Methimazole

Identification

Summary

Methimazole is a thionamide antithyroid agent that inhibits the actions of thyroid peroxidase, leading to a reduction in thyroid hormone synthesis and amelioration of hyperthyroidism.

Brand Names

Tapazole

Generic Name

Methimazole

DrugBank Accession Number

DB00763

Background

Methimazole is a thionamide antithyroid agent that inhibits the synthesis of thyroid hormones.^6,14,12 It was first introduced as an antithyroid agent in 1949² and is now commonly used in the management of hyperthyroidism, particularly in those for whom more aggressive options such as surgery or radioactive iodine therapy are inappropriate.^18,19

On a weight basis, methimazole is 10 times more potent than the other major antithyroid thionamide used in North America, propylthiouracil,¹⁹ 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.¹⁴ Traditionally, methimazole has been preferentially used over propylthiouracil due to the risk of fulminant hepatotoxicity carried by the latter,¹⁵ with propylthiouracil being preferred in pregnancy due to a perceived lower risk of teratogenic effects. Despite documented teratogenic effects in its published labels,^18,19 the true teratogenicity of methimazole appears to be unclear^11,15,16 and its place in therapy may change in the future.

Type

Small Molecule

Groups

Approved

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Methimazole (DB00763)

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Weight

Average: 114.169
Monoisotopic: 114.025168892

Chemical Formula

C₄H₆N₂S

Synonyms

• 1-Methylimidazole-2(3H)-thione
• Methimazole
• Thiamazol
• Thiamazole
• Thiamazolum
• Tiamazol

External IDs

• NSC 38608
• USAF el-30

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Pharmacology

Indication

In the United States, methimazole is indicated for the treatment of hyperthyroidism in patients with Graves' disease or toxic multinodular goiter for whom thyroidectomy or radioactive iodine therapy are not appropriate treatment options. Methimazole is also indicated for the amelioration of hyperthyroid symptoms in preparation for thyroidectomy or radioactive iodine therapy.¹⁸

In Canada, methimazole carries the above indications and is also indicated for the medical treatment of hyperthyroidism regardless of other available treatment options.¹⁹

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Management of	Graves' disease		••••••••••••		••• • ••••••••• ••• ••••••• •• ••••••••••• •••••• •••••••
Treatment of	Hyperthyroidism		••••••••••••
Symptomatic treatment of	Hyperthyroidism		••••••••••••
Treatment of	Toxic multinodular goiter		••••••••••••		••• • ••••••••• ••• ••••••• •• ••••••••••• •••••• •••••••

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Pharmacodynamics

Methimazole inhibits the synthesis of thyroid hormones resulting in an alleviation of hyperthyroidism.¹⁸¹⁹ Onset of action occurs within 12 to 18 hours, and its duration of action is 36 to 72 hours, likely due to concentration of methimazole and some metabolites within the thyroid gland after administration.¹¹

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.^18,19

Mechanism of action

Methimazole's primary mechanism of action appears to be interference in an early step in thyroid hormone synthesis involving thyroid peroxidase (TPO), however the exact method through which methimazole inhibits this step is unclear.⁶ TPO, along with hydrogen peroxide, normally catalyzes the conversion of iodide to iodine and then further catalyzes the incorporation of this iodine onto the 3 and/or 5 positions of the phenol rings of tyrosine residues in thyroglobulin. These thyroglobulin molecules then degrade within thyroid follicular cells to form either thyroxine (T₄) or tri-iodothyronine (T₃), which are the main hormones produced by the thyroid gland.¹³

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.⁶ 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.¹² Other proposed mechanisms with weaker evidence include methimazole binding directly to thyroglobulin or direct inhibition of thyroglobulin itself.⁶

Target	Actions	Organism
AThyroid peroxidase	substrate inhibitor	Humans

Absorption

Absorption of methimazole after oral administration is rapid and extensive,^3,5,1 with an absolute bioavailability of approximately 0.93¹ and a T_max ranging from 0.25 to 4.0 hours.^3,1 C_max is slightly, but not significantly, higher in hyperthyroid patients, and both C_max and AUC are significantly affected by the oral dose administered.³

Volume of distribution

The apparent volume of distribution of methimazole has been reported as roughly 20 L.⁵ 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.⁶

Protein binding

Methimazole exhibits little-to-no protein binding, existing primarily as free drug in the serum.^4,5,11

Metabolism

Methimazole is rapidly and extensively metabolized by the liver, mainly via the CYP450 and FMO enzyme systems.^7,8 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.⁵

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.^7,8

Hover over products below to view reaction partners

• Methimazole
  • Methimazole Epoxide Metabolite
    • Methimazole Dihydrodiol Metabolite
      • Methimazole N-methyl Thiourea Metabolite
        • Methimazole Sulfenic Acid Metabolite (Open)
          • Methimazole Sulfinic Acid Metabolite (Open)
      • Methimazole Glyoxal Metabolite
  • Methimazole Sulfenic Acid Metabolite (Ring)
    • Methimazole Sulfinic Acid Metabolite (Ring)
  • 3-methyl-2-thiohydantoin

Route of elimination

Urinary excretion of unchanged methimazole has been reported to be between 7% and 12%. Elimination via feces appears to be limited, with a cumulative fecal excretion of 3% after administration of methimazole.³ 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.¹¹

Half-life

Following a single intravenous bolus injection of 10mg of methimazole, the t_1/2 of the distribution phase was 0.17 hours and the t_1/2 of the elimination phase was 5.3 hours.¹ Methimazole's primary active metabolite, 3-methyl-2-thiohydantoin, has a half-life approximately 3 times longer than its parent drug.⁵ 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 t_1/2 of 7.1 hours, while severe insufficiency resulted in an elimination t_1/2 of 22.1 hours.¹

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).^1,2,3

Clearance

Following a single intravenous bolus injection of 10mg of methimazole, clearance was found to be 5.70 L/h.¹ 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.¹

There does not appear to be any significant differences in clearance based on thyroid status (i.e. no difference between euthyroid and hyperthyroid patients).^1,2,3

Adverse Effects

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Toxicity

The oral LD₅₀ of methimazole in rats is 2250 mg/kg.¹⁷ 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.^18,19 Hepatitis, nephrotic syndrome, exfoliative dermatitis, and CNS effects such as neuropathy or CNS depression/stimulation are also potential, albeit less frequent, results of overdose.^18,19

Management of overdose involves supportive treatment as dictated by the patient's status.^18,19 This may involve monitoring of the patient's vital signs, blood gases, serum electrolytes, or bone marrow function as indicated.¹⁹

Pathways

Not Available

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Interactions

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This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Drug	Interaction
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1,2-Benzodiazepine	The metabolism of 1,2-Benzodiazepine can be decreased when combined with Methimazole.
Abacavir	Methimazole may decrease the excretion rate of Abacavir which could result in a higher serum level.
Abatacept	The risk or severity of adverse effects can be increased when Methimazole is combined with Abatacept.
Abciximab	Methimazole may increase the anticoagulant activities of Abciximab.
Abemaciclib	The metabolism of Abemaciclib can be decreased when combined with Methimazole.

Food Interactions

No interactions found.

Products

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Product Images

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International/Other Brands

Danantizol (Gador S.A.) / Favistan (Temmler) / Metizol (ICN) / Strumazol (Organon) / Strumazole / Thacapzol (Recip) / Thycapzol (Sandoz) / Thyrozol (Merck) / Tirozol (Merck)

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Methimazole	Tablet	10 mg/1	Oral	United Research Laboratories, Inc.	2006-04-19	Not applicable
Methimazole	Tablet	5 mg/1	Oral	United Research Laboratories, Inc.	2006-04-19	Not applicable
Methimazole Tablets USP	Tablet	5 mg	Oral	Endo Ventures Ltd.	Not applicable	Not applicable
Methimazole Tablets USP	Tablet	20 mg	Oral	Endo Ventures Ltd.	Not applicable	Not applicable
Methimazole Tablets USP	Tablet	10 mg	Oral	Endo Ventures Ltd.	Not applicable	Not applicable

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Apo-methimazole	Tablet	5 mg	Oral	Apotex Corporation	2005-03-18	Not applicable
Dom-methimazole	Tablet	5 mg	Oral	Dominion Pharmacal	Not applicable	Not applicable
Jamp Methimazole	Tablet	10 mg	Oral	Jamp Pharma Corporation	2021-08-21	Not applicable
Jamp Methimazole	Tablet	5 mg	Oral	Jamp Pharma Corporation	2020-08-21	Not applicable
Mar-methimazole	Tablet	5 mg	Oral	Marcan Pharmaceuticals Inc	2018-10-19	Not applicable

Categories

ATC Codes

H03BB52 — Thiamazole, combinations

• H03BB — Sulfur-containing imidazole derivatives
• H03B — ANTITHYROID PREPARATIONS
• H03 — THYROID THERAPY
• H — SYSTEMIC HORMONAL PREPARATIONS, EXCL. SEX HORMONES AND INSULINS

H03BB02 — Thiamazole

• H03BB — Sulfur-containing imidazole derivatives
• H03B — ANTITHYROID PREPARATIONS
• H03 — THYROID THERAPY
• H — SYSTEMIC HORMONAL PREPARATIONS, EXCL. SEX HORMONES AND INSULINS

Drug Categories

• Antithyroid agents
• Cytochrome P-450 CYP1A2 Inhibitors
• Cytochrome P-450 CYP1A2 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2A6 Inhibitors
• Cytochrome P-450 CYP2A6 Inhibitors (weak)
• Cytochrome P-450 CYP2B6 Inhibitors
• Cytochrome P-450 CYP2B6 Inhibitors (strong)
• Cytochrome P-450 CYP2C19 Inhibitors
• Cytochrome P-450 CYP2C19 inhibitors (strength unknown)
• Cytochrome P-450 CYP2C9 Inhibitors
• Cytochrome P-450 CYP2C9 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2D6 Inhibitors
• Cytochrome P-450 CYP2D6 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2D6 Inhibitors (weak)
• Cytochrome P-450 CYP2E1 Inhibitors
• Cytochrome P-450 CYP2E1 Inhibitors (weak)
• Cytochrome P-450 CYP3A Inhibitors
• Cytochrome P-450 CYP3A4 Inhibitors
• Cytochrome P-450 CYP3A4 Inhibitors (strong)
• Cytochrome P-450 CYP3A4 Inhibitors (weak)
• Cytochrome P-450 Enzyme Inhibitors
• Drugs that are Mainly Renally Excreted
• Hormone Antagonists
• Hormones, Hormone Substitutes, and Hormone Antagonists
• Imidazoles
• Immunosuppressive Agents
• Myelosuppressive Agents
• Sulfur Compounds
• Sulfur-Containing Imidazole Derivatives
• Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins
• Thyroid Hormone Synthesis Inhibitor
• Thyroid Hormone Synthesis Inhibitors
• Thyroid Products

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as imidazolethiones. These are aromatic compounds containing an imidazole ring which bears a thioketone group.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Azolines

Sub Class

Imidazolines

Direct Parent

Imidazolethiones

Alternative Parents

N-substituted imidazoles / Heteroaromatic compounds / Thioureas / Azacyclic compounds / Organopnictogen compounds / Organonitrogen compounds / Hydrocarbon derivatives

Substituents

Aromatic heteromonocyclic compound / Azacycle / Azole / Heteroaromatic compound / Hydrocarbon derivative / Imidazole / Imidazole-2-thione / N-substituted imidazole / Organic nitrogen compound / Organonitrogen compound

Molecular Framework

Aromatic heteromonocyclic compounds

External Descriptors

imidazoles, thioureas (CHEBI:50673) / a small molecule (CPD-11282)

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

554Z48XN5E

CAS number

60-56-0

InChI Key

PMRYVIKBURPHAH-UHFFFAOYSA-N

InChI

InChI=1S/C4H6N2S/c1-6-3-2-5-4(6)7/h2-3H,1H3,(H,5,7)

IUPAC Name

1-methyl-2,3-dihydro-1H-imidazole-2-thione

SMILES

CN1C=CNC1=S

References

Synthesis Reference

李光文李剑平倪国成, "Methimazole synthesizing and purifying method." Chinese Patent CN107162983A, published September, 2017.

General References

1. Jansson R, Lindstrom B, Dahlberg PA: Pharmacokinetic properties and bioavailability of methimazole. Clin Pharmacokinet. 1985 Sep-Oct;10(5):443-50. doi: 10.2165/00003088-198510050-00006. [Article]
2. Cooper DS, Bode HH, Nath B, Saxe V, Maloof F, Ridgway EC: Methimazole pharmacology in man: studies using a newly developed radioimmunoassay for methimazole. J Clin Endocrinol Metab. 1984 Mar;58(3):473-9. doi: 10.1210/jcem-58-3-473. [Article]
3. Okamura Y, Shigemasa C, Tatsuhara T: Pharmacokinetics of methimazole in normal subjects and hyperthyroid patients. Endocrinol Jpn. 1986 Oct;33(5):605-15. doi: 10.1507/endocrj1954.33.605. [Article]
4. Okosieme OE, Lazarus JH: Current trends in antithyroid drug treatment of Graves' disease. Expert Opin Pharmacother. 2016 Oct;17(15):2005-17. doi: 10.1080/14656566.2016.1232388. Epub 2016 Sep 14. [Article]
5. Skellern GG, Knight BI, Low CK, Alexander WD, McLarty DG, Kalk WJ: The pharmacokinetics of methimazole after oral administration of carbimazole and methimazole, in hyperthyroid patients. Br J Clin Pharmacol. 1980 Feb;9(2):137-43. doi: 10.1111/j.1365-2125.1980.tb05823.x. [Article]
6. Burch HB, Cooper DS: ANNIVERSARY REVIEW: Antithyroid drug therapy: 70 years later Eur J Endocrinol. 2018 Oct 12;179(5):R261-R274. doi: 10.1530/EJE-18-0678. [Article]
7. Heidari R, Niknahad H, Jamshidzadeh A, Eghbal MA, Abdoli N: An overview on the proposed mechanisms of antithyroid drugs-induced liver injury. Adv Pharm Bull. 2015 Mar;5(1):1-11. doi: 10.5681/apb.2015.001. Epub 2015 Mar 5. [Article]
8. Mizutani T, Yoshida K, Murakami M, Shirai M, Kawazoe S: Evidence for the involvement of N-methylthiourea, a ring cleavage metabolite, in the hepatotoxicity of methimazole in glutathione-depleted mice: structure-toxicity and metabolic studies. Chem Res Toxicol. 2000 Mar;13(3):170-6. [Article]
9. Guo Z, Raeissi S, White RB, Stevens JC: Orphenadrine and methimazole inhibit multiple cytochrome P450 enzymes in human liver microsomes. Drug Metab Dispos. 1997 Mar;25(3):390-3. [Article]
10. Rendic S: Summary of information on human CYP enzymes: human P450 metabolism data. Drug Metab Rev. 2002 Feb-May;34(1-2):83-448. [Article]
11. Clark SM, Saade GR, Snodgrass WR, Hankins GD: Pharmacokinetics and pharmacotherapy of thionamides in pregnancy. Ther Drug Monit. 2006 Aug;28(4):477-83. [Article]
12. Manna D, Roy G, Mugesh G: Antithyroid drugs and their analogues: synthesis, structure, and mechanism of action. Acc Chem Res. 2013 Nov 19;46(11):2706-15. doi: 10.1021/ar4001229. Epub 2013 Jul 24. [Article]
13. Carvalho DP, Dupuy C: Thyroid hormone biosynthesis and release. Mol Cell Endocrinol. 2017 Dec 15;458:6-15. doi: 10.1016/j.mce.2017.01.038. Epub 2017 Jan 31. [Article]
14. Cooper DS: Antithyroid drugs. N Engl J Med. 2005 Mar 3;352(9):905-17. doi: 10.1056/NEJMra042972. [Article]
15. Cooper DS, Laurberg P: Hyperthyroidism in pregnancy. Lancet Diabetes Endocrinol. 2013 Nov;1(3):238-49. doi: 10.1016/S2213-8587(13)70086-X. Epub 2013 Oct 18. [Article]
16. Mallela MK, Strobl M, Poulsen RR, Wendler CC, Booth CJ, Rivkees SA: Evaluation of developmental toxicity of propylthiouracil and methimazole. Birth Defects Res B Dev Reprod Toxicol. 2014 Aug;101(4):300-7. doi: 10.1002/bdrb.21113. Epub 2014 Jun 30. [Article]
17. CaymenChem: Methimazole MSDS [Link]
18. FDA Approved Drug Products: TAPAZOLE (methimazole) oral tablet [Link]
19. DPD Approved Drugs: Methimazole [Link]

External Links

Human Metabolome Database

HMDB0014901

KEGG Drug

D00401

KEGG Compound

C07190

PubChem Compound

1349907

PubChem Substance

46506536

ChemSpider

1131173

BindingDB

50241361

RxNav

6835

ChEBI

50673

ChEMBL

CHEMBL1515

ZINC

ZINC000001187543

Therapeutic Targets Database

DNC001429

PharmGKB

PA450422

PDBe Ligand

MMZ

RxList

RxList Drug Page

Drugs.com

Drugs.com Drug Page

Wikipedia

Thiamazole

PDB Entries

2gvc / 5ff1 / 5gsn

Clinical Trials

Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">

Phase	Status	Purpose	Conditions	Count
4	Completed	Prevention	Graves´ Disease	1
4	Completed	Treatment	Graves' Disease	1
4	Completed	Treatment	Graves' Disease / Toxic Nodular Goitre	2
4	Recruiting	Treatment	Drug Relapse / Drug Withdrawal Symptoms / Graves' Disease / Treatments	1
4	Unknown Status	Diagnostic	Healthy Subjects (HS)	1

Pharmacoeconomics

Manufacturers

• Actavis totowa llc
• Caraco pharmaceutical laboratories ltd
• Cedar pharmaceuticals llc
• Mylan pharmaceuticals inc
• Sandoz inc
• King pharmaceuticals inc
• King pharmaceuticals research and development inc sub king pharmaceuticals inc

Packagers

• AAIPharma Inc.
• Actavis Group
• Amerisource Health Services Corp.
• Caraco Pharmaceutical Labs
• Cedar Pharmaceuticals LLC
• Centrix Pharmaceuticals
• Dispensing Solutions
• Eon Labs
• Heartland Repack Services LLC
• Kaiser Foundation Hospital
• King Pharmaceuticals Inc.
• Medisca Inc.
• Mikart Inc.
• Murfreesboro Pharmaceutical Nursing Supply
• Mylan
• Nucare Pharmaceuticals Inc.
• Par Pharmaceuticals
• Philopharm GmbH
• Physicians Total Care Inc.
• Remedy Repack
• Resource Optimization and Innovation LLC
• Southwood Pharmaceuticals
• United Research Laboratories Inc.
• Vangard Labs Inc.

Dosage Forms

Form	Route	Strength
Tablet	Oral	10 mg/1
Tablet	Oral	5 mg/1
Tablet	Oral	10.000 mg
Tablet	Oral	10 mg
Tablet	Oral	20 mg
Tablet, film coated	Oral	20 MG
Tablet, film coated	Oral	5 MG
Tablet, film coated	Oral	10 Mg
Tablet	Oral	5.000 mg
Tablet	Oral
Tablet, film coated	Oral
Tablet	Oral	5 mg

Prices

Unit description	Cost	Unit
Methimazole powder	9.49USD	g
Methimazole 20 mg tablet	1.9USD	tablet
Tapazole 10 mg tablet	1.45USD	tablet
Northyx 20 mg tablet	0.94USD	tablet
Northyx 15 mg tablet	0.82USD	tablet
Methimazole 10 mg tablet	0.78USD	tablet
Tapazole 5 mg tablet	0.66USD	tablet
Northyx 10 mg tablet	0.47USD	tablet
Methimazole 5 mg tablet	0.45USD	tablet
Northyx 5 mg tablet	0.29USD	tablet

DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.

Patents

Not Available

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	143-146 °C	DPD Label (Canada)
water solubility	Freely soluble	DPD Label (Canada)

Predicted Properties

Property	Value	Source
Water Solubility	11.3 mg/mL	ALOGPS
logP	-0.38	ALOGPS
logP	0.75	Chemaxon
logS	-1	ALOGPS
pKa (Strongest Acidic)	10.41	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	0	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	15.27 Å2	Chemaxon
Rotatable Bond Count	0	Chemaxon
Refractivity	33.23 m3·mol-1	Chemaxon
Polarizability	11.64 Å3	Chemaxon
Number of Rings	1	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	Yes	Chemaxon
MDDR-like Rule	No	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.9156
Blood Brain Barrier	+	0.9731
Caco-2 permeable	+	0.6156
P-glycoprotein substrate	Non-substrate	0.8213
P-glycoprotein inhibitor I	Non-inhibitor	0.7552
P-glycoprotein inhibitor II	Non-inhibitor	0.944
Renal organic cation transporter	Non-inhibitor	0.7662
CYP450 2C9 substrate	Non-substrate	0.7919
CYP450 2D6 substrate	Non-substrate	0.8985
CYP450 3A4 substrate	Non-substrate	0.7849
CYP450 1A2 substrate	Non-inhibitor	0.9045
CYP450 2C9 inhibitor	Non-inhibitor	0.9071
CYP450 2D6 inhibitor	Non-inhibitor	0.9232
CYP450 2C19 inhibitor	Non-inhibitor	0.9025
CYP450 3A4 inhibitor	Non-inhibitor	0.8309
CYP450 inhibitory promiscuity	High CYP Inhibitory Promiscuity	0.7105
Ames test	Non AMES toxic	0.8582
Carcinogenicity	Non-carcinogens	0.9348
Biodegradation	Not ready biodegradable	0.9815
Rat acute toxicity	1.8215 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.9401
hERG inhibition (predictor II)	Non-inhibitor	0.8416

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Download (8.12 KB)

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted GC-MS Spectrum - GC-MS	Predicted GC-MS	splash10-03di-9400000000-2a587b1850e13e97c2cf
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-066r-8900000000-9230df83b87c13377bfb
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-014i-0900000000-275f9771b8d1d7486052
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-014i-0900000000-1763fdc1a812fa765250
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-014i-0900000000-78877e6d65fda61a0e67
LC-MS/MS Spectrum - LC-ESI-QQ , positive	LC-MS/MS	splash10-014i-1900000000-c979e7cdbceb656b6a1e
LC-MS/MS Spectrum - LC-ESI-QQ , positive	LC-MS/MS	splash10-014i-1900000000-1447e5774eda5dc3fe26
LC-MS/MS Spectrum - LC-ESI-QQ , positive	LC-MS/MS	splash10-066r-9300000000-41d253a513ee17fed774
LC-MS/MS Spectrum - LC-ESI-QQ , positive	LC-MS/MS	splash10-0a4i-9000000000-11684a341cebaa28c427
LC-MS/MS Spectrum - LC-ESI-QQ , positive	LC-MS/MS	splash10-0a60-9000000000-7637560408e70990bc27
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-014i-0900000000-070cffaa5a2a45ea0bae
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0bt9-9300000000-a15d2e5e95d919cfd539
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-060u-9100000000-5f4baf04056cb29a437d
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4i-9100000000-f2693cd2cbbbb999def8
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4i-9000000000-dc413cda6cb435459863
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0zfr-9000000000-26bfb8bb49ab9efffa1c
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å2)	Source type	Source
[M-H]-	113.947035	predicted	DarkChem Lite v0.1.0
[M-H]-	113.940135	predicted	DarkChem Lite v0.1.0
[M-H]-	113.852935	predicted	DarkChem Lite v0.1.0
[M-H]-	121.80206	predicted	DeepCCS 1.0 (2019)
[M+H]+	115.061335	predicted	DarkChem Lite v0.1.0
[M+H]+	115.034235	predicted	DarkChem Lite v0.1.0
[M+H]+	114.982635	predicted	DarkChem Lite v0.1.0
[M+H]+	123.73746	predicted	DeepCCS 1.0 (2019)
[M+Na]+	114.355235	predicted	DarkChem Lite v0.1.0
[M+Na]+	114.340035	predicted	DarkChem Lite v0.1.0
[M+Na]+	114.253835	predicted	DarkChem Lite v0.1.0
[M+Na]+	131.78075	predicted	DeepCCS 1.0 (2019)

Targets

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Details1. Thyroid peroxidase

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Substrate

Inhibitor

General Function

Peroxidase activity

Specific Function

Iodination and coupling of the hormonogenic tyrosines in thyroglobulin to yield the thyroid hormones T(3) and T(4).

Gene Name

TPO

Uniprot ID

P07202

Uniprot Name

Thyroid peroxidase

Molecular Weight

102961.63 Da

References

1. Sugawara M, Sugawara Y, Wen K: Methimazole and propylthiouracil increase cellular thyroid peroxidase activity and thyroid peroxidase mRNA in cultured porcine thyroid follicles. Thyroid. 1999 May;9(5):513-8. [Article]
2. Manzon RG, Holmes JA, Youson JH: Variable effects of goitrogens in inducing precocious metamorphosis in sea lampreys (Petromyzon marinus). J Exp Zool. 2001 Apr 15;289(5):290-303. [Article]
3. Ferreira AC, de Carvalho Cardoso L, Rosenthal D, de Carvalho DP: Thyroid Ca2+/NADPH-dependent H2O2 generation is partially inhibited by propylthiouracil and methimazole. Eur J Biochem. 2003 Jun;270(11):2363-8. [Article]
4. Magnusson RP, Yu B, Brennan V: Effect of serum thyrotropin levels on the concentration of messenger RNA for thyroid peroxidase in the rat. Acta Endocrinol (Copenh). 1992 May;126(5):460-6. [Article]
5. Chiovato L, Pinchera A: The microsomal/peroxidase antigen: modulation of its expression in thyroid cells. Autoimmunity. 1991;10(4):319-31. [Article]
6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
7. Burch HB, Cooper DS: ANNIVERSARY REVIEW: Antithyroid drug therapy: 70 years later Eur J Endocrinol. 2018 Oct 12;179(5):R261-R274. doi: 10.1530/EJE-18-0678. [Article]

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Drug created at June 13, 2005 13:24 / Updated at February 20, 2024 23:55