Page last updated: 2024-11-05

carbimazole

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

Carbimazole is a thioureylene derivative that acts as an antithyroid agent. It is a prodrug that is metabolized in the body to its active form, methimazole. Carbimazole inhibits the synthesis of thyroid hormones by blocking the incorporation of iodine into the thyroid gland. This effect is due to its inhibition of the enzyme thyroid peroxidase, which is crucial for the iodination of tyrosine residues in thyroglobulin. Carbimazole is used to treat hyperthyroidism, a condition where the thyroid gland produces too much thyroid hormone. It can also be used to prevent hyperthyroidism in people who are about to have surgery on their thyroid gland. Carbimazole is available as tablets and is typically taken by mouth. It is generally well tolerated, but common side effects include skin rash, itching, headache, and joint pain. Carbimazole can also cause serious side effects, such as liver damage, blood disorders, and a decrease in white blood cell count. Carbimazole is not recommended for pregnant women or breastfeeding mothers. It is also not recommended for people with certain medical conditions, such as liver disease, kidney disease, and bone marrow suppression. Carbimazole is a commonly used and effective treatment for hyperthyroidism. It is important to note that Carbimazole should only be taken under the supervision of a qualified healthcare professional. The mechanism of action, clinical applications, and side effects of Carbimazole are well-studied and documented in scientific literature.'

Carbimazole: An imidazole antithyroid agent. Carbimazole is metabolized to METHIMAZOLE, which is responsible for the antithyroid activity. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

carbimazole : A member of the class of imidazoles that is methimazole in which the nitrogen bearing a hydrogen is converted into its ethoxycarbonyl derivative. A prodrug for methimazol, carbimazole is used for the treatment of hyperthyroidism. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID31072
CHEMBL ID508102
CHEBI ID617099
SCHEMBL ID44211
MeSH IDM0003346

Synonyms (133)

Synonym
BRD-K87156652-001-05-1
1h-imidazole-1-carboxylic acid, 2,3-dihydro-3-methyl-2-thioxo-, ethyl ester
ethyl 3-methyl-2-thioxo-2,3-dihydro-1h-imidazole-1-carboxylate
tyrazol
atirozidina
brn 0144339
3-methyl-2-thioxo-4-imidazoline-1-carboxylic acid ethyl ester
carbimazolum [inn-latin]
basolest
neomercazole
neo-mercazole
mertiran
carbimazol
thyrostat
1-ethoxycarbonyl-3-methyl-2-thioimidazol
carbotiroid
einecs 244-854-4
neo-thyreostat
carbimazol [inn-spanish, french]
carbimazol spofa
neo-tireol
4-imidazoline-1-carboxylic acid, 3-methyl-2-thioxo-, ethyl ester
1h-imidazole-1-carboxylic acid, 2,3-dihydro-3-methyl-2-thioxo, ethyl ester
carbimazole [inn:ban:dcf]
CG1 ,
PRESTWICK_788
NCGC00016760-01
cas-22232-54-8
PRESTWICK3_000439
BPBIO1_000504
BSPBIO_003568
D07616
carbimazole (inn)
carbimazol henning (tn)
BSPBIO_000458
PRESTWICK2_000439
C07615
22232-54-8
carbimazole
carbinazole
ethyl 3-methyl-2-thioimidazoline-1-carboxylate
carbethoxymethimazole
DB00389
athyromazole
NCGC00095167-02
NCGC00095167-01
KBIO3_002918
SPECTRUM2_001251
PRESTWICK0_000439
PRESTWICK1_000439
SPECTRUM3_001968
SPBIO_002397
SPBIO_001182
SPECTRUM1505323
NCGC00177988-01
NCGC00177988-02
CHEBI:617099 ,
carbimazolum
1-ethoxycarbonyl-3-methyl-2-thioxo-4-imidazoline
bdbm50275889
HMS1922D12
HMS1569G20
CHEMBL508102 ,
carbimazol henning
nsc-758966
ethyl 3-methyl-2-sulfanylideneimidazole-1-carboxylate
AKOS001647527
HMS2096G20
dtxsid9022736 ,
NCGC00255133-01
dtxcid902736
tox21_302320
A816030
ethyl 3-methyl-2-thioxo-imidazole-1-carboxylate;carbimazole
pharmakon1600-01505323
nsc758966
tox21_110596
smr001233183
MLS004734638
S4048 ,
CCG-39106
NCGC00016760-02
NCGC00016760-04
NCGC00016760-03
NCGC00016760-05
4-24-00-00064 (beilstein handbook reference)
unii-8kq660g60g
8kq660g60g ,
nsc 758966
FT-0602919
EPITOPE ID:116890
AM84794
3-methyl-2-thioi-midazoline-1-carboxylate
carbimazole [mart.]
carbimazole [inn]
carbimazole [mi]
carbimazole [who-dd]
carbimazole [ep monograph]
HY-B0558
SCHEMBL44211
tox21_110596_1
NCGC00016760-08
ethyl 3-methyl-2-thionoimidazoline-1-carboxylate
W-107493
CFOYWRHIYXMDOT-UHFFFAOYSA-N
ethyl 3-methyl-2-thioxo-2,3-dihydro-1h-imidazole-1-carboxylate #
mfcd00027421
ethyl 3-methyl-2-sulfanylidene-2,3-dihydro-1h-imidazole-1-carboxylate
ethyl 3-methyl-2-thioxo-2,3-dihydro-1h-imidazole-1-carboxylate, aldrichcpr
SR-01000872660-1
AC-8348
sr-01000872660
SR-01000872660-2
HMS3652G04
SBI-0207026.P001
HMS3713G20
SW196926-3
Q414013
AS-13267
BCP12935
BRD-K87156652-001-06-9
A16427
C74138
carbimazole 3-methyl-2-thionoimidazoline-1-carboxylic acid ethyl ester
fenobucarb bassa bpmc
BE164282
EN300-7816879
h03bb01
carbimazole (ep monograph)
carbimazolo
carbimazol (inn-spanish, french)
carbimazole (mart.)
carbimazolum (inn-latin)

Research Excerpts

Overview

Carbimazole is an antithyroid drug of the thionamide class which is used in the treatment of hyperthyroidism. It is a drug that is widely used forhyperthyroid disorders, such as Graves' disease.

ExcerptReferenceRelevance
"Carbimazole is an anti-thyroid medication used to treat hyperthyroidism in adults and children."( Severe Neutropenia and Hepatotoxicity After Carbimazole Drug Therapy for Hyperthyroidism in a Pediatric Patient: A Case Report.
AlAboud, M; Alanizi, A; Alasqah, MA; Alhubaishi, AA; Alkahtani, R; Alnajjar, LI; Alwahhabi, B; Bin Sheraim, N, 2023
)
1.89
"Carbimazole is a widespread drug utilized for treating hyperthyroidism. "( The Protective Effect of Turmeric against Carbimazole Induced Toxicity in Male Rats.
Abed Al-Kareem, Z; Aziz, ND; Hussein Naser, I, 2022
)
2.43
"Carbimazole is an antithyroid drug of the thionamide class which is used in the treatment of hyperthyroidism. "( Fatality complicating agranulocytosis in the setting of carbimazole therapy.
Lynch, MJ; Woodford, NW, 2008
)
2.03
"Carbimazole is a drug that is widely used for hyperthyroid disorders, such as Graves' disease. "( Carbimazole-induced agranulocytosis: does antineutrophil cytoplasmic antibody have a role?
Ekinci, E; Grossmann, M; Jerums, G; Lee, ST; Yip, G, 2010
)
3.25
"Carbimazole is an antithyroid drug used in treatment of hyperthyroidism. "( Effect of selenium on carbimazole-induced testicular damage and oxidative stress in albino rats.
Mahran, HA; Nofal, AE; Sakr, SA, 2011
)
2.13
"Carbimazole is a methimazole derivative that is rapidly metabolized to methimazole in vivo."( Serum concentrations of methimazole in cats after a single oral dose of controlled-release carbimazole or sugar-coated methimazole (thiamazole).
Longhofer, SL; Martín-Jiménez, T; Soni-Gupta, J, 2010
)
1.3
"Carbimazole embryopathy is a recently recognized and defined phenotype. "( Antenatal carbimazole and choanal atresia: a new embryopathy.
Daya, H; Foulds, N; Wolf, D, 2006
)
2.18
"Carbimazole is a useful antithyroid drug with a rare potentially fatal complication of agranulocytosis. "( Carbimazole-induced agranulocytosis--a report of 2 recent cases.
Chew, LS; Rajasoorya, C; Tavintharan, S, 1997
)
3.18

Effects

Carbimazole has no effect on the conversion process, whereas propylthiouracil (50 microM) inhibits the conversion. BM-MSCs are capable to mend these destructive outcomes in time dependent manner.

ExcerptReferenceRelevance
"Carbimazole has damaging effects and BM-MSCs are capable to mend these destructive outcomes in time dependent manner."( Histological, Histochemical and Immunohistochemical Evaluation of the Role of Bone Marrow-Derived Mesenchymal Stem Cells on the Structure of Periodontal Tissues in Carbimazole-Treated Albino Rats.
Rabea, AA, 2020
)
2.2
"Carbimazole has to be added to the list of drugs capable of inducing acute pancreatitis, and should be emphasized the need to discontinue this medication as soon as there is evidence of pancreatic dysfunction."( Acute pancreatitis, hepatic cholestasis, and erythema nodosum induced by carbimazole treatment for Graves' disease.
Carraro, R; Fernández-Herrera, J; Gómez-Pan, A; Jiménez, I; Marazuela, M; Pajares, JM; Sánchez de Paco, G, 2002
)
1.27
"Carbimazole (50 microM) has no effect on the conversion process, whereas propylthiouracil (50 microM) inhibits the conversion."( Propranolol inhibits the in vitro conversion of thyroxine into triiodothyronine by isolated rat liver parenchymal cells.
Touber, JL; van Noorden, CJ; Wiersinga, WM, 1979
)
0.98

Treatment

Carbimazole treatment followed by thyroidectomy resulted in a quick weight gain and general improvement in health status.

ExcerptReferenceRelevance
"Carbimazole treatment followed by thyroidectomy resulted in a quick weight gain and general improvement in health status."( Evidence for the possible occurrence of Grave's disease in a blue-eyed black lemur (Eulemur flavifrons).
Feirrera, X; Giorgiadis, M; Lefaux, B; Lemberger, K; Quintard, B; Schohn, C, 2018
)
1.2
"Carbimazole treatment had little effect and his symptoms worsened to include severe shortness of breath."( Testicular germ cell tumour presenting as thyrotoxicosis.
Blainey, AD; Slater, J; Tilbrook, LK, 2004
)
1.04
"from carbimazole treated mothers (X), carbimazole plus thyroxine treated mothers (Y), and controlled mothers (Z)."( Carbimazole-induced hypothyroidism causes the adrenal atrophy in 10 days' prenatally treated albino rats.
Parveen, S; Sarwar, G, 2005
)
2.23
"Carbimazole pretreatment for eight weeks did not appear to protect against hypothyroidism, in our study."( Thyrotoxicosis--treatment by I131 therapy and early prediction of hypothyroidism following this therapy.
Jain, SK; Khanna, CM; Walia, RP, 1994
)
1.01
"Li-carbimazole treatment brought about a fall in the mean total serum T4 of 57.4% compared with a drop of 32.8% in patients treated with carbimazole alone."( Low dose lithium-carbimazole in the treatment of thyrotoxicosis.
Brownlie, BE; Hedley, JM; Sadler, WA; Turner, JG, 1978
)
1.11
"In carbimazole-treated patients, the appearance of functional suppressor T cells was delayed slightly, but the overall suppression ratios on the 16th and 20th days were normal."( Normal suppressive T cell function of Epstein-Barr virus-induced B cell activation in Graves' disease.
Charreire, J; Kahan, A; Lefloch, JP, 1987
)
0.79
"Treatment with carbimazole along with thyroxine was followed by a live birth at 35 wk; but the baby developed severe fatal neonatal thyrotoxicosis with crisis on day 9 and died on day 12."( Fetal Hyperthyroidism: Intrauterine Treatment with Carbimazole in Two Siblings.
Batra, CM; Gupta, N; Gupta, V; Menon, PS, 2015
)
1.01
"Treatment with Carbimazole 30 mg/day was initiated."( Acute cholestatic hepatitis along with agranulocytosis: a rare side effect of carbimazole.
Chakrapani, M; Jain, K; Smitha, K,
)
0.7
"Treatment with carbimazole ointment resulted in disappearance of signs of hyperthyroidism; plasma concentrations of urea and creatinine increased significantly."( [Transdermal carbimazole for the treatment of feline hyperthyroidism].
Buijtels, JJ; Galac, S; Kooistra, HS; Kurvers, IA; Winter, EA, 2006
)
1.04
"Treatment with carbimazole 30 mg/day was initiated."( Concomitant agranulocytosis and hepatotoxicity after treatment with carbimazole.
Aguilar-Diosdado, M; de Los Santos, A; Garcia-Valero, A; López-Tinoco, C; Torres, I; Vilchez, FJ, 2006
)
0.91
"Pre-treatment with carbimazole did not protect against the development of hypothyroidism (carbimazole treated 69% hypothyroid at 4 months, untreated 62% hypothyroid at 4 months)."( Hyperthyroidism and radio-iodine therapy in a district general hospital.
Child, DF; Harvey, JN; Hudson, P; Mughni, MA; Williams, CP, 1994
)
0.61
"Treatment with carbimazole resulted in complete resolution of symptoms and return of muscle power to normal."( Inflammatory myopathy in thyrotoxicosis.
Brett, F; Farrell, M; Hardiman, O; Molloy, F, 1997
)
0.64
"Treatment with carbimazole produced a significant rise in LSH and SOD."( Free radicals and Graves' disease: the effects of therapy.
Bradley, H; Chopra, M; McKillop, JH; Smith, WE; Thomson, JA; Wilson, R, 1989
)
0.62
"Pretreatment with carbimazole of patients given radioiodine (131I) therapy for thyrotoxicosis reduces the incidence of early hypothyroidism. "( Radioprotective action of carbimazole in radioiodine therapy for thyrotoxicosis--influence of the drug on iodine kinetics.
Alexander, WD; Coghill, G; Connell, JM; Hilditch, TE; Robertson, J, 1987
)
0.91

Toxicity

Once daily application of a novel formulation of transdermal methimazole applied to the pinnae was as effective and safe as twice daily oral carbimazoles. Within six weeks following the start of therapy, patient developed potentially life-threatening acute cholestatic hepatitis.

ExcerptReferenceRelevance
" Possible adverse effects of this therapy include cardiovascular changes (shortening of systolic time intervals, increased frequency of atrial premature beats and, possibly, left ventricular hypertrophy) and bone changes (reduced bone density and bone mass), but the risk of these adverse effects can be minimised by carefully monitoring serum free thyroxine and free liothyronine (triiodothyronine) measurements and adjusting the dosage accordingly."( Adverse effects of thyroid hormone preparations and antithyroid drugs.
Bartalena, L; Bogazzi, F; Martino, E, 1996
)
0.29
" Within 15 days following the start of therapy, both minor (eg, pruritus, rash, urticaria, fever, arthralgias) and potentially life-threatening (eg, agranulocytosis, severe mixed hepatotoxicity with severe cholestatic jaundice) adverse effects developed."( Concomitant agranulocytosis and hepatotoxicity after treatment with carbimazole.
Aguilar-Diosdado, M; de Los Santos, A; Garcia-Valero, A; López-Tinoco, C; Torres, I; Vilchez, FJ, 2006
)
0.57
"Agranulocytosis and hepatotoxicity are rare adverse effects associated with carbimazole treatment and are usually dose- and age-related."( Concomitant agranulocytosis and hepatotoxicity after treatment with carbimazole.
Aguilar-Diosdado, M; de Los Santos, A; Garcia-Valero, A; López-Tinoco, C; Torres, I; Vilchez, FJ, 2006
)
0.8
"Major adverse effects associated with carbimazole are infrequent."( Concomitant agranulocytosis and hepatotoxicity after treatment with carbimazole.
Aguilar-Diosdado, M; de Los Santos, A; Garcia-Valero, A; López-Tinoco, C; Torres, I; Vilchez, FJ, 2006
)
0.84
" Twenty-one adverse reactions possibly (20) or probably (1) related to treatment were reported."( Clinical efficacy and safety of a once-daily formulation of carbimazole in cats with hyperthyroidism.
Burgaud, S; Frénais, R; Horspool, LJ; Rosenberg, D, 2009
)
0.6
" Within six weeks following the start of therapy, patient developed potentially life-threatening acute cholestatic hepatitis and agranulocytosis as adverse effects to carbimazole."( Acute cholestatic hepatitis along with agranulocytosis: a rare side effect of carbimazole.
Chakrapani, M; Jain, K; Smitha, K,
)
0.55
"Once daily transdermal administration of a novel lipophilic formulation of methimazole is as safe and effective as oral carbimazole in treating hyperthyroidism in cats."( The efficacy and safety of a novel lipophilic formulation of methimazole for the once daily transdermal treatment of cats with hyperthyroidism.
Bridges, J; Chambers, P; Gieseg, MA; Hill, KE; Kingsbury, D; Lopez-Villalobos, N,
)
0.34
"In this 12-week trial, once daily application of a novel formulation of transdermal methimazole applied to the pinnae was as effective and safe as twice daily oral carbimazole in the treatment of cats with hyperthyroidism."( The efficacy and safety of a novel lipophilic formulation of methimazole for the once daily transdermal treatment of cats with hyperthyroidism.
Bridges, J; Chambers, P; Gieseg, MA; Hill, KE; Kingsbury, D; Lopez-Villalobos, N,
)
0.33
" It is a thionamide associated with rare adverse effects such as neutropenia, leukopenia, agranulocytosis, and hepatotoxicity."( Severe Neutropenia and Hepatotoxicity After Carbimazole Drug Therapy for Hyperthyroidism in a Pediatric Patient: A Case Report.
AlAboud, M; Alanizi, A; Alasqah, MA; Alhubaishi, AA; Alkahtani, R; Alnajjar, LI; Alwahhabi, B; Bin Sheraim, N, 2023
)
1.17
" However, carbimazole usage could be associated with adverse effects such as liver damage and nephritis in rats."( The Protective Effect of Turmeric against Carbimazole Induced Toxicity in Male Rats.
Abed Al-Kareem, Z; Aziz, ND; Hussein Naser, I, 2022
)
1.39

Pharmacokinetics

ExcerptReferenceRelevance
" Simulations of carbamazepine dosing regimen based on the pharmacokinetic parameters of this patient were performed to allow individualization of drug therapy."( Slow carbamazepine clearance in a nonadherent Malay woman with epilepsy and thyrotoxicosis.
Hui-Ping Khor, A; Lim, KS; Lo, YL; Ng, CC; Yeap, LL, 2014
)
0.4
" The time at maximal concentration and elimination half-life were longer for 10 mg transdermal methimazole (5."( The pharmacokinetics of methimazole in a novel lipophilic formulation administered transdermally to healthy cats.
Bridges, J; Chambers, JP; Gieseg, MA; Hill, KE, 2014
)
0.4

Compound-Compound Interactions

TSH suppressive therapy combined with carbimazole (CBZ) had a positive effect on Graves' disease. Graves' Disease was treated with 131I in combination withcarbimazoles in 22 patients.

ExcerptReferenceRelevance
" Graves' disease was treated with 131I in combination with carbimazole in 22 patients."( Prognostic value of thyrotrophin binding inhibiting immunoglobulins (TBII) in longterm antithyroid treatment, 131I therapy given in combination with carbimazole and in euthyroid ophthalmopathy.
Bliddal, H; Friis, T; Kirkegaard, C; Siersbaek-Nielsen, K, 1981
)
0.71
"We studied the influence of TSH suppressive therapy combined with carbimazole (CBZ) on treatment outcome in Graves' disease."( TSH suppression combined with carbimazole for Graves' disease: effect on remission and relapse rates.
Baldet, L; Boegner, C; Bringer, J; Daurès, JP; Galtier-Dereure, F; Grabar, S; Jaffiol, C; Osman, A; Pujol, P; Raye, R, 1998
)
0.83
"TSH suppression combined with CBZ has little or no effect on remission and relapse rates in Graves' disease patients."( TSH suppression combined with carbimazole for Graves' disease: effect on remission and relapse rates.
Baldet, L; Boegner, C; Bringer, J; Daurès, JP; Galtier-Dereure, F; Grabar, S; Jaffiol, C; Osman, A; Pujol, P; Raye, R, 1998
)
0.59

Bioavailability

The oral bioavailability of two antithyroid drugs, methimazole and carbimazoles, was investigated in seven euthyroid subjects. The mean relativeBioavailability of 10 mg transdermal methiazole compared to oral carbimzole was 48 (min 43, max 55)%.

ExcerptReferenceRelevance
" The bioavailability of two 5 mg tablet formulations of carbimazole (Neomercazole [A] and Carbazole [B]) have been compared in six euthyroid subjects."( Bioavailability of two tablet preparations of carbimazole in man.
Ilett, KF; Shenfield, GM; Tearne, P; Tjokrosetio, R,
)
0.64
"In this study we investigated the oral bioavailability of therapeutic doses of two antithyroid drugs, methimazole and carbimazole, in seven euthyroid subjects."( Comparative bioavailability of carbimazole and methimazole.
Dahlberg, PA; Jansson, R; Lindström, B, 1983
)
0.76
" The absolute bioavailability of carbimazole was around 88 +/- 11%."( Pharmacokinetics of controlled-release carbimazole tablets support once daily dosing in cats.
Burgaud, S; Frénais, R; Horspool, LJ, 2008
)
0.9
" The authors also extensively discuss the details regarding the pharmacology, bioactivation, biodisposition, bioavailability and pharmacokinetic properties of the two main ATD (MMI and PTU)."( Toxicological considerations for antithyroid drugs in children.
Karras, S; Krassas, GE; Tzotzas, T, 2011
)
0.37
" The mean relative bioavailability of 10 mg transdermal methimazole compared to oral carbimazole was 48 (min 43, max 55)%."( The pharmacokinetics of methimazole in a novel lipophilic formulation administered transdermally to healthy cats.
Bridges, J; Chambers, JP; Gieseg, MA; Hill, KE, 2014
)
0.63
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

The influence of synthetic antithyroid drug dosage on the course of Graves' disease was evaluated by comparing two groups of matched patients treated with carbimazole. Five dosage regimens ranging from 5 mg carbimzole twice daily to 15 mg methimazoles twice daily were studied. The dosage of carbimZole needed to achieve euthyroidism ranged from 4 to 17 mg twice daily.

ExcerptRelevanceReference
" Five dosage regimens ranging from 5 mg carbimazole twice daily to 15 mg methimazole twice daily were studied."( Kinetics of [123I]iodide uptake and discharge by perchlorate in studies of inhibition of iodide binding by antithyroid drugs.
Alexander, WD; Connell, JM; Hilditch, TE; McCruden, DC, 1985
)
0.54
" Although most side effects were not dangerous, in normal instances the lowest possible dosage should be administered to control hyperthyroid metabolism."( [Side effects of antithyroid therapy of hyperthyroidism. A study of 1256 continuously treated patients].
Benker, G; Cissewski, K; Meyer-Gessner, M; Olbricht, T; Reiners, C; Reinwein, D; Windeck, R, 1989
)
0.28
" The antithyroid treatment was given in low dosage without supplementary thyroxine."( [Severe adverse effects of low-dose carbimazole treatment in hyperthyroidism. A retrospective study of 476 patients].
Bregengård, C; Eigtved, A; Poulsen, S, 1989
)
0.55
"The influence of synthetic antithyroid drug dosage on the course of Graves' disease was evaluated by comparing two groups of matched patients treated with carbimazole."( [Improvement of the prognosis of Basedow's disease by using high doses of carbimazole].
Ducornet, B; Duprey, J; Izembart, M; Lifchitz, E; Louis, MF; Mossé, A; Sultan, M, 1988
)
0.7
" Dose-response studies in 17 sera showed that both receptor binding and thyroid stimulating responses always increased with increasing doses of serum."( An analysis of thyrotrophin receptor binding and thyroid stimulating activities in a series of Graves' sera.
Creagh, F; Didcote, S; Hashim, F; Perkins, W; Rees Smith, B; Teece, M; Williams, S, 1985
)
0.27
" This diabetes insipidus is reversible, non-progressive, unrelated to plasma level, and distinct in attack from lithium-induced hypothyroidism, which may occur at low dosage but is also usually of late onset and reversible or treatable with thyroxine while lithium is continued."( Blood levels and management of lithium treatment.
Crammer, JL; Crane, G; Rosser, RM, 1974
)
0.25
" The two groups of patients were fully comparable in regard to age, size of goitre and time of observation, and the same diagnostic criteria and dosage regimen of 131I were used."( 131I treatment of diffuse and nodular toxic goitre with or without antithyroid agents.
Bliddal, H; Friis, T; Hansen, JM; Johansen, K; Rogowski, P; Siersbaek-Nielsen, K, 1982
)
0.26
" High pretreatment T3 values were comparatively common among patients in whom a fixed CMI dosage had a insufficient effect."( Studies of thyroid hormone and methimazole levels in patients with Graves' disease on a standardized anti-thyroid drug regimen.
Dahlberg, PA; Karlsson, FA; Lindström, B; Wide, L, 1981
)
0.26
" Conventional propranolol at a dosage of 160 mg/day was frequently insufficient to produce a high degree of beta-adrenergic blockade, particularly in severely thyrotoxic patients."( Propranolol in the surgical treatment of hyperthyroidism, including severely thyrotoxic patients.
Crooks, J; Feely, J; Forrest, AL; Gunn, A; Hamilton, WF, 1981
)
0.26
" Possible adverse effects of this therapy include cardiovascular changes (shortening of systolic time intervals, increased frequency of atrial premature beats and, possibly, left ventricular hypertrophy) and bone changes (reduced bone density and bone mass), but the risk of these adverse effects can be minimised by carefully monitoring serum free thyroxine and free liothyronine (triiodothyronine) measurements and adjusting the dosage accordingly."( Adverse effects of thyroid hormone preparations and antithyroid drugs.
Bartalena, L; Bogazzi, F; Martino, E, 1996
)
0.29
"The optimal dosage regimen for carbimazole (CBZ) in the treatment of hyperthyroidism remains uncertain, despite clinical use of the drug for approximately fifty years."( A comparison of 20 or 40 mg per day of carbimazole in the initial treatment of hyperthyroidism.
Herbert, M; Hopton, M; Jeffcoate, WJ; Page, SR; Sheard, CE, 1996
)
0.85
" Mean initial carbimazole dosage was about 34 +/- 8 mg/d."( [Hyperthyroidism in people over 50 years of age in Senegal. Study of 31 cases observed over a 14-year period].
Fall, L; Sidibe, EH; Sow, AM; Toure-Sow, H, 1998
)
0.66
" The dosage of carbimazole needed to achieve euthyroidism ranged from 4 to 17 mg twice daily."( [Transdermal carbimazole for the treatment of feline hyperthyroidism].
Buijtels, JJ; Galac, S; Kooistra, HS; Kurvers, IA; Winter, EA, 2006
)
1.06
" Failure to recommend increased thyroxine dosage early in pregnancy (thus placing the offspring of women being treated for hypothyroidism at risk of impaired fetal brain development)."( Barriers in the quest for quality drug information: salutary lessons from TGA-approved sources for thyroid-related medications.
Stockigt, JR, 2007
)
0.34
"There is little consensus regarding the most appropriate dosage regimen for radioiodine treatment in Graves' disease."( Early treatment with low fixed dose (5 mCi) radioiodine therapy is effective in Indian subjects with Graves' disease.
Chatterjee, J; Chowdhury, S; Mukherjee, S; Mukhhopadhyay, P; Pandit, K; Raychaudhuri, M; Sanyal, D, 2008
)
0.35
" Simulations of carbamazepine dosing regimen based on the pharmacokinetic parameters of this patient were performed to allow individualization of drug therapy."( Slow carbamazepine clearance in a nonadherent Malay woman with epilepsy and thyrotoxicosis.
Hui-Ping Khor, A; Lim, KS; Lo, YL; Ng, CC; Yeap, LL, 2014
)
0.4
" The effect of adjunctive carbimazole treatment with regard to its use and timing with RAI dosing was analysed."( The adjunctive use of carbimazole during radioactive iodine treatment reduces the cure rate of Graves' disease.
Ankrah, AO; Docrat, F; Karusseit, VOL; Mokoena, T, 2021
)
1.24
" MET in a dose-response manner improved the LT4/CMZ-induced testicular toxicity by increasing the steroidogenic acute regulatory protein (StAR), and 17-β-hydroxysteroid dehydrogenase (17βHSD) activities, the proliferating cell nuclear antigen (PCNA), sperm count and motility, sex hormones, and gonadotropin levels."( Metformin alleviates the dysregulated testicular steroidogenesis and spermatogenesis induced by carbimazole in levothyroxine-primed rats.
Ameen, AM; Amin, MK; El Sherif, I; Elaidy, SM; Elkholy, SE; Hassan, WA; Tawfik, MM, 2022
)
0.94
" Group A and B were further subdivided depending on the reduction of dosage of thionamides."( The influence of thionamides on intra-thyroidal uptake of
Bockisch, B; Groener, D; Grünwald, F; Happel, C; Leonhäuser, B; Sabet, A, 2023
)
0.91
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
prodrugA compound that, on administration, must undergo chemical conversion by metabolic processes before becoming the pharmacologically active drug for which it is a prodrug.
antithyroid drugA drug used to treat hyperthyroidism by reducing the excessive production of thyroid hormones.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (2)

ClassDescription
carbamate esterAny ester of carbamic acid or its N-substituted derivatives.
1,3-dihydroimidazole-2-thionesA member of the class of imidazoles that is 1,3-dihydroimidazole-2-thione and its derivatives by substitution.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (12)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASEHomo sapiens (human)Potency0.89130.003245.467312,589.2998AID2517
USP1 protein, partialHomo sapiens (human)Potency39.81070.031637.5844354.8130AID504865
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency54.94100.000214.376460.0339AID720691
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency26.60320.003041.611522,387.1992AID1159552
estrogen nuclear receptor alphaHomo sapiens (human)Potency0.25650.000229.305416,493.5996AID743069
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency24.54120.001019.414170.9645AID743191
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency50.79640.000323.4451159.6830AID743065; AID743067
gemininHomo sapiens (human)Potency7.17670.004611.374133.4983AID624297
lamin isoform A-delta10Homo sapiens (human)Potency8.91250.891312.067628.1838AID1487
Cellular tumor antigen p53Homo sapiens (human)Potency10.12350.002319.595674.0614AID651631
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Bile salt export pumpHomo sapiens (human)IC50 (µMol)1,000.00000.11007.190310.0000AID1449628
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (151)

Processvia Protein(s)Taxonomy
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
detection of chemical stimulus involved in sensory perception of bitter tasteLactoperoxidaseHomo sapiens (human)
response to oxidative stressLactoperoxidaseHomo sapiens (human)
thiocyanate metabolic processLactoperoxidaseHomo sapiens (human)
defense response to bacteriumLactoperoxidaseHomo sapiens (human)
hydrogen peroxide catabolic processLactoperoxidaseHomo sapiens (human)
cellular oxidant detoxificationLactoperoxidaseHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (45)

Processvia Protein(s)Taxonomy
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
heme bindingLactoperoxidaseHomo sapiens (human)
thiocyanate peroxidase activityLactoperoxidaseHomo sapiens (human)
metal ion bindingLactoperoxidaseHomo sapiens (human)
lactoperoxidase activityLactoperoxidaseHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (33)

Processvia Protein(s)Taxonomy
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
extracellular regionLactoperoxidaseHomo sapiens (human)
extracellular spaceLactoperoxidaseHomo sapiens (human)
cytoplasmLactoperoxidaseHomo sapiens (human)
basolateral plasma membraneLactoperoxidaseHomo sapiens (human)
extracellular exosomeLactoperoxidaseHomo sapiens (human)
extracellular spaceLactoperoxidaseHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (72)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID345301Inhibition of lactoperoxidase-catalyzed iodination of L-tyrosine assessed as 3,5-diiodo-L-tyrosine formation by HPLC2008Journal of medicinal chemistry, Nov-27, Volume: 51, Issue:22
Antithyroid drug carbimazole and its analogues: synthesis and inhibition of peroxidase-catalyzed iodination of L-tyrosine.
AID678715Inhibition of human CYP2D6 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 4-methylaminoethyl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID678713Inhibition of human CYP2C9 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-methoxy-4-trifluoromethylcoumarin-3-acetic acid as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID678712Inhibition of human CYP1A2 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using ethoxyresorufin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1449628Inhibition of human BSEP expressed in baculovirus transfected fall armyworm Sf21 cell membranes vesicles assessed as reduction in ATP-dependent [3H]-taurocholate transport into vesicles incubated for 5 mins by Topcount based rapid filtration method2012Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 40, Issue:12
Mitigating the inhibition of human bile salt export pump by drugs: opportunities provided by physicochemical property modulation, in silico modeling, and structural modification.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID678714Inhibition of human CYP2C19 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 3-butyryl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID678717Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-benzyloxyquinoline as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID678716Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using diethoxyfluorescein as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID678722Covalent binding affinity to human liver microsomes assessed per mg of protein at 10 uM after 60 mins presence of NADPH2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID678718Metabolic stability in human liver microsomes assessed as high signal/noise ratio (S/N of >100) by measuring GSH adduct formation at 100 uM after 90 mins by HPLC-MS analysis2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,060)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990522 (49.25)18.7374
1990's176 (16.60)18.2507
2000's177 (16.70)29.6817
2010's145 (13.68)24.3611
2020's40 (3.77)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 99.53

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index99.53 (24.57)
Research Supply Index7.10 (2.92)
Research Growth Index4.39 (4.65)
Search Engine Demand Index183.49 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (99.53)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials67 (5.85%)5.53%
Reviews71 (6.20%)6.00%
Case Studies355 (30.98%)4.05%
Observational0 (0.00%)0.25%
Other653 (56.98%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (5)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Thyroid Function Tests in Infants of COVID-19 Positive Pregnant Mothers [NCT05385029]95 participants (Actual)Observational [Patient Registry]2020-05-01Completed
Thyroid-Associated Ophthalmopathy Subtypes and Orbital Antibodies [NCT00430547]60 participants Interventional2003-08-31Completed
The Role of Thyroid Status in Regulating Brown Adipose Tissue Activity, White Adipose Tissue Partitioning and Resting Energy Expenditure [NCT03064542]30 participants (Actual)Observational [Patient Registry]2015-10-13Completed
A Randomised Study of Two Anti-thyroid Drug Treatment Regimens in Young People [NCT01436994]Phase 381 participants (Actual)Interventional2004-07-31Completed
A Multi-center, Open Label, Randomised Parallel- Group Study to Compare the Efficacy of Cholestyramine Plus Standard Treatment Versus Prednisolone Plus Standard Treatment Versus Standard Treatment Alone in Treatment of Overt Hyperthyroidism [NCT03303053]Phase 3135 participants (Anticipated)Interventional2017-05-11Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]