Desogestrel 75microgram tablets
Requires a prescription from a doctor or prescriber
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Desogestrel
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Desogestrel
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Desogestrel
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
25 branded products available
MHRA licensed products
View all licensed products for Desogestrel on the MHRA register
Cerazette 75microgram tablets
Cerelle 75microgram tablets
Desomono 75microgram tablets
Desorex 75microgram tablets
Lovima 75microgram tablets
Zelleta 75microgram tablets
Desogestrel 75microgram tablets
Desogestrel 75microgram tablets
Desogestrel 75microgram tablets
Desogestrel 75microgram tablets
Desogestrel 75microgram tablets
Desogestrel 75microgram tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 11 · Randomised trials: 16 · 1983–2026
Showing the 50 most relevant studies, sorted by most relevant.
Li B, Xu X, Xu K, et al.
2025
- Contraceptives, Oral, Combined
- Progestins
- Androstenes
PurposeThis systematic review and network meta-analysis (NMA) compares four progestins-gestodene (GSD), desogestrel (DSG), drospirenone (DRSP), and levonorgestrel (LNG)-in combined oral contraceptives (COCs) regarding safety, and efficacy for personalized contraceptive selection.MethodsThis systematic review, which searched PubMed, Cochrane, Embase and Medline through Jan 28, 2025, to identify published and unpublished randomised controlled trials (RCTs). We assessed the certainty of evidence using the confidence in network meta-analysis (CINeMA) framework. We estimated summary standardised mean differences (SMDs) and odds ratios (ORs) using NMA with random effects by STATA and GeMTC software. The outcomes included breakthrough bleeding (BTB), irregular bleeding (IB), withdrawal bleeding days, pregnancy rates, and adverse events.ResultsEighteen RCTs were included. GSD demonstrated the lowest incidence of BTB and IB (OR 0.41 (0.26, 0.66); OR 0.67 (0.52, 0.86)). For withdrawal bleeding days, DRSP ranked highest (SUCRA 40.1; I2 = 27%, p = 0.222), followed by GSD, LNG and DSG. Contraceptive efficacy was highest for DSG (OR 0.74, (0.31-1.73); SUCRA = 51.3%) followed by DRSP and GSD, with LNG being the least effective. Regarding safety, DRSP had the lowest adverse event rate (OR 0.84, 0.60-1.19); SUCRA = 66.9%), followed by LNG and DSG, while GSD was associated with the highest.ConclusionThe four progestogens demonstrate comparable contraceptive efficacy while exhibiting distinct therapeutic advantages in their respective clinical applications. DSG for routine use, GSD for bleeding control, DRSP for minimizing androgenic effects, and LNG for emergency contraception.Trial registrationPROSPERO ID: CRD42024582991.
Abstract licence: CC BY-NC-ND
S. Hennessy, J. Berlin, J. Kinman, et al.
Contraception, 2001
Rogerio A. Lobo, J. B. Skinner, J. Lippman, et al.
Fertility and sterility, 1996
G. B. Dikke
Акушерство, гинекология и репродукция, 2022
S. Palacios, E. Colli, P. Regidor
Archives of Gynecology and Obstetrics, 2019
Farahnaz Mardanian, Ferdous Mehrabian, Safura Rouholamin, et al.
Advanced Biomedical Research, 2024
Valeria Lombardi Fäh, Rosa Catarino, Sarah Castillo, et al.
BMC Research Notes, 2023
Humart P, Petyim S, Boriboonhirunsan D
2025
- Ovarian Cysts
- Contraceptives, Oral, Combined
- Oocyte Retrieval
The objective was to compare the preventive effect of combined oral contraceptive pills (COCs) to the expectant management approach on the incident of corpus luteal cysts following oocyte retrieval in in vitro fertilization (IVF). A total of 130 IVF patients at the Infertility Unit of Siriraj Hospital were randomized into two groups following ovarian stimulation and oocyte retrieval. Participants in the study group received COCs containing 0.15 mg desogestrel and 0.02 mg ethinyl oestradiol per pill for 21 days (n = 65), while the comparison group underwent expectant management (n = 65). Transvaginal ultrasonography was performed to detect corpus luteal cysts (mean cyst diameter ≥ 10 mm) at 2 and 4 weeks after oocyte retrieval. Baseline characteristics were similar between groups. At 2 weeks, the incidence of persistent corpus luteal cysts was 58.4% in the COC group and 69.2% in the expectant management group (p = 0.2). A comparable, non-significant difference was also observed at 4 weeks (26.2% vs. 36.9%, p = 0.19). However, the mean cyst diameter at 4 weeks was significantly smaller in the COC group (5.74 mm vs. 9.39 mm, p < 0.01). The use of COCs does not effectively prevent the formation of corpus luteal cysts at 2 and 4 weeks after oocyte retrieval in the IVF process.
Abstract licence: CC BY
S. Middeldorp, J. Meijers, A. van den Ende, et al.
Thrombosis and Haemostasis, 2000
G. Tans, J. Curvers, S. Middeldorp, et al.
Thrombosis and Haemostasis, 2000
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
30 hours
Mechanism
Desogestrel enters the cell passively and acts by binding selectively to the pro…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
2 ng/ml
Half-life
30 hours
Protein binding
96-98%
Volume of distribution
1.5 L/kg
Metabolism
Elimination
85%
Clearance
2 ml/min/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Desogestrel is part of the combined oral contraceptives that contain a mix of estrogen and progestin which inhibit ovulation.
[L5698]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 844 interactions
Most reports haven't linked the administration of desogestrel with the increased risk of breast cancer. The increased risk has been reported to be related to the duration of use.
However, several reports indicate a desogestrel-driven increased risk in cervical intra-epithelial neoplasia but the results are still not conclusive.[FDA label]
The active metabolite of desogestrel, [etonogestrel], presents a combination of high progestational activity with minimal intrinsic androgenicity.[FDA label]
Desogestrel main therapeutic effect due to its mechanism of action is known to be related to the inhibition of the ovulation in 97% of the cycles. This effect was proven in clinical trials in non-breastfeeding women from which the Pearl failure rate was reported to be of 0.17 per 100 women-years. This result indicated that desogestrel is more efficient when compared to other progestogen-only pills.[A176345] All the therapeutic effect is produced by a transformation of the endometrium followed by an inhibition of the ovulation due to the suppression of other hormones.[T521]
Desogestrel has been widely confirmed to be related to an increase in the risk of venous thromboembolism due to the driven increased in blood coagulation factors, leading to a pronounced prothrombotic state.[A176315] However, the effects of desogestrel are known to not impact significantly the level of total cholesterol remaining in the range of change of 10% which allows it to be a molecule that presents a favorable lipid profile.[A176339]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A176423]
[A176333][A176336]
This modification is described by the hydroxylation in C3 of the desogestrel molecule.
[A176423]
Later, etonogestrel is metabolized following the normal pathways of steroid metabolism. On the other hand, due to the 11-methylene side chain, desogestrel cannot be metabolized to other progestins.[F4127]
Proteins and enzymes this drug interacts with in the body
Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter.
Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP.
Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3 .
PMID:17922032
Maintains neuronal survival in response to ischemic reperfusion injury when in the presence of circulating estradiol (17-beta-estradiol/E2) (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Regulates the plasma metabolic clearance rate of steroid hormones by controlling their plasma concentration
ATC G03AC09
ATC G03FB10
ATC G03AB05
ATC G03AA09
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Desogestrel
Additional database identifiers
Drugs Product Database (DPD)
660
ChemSpider
37400
BindingDB
50423510
ZINC
ZINC000004097416
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8910
GenAtlas
PGR
GeneCards
PGR
GenBank Gene Database
X51730
GenBank Protein Database
35652
Guide to Pharmacology
627
UniProt Accession
PRGR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3467
GenAtlas
ESR1
GeneCards
ESR1
GenBank Gene Database
X03635
GenBank Protein Database
31234
Guide to Pharmacology
620
UniProt Accession
ESR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10839
GenAtlas
SHBG
GeneCards
SHBG
GenBank Gene Database
X16349
GenBank Protein Database
296673
UniProt Accession
SHBG_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72