Thiamazole 5mg 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
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 Thiamazole
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 Thiamazole
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.
1 branded products available
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.
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. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. 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 all 23 studies.
Reviews & meta-analyses: 2 · 2023–2026
Showing all 23 studies, sorted by most relevant.
Mingzhe Li, Bingchen Wei, Tianshu Gao, et al.
Frontiers in Pharmacology, 2025
Objective This study aims to conduct a systematic review of the effectiveness and safety of Tripterygium Glycosides interventions in the treatment of Chinese patients with thyroid-associated orbitopathy (TAO). Methods A literature search was conducted using PubMed for English sources, and the CNKI, Chinese Biomedical Database, Wanfang Database, and VIP Database for Chinese sources. The search period extended from the beginning of the databases’ creation to Dec. 2023. The keywords used in the search were hyperthyroidism, thyroid-related immune orbitopathy (TRIO), ophthalmopathy, and Tripterygium Glycosides. Various combinations of search terms were used, depending on the database being queried. All the trials included in the study were clinical randomized controlled trials (RCTs). Results 33 RCTs or quasi-RCTs that met the inclusion criteria were included. The meta-analysis included 27 RCTs. 6 RCTs were excluded from the analysis due to the absence of a control group, but they were still included in the systematic review. 27 RCTs or quasi-RCTs involving 2,134 patients were included in the meta-analysis. The TRIO patients in the treatment group received Tripterygium Glycosides in combination with Thiamazole, Prednisone, Levothyroxine sodium, or a combination of these medications. While the TRIO patients in the control group were treated with Thiamazole, Prednisone, Levothyroxine sodium, or a combination of these treatments, the meta-analysis results show that the overall effectiveness rate of the treatment group and the control group was P = 0.05, I 2 = 0.33 < 0.5 [MD = 4.45, 95% CI (3.31, 5.99), P < 0.00001]. The former was significantly superior to the latter. At the same time, a risk assessment was conducted for the study of the 2 groups. The former was significantly superior to the latter. Furthermore, the clinical effectiveness rate of eyeball prominence was P < 0.00001, I 2 = 0.98 > 0.5 [MD = 2.40, 95% CI (2.28, 2.51), P < 0.00001]. The clinical effectiveness rate of CAS score was P < 0.00001, I 2 = 0.89 > 0.5 [MD = 1.68, 95% CI (1.50, 1.85), P < 0.00001]. The clinical effectiveness rate of FT 3 was P < 0.00001, I 2 = 0.98 > 0.5 [MD = 0.95, 95% CI (0.81, 1.08), P < 0.00001], the clinical effectiveness rate of FT 4 was P < 0.00001, I 2 = 0.95 > 0.5 [MD = 2.12, 95% CI (1.99, 2.25), P < 0.00001], and the clinical effectiveness rate of TSH was P < 0.00001, I 2 = 0.89 > 0.5 [MD = −0.19, 95% CI (−0.21, −0.17), P < 0.00001]. Conclusion The experience with the treatment of TAO using Tripterygium Glycosides was promising. The existing evidence suggests that treatment with Tripterygium Glycosides may be more effective in enhancing the response rate, quality of life, and FT 3 levels compared to treatment with Prednisone, Levothyroxine sodium, and/or Thiamazole alone.
Abstract licence: CC BY
Matsui D, Mugikura S, Goshima T, et al.
2025
Thyrotoxic periodic paralysis (TPP) is a potentially life-threatening complication of hyperthyroidism. It is characterized by hypokalemia-induced muscle weakness that typically begins in the proximal lower limbs and may progress to paralysis of all four extremities and involvement of the respiratory muscles. We present a case of a 37-year-old man with a history of TPP, presenting with acute muscle weakness and hypokalemia. The patient reported acute-onset bilateral lower extremity weakness from the previous day. Physical examination revealed normal deep tendon reflexes, but marked muscle weakness was observed in both lower limbs. Laboratory workup revealed severe hypokalemia at 2.1 mEq/L and thyrotoxicosis, while the electrocardiogram showed a prolonged QTc interval. The patient received thiamazole, potassium iodide, and propranolol for thyrotoxicosis and a total dose of 122 mEq of potassium repletion. His potassium level rose from 1.7 mEq/L to 5.6 mEq/L within six hours post-repletion cessation, highlighting the risk of rebound hyperkalemia and the importance of close monitoring. This case underscores the danger of rebound hyperkalemia after aggressive potassium repletion in TPP and supports a cautious, stepwise correction strategy.
Abstract licence: CC BY
Dietlein M, Schmidt M, Drzezga A, et al.
2025
Graves' disease and hyperthyroidism in women with childbearing potential are a challenge in pre-conceptional counseling. The non-surgical alternatives are radioiodine therapy or antithyroid drugs. Here, we focus on the TSH receptor antibody (TRAb) level-without or after radioiodine therapy-and the probability of fetal or neonatal hyperthyroidism. This immunological effect should be weighed against the risk of congenital malformation taking propylthiouracil during pregnancy. For up to 2 years after radioiodine therapy for Graves' disease, TRAb levels may remain above the pre-therapeutic level. The time of conception after radioiodine therapy and a high TRAb level are associated with the likelihood of neonatal hyperthyroidism: 8.8% probability if conception occurred 6-12 months after radioiodine therapy, with a 5.5% probability for 12-18 months, and 3.6% probability for 18-24 months. The TRAb value above 10 U/L in the third trimester is the main risk factor for neonatal hyperthyroidism. If a woman does not wish to postpone her family planning, the pre-conceptional counseling has to describe the risk of propylthiouracil, thiamazole, or of an uncontrolled hyperthyroidism. According to some national cohort studies (Danish, Swedish, Korean), the risk for fetal malformations (ear, urinary tract) under propylthiouracil is increased by 1.1-1.6%, in addition to the spontaneous risk for unexposed pregnant women. For thiamazole, the additional risk for fetal malformation was about 2-3%, depending on the dose of thiamazole. Propylthiouracil has posed a lower risk for congenital malformation than an uncontrolled hyperthyroidism. To minimize the risk for the newborn, women with Graves' disease and hyperthyroidism should offer a definitive therapy strategy (e.g., radioiodine therapy) long before planning a pregnancy.
Abstract licence: CC BY
Fedorczak A, Kruk B, Mazurek-Kula A, et al.
2025
Background: Resistance to thyroid hormones (RTH) is a rare, genetically determined disease characterised by reduced tissue sensitivity to thyroid hormones (THs). It is caused by mutations in genes encoding the receptors for thyroid hormones, α (THRα) or β (THRβ), the distribution of which varies between tissues. Therefore, patients present with elevated TH levels with unsuppressed TSH levels, and symptoms of both hypothyroidism and hyperthyroidism may be present. Methods: Hence, we report the case of a boy with a complex, cyanotic, congenital heart defect who was also diagnosed with TH resistance syndrome. Results: Because of the clinical features of hyperthyroidism in preparation for cardiac surgery, thiamazole was administered, resulting in the normalisation of TH effects on the α-receptor for HTs. Due to the effectiveness of the proposed treatment, it was further introduced before the further stages of cardiac surgeries. Conclusions: The management of RTH is a constant challenge for clinicians and must be individualised.
Abstract licence: CC BY
Yuka Ono, Norio Wada, Shuhei Baba, et al.
Endocrinology, Diabetes & Metabolism Case Reports, 2025
Summary: We report the case of a 41-year-old Japanese woman with visual field disturbances during late pregnancy. At 39 weeks of gestation, she was diagnosed with bitemporal hemianopsia at the ophthalmology department. An MRI revealed a symmetrical pituitary gland enlargement, compressing the optic chiasm. An emergency cesarean section was performed immediately, resulting in the delivery of a male infant weighing 3,112 grams. Laboratory tests indicated low serum free thyroxine (T4), thyroid-stimulating hormone (TSH), cortisol, luteinizing hormone, and follicle-stimulating hormone. The patient was clinically diagnosed with lymphocytic hypophysitis (LHy). Due to her visual field impairment, she was administered 60 mg of prednisolone daily. After 2 days, her visual field impairment improved rapidly, leading to a gradual tapering of the dose. Six months after treatment initiation, an MRI showed shrinkage of the pituitary gland. Her prednisolone dose was reduced to 5 mg daily, and she was switched to hydrocortisone at 15 mg daily. Twelve months after starting treatment, the patient developed thyrotoxicosis. Testing revealed a positive TSH receptor antibody, resulting in a diagnosis of Graves' disease (GD). Treatment with thiamazole (15 mg daily) and potassium iodide (76 mg daily) was initiated, and her thyroid function normalized after 2 months. LHy is believed to have an autoimmune mechanism and is frequently associated with other autoimmune diseases; however, the development of GD is rare. Development of Graves' disease should be considered in patients with LHy, particularly during the postpartum period and the glucocorticoid treatment process. Learning points: Females with lymphocytic hypophysitis often experience local symptoms, such as visual field disorders, when pregnant. This condition is frequently associated with autoimmune diseases, particularly autoimmune thyroid disorders. However, reports explicitly linking it to Graves' disease have been limited. The postpartum period is considered a trigger of the onset of Graves' disease. In addition, the high-dose glucocorticoid treatment and its tapering may affect it.
Abstract licence: CC BY-NC-ND
Yan Wang, Haojun Xu, Junjun Li, et al.
Materials & Design, 2026
• Near-infrared light improves local drug diffusion and enhances therapeutic efficacy. • The therapy restores thyroid hormone balance and tissue structure while alleviating liver injury. • The system reduces oxidative stress and apoptosis, providing a safer alternative to oral treatment.
Abstract licence: CC BY-NC-ND
Shigeru Nagaki, Makiko Osawa, Satoru Nagata
SAGE Open Medical Case Reports, 2024
We present two cases of epilepsy associated with Graves' disease. Case 1 is a 22-year-old woman. She had three epileptic seizures and was diagnosed with idiopathic generalized epilepsy. She was treated with valproic acid (VPA). She was later diagnosed with Graves' disease, and treated with antithyroid medication (thiamazole). We added a thyroid medication (levothyroxine) because of a decrease in free thyroxine observed with antithyroid medication. Case 2 is an 18-year-old woman. She had three epileptic seizures and was diagnosed with juvenile myoclonic epilepsy and treated with VPA. Then, she was diagnosed with Graves' disease and was treated with thiamazole. Levothyroxine was added due to low fT4 induced by thiamazole. Due to poor compliance with antithyroid medication, the thyroid functional status was not stable. Both patients became seizure-free and euthyroid after VPA and thiamazole treatments.
Abstract licence: CC BY-NC
E. I. Surikova, E. M. Frantsiyants, V. A. Bandovkina, et al.
Исследования и практика в медицине, 2023
Objective . Studying the levels of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF-β), and neurotrophin 3 (NT3) in the cerebral cortex and subcortical substance of female rats in an experimental model of extracerebral growth of malignant tumor under conditions of induced hypothyroidism. Materials and methods . An experiment was performed on 47 white non-linear female rats: 10 rats each in the intact group, control group 1 (induced hypothyroidism), control group 2 (subcutaneous growth of Guerin’s carcinoma), main group (combination of pathologies); 7 rats in the group with subcutaneous tumor growth to assess life expectancy. Hypothyroidism was induced by per os administration of thiamazole (mercazolil, Akrikhin, Russia), daily dose of 2.5 mg/100 g of body weight, course of 30 days; total thyroxine and thyroid stimulating hormone were determined in blood serum by RIA (Immunotech, Czech Republic). When persistent hypothyroidism was achieved, Guerin’s carcinoma was transplanted under the skin as standard. Aſter decapitation on the 18th day aſter transplantation, the content of BDNF, NGF-β, NT3 (R&D System, RayBiotech, USA) was determined in 10 % homogenates of the cortex and subcortical substance subcortex of the brain (R&D System, RayBiotech, USA). Results . In the cortex in control groups 1 and 2, the level of BDNF was 2.6- and 1.6-fold lower, respectively, and NGF-β was 2.2-fold higher on average than in the intact group. NT3 levels in the control group 1 were 3.0- and 1.6-fold lower in the cortex and subcortical substance, respectively. In the control group 2, the levels of NT3 and NGF-β were higher in the subcortical matter than in the intact group by 2.4-fold and 3.1-fold, respectively. In the cortex and subcortical substance in the main group, only NGF-β levels were higher on average by 1.7 times, with values being intermediate between the corresponding values in control groups 1 and 2. Conclusion . Changes in the levels of all neurotrophins in hypothyroidism were most pronounced in the cortex, while in independent tumor growth, NGF-β in the cortex and subcortical substance and NT3 only in subcortical substance changed the most. When the pathologies were combined, only NGF-β was altered in the cortex and subcortical substance. Apparently, there is an interaction of the tumor and the CNS with changes in the balance of regulatory signals in the subcortical areas of the brain, that reflecting the connection with the biological characteristics of an active or inhibited (in presence of hypothyroidism) tumor growth.
Abstract licence: CC BY
Toshihiko Kasahara
European Thyroid Journal, 2025
- Hypothyroidism
- Thyroxine
- Thyroid Function Tests
Objective: This study examined the relationship between levothyroxine dosage and free thyroxine levels in hypothyroid patients. The aim was to ascertain whether elevated free thyroxine in treated patients suggests overmedication or is essential for maintaining appropriate free triiodothyronine levels, guiding improved monitoring practices during therapy. Methods: A retrospective analysis was conducted on 3,020 free thyroxine measurements from 1,409 patients between July 2021 and March 2024. Patients with thyrotropin receptor antibodies or treated with antithyroid drugs such as thiamazole, propylthiouracil, and potassium iodide were excluded. Measurements were performed using the Elecsys FT4 III immunoassay, and statistical comparisons were made between levothyroxine-treated and untreated groups. Results: Levothyroxine-treated patients showed significantly higher median free thyroxine levels (17.9 pmol/L, interquartile range (IQR): 15.6-20.1) than untreated patients (16.2 pmol/L, IQR: 14.5-17.9, P < 0.0001). In addition, the free triiodothyronine/free thyroxine ratio was significantly lower in levothyroxine-treated patients (0.24, IQR: 0.20-0.29) than in untreated patients (0.28, IQR: 0.25-0.32, P < 0.0001). Free thyroxine levels increased with levothyroxine dosage, whereas the free triiodothyronine/free thyroxine ratio decreased. Although thyroid-stimulating hormone levels did not differ significantly between the groups, higher levothyroxine doses were associated with mild suppression. Conclusion: The findings emphasize the importance of higher free thyroxine levels for maintaining adequate free triiodothyronine in levothyroxine-treated patients, underscoring the need to monitor free thyroxine, free triiodothyronine, and their ratio during therapy to optimize treatment outcomes. In addition, clinicians should recognize that higher levothyroxine doses may elevate free thyroxine levels beyond the reference range.
Abstract licence: CC BY
Aimi Ohya, Makoto Ohtake, Yusuke Kawamura, et al.
International Journal of Emergency Medicine, 2023
BACKGROUND: Subarachnoid hemorrhage and thyroid storm are similar in their clinical symptomatology, and diagnosis of these conditions, when they occur simultaneously, is difficult. Here, we report a rare case of concurrent subarachnoid hemorrhage and thyroid storm we encountered at our hospital. CASE PRESENTATION: The patient was a 52-year-old woman. While bathing at home, the patient experienced a sudden disturbance of consciousness and was brought to our hospital. The main physical findings upon admittance were Glasgow Coma Scale score of E1V2M4, elevated blood pressure (208/145 mmHg), and tachycardia with atrial fibrillation (180 bpm) along with body temperature of 36.1 °C. Brain computed tomography revealed subarachnoid hemorrhage associated with a ruptured aneurysm of the posterior communicating artery branching from the left internal carotid artery, and aneurysm clipping was performed. Blood tests upon admission revealed high levels of free T3 and free T4 and low levels of thyroid-stimulating hormone. Upon determining that the patient had hyperthyroidism, thiamazole was administered. However, due to continuous impaired consciousness, fever, and persistence of tachycardia, the patient was diagnosed with thyroid storm. Oral potassium iodide and hydrocortisone were added to the treatment. The treatment was successful as the patient's symptoms improved, and she became lucid. In this case, we believe that in the presence of untreated hyperthyroidism, the onset of subarachnoid hemorrhage induced thyroid storm. Tachycardia of 130 bpm or higher, which is the diagnostic criterion for thyroid storm, rarely occurs with subarachnoid hemorrhage. Therefore, we believe it is an important factor for recognizing the presence of the thyroid storm. In this case, clipping surgery was prioritized which resulted in a favorable outcome. However, it is possible that invasive surgery may have exacerbated thyroid storm, suggesting that treatment should be tailored as per patient's condition. CONCLUSION: If a pulse rate of 130 bpm or higher is observed alongside subarachnoid hemorrhage, we recommend considering the possibility of concomitant thyroid storm and testing for thyroid hormone. If concomitant thyroid storm is present, we believe that a treatment plan tailored to the patient's condition is critical, and early diagnosis will lead to a favorable outcome for the patient.
Abstract licence: CC BY
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
1 found
Half-life
0.17 hours
Mechanism
Methimazole's primary mechanism of action appears to be interference in an early…
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.25 to 4.0 hours
Half-life
10mg
Protein binding
[A184526][A184541][A184643]
Volume of distribution
20 L
[A184541]…
Metabolism
[A184571][A184574]…
Elimination
7%
Clearance
10mg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
On a weight basis, methimazole is 10 times more potent than the other major antithyroid thionamide used in North America, [propylthiouracil],[L8339] and is the active metabolite of the pro-drug [carbimazole], which is an antithyroid medication used in the United Kingdom and parts of the former British Commonwealth.[A184733] Traditionally, methimazole has been preferentially used over propylthiouracil due to the risk of fulminant hepatotoxicity carried by the latter,[A184757] with propylthiouracil being preferred in pregnancy due to a perceived lower risk of teratogenic effects. Despite documented teratogenic effects in its published labels,[L8336][L8339] the true teratogenicity of methimazole appears to be unclear[A184643][A184757][A184763] and its place in therapy may change in the future.
[L8336]
In Canada, methimazole carries the above indications and is also indicated for the medical treatment of hyperthyroidism regardless of other available treatment options.
[L8339]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1982 interactions
[L8333]
Signs and symptoms of methimazole overdose may include gastrointestinal distress, headache, fever, joint pain, pruritus, and edema. More serious adverse effects, such as aplastic anemia or agranulocytosis, may manifest within hours to days.
[L8336][L8339]
Hepatitis, nephrotic syndrome, exfoliative dermatitis, and CNS effects such as neuropathy or CNS depression/stimulation are also potential, albeit less frequent, results of overdose.
[L8336][L8339]
Management of overdose involves supportive treatment as dictated by the patient's status.
[L8336][L8339]
This may involve monitoring of the patient's vital signs, blood gases, serum electrolytes, or bone marrow function as indicated.
[L8339]
Methimazole may directly inhibit TPO, but has been shown in vivo to instead act as a competitive substrate for TPO, thus becoming iodinated itself and interfering with the iodination of thyroglobulin.[A184559] Another proposed theory is that methimazole’s sulfur moiety may interact directly with the iron atom at the centre of TPO’s heme molecule, thus inhibiting its ability to iodinate tyrosine residues.[A184694] Other proposed mechanisms with weaker evidence include methimazole binding directly to thyroglobulin or direct inhibition of thyroglobulin itself.[A184559]
The most serious potential side effect of methimazole therapy is agranulocytosis, and patients should be instructed to monitor for, and report, any signs or symptoms of agranulocytosis such as fever or sore throat. Other cytopenias may also occur during methimazole therapy. There also exists the potential for severe hepatic toxicity with the use of methimazole, and monitoring for signs and symptoms of hepatic dysfunction, such as jaundice, anorexia, pruritus, and elevation in liver transaminases, is prudent in patients using this therapy.[L8336][L8339]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A184514][A184499]
Cmax is slightly, but not significantly, higher in hyperthyroid patients, and both Cmax and AUC are significantly affected by the oral dose administered.
[A184514]
[A184499]
Methimazole's primary active metabolite, 3-methyl-2-thiohydantoin, has a half-life approximately 3 times longer than its parent drug.
[A184541]
Renal impairment does not appear to alter the half-life of methimazole, but patients with hepatic impairment showed an increase in half-life roughly proportional to the severity of their impairment - moderate insufficiency resulted in a elimination t1/2 of 7.1 hours, while severe insufficiency resulted in an elimination t1/2 of 22.1 hours.
[A184499]
There does not appear to be any significant differences in half-life based on thyroid status (i.e. no difference between euthyroid and hyperthyroid patients).
[A184499][A184502][A184514]
[A184526][A184541][A184643]
[A184541]
Following oral administration, methimazole is highly concentrated in the thyroid gland - intrathyroidal methimazole levels are approximately 2 to 5 times higher than peak plasma levels, and remain high for 20 hours after ingestion.
[A184559]
[A184571][A184574]
Several metabolites have been identified, though the specific enzyme isoforms responsible for their formation are not entirely clear. One of the first methimazole metabolites identified, 3-methyl-2-thiohydantoin, may contribute to antithyroid activity - its antithyroid activity has been demonstrated in rats and may explain the prolonged duration of iodination inhibition following administration despite methimazole's relatively short half-life.
[A184541]
A number of metabolites have been investigated as being the culprits behind methimazole-induced hepatotoxicity. Both glyoxal and N-methylthiourea have established cytotoxicity and are known metabolic products of methimazole's dihydrodiol intermediate.
Sulfenic and sulfinic acid derivatives of methimazole are thought to be the ultimate toxicants responsible for hepatotoxicity, though their origin is unclear - they may arise from direct oxidation of methimazole via FMO, or from oxidation of N-methylthiourea further downstream in the metabolic process.
[A184571][A184574]
[A184514]
Enterohepatic circulation also appears to play a role in the elimination of methimazole and its metabolites, as significant amounts of these substances are found in the bile post-administration.
[A184643]
[A184499]
Renal impairment does not appear to alter clearance of methimazole, but patients with hepatic impairment showed a reduction in clearance roughly proportional to the severity of their impairment - moderate insufficiency resulted in a clearance of 3.49 L/h, while severe insufficiency resulted in a clearance of 0.83 L/h.
[A184499]
There does not appear to be any significant differences in clearance based on thyroid status (i.e. no difference between euthyroid and hyperthyroid patients).
[A184499][A184502][A184514]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC H03BB52
ATC H03BB02
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)
Methimazole
Matched from: Thiamazole
Additional database identifiers
Drugs Product Database (DPD)
14593
Drugs Product Database (DPD)
9107
ChemSpider
1131173
BindingDB
50241361
PDB
MMZ
ZINC
ZINC000001187543
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12015
GenAtlas
TPO
GeneCards
TPO
GenBank Gene Database
J02969
GenBank Protein Database
339867
Guide to Pharmacology
2526
UniProt Accession
PERT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2610
GenAtlas
CYP2A6
GeneCards
CYP2A6
GenBank Gene Database
X13897
Guide to Pharmacology
1321
UniProt Accession
CP2A6_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:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_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:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2631
GeneCards
CYP2E1
GenBank Gene Database
J02625
GenBank Protein Database
181360
Guide to Pharmacology
1330
UniProt Accession
CP2E1_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:3771
GeneCards
FMO3
GenBank Gene Database
M83772
GenBank Protein Database
188631
UniProt Accession
FMO3_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q419663), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.