Testosterone acetate, a testosterone ester, is an androgen. It is a steroid lipid molecule considered to be practically insoluble (in water) and basic. It is an anabolic steroid and testosterone prodrug. Testosterone acetate has a faster rate of absorption in the body then other esters. In combination with two other testosterone esters, testosterone valerate and testosterone undecanoate, it is a part of Deposterona, an injectable veterinary blend steroid preparation marketed in Mexico. With its blend of slow and fast-acting esters, Deposterona is essentially a low dosed alternative to Sustanon and is used primarily to treat impotence, weakness, fatigue, and hypogonadism in male breeding animals (cows, pigs, canines, and sheep), and also as a general protein-sparing anabolic. Testosterone acetate is classified as a Schedule III drug by the United States Drug Enforcement Agency and is only legal with a prescription due to his potential for misuse and abuse.

FLUROGESTONE (9α-FLUORO-11β,17α-DIHYDROXYPROGESTERONE) is a steroidal progestin of the 17α-hydroxyprogesterone group that was never marketed. An acetate ester, flurogestone acetate, is used in veterinary medicine. It has progestational action higher than that of progesterone itself. It is intended for intravaginal use in sheep and goats to induce oestrus synchronisation. The proposed dosage is 1 sponge, impregnated with 30, 40 (for sheep) or 45 mg (for goats) flugestone acetate, which is to be removed after 12 to 14 days from ewes and after 17 to 21 days from goats. Flugestone acetate is not indicated for use in humans.

Fluperolone (P-1742 or Methral) is a topical fluorinated prednisolone derivative exerting an anti-inflammatory activity. It demonstrated effectivity in the treatment of various dermatoses.

Clostebol acetate (4-chloro-testosterone acetate), an anabolic androgenic agent used for fattening purposes in cattle breeding or applied topically in ophthalmological and dermatological treatments. The European Commission has prohibited its use since 1986.

Methadyl Acetate is a narcotic analgesic with a long onset and duration of action. Methadyl Acetate is primarily a mu-type opioid receptor agonist and the drug decreases a patient's opioid use by preventing opioid withdrawal. Levacetylmethadol, the enantiomer of Methadyl Acetate, was approved in 1993 by the U.S. Food and Drug Administration for use in the treatment of opioid dependence. In 2001, levacetylmethadol was removed from the U.S. market due to reports of life-threatening ventricular rhythm disorders.

Fluprednidene (used in a form of fluprednidene 21-acetate) is a glucocorticoid developed for the treatment of inflammatory skin diseases. The drug is marketed under the name Decoderm in Europe.

Chloroprednisone acetate is the 21-acetate ester of chloroprednisone. Chloroprednisone acetate was sold under the brand name Topilan as an anti-inflammatory agent.

Cyproterone belongs to a group of medications known as steroidal antiandrogens. It suppresses testosterone and its metabolites. It has approximately three-fold lower potency as an antagonist of the androgen receptor relative to cyproterone acetate. Cyproterone acetate is used to treat advanced prostate cancer and acne.

Loteprednol (as the ester loteprednol etabonate) is a corticosteroid used to treat inflammations of the eye. It is marketed by Bausch and Lomb as Lotemax. It is a topical corticoid anti-inflammatory. It is used in ophthalmic solution for the treatment of steroid responsive inflammatory conditions of the eye such as allergic conjunctivitis, uveitis, acne rosacea, superficial punctate keratitis, herpes zoster keratitis, iritis, cyclitis, and selected infective conjunctivitis’s. Lotemax is less effective than prednisolone acetate 1% in two 28-day controlled clinical studies in acute anterior uveitis, where 72% of patients treated with Lotemax experienced resolution of anterior chamber cells, compared to 87% of patients treated with prednisolone acetate 1%. Lotemax is also indicated for the treatment of post-operative inflammation following ocular surgery. Corticosteroids inhibit the inflammatory response to a variety of inciting agents and probably delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, deposition of collagen, and scar formation associated with inflammation. There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Corticosteroids are capable of producing a rise in intraocular pressure (IOP). Loteprednol etabonate is structurally similar to other corticosteroids. However, the number 20 position ketone group is absent. It is highly lipid soluble, which enhances its penetration into cells. Loteprednol etabonate is synthesized through structural modifications of prednisolone-related compounds so that it will undergo a predictable transformation to an inactive metabolite. Based upon in vivo and in vitro preclinical metabolism studies, loteprednol etabonate undergoes extensive metabolism to inactive carboxylic acid metabolites. Lotemax possesses some adverse reactions associated with ophthalmic steroids include elevated intraocular pressure, which may be associated with optic nerve damage, visual acuity and field defects, posterior subcapsular cataract formation, secondary ocular infection from pathogens including herpes simplex, and perforation of the globe where there is thinning of the cornea or sclera.

Anagestone acetate is a progestin medication, used in the 1960s in combination with the estrogen mestranol as a combined birth control pill. Toxicological study of chronic administration in dogs and monkeys showed the increased risk of developing malignant tumors in the mammary glands and a dose-dependent, nonprogressive decrease in hemoglobin and hematocrits. The drug was voluntarily withdrawn from the market in 1969.