S are much lower than those of E1S. High concentrations of E2S are present in breast tissue, and E2S has been implicated in the biology of breast cancer via serving as an active reservoir of<unk> . As the sodium salt, sodium<unk> , E2S is present as a minor constituent (0.9%) of conjugated equine estrogens (CEEs), or Premarin. It effectively functions as a prodrug to<unk>  in this preparation, similarly to E1S. E2S is also formed as a metabolite of<unk> , as well as of estrone and E1S. Aside from its presence in CEEs, E2S is not available as a commercial pharmaceutical drug. E2S shows about 10,000-fold lower potency in activating the estrogen receptors relative to<unk>  in vitro. It is 10-fold less potent than estrone<unk>  orally in terms of in vivo uterotrophic effect in rats. Estrogen<unk> s like<unk>  or estrone<unk>  are about twice as potent as the corresponding free estrogens in terms of estrogenic effect when given orally to rodents. This in part led to the introduction of conjugated estrogens (Premarin), which are primarily estrone<unk> , in 1941. Although inactive at steroid hormone receptors, E2S has been found to act as a potent inhibitor of glutathione S-transferase, an enzyme that contributes to the inactivation of<unk>  via conversion of it into an<unk> -glutathione conjugate. As such, E2S can indirectly serve as a positive effector of estrogen signaling.<unk>  levels are about 1.5- to 4-fold higher than E2S levels in women. This is in contrast to E1S, the levels of which are about 10 to 15 times higher than those of estrone. E2S at an oral dosage of 5 mg/day in women resulted in inhibition of ovulation in 89% of cycles (47 of 53).
Estradiol sulfate
Estradiol acetate
Alfatradiol
Estradiol undecylate
Estradiol dienantate
Estradiol furoate
Estradiol valerate
Estradiol enantate