β-Estradiol 17-acetate is a natural metabolite of estradiol. Hydrolytic enzymes in human cadaver, hairless dog, rat and hairless mouse skin can metabolize β-Estradiol 17-acetate to β-Estradiol. β-Estradiol 17-acetate transported across the human and hairless dog skin can be effectively metabolized before entering the capillary.

Estradiol mustard (developmental code name NSC-112259), also known as chlorphenacyl estradiol diester, as well as estradiol 3,17β-bis(4-(bis(2-chloroethyl)amino)phenyl)acetate, is a synthetic, steroidal estrogen and alkylating antineoplastic agent and a nitrogen mustard-coupled estrogen ester that was never marketed.[1] It is selectively distributed into estrogen receptor (ER)-positive tissues such as ER-expressing tumors like those seen in breast and prostate cancers. For this reason, estradiol mustard and other cytostatic-linked estrogens like estramustine phosphate have reduced toxicity relative to non-linked nitrogen mustard alkylating antineoplastic agents. However, they may stimulate breast tumor growth due to their inherent estrogenic activity and are said to be devoid of major therapeutic efficacy in breast cancer,[3] although estramustine phosphate has been approved for and is used (almost exclusively) in the treatment of prostate cancer.

Estradiol-glucoside, also known as E2-3beta-glucoside, is a novel conjugated estrogen synthesized by attaching a glucose molecule to the 3beta position of estradiol. This glucoside derivative is a water-soluble estrogen that is easily absorbed from the gastrointestinal tract and achieves favorable systemic estrogen levels. The results of a randomized, double-blinded controlled pilot study have revealed, that estradiol-glucoside reduced serum gonadotropin levels in the premenopausal range and could be effective at reducing postmenopausal symptoms. As a conclusion, was made the assumption, that estradiol-glucoside can serve as a hormone replacement therapy.