Relugolix 120mg tablets
Requires a prescription from a doctor or prescriber
Relugolix is a gonadotropin-releasing hormone (GnRH) receptor antagonist used in the treatment of several hormone-responsive conditions.
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Relugolix
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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.
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Suspected adverse reactions reported for Relugolix
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3 branded products available
MHRA licensed products
View all licensed products for Relugolix on the MHRA register
Orgovyx 120mg tablets
Relugolix 120mg tablets
Relugolix 120mg tablets
Therapeutically similar medicines
Tablets & capsules
(3)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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(7)
Relugolix for treating hormone-sensitive prostate cancer (TA995)
Relugolix–estradiol–norethisterone for treating symptoms of endometriosis (TA1057)
Linzagolix for treating symptoms of endometriosis (TA1067)
Relugolix–estradiol–norethisterone acetate for treating moderate to severe symptoms of uterine fibroids (TA832)
Linzagolix for treating moderate to severe symptoms of uterine fibroids (TA996)
Heavy menstrual bleeding: assessment and management (NG88)
Endometriosis: diagnosis and management (NG73)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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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: 31 · Randomised trials: 11 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
I. Kyriazis, T. Bellos, Stamatios Katsimperis, et al.
Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica, 2025
- Prostatic Neoplasms
- Antineoplastic Agents, Hormonal
- Gonadotropin-Releasing Hormone
Aachal Bhavsar, C. Patel, Khushbu K. Patel, et al.
International Journal of Sciences and Innovation Engineering, 2026
Betiuk Z, Błażyca M, Bartoszczyk M, et al.
2026
Background: Endometriosis affects 190 million women worldwide, so there is a need for accessible and more comprehensive knowledge regarding the pharmacotherapeutic options that can be offered to patients. This systematic review (2019-2025) synthesizes research results regarding the efficacy and safety of dienogest (DNG) and GnRH antagonists, while also summarizing research on new directions in endometriosis treatment. Methods: Following PRISMA 2020 guidelines, we searched Medline for clinical evidence on established standards and emerging therapies. A structured narrative synthesis was performed. Quality was assessed using Cochrane RoB 2 and ROBINS-I tools. Results: A total of 44 out of 926 records were analyzed. The review confirms the efficacy of DNG as a first-line treatment for endometriosis. Relugolix combination therapy appears to be a more effective and safer option than elagolix or relugolix monotherapy in reducing dysmenorrhea and pelvic pain. Research concerning immunotherapy for endometriosis (using tocilizumab, anakinra, bevacizumab, and anti-CD47 antibodies) is subject to a high risk of bias and very low GRADE certainty. Nevertheless, these findings may serve as a foundation for further studies, which are necessary to evaluate their efficacy and safety in the treatment of endometriosis. Conclusions: DNG is generally well-tolerated, but further studies are needed to unequivocally determine the impact of DNG on BMD loss and cancer risk. Research on GnRH antagonists indicates their increasing role in the future management of endometriosis. There are new perspectives in endometriosis pharmacotherapy-including immunotherapy; however, there is a fundamental need for their further development and evaluation.
Abstract licence: CC BY
Sánchez Martín MJ, Huerga López C, Cristóbal García I, et al.
2025
- Leiomyoma
- Uterine Neoplasms
- Hormone Antagonists
PurposeUterine fibroids are the most common pelvic tumors in women, representing the primary indication of hysterectomy. Gonadotropin-releasing hormone (GnRH) antagonists represent a new therapeutic option for premenopausal women. The aim of this review is to evaluate the efficacy and safety of GnRH antagonists in the treatment of uterine fibroids (size reduction and symptom control).MethodsA review of studies from electronic databases (PubMed and Cochrane Central) published up to December 2023 was performed. Eleven randomized clinical trials with a total of 4164 patients were included in the review, which evaluated GnRH antagonists (Relugolix, Elagolix, Linzagolix and Cetrorelix) against placebo or GnRH agonists in premenopausal women with uterine fibroids and heavy menstrual bleeding.ResultsThe results of the measures evaluated to determine the efficacy and safety of GnRH antagonists versus placebo are favorable for the variables of control of uterine bleeding (Relative risk (RR) = 5.09; 95% CI 3.19 to 8.14), percentage reduction of fibroid volume (Mean difference (MD) = -27.36; 95% CI -38.89 to -15.83) and lower reduction of bone density (MD -0.35; 95% CI -0.47 to -0.24). The results do not allow us to conclude whether there are differences between the alternatives compared in the control of vasomotor symptoms.ConclusionsGnRH antagonists represent an effective alternative for uterine fibroids treatment as they allow a superior reduction in menstrual bleeding and uterine fibroid volume compared to the placebo group.
Abstract licence: CC BY-NC-ND
Jiani Xie, Xiaorong Ni, Qunhuan Huang, et al.
Frontiers in Endocrinology, 2025
- Endometriosis
- Pelvic Pain
- Quality of Life
M. V. S. Sobral, João Pedro Pereira dos Santos, Tânia Aparecida Alves Vilela, et al.
American Journal of Therapeutics, 2024
Reza Sari Motlagh, Mohammad Abufaraj, Keiichiro Mori, et al.
European Urology Oncology, 2022
David P. Dearnaley, Daniel R. Saltzstein, John E. Sylvester, et al.
European Urology, 2020
Neal D. Shore, Fred Saad, Michael S. Cookson, et al.
New England Journal of Medicine, 2020
Ayman Al-Hendy, Andrea S. Lukes, Alfred N. Poindexter, et al.
New England Journal of Medicine, 2021
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
25 hours
Mechanism
The pathogenesis and progression of prostate cancer appear driven, at least in part, by the effects of testosterone.
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
120mg
Half-life
25 hours
[L27991]
Protein binding
68-71%
[L27991]
Metabolism
[L27991]
Elimination
81%
Clearance
8 L/h
[L27991]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Relugolix is the first (and currently only) orally-administered GnRH receptor antagonist approved for the treatment of prostate cancer - similar therapies such as [degarelix] require subcutaneous administration - and therefore provides a less burdensome therapeutic option for patients who might otherwise require clinic visits for administration by healthcare professionals.[L27996] In addition to its relative ease-of-use, relugolix was shown to be superior in the depression of testosterone levels when compared to [leuprolide], another androgen deprivation therapy used in the treatment of prostate cancer.[A225926] In May 2021, the FDA approved the combination product made up of relugolix, [estradiol], and [norethindrone] under the market name Myfembree for the first once-daily treatment for the management of heavy menstrual bleeding associated with uterine fibroids in premenopausal women.[L34289]
[L27991][L42145]
In a combination product with [estradiol] and [norethindrone], relugolix is indicated for the once-daily treatment for the management of heavy menstrual bleeding associated with uterine fibroids in premenopausal women.
[L34289]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 748 interactions
Testosterone production in males is carried out in the Leydig cells of testes and is stimulated by luteinizing hormone (LH), which itself is produced in the pituitary gland following the binding of gonadotropin-releasing hormone (GnRH) to corresponding GnRH receptors.[L28011] Relugolix is a competitive antagonist of these GnRH receptors, thereby decreasing the release of LH and, ultimately, testosterone.[L27991]
Androgen deprivation therapies may prolong the QTc interval and should therefore be used with caution in patients having a high baseline risk of QTc prolongation, such as those with electrolyte abnormalities, congestive heart failure, or using other medications known to prolong the QTc interval.[L27991] Based on its mechanism of action and data from animal studies, relugolix may result in fetal harm if administered to pregnant females - male patients with female partners should be advised to use effective contraception throughout therapy and for 2 weeks following cessation of therapy to prevent inadvertent fetal exposure.[L27991]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L27991]
Following the administration of 120mg once daily, the steady-state AUC and Cmax of relugolix were 407 (± 168) ng.hr/mL and 70 (± 65) ng/mL, respectively.
The absolute oral bioavailability of relugolix is approximately 12% and the median Tmax following oral administration is 2.25 hours.
[L27991]
[L27991]
[L27991]
[L27991]
[L27991]
[L27991]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
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
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC H01CC54
ATC L02BX04
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)
Relugolix
Additional database identifiers
Drugs Product Database (DPD)
23873
ChemSpider
8524431
BindingDB
50347982
ZINC
ZINC000043206033
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4421
GenAtlas
GNRHR
GeneCards
GNRHR
GenBank Gene Database
L03380
GenBank Protein Database
183422
Guide to Pharmacology
256
UniProt Accession
GNRHR_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:17450
GeneCards
CYP3A43
GenBank Gene Database
AF319634
GenBank Protein Database
12642642
UniProt Accession
CP343_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_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:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_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