- Progesterone Receptor (PR): As a progestin, Desogestrel exerts biological effects by binding to PR; specific Ki/EC50 values were not available in the abstract [2][3][4][5]
- PHOX2B (Paired-Like Homeobox 2B): Desogestrel downregulates the expression of PHOX2B and its target genes (e.g., DBH, TH) in progesterone-responsive neuroblastoma cells; specific binding affinity (Ki) or regulatory activity (EC50) values were not available in the abstract [6]

- Metabolism experiments: In vitro metabolism of Desogestrel was investigated using liver microsomes or hepatocytes from several species (e.g., rat, dog, human). The main metabolite identified was 3-keto-desogestrel (3-KD), and the metabolic pathways involved cytochrome P450 (CYP) enzymes (specific CYP isoforms not detailed in the abstract). The metabolic rate and metabolite profile varied among species [1]
- Neuroblastoma cell experiments: Desogestrel was treated to progesterone-responsive neuroblastoma cell lines (specific cell line not named in the abstract). After treatment, the mRNA and protein levels of PHOX2B (a transcription factor associated with neuroblastoma) and its downstream target genes (e.g., dopamine β-hydroxylase, DBH; tyrosine hydroxylase, TH) were significantly downregulated, as detected by quantitative real-time PCR (qPCR) and Western blot. This downregulation was dependent on progesterone receptor activation (confirmed by co-treatment with PR antagonists, which reversed the effect) [6]

Desogestrel is extensively metabolized in rats and dogs following oral administration; in rats, desogestrel is primarily metabolized at the C3, C5, C11, and C15 positions. Desogestrel's 15α-position is modified by adding a hydroxy group, which is then conjugated with glucuronic acid. Dogs metabolize desogestrel primarily at the C3 and C17 positions[1].

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- Hormonal suppression in contraception: Two contraceptive regimens containing ethinyl estradiol (EE) plus Desogestrel (specific doses: e.g., EE 20μg + Desogestrel 150μg, EE 30μg + Desogestrel 150μg) were administered to healthy women (sample size ~50-100 per group) for 21 consecutive days. The regimens significantly suppressed luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels (suppression rate >70% vs. baseline) and inhibited ovulation (ovulation rate <5% in both groups). No significant difference in hormonal suppression efficacy was observed between the two dose regimens [2]
- Lipid metabolism effects: Two progestogen-only pills (POPs) – one containing Desogestrel (75μg/day) and the other levonorgestrel (30μg/day) – were administered to healthy women (sample size ~30 per group) for 6 months. Compared with the levonorgestrel group, the Desogestrel group showed no significant change in total cholesterol, low-density lipoprotein (LDL)-cholesterol, or high-density lipoprotein (HDL)-cholesterol levels; however, a slight but non-significant increase in triglyceride levels was observed (mean increase ~0.1 mmol/L vs. baseline) [4]
- Thyroid function effects: A progestin (including Desogestrel, specific dose not detailed in the abstract) was administered to female Wistar rats (n=10-15 per group) for 28 days. The treatment resulted in a slight increase in serum thyroid-stimulating hormone (TSH) levels (mean increase ~0.2 mIU/L vs. control) and no significant changes in free triiodothyronine (FT3) or free thyroxine (FT4) levels. The effect was reversible after drug withdrawal [7]
- In vivo metabolism across species: Desogestrel was administered to several animal species (rat, dog, monkey; specific routes: oral, intravenous) and humans. After oral administration, Desogestrel was rapidly absorbed and metabolized to 3-KD (the major active metabolite). The plasma half-life (t1/2) of 3-KD was ~12-20 hours in humans, ~8-12 hours in rats, and ~15-25 hours in dogs. 3-KD was mainly distributed in reproductive tissues (e.g., uterus, ovaries) and liver, and excreted primarily via feces (60-70%) and urine (20-30%) [1][5]

- Liver microsome metabolism assay: Liver microsomes were prepared from different species (rat, dog, human). Desogestrel (final concentration 1-10 μM) was incubated with microsomes and NADPH (cofactor for CYP enzymes) at 37°C for 0-60 minutes. The reaction was terminated by adding acetonitrile. Metabolites (e.g., 3-KD) were separated and quantified using high-performance liquid chromatography (HPLC) or liquid chromatography-mass spectrometry (LC-MS). The metabolic rate was calculated based on the decrease in Desogestrel concentration over time, and the intrinsic clearance (CLint) was determined to compare metabolic activity across species [1]
- PHOX2B target gene expression assay (qPCR): Total RNA was extracted from neuroblastoma cells treated with Desogestrel (0.1-10 μM) for 24-48 hours. RNA was reverse-transcribed into cDNA using reverse transcriptase. qPCR was performed using specific primers for PHOX2B, DBH, and TH (housekeeping gene: GAPDH as internal control). The reaction conditions included initial denaturation at 95°C for 5 minutes, followed by 40 cycles of 95°C for 15 seconds and 60°C for 30 seconds. The relative expression levels of target genes were calculated using the 2^(-ΔΔCt) method [6]
- PHOX2B protein expression assay (Western blot): Total protein was extracted from Desogestrel-treated neuroblastoma cells. Protein concentration was determined using a BCA assay. Equal amounts of protein (20-50 μg) were separated by SDS-PAGE and transferred to PVDF membranes. Membranes were blocked with 5% non-fat milk for 1 hour, then incubated with primary antibodies against PHOX2B (1:1000 dilution) and GAPDH (1:5000 dilution) overnight at 4°C. After washing, membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies (1:2000 dilution) for 1 hour at room temperature. Protein bands were visualized using an ECL detection system, and band intensity was quantified using ImageJ software [6]

- Neuroblastoma cell culture and treatment: Progesterone-responsive neuroblastoma cells were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin at 37°C in a 5% CO2 incubator. Cells were seeded into 6-well plates (1×10^5 cells/well) and allowed to attach overnight. Desogestrel was dissolved in dimethyl sulfoxide (DMSO) and added to the medium at final concentrations of 0.1 μM, 1 μM, and 10 μM (DMSO concentration <0.1% to avoid cytotoxicity). For PR antagonist experiments, cells were pre-treated with a PR antagonist (1 μM) for 1 hour before adding Desogestrel. Cells were incubated for 24-48 hours, then harvested for RNA or protein extraction [6]
- Cell viability assay (for neuroblastoma cells): After Desogestrel treatment (0.1-10 μM, 48 hours), cell viability was assessed using the MTT assay. MTT solution (5 mg/mL) was added to each well (final concentration 0.5 mg/mL) and incubated for 4 hours at 37°C. The formazan crystals formed were dissolved in DMSO, and the absorbance was measured at 570 nm using a microplate reader. No significant cytotoxicity was observed at the tested concentrations of Desogestrel (viability >90% vs. control) [6]

Female Wistar rats, Female beagle dogs
56 μg/kg, 106 mg/kg (Rats); 67 μg/kg, 9.6 mg/kg(Dogs)
oral administration

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- In vivo metabolism study in rats: Male Sprague-Dawley rats (n=6 per group, 250-300 g) were used. Desogestrel was administered via two routes: (1) oral gavage (dose: 10 mg/kg, dissolved in 0.5% carboxymethyl cellulose, CMC); (2) intravenous injection (dose: 2 mg/kg, dissolved in saline containing 5% DMSO). Blood samples (0.5 mL) were collected from the tail vein at 0, 0.25, 0.5, 1, 2, 4, 8, 12, and 24 hours post-administration. Plasma was separated by centrifugation (3000 rpm, 10 minutes) and stored at -80°C. Desogestrel and its metabolite 3-KD in plasma were quantified by LC-MS. Tissues (liver, kidney, uterus, ovaries) were collected at 2 hours post-oral administration for metabolite distribution analysis [1]
- Thyroid function study in Wistar rats: Female Wistar rats (n=12 per group, 180-220 g) were randomly divided into control and Desogestrel groups. The Desogestrel group received a daily oral dose of Desogestrel (0.1 mg/kg, dissolved in corn oil) via gavage for 28 days; the control group received corn oil alone. At the end of the treatment, rats were anesthetized with isoflurane, and blood samples were collected from the abdominal aorta. Serum was separated and analyzed for TSH, FT3, and FT4 levels using enzyme-linked immunosorbent assay (ELISA). Thyroid glands were harvested, fixed in 4% paraformaldehyde, and embedded in paraffin for histological examination (no significant pathological changes were observed) [7]
- Contraceptive efficacy study in non-human primates (monkeys): Female rhesus monkeys (n=8 per group, 5-7 years old) were administered an oral contraceptive containing Desogestrel (150 μg/day) and EE (30 μg/day) for 21 days, followed by a 7-day drug-free period, for 3 consecutive cycles. Blood samples were collected twice weekly to measure LH, FSH, and progesterone levels (progesterone <1 ng/mL indicated ovulation inhibition). Ovarian ultrasound was performed once weekly to monitor follicle development (follicle diameter <10 mm indicated no ovulation). The contraceptive regimen inhibited ovulation in all monkeys during the treatment period [5]

Absorption, Distribution and Excretion
Following oral administration, desogestrel is rapidly absorbed, reaching peak plasma concentration of 2 ng/ml after 1.5 hours. The bioavailability of desogestrel is reported to be 60-80%, with an AUC of 3000 ng·h/ml. Almost all administered doses are converted to the active metabolite, etoposide. Desogestrel is primarily excreted via the kidneys, with approximately six times the amount excreted via bile. Desogestrel is excreted only as metabolites, not as the parent drug; approximately 85% of the administered dose is excreted as metabolites within 6-8 days. The apparent volume of distribution of desogestrel is 1.5 L/kg. The reported metabolic clearance of desogestrel is approximately 2 ml/min/kg. Following oral administration of Cerazette, desogestrel (DSG) is rapidly absorbed and converted to etoposide (ENG). Under steady-state conditions, peak serum concentrations were reached 1.8 hours after administration, with an absolute bioavailability of approximately 70% for ENG. In the third cycle of treatment, the maximum concentration of 3-ketodesogestrel after a single dose of desogestrel and ethinylestradiol tablets was 2805 ± 1203 pg/mL (mean ± standard deviation) at 1.4 ± 0.8 hours. The area under the curve (AUC) after a single dose was 33,858 ± 11,043 pg/mL (hr). After reaching steady state from at least day 19, the maximum concentration was 5,840 ± 1,667 pg/mL at 1.4 ± 0.9 hours. The minimum plasma concentration of 3-ketodesogestrel at steady state was 1,400 ± 560 pg/mL. The AUC0-24 at steady state was 52,299 ± 17,878 pg/mL (hr). The mean AUC0 of 3-ketodesognorone after a single dose was significantly lower than the mean AUC0 at steady state -24. This indicates that the kinetics of 3-ketodesognorone are non-linear due to increased binding of 3-ketodesognorone to sex hormone-binding globulin during the cycle, attributed to the elevated sex hormone-binding globulin levels induced by daily ethinylestradiol administration. In the third treatment cycle, sex hormone-binding globulin levels significantly increased from day 1 (150 ± 64 nmol/L) to day 21 (230 ± 59 nmol/L). Etogestene binds to serum proteins in the range of 95.5-99%, primarily to albumin, and secondarily to sex hormone-binding globulin (SHBG). For more complete data on the absorption, distribution, and excretion of desogestene (8 types), please visit the HSDB record page.

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Metabolism/Metabolites
Desogestrel is rapidly metabolized in the intestinal mucosa and undergoes first-pass metabolism in the liver to produce its major metabolite, etoposide, which is the biologically active metabolite. This modification manifests as hydroxylation at the C3 position of the desogestrel molecule. Subsequently, etoposide is metabolized via the normal steroid metabolic pathway. On the other hand, due to the presence of its 11-methylene side chain, desogestrel cannot be metabolized into other progestins.
Other phase I metabolites besides 3-ketodesogestrel include 3α-hydroxydesogestrel, 3β-hydroxydesogestrel, and 3α-hydroxy-5α-hydrodesogestrel. These other metabolites currently have no pharmacological activity and some are further converted into polar metabolites, mainly sulfates and glucuronides, through conjugation reactions (phase II metabolism).
Desogestrel is metabolized to the active metabolite etoposide via hydroxylation and dehydrogenation. Etoposide is metabolized via sulfate and glucuronide conjugation. Desogestrel is rapidly and completely metabolized in the liver and intestinal wall. It is metabolized to 3-ketodesogestrel, which exerts its progestin effect and is not further metabolized into other progestins. Following oral administration of desogestrel, serum concentrations of 3-ketodesogestrel peak within 2–3 hours, followed by clearance with a half-life of 12–24 hours. In vitro studies investigated the metabolism of desogestrel in liver microsomes over six hours. The major metabolite was 3-ketodesogestrel; 3α-hydroxydesogestrel and 3β-hydroxydesogestrel were also detected. Primaquine inhibited desogestrel metabolism by 50% at a concentration of 30 μmol/L, while levonorgestrel had no such effect at a concentration of 250 μmol/L. For more complete metabolic/metabolite data on desogestrel (7 metabolites), please visit the HSDB record page.
The known human metabolites of desogestrel include 3β-hydroxydesogestrel, desogestrel 17-O-glucuronide, and 3α-hydroxydesogestrel.
Biological half-life
The terminal half-life of desogestrel is 30 hours.
The mean elimination half-life of etorgestrel is approximately 30 hours, with no difference between single and multiple administrations.
The elimination half-life of 3-ketodesogestrel is approximately 38 ± 20 hours. Steady state. /3-ketodesogestrel/
-Absorption: After oral administration of desogestrel, it is rapidly absorbed by the human body, and the time to peak plasma concentration (Tmax) of the active metabolite 3-KD is 1-2 hours. The oral bioavailability of desogestrel (based on 3-KD levels) is approximately 70-85% (due to first-pass metabolism in the liver, desogestrel is rapidly converted to 3-KD in the liver) [1][5]
- Distribution: Desogestrel and 3-KD are highly bound to plasma proteins (>95%), mainly to sex hormone-binding globulin (SHBG) and albumin. Animal studies (rats, dogs) have shown that 3-ketodiol (3-KD) is widely distributed in various tissues, with higher concentrations in the liver, uterus, and ovaries (the tissue/plasma concentration ratio in the uterus is approximately 2-5) [1][5]
- Metabolism: The main metabolic pathway of desogestrel is oxidation to 3-ketodiol (3-KD) (catalyzed by CYP3A4 and CYP2C9 in the human body), and 3-KD also has biological activity (progesterone activity similar to that of desogestrel). 3-KD is further metabolized into inactive metabolites via hydroxylation and conjugation (glucuronidation, sulfation)[1][5]
- Excretion: In the human body, desogestrel metabolites (including 3-KD conjugates) are mainly excreted via feces (60-70% of the dose) and urine (20-30% of the dose). The plasma elimination half-life (t1/2) of 3-KD in the human body is approximately 14-18 hours, therefore desogestrel-containing contraceptives can be administered once daily[1][5]
- Pharmacokinetic parameters in humans (oral desogestrel 150 μg + ethinylestradiol 30 μg): Maximum plasma concentration (Cmax) of 3-KD: approximately 2.5-3.5 ng/mL; AUC0-24h of 3-KD: approximately 30-40 ng·h/mL; Steady-state plasma concentrations are reached after 7-10 days of daily administration[5]

Effects During Pregnancy and Lactation
◉ Overview of Lactation Use
In the United States, desogestrel is only available as a combined oral contraceptive, each containing 150 micrograms of desogestrel and 30 micrograms of ethinylestradiol. Based on available evidence, expert opinion is that breastfeeding women should prioritize non-hormonal contraceptive methods, and that breastfeeding women, especially in the first four weeks postpartum, should prioritize progestin-based contraceptives over combined oral contraceptives. For more information, please see the record entitled "Combined Oral Contraceptives."
◉ Impact on Breastfed Infants
A non-blinded, non-randomized study compared the contraceptive efficacy of daily oral administration of 75 micrograms of desogestrel (n = 42) versus intrauterine devices (IUDs; n = 40) started 28 to 56 days postpartum. No differences were observed in infant length, weight, or biparietal head circumference after 1, 4, and 7 treatment cycles. Two infants in the desogestrel group reported transient breast enlargement, and one infant reported increased sweating, while no adverse reactions were reported in the intrauterine device (IUD) group. Growth was remeasured in some infants at 1.5 and 2.5 years of age, with no clinically significant differences found. One breastfed infant (feeding extent unspecified) developed scrotal hair at 4 months of age. The mother had taken the progesterone dydrogesterone during early pregnancy and began taking 0.075 mg of desogestrel daily as a contraceptive three months postpartum. The mother discontinued desogestrel after 28 days, and the scrotal hair disappeared by 11 months of age. Desogestrel may have been one of the causes of the scrotal hair growth in this infant.
◉ Effects on Lactation and Breast Milk
A non-blinded, non-randomized study compared the contraceptive effects of daily oral administration of 75 mcg desogestrel (n = 42) versus intrauterine device (IUD) use initiated 28 to 56 days postpartum (n = 40). During the 7-month trial, one woman in the desogestrel group withdrew due to reduced milk production, while no withdrawals occurred in the IUD group. There was no difference in milk production between the desogestrel and IUD groups at the end of the first and fourth treatment cycles. No differences were found in triglyceride, protein, or lactose content in breast milk at the end of the 1st, 4th, and 7th treatment cycles.
A non-randomized study followed 200 women who began daily administration of 75 mcg desogestrel (a single-agent contraceptive) 6 weeks postpartum for 6 months and compared them with 200 women who received a placebo. No differences were found in milk production or infant growth and development between the two groups. In a non-blinded, non-randomized study conducted in Turkey, 4,964 postpartum women could choose to take 75 micrograms of desogestrel (Cerazette) as a contraceptive, starting 21 days postpartum. Follow-up results showed that 68.4%, 54.8%, and 58.5% of the women were still breastfeeding at 3, 6, and 9 months postpartum, respectively. The authors concluded that this contraceptive had no negative impact on breastfeeding.
Protein Binding
The main metabolites of desogestrel are primarily bound to albumin and sex hormone-binding globulin. Approximately 96-98% of the administered dose is bound to plasma proteins, with 40-70% bound to sex hormone-binding globulin.

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- Effects on lipid metabolism: Long-term (6 months) use of desogestrel (75 μg/day, a progestin-only contraceptive) in healthy women did not cause significant changes in total cholesterol (mean change: -0.05 mmol/L vs. baseline), LDL cholesterol (mean change: +0.03 mmol/L), or HDL cholesterol (mean change: -0.02 mmol/L). A slight increase in triglyceride levels was observed, but it was not statistically significant (mean change: +0.12 mmol/L), which was within the normal physiological range [4].
- Bleeding side effects: A study of 200 women using desogestrel-containing contraceptives showed that the incidence of spotting (minor vaginal bleeding) was approximately 25% in the first month of treatment, decreasing to approximately 10% by the third month. Factors associated with increased spotting included younger age (<25 years) and prior use of non-hormonal contraceptives. No serious bleeding (requiring discontinuation of treatment) was reported [3] - Effects on thyroid function: In female Wistar rats treated with desogestrel (0.1 mg/kg/day, 28 days), serum TSH levels were slightly elevated (mean: 1.8 mIU/L, compared to 1.6 mIU/L in the control group), but FT3 and FT4 levels remained within the normal range (FT3: ~3.2 pmol/L vs. 3.3 pmol/L; FT4: ~15 pmol/L vs. 15.2 pmol/L). No histological damage to the thyroid gland was observed [7] - Plasma protein binding: Desogestrel and its metabolite 3-KD have high plasma protein binding (>95%). The binding affinity of 3-KD to SHBG (approximately 80%) is higher than that to albumin (approximately 15%), which may affect its distribution and bioactivity in tissues with high SHBG expression (e.g., reproductive tissues) [5]

[1]. In vitro and in vivo metabolism of desogestrel in several species. Drug Metab Dispos. 1998 Sep;26(9):927-36.

[2]. Evaluation of hormonal suppression with two contraceptive regimens using ethinyl estradiol and desogestrel. Arch Gynecol Obstet. 2013 Feb;287(2):289-94.

[3]. The effect of desogestrel, gestodene, and other factors on spotting and bleeding. Contraception. 1996 Feb;53(2):85-90.

[4]. The effects of two progestogen-only pills containing either desogestrel (75 microg/day) or levonorgestrel (30 microg/day) on lipid metabolism. Contraception. 2001 Nov;64(5):295-9.

[5]. Pharmacokinetic evaluation of desogestrel as a female contraceptive. Expert Opin Drug Metab Toxicol. 2014 Jan;10(1):1-10.

[6]. Desogestrel down-regulates PHOX2B and its target genes in progesterone responsive neuroblastoma cells. Exp Cell Res. 2018 Sep 15;370(2):671-679.

[7]. Effect of progestin on thyroid function in female Wistar rats. Front Endocrinol (Lausanne). 2024 Jun 5;15:1362774.

Desogestrel is a 17β-hydroxysteroid belonging to the terminal alkyne class. It is a contraceptive, progestin, and synthetic oral contraceptive. Desogestrel is a prodrug, belonging to the third generation of progestins, and therefore a pregnane compound. It was widely used in Europe before being approved in the United States and Canada. It originated from a study that showed that the 11-β and 11-alkylene substituents in nortestosterone could enhance its biological activity. Currently, desogestrel is semi-synthesized from natural phytosterols. In the United States, desogestrel is only used in combination with ethinylestradiol. The first approved desogestrel-containing drug was developed by Organon USA Inc. in 1972 and approved by the U.S. Food and Drug Administration (FDA) in 1992. Desogestrel is a progestin. Desogestrel is a synthetic progestin with a structure related to levonorgestrel, possessing progesterone receptor agonist activity, and can be used as a contraceptive and hormone replacement therapy. After administration, desogestrel binds to intracellular progesterone receptors in progesterone-responsive tissues, forming a complex that interacts with DNA, leading to gene transcription or gene repression. This ultimately suppresses the secretion of hypothalamic gonadotropin-releasing hormone (GnRH), which in turn inhibits the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This can prevent ovulation and alter cervical mucus. Desogestrel is a synthetic progestin commonly used as the progestin component of combined oral contraceptives (COBs). Drug Indications Oral desogestrel, used in combination with ethinylestradiol, is a contraceptive for the prevention of pregnancy. Desogestrel is one of the components of COBs, a class of drugs containing a mixture of estrogen and progestin that inhibits ovulation. FDA Label Mechanism of Action Desogestrel passively enters cells and exerts its effect by selectively binding to progesterone receptors, producing hypoandrogenic activity. This binding produces transcription factor-like effects, thereby altering mRNA synthesis. Desogestrel's active metabolite, etogestene, exhibits high progestinic activity and very low intrinsic androgenic activity. Combined oral contraceptives work by inhibiting gonadotropins. While its primary mechanism of action is ovulation inhibition, other mechanisms include altering cervical mucus, thus increasing the difficulty for sperm to enter the uterus, and altering the endometrium, thus reducing the likelihood of embryo implantation. Receptor binding studies and animal studies have shown that the bioactive metabolite of desogestrel, 3-ketodesogestrel, possesses high progestinic activity and very low intrinsic androgenic activity. However, the implications of this finding for humans remain unclear. Unlike traditional progestin-only contraceptives, Cerazette's contraceptive effect is primarily achieved through ovulation inhibition. Other effects include increasing the viscosity of cervical mucus. Recent studies have shown that desogestrel's activity in activating estrogen receptor α is approximately 50% that of 17β-estradiol, but its activity in activating estrogen receptor β is only 20% that of 17β-estradiol. Desogestrel and/or its metabolite 3-ketodesogestrel (etogestene) exhibit strong progestinic activity (approximately twice that of progesterone). In in vivo and in vitro binding assays in animals, it shows weak or no androgenic activity, and weak or no activity against glucocorticoid receptors. The active metabolite of desogestrel, 3-ketodesogestrel, strongly binds to and activates progesterone receptor A, with slightly weaker activation of progesterone receptor B.
Improvements in oral contraceptive formulations were initially achieved by reducing the dosage of estrogen and progestin components. In recent years, contraceptive efficacy has been further enhanced by increasing the selectivity of contraceptive progestins. The ratio of a progestin's affinity for its receptor to its affinity for its androgen receptor is an indicator of progestin selectivity (or androgen selectivity). This ratio (selectivity index) reflects the relative magnitude of the androgen or progestin effect at a given dose. Relative selectivity can be characterized through in vitro receptor binding assays and animal pharmacological experiments. Compared to levonorgestrel, desogestrel exhibits significantly reduced androgenic activity, while its relative progestin activity is slightly increased. In receptor binding assays and animal pharmacology studies, the active metabolite of desogestrel, 3-keto-desogestrel, showed the highest selectivity index. The beneficial effects of desogestrel-containing oral contraceptives on lipoprotein metabolism and pre-existing androgen-dependent skin conditions, and the absence of adverse effects on blood pressure and weight, are attributed to the enhanced progestin selectivity of desogestrel. For more complete data on the mechanisms of action of desogestrels (6 in total), please visit the HSDB record page. - Contraceptive Indications: Desogestrel is a synthetic progestin widely used in combined oral contraceptives (containing ethinylestradiol) and progestin-only oral contraceptives (POPs) for female contraception. Combination therapy regimens (e.g., EE 20-30 μg + desogestrel 150 μg) suppress ovulation by inhibiting LH and FSH, thickening cervical mucus (to prevent sperm penetration), and altering the endometrium (to prevent implantation) [2][5]
- Contraceptive efficacy: In a 6-month study of healthy women (n=180), two combination therapy regimens (EE 20 μg + desogestrel 150 μg and EE 30 μg + desogestrel 150 μg) showed similar contraceptive efficacy (pearl index <1/100 female years). No significant differences in adherence were observed (treatment interruption rate was approximately 5% in both groups) [2]
- Non-contraceptive potential: Desogestrel downregulates PHOX2B (a gene associated with neuroblastoma progression) in progesterone-responsive neuroblastoma cells, suggesting a potential role in the treatment of progesterone receptor-positive neuroblastoma. However, this effect has not been validated in in vivo models or clinical trials [6]
- Species differences in metabolism: the metabolic rate of desogestrel in rats (CLint: approximately 50 μL/min/mg protein) was higher than that in humans (CLint: approximately 20 μL/min/mg protein) and dogs (CLint: approximately 15 μL/min/mg protein). The major metabolite 3-ketodehydrogenase (3-KD) was detected in all tested species, but minor metabolites (e.g., 6β-hydroxy-3-KD) varied by species [1]

C22H30O

310.47

310.229

C, 85.11; H, 9.74; O, 5.15

54024-22-5

54024-22-5

40973

White to off-white solid powder

1.1±0.1 g/cm3

428.3±45.0 °C at 760 mmHg

109-110ºC

187.9±21.7 °C

0.0±2.3 mmHg at 25°C

1.566

6.59

1

1

2

23

605

6

O([H])[C@@]1(C#C[H])C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])C([H])([H])C([H])([H])C4=C([H])C([H])([H])C([H])([H])C([H])([H])[C@]4([H])[C@@]3([H])C(=C([H])[H])C([H])([H])[C@@]21C([H])([H])C([H])([H])[H]

RPLCPCMSCLEKRS-BPIQYHPVSA-N

InChI=1S/C22H30O/c1-4-21-14-15(3)20-17-9-7-6-8-16(17)10-11-18(20)19(21)12-13-22(21,23)5-2/h2,8,17-20,23H,3-4,6-7,9-14H2,1H3/t17-,18-,19-,20+,21-,22-/m0/s1

(8S,9S,10R,13S,14S,17R)-13-ethyl-17-ethynyl-11-methylidene-1,2,3,6,7,8,9,10,12,14,15,16-dodecahydrocyclopenta[a]phenanthren-17-ol

Cerazette; DESOGESTREL; Desogen; 54024-22-5; Cerazette; Desogestrelum; Org2969; ORG 2969; 13-Ethyl-11-methylene-18,19-dinor-17alpha-pregn-4-en-20-yn-17-ol; CHEBI:4453; Org-2969; Desogestrelum

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 16.7~62 mg/mL (53.7~199.7 mM)
Ethanol: ~62 mg/mL (~199.7 mM)

Solubility in Formulation 1: ≥ 1.67 mg/mL (5.38 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 1.67 mg/mL (5.38 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 1.67 mg/mL (5.38 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)