[1] Side effects of desogestrel include menstrual irregularities, headaches, nausea, breast tenderness, mood changes, acne, increased hair growth, and others.

[21] Like norethisterone and Norgestrel, Desogestrel is widely available as a progestogen-only "mini pill" for birth control.

[34] Common side effects of desogestrel may include menstrual irregularities, amenorrhea, headaches, nausea, breast tenderness, and mood changes (e.g., depression), as well as weight gain, acne, and hirsutism.

[1] Uncommon side effects of desogestrel may include vaginal infection, contact lens intolerance, vomiting, hair loss, dysmenorrhea, ovarian cysts, and fatigue, while rare side effects include rash, urticaria, and erythema nodosum.

[4] Inducers of liver enzymes can increase the metabolism of desogestrel and etonogestrel and reduce their circulating levels.

[4] Examples of liver enzyme inducers include barbiturates (e.g., phenobarbital), bosentan, carbamazepine, efavirenz, phenytoin, primidone, rifampicin, and possibly also felbamate, griseofulvin, oxcarbazepine, rifabutin, St. John's Wort, and topiramate.

[4] Many antivirals for HIV/AIDS and HCV, such as boceprevir, nelfinavir, nevirapine, ritonavir, and telaprevir, may increase or decrease levels of desogestrel and etonogestrel.

[13][35] However, these activities are relatively weak, and desogestrel is said to be one of the most selective and pure progestogens used in oral contraceptives.

[14] In addition, desogestrel has been extensively investigated as an antigonadotropin at dosages of 150 to 300 μg/day in combination with testosterone in male contraceptive regimens.

[39] A previous study by the same authors found that increasing the dosage of desogestrel from 300 μg/day to 450 μg/day resulted in no further suppression of gonadotropin concentrations.

[39] Upon cessation of treatment, levels of LH, FSH, and testosterone all recovered to baseline values within 4 weeks.

[1][14][37] Although etonogestrel has about the same affinity for the AR as norethisterone, due to the relatively increased progestogenic potency and decreased androgenic activity of etonogestrel, the drug has markedly higher selectivity for the PR over the AR than older 19-nortestosterone progestins like norethisterone and levonorgestrel.

[18][40] It has been estimated that 150 μg/day desogestrel has less than one-sixth of the androgenic effect of 1 mg/day norethisterone (these being common dosages of the drugs used in combined oral contraceptives).

[40] Clinical studies with norethisterone even at very high dosages (e.g., 10 to 60 mg/day) have observed only mild androgenic effects in a minority of women including acne, increased sebum production, hirsutism, and slight virilization of female fetuses.

[14] However, at the dosages used in oral contraceptives and in combination with ethinylestradiol, which has potent functional antiandrogenic effects mainly due to increased SHBG levels, the androgenic activity of desogestrel is said to be essentially without any clinical relevance.

[35] The affinity of etonogestrel for the glucocorticoid receptor is a product of its C11 methylene substitution, as substitutions at the C11 position are a common feature of corticosteroids and as levonorgestrel, which is etonogestrel without the C11 methylene group (17α-ethynyl-18-methyl-19-nortestosterone), has only 1% of the affinity of dexamethasone for the receptor and hence is considered to have negligible glucocorticoid activity.

[14][35] Desogestrel stimulates the proliferation of MCF-7 breast cancer cells in vitro, an action that is independent of the classical PRs and is instead mediated via the progesterone receptor membrane component-1 (PGRMC1).

[47][48] It is unclear if these findings may explain the different risks of breast cancer observed with progesterone and progestins in clinical studies.

[14] Desogestrel is a prodrug of etonogestrel (3-ketodesogestrel) and upon ingestion is rapidly and completely transformed into this metabolite in the intestines and liver.

[1] Following further metabolism of etonogestrel, which occurs mainly by reduction of the Δ4-3-keto group (by 5α- and 5β-reductases) and hydroxylation (by monooxygenases), the major metabolite of desogestrel is 3α,5α-tetrahydroetonogestrel.

[50][51][25] Desogestrel is marketed under a variety of brand names throughout the world including Alenvona, Apri, Azalia, Azurette, Bekyree, Caziant, Cerazette,[4] Cerelle, Cesia, Cyclessa, Cyred, Denise, Desogen, Desirett, Diamilla, Emoquette, Enskyce, Feanolla, Gedarel, Gracial, Hana,[5] Isibloom, Juleber, Kalliga, Kariva, Laurina, Lovima, Marvelon,[2] Mercilon,[3] Mircette, Mirvala, Novynette, Ortho-Cept, Pimtrea, Reclipsen, Regulon, Simliya, Solia, Velivet, Viorele, and Volnea among others.

[34][61] In the UK, in July 2021, some Desogestrel pills were made available to purchase over the counter,[62] without requiring a prescription from a doctor beforehand.

In February 2007, the consumer advocacy group Public Citizen released a petition requesting that the Food and Drug Administration ban oral contraceptives containing desogestrel in the United States, citing studies going as far back as 1995 that suggest the risk of dangerous blood clots is doubled for women on such pills in comparison to other oral contraceptives.

[63] In 2009, Public Citizen released a list of recommendations that included numerous alternative, second-generation birth control pills that women could take in place of oral contraceptives containing desogestrel.

[64] Most of those second-generation medications have been on the market longer and have been shown to be as effective in preventing unwanted pregnancy, but with a lower risk of blood clots.

[64] Medications cited specifically in the petition include Apri-28, Cyclessa, Desogen, Kariva, Mircette, Ortho-Cept, Reclipsen, Velivet, and some generic pills, all of which contain desogestrel in combination with ethinylestradiol.