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a drug (trade name Tagamet) used to treat peptic ulcers by decreasing the secretion of stomach acid (同)Tagamet

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/08/31 02:40:22」(JST)

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Cimetidine, sold under the brand name Tagamet among others, is a histamine H₂ receptor antagonist that inhibits stomach acid production.^[1]^[3]^[4] It is available over-the-counter and is mainly used in the treatment of heartburn and peptic ulcers.^[1]^[4]^[5]

The development of longer-acting H₂ receptor antagonists with fewer drug interactions and adverse effects, such as ranitidine and famotidine, decreased the use of cimetidine, and though it is still used, cimetidine is no longer among the more widely used of the H₂-receptor antagonists.^{[citation needed]}

Cimetidine was discovered in 1971 and came into commercial use in 1977.^[6]^[7] Cimetidine was approved in the United Kingdom in 1976, and was approved in the United States by the Food and Drug Administration for prescriptions in 1979.^{[citation needed]}

1 Medical uses
- 1.1 Other uses
2 Side effects
- 2.1 Overdose
3 Interactions
4 Pharmacology
- 4.1 Pharmacodynamics
  - 4.1.1 Histamine H2 receptor antagonism
  - 4.1.2 Antiandrogenic and estrogenic effects
- 4.2 Pharmacokinetics
  - 4.2.1 Metabolism
  - 4.2.2 Enzyme inhibition
5 History
6 References
7 External links

Medical uses

Other uses

Some evidence suggests cimetidine could be effective in the treatment of common warts, but more rigorous double-blind clinical trials found it to be no more effective than a placebo.^[8]^[9]^[10]

Another study used cimetidine for the treatment of chronic calcific tendinitis of the shoulder.^[11] The small-scale study took 16 individuals with calcific tendinitis in one shoulder, all of which had previously attempted other forms of therapy, including steroid injection and arthroscopic lavage. During the course of the study, 10 patients reported an elimination of pain and nine displayed a complete disappearance of calcium deposits. With results being on a small scale, cimetidine, for the treatment of chronic calcific tendinitis of the shoulder, has been recommended to be opened to large-scale clinical trials.^[12]

Tentative evidence supports a beneficial role as add-on therapy in colorectal cancer.^[13]

Side effects

Reported side effects of cimetidine include diarrhea, rashes, dizziness, fatigue, constipation, and muscle pain, all of which are usually mild and transient.^[14] It has been reported that mental confusion may occur in the elderly.^[14] Because of its hormonal effects, cimetidine rarely may cause sexual dysfunction including loss of libido and erectile dysfunction and gynecomastia (0.1–0.2%) in males during long-term treatment.^[14]^[15]^[16] Rarely, interstitial nephritis, urticaria, and angioedema have been reported with cimetidine treatment.^[14] Cimetidine is also commonly associated with transient raised aminotransferase activity; hepatotoxicity is rare.^[17]

Overdose

Cimetidine appears to be very safe in overdose, producing no symptoms even with massive overdoses (e.g., 20 g).^[18]

Interactions

Cimetidine affects the metabolism of methadone, sometimes resulting in higher blood levels and a higher incidence of side effects, and may interact with the antimalarial medication hydroxychloroquine.^[19]
Cimetidine can also interact with a number of psychoactive medications, including tricyclic antidepressants and selective serotonin reuptake inhibitors, causing increased blood levels of these drugs and the potential of subsequent toxicity.^{[citation needed]}
Following administration of cimetidine, the half-life and area-under-curve of zolmitriptan and its active metabolites were roughly doubled.^[20]
Cimetidine is a potent inhibitor of tubular creatinine secretion. Creatinine is a metabolic byproduct of creatine breakdown. Accumulation of creatinine is associated with uremia, but the symptoms of creatinine accumulation are unknown, as they are hard to separate from other nitrogenous waste buildups.^[21]
Like several other medications, the most obvious being erythromycin, cimetidine interferes with the body's metabolization of sildenafil, causing its strength and duration to increase (therefore also its side effects to be more likely and prominent).^{[citation needed]}
Clinically significant drug interactions with the CYP1A2 substrate theophylline, the CYP2C9 substrate tolbutamide, the CYP2D6 substrate desipramine, and the CYP3A4 substrate triazolam have all been demonstrated with cimetidine, and interactions with other substrates of these enzymes are likely as well.^[22]
Cimetidine has been shown clinically to reduce the clearance of mirtazapine, imipramine, timolol, nebivolol, sparteine, loratadine, nortriptyline, gabapentin, and desipramine in humans.^[23]
Cimetidine inhibits the renal excretion of metformin and procainamide, resulting in increased circulating levels of these drugs.^[14]
Interactions of potential clinical importance with cimetidine include warfarin, theophylline, phenytoin, carbamazepine, pethidine and other opioid analgesics, tricyclic antidepressants, lidocaine, terfenadine, amiodarone, flecainide, quinidine, fluorouracil, and benzodiazepines.^[14]^[24]
Cimetidine may decrease the effects of CYP2D6 substrates that are prodrugs, such as codeine, tramadol, and tamoxifen.^[25]
Cimetidine reduces the absorption of ketoconazole and itraconazole (which require a low pH).^[14]
Cimetidine has a theoretical but unproven benefit in paracetamol toxicity.^[17] This is because N-acetyl-p-benzoquinone imine (NAPQI), a metabolite of paracetamol (acetaminophen) that is responsible for its hepatotoxicity, is formed from it by the cytochrome P450 system (specifically, CYP1A2, CYP2E1, and CYP3A4).^[26]
Numerous other drug interactions.

Pharmacology

Pharmacodynamics

Histamine H2 receptor antagonism

Cimetidine's mechanism of action as an antacid is as a histamine H₂ receptor antagonist.^[27]

Antiandrogenic and estrogenic effects

Cimetidine has been found to possess clinically significant albeit weak antiandrogen activity at high doses.^[27]^[28]^[29]^[30] It has been found to directly and competitively displace testosterone and dihydrotestosterone (DHT) and antagonize the androgen receptor (AR) in animals.^[31]^[32] In addition, cimetidine has been found to inhibit 2-hydroxylation of estradiol (via inhibition of CYP450 enzymes, which are involved in the metabolic inactivation of estradiol), resulting in increased levels of estrogen.^[33]^[34]^[35]^[36]^[37]^[38] By increasing estrogen levels, cimetidine can also decrease testosterone and increase prolactin levels.^[39]

Pharmacokinetics

Metabolism

Cimetidine is S-oxygenated by human flavin-containing monooxygenases, specifically FMO1 and FMO3.^[40]

Enzyme inhibition

Cimetidine is a potent inhibitor of certain cytochrome P450 (CYP450) enzymes,^[18]^[41] including CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4.^[18]^[41]^[42] The drug appears to primarily inhibit CYP1A2, CYP2D6, and CYP3A4,^[43] of which it is described as a moderate inhibitor.^[2] This is notable since these three CYP450 isoenzymes are involved in CYP450-mediated drug biotransformations;^[44] however, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 are also involved in the oxidative metabolism of many commonly used drugs.^[45] As a result, cimetidine has the potential for a large number of pharmacokinetic interactions.^[18]^[41]^[42]

Cimetidine is reported to be a competitive and reversible inhibitor of several CYP450 enzymes,^[17]^[24]^[41]^[46] although mechanism-based (suicide) irreversible inhibition has also been identified for cimetidine's inhibition of CYP2D6.^[23] It reversibly inhibits CYP450 enzymes by binding directly with the complexed heme-iron of the active site via one of its imidazole ring nitrogen atoms, thereby blocking the oxidation of other drugs.^[41]^[46]^[47]

History

Cimetidine, approved by the FDA for inhibition of gastric acid secretion, has been advocated for a number of dermatological diseases.^[48] Cimetidine was the prototypical histamine H₂ receptor antagonist from which the later members of the class were developed. Cimetidine was the culmination of a project at Smith, Kline and French (SK&F) Laboratories in Welwyn Garden City (now part of GlaxoSmithKline) by James W. Black, C. Robin Ganellin, and others to develop a histamine receptor antagonist to suppress stomach acid secretion.^[49] This was one of the first drugs discovered using a rational drug design approach. Sir James W. Black shared the 1988 Nobel Prize in Physiology or Medicine for the discovery of propranolol and also is credited for the discovery of cimetidine.

At the time (1964), histamine was known to stimulate the secretion of stomach acid, but also that traditional antihistamines had no effect on acid production. In the process, the SK&F scientists also proved the existence of histamine H₂ receptors.

The SK&F team used a rational drug-design structure starting from the structure of histamine — the only design lead, since nothing was known of the then hypothetical H₂ receptor. Hundreds of modified compounds were synthesized in an effort to develop a model of the receptor. The first breakthrough was N^α-guanylhistamine, a partial H₂ receptor antagonist. From this lead, the receptor model was further refined and eventually led to the development of burimamide, the first H₂ receptor antagonist. Burimamide, a specific competitive antagonist at the H₂ receptor, 100 times more potent than N^α-guanylhistamine, proved the existence of the H₂ receptor.

Burimamide was still insufficiently potent for oral administration, and further modification of the structure, based on modifying the pKa of the compound, led to the development of metiamide. Metiamide was an effective agent; it was associated, however, with unacceptable nephrotoxicity and agranulocytosis.^[49] The toxicity was proposed to arise from the thiourea group, and similar guanidine analogues were investigated until the ultimate discovery of cimetidine. The compound was synthesized in 1972 and evaluated for toxicology by 1973. It passed all trials.

Cimetidine was first marketed in the United Kingdom in 1976, and in the U.S. in August 1977; therefore, it took 12 years from initiation of the H₂ receptor antagonist program to commercialization. By 1979, Tagamet was being sold in more than 100 countries and became the top-selling prescription product in the U.S., Canada, and several other countries. In November 1997, the American Chemical Society and the Royal Society of Chemistry in the U.K. jointly recognized the work as a milestone in drug discovery by designating it an International Historic Chemical Landmark during a ceremony at SmithKline Beecham's New Frontiers Science Park research facilities in Harlow, England.^[50]

The commercial name "Tagamet" was decided upon by fusing the two words "antagonist" and "cimetidine".^[49] Subsequent to the introduction onto the U.S. drug market, two other H₂ receptor antagonists were approved, ranitidine (Zantac, Glaxo Labs) and famotidine (Pepcid, Yamanouchi, Ltd.) Cimetidine became the first drug ever to reach more than $1 billion a year in sales, thus making it the first blockbuster drug.^[51]

In a deal expected to take effect in 2012, GlaxoSmithKline sold Tagamet and 16 other brands to Prestige Brands.^[52]

Tagamet has now been largely replaced by the proton pump inhibitors for treating peptic ulcers, but is now available as an over-the-counter medicine for heartburn in many countries.^[50]

References

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^ Index Nominum 2000: International Drug Directory. Taylor & Francis. January 2000. pp. 234–. ISBN 978-3-88763-075-1.
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^ Burchum J, Rosenthal L (2 December 2014). Lehne's Pharmacology for Nursing Care. Elsevier Health Sciences. pp. 952–. ISBN 978-0-323-34026-7.
^ Fischer J, Ganellin CR (24 August 2010). Analogue-based Drug Discovery II. John Wiley & Sons. p. 4. ISBN 978-3-527-63212-1.
^ Fischer, Janos; Ganellin, C. Robin (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 444. ISBN 9783527607495.
^ Fit KE, Williams PC (July 2007). "Use of histamine2-antagonists for the treatment of verruca vulgaris". The Annals of Pharmacotherapy. 41 (7): 1222–6. PMID 17535844. doi:10.1345/aph.1H616.
^ Glass AT, Solomon BA (June 1996). "Cimetidine therapy for recalcitrant warts in adults". Archives of Dermatology. 132 (6): 680–2. PMID 8651718. doi:10.1001/archderm.1996.03890300108014.
^ Karabulut AA, Sahin S, Ekşioglu M (April 1997). "Is cimetidine effective for nongenital warts: a double-blind, placebo-controlled study". Archives of Dermatology. 133 (4): 533–4. PMID 9126017. doi:10.1001/archderm.133.4.533.
^ Yokoyama M, Aono H, Takeda A, Morita K (2003). "Cimetidine for chronic calcifying tendinitis of the shoulder". Regional Anesthesia and Pain Medicine. 28 (3): 248–52. PMID 12772145. doi:10.1053/rapm.2003.50048.
^ "Musculoskeletal Pain". Archived from the original on 2 October 2008. Retrieved 2008-10-22.
^ Deva S, Jameson M (15 August 2012). "Histamine type 2 receptor antagonists as adjuvant treatment for resected colorectal cancer". The Cochrane Database of Systematic Reviews. 8 (8): CD007814. PMID 22895966. doi:10.1002/14651858.CD007814.pub2.
^ ^a ^b ^c ^d ^e ^f ^g Ritter J, Lewis L, Mant T, Ferro A (25 April 2008). A Textbook of Clinical Pharmacology and Therapeutics (5 ed.). CRC Press. pp. 250–. ISBN 978-1-4441-1300-6.
^ Sawyer D, Conner CS, Scalley R (February 1981). "Cimetidine: adverse reactions and acute toxicity". American Journal of Hospital Pharmacy. 38 (2): 188–97. PMID 7011006.
^ Sabesin SM (1993). "Safety issues relating to long-term treatment with histamine H2-receptor antagonists". Alimentary Pharmacology & Therapeutics. 7 Suppl 2: 35–40. PMID 8103374. doi:10.1111/j.1365-2036.1993.tb00597.x.
^ ^a ^b ^c Kelly D (26 January 2009). Diseases of the Liver and Biliary System in Children. John Wiley & Sons. pp. 224–. ISBN 978-1-4443-0054-3.
^ ^a ^b ^c ^d Dart RC (2004). Medical Toxicology. Lippincott Williams & Wilkins. pp. 402–. ISBN 978-0-7817-2845-4.
^ Furst DE (June 1996). "Pharmacokinetics of hydroxychloroquine and chloroquine during treatment of rheumatic diseases". Lupus. 5 Suppl 1: S11–5. PMID 8803904. doi:10.1177/096120339600500104.
^ See complete drug interactions for Zomig (zolmitriptan succinate used for migraine relief) in package insert: "Highlights of Zomig Prescribing Information" (PDF). AstraZeneca.
^ Urakami Y, Kimura N, Okuda M, Masuda S, Katsura T, Inui K (June 2005). "Transcellular transport of creatinine in renal tubular epithelial cell line LLC-PK1". Drug Metabolism and Pharmacokinetics. 20 (3): 200–5. PMID 15988122. doi:10.2133/dmpk.20.200.
^ Rodrigues AD (8 February 2008). Drug-Drug Interactions, Second Edition. CRC Press. pp. 277, 294. ISBN 978-0-8493-7594-1.
^ ^a ^b Shufeng Zhou (6 April 2016). Cytochrome P450 2D6: Structure, Function, Regulation and Polymorphism. CRC Press. pp. 299–. ISBN 978-1-4665-9788-4.
^ ^a ^b Rosenfeld GC, Loose DS (2007). Pharmacology. Lippincott Williams & Wilkins. pp. 202–. ISBN 978-0-7817-8074-2.
^ Fuller MA, Sajatovic M (2005). Drug Information Handbook for Psychiatry. Lexi-Comp. p. 285.
^ Cameron R, Feuer G, de la Iglesias F (6 December 2012). Drug-Induced Hepatotoxicity. Springer Science & Business Media. pp. 140–. ISBN 978-3-642-61013-4.
^ ^a ^b Richards DA (1983). "Comparative pharmacodynamics and pharmacokinetics of cimetidine and ranitidine". Journal of Clinical Gastroenterology. 5 Suppl 1: 81–90. PMID 6317740. doi:10.1097/00004836-198312001-00008.
^ Becker KL (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 1196–. ISBN 978-0-7817-1750-2.
^ Jensen RT, Collen MJ, McArthur KE, Howard JM, Maton PN, Cherner JA, Gardner JD (November 1984). "Comparison of the effectiveness of ranitidine and cimetidine in inhibiting acid secretion in patients with gastric hypersecretory states". The American Journal of Medicine. 77 (5B): 90–105. PMID 6150641.
^ Biagi P, Milani G (March 1985). "[Dysfunction of the hypothalamo-hypophyseal-gonadal axis induced by histamine H2 antagonists. Review of the literature and personal observations]". Minerva Medica (in Italian). 76 (12): 579–86. PMID 3921876.
^ Winters SJ, Banks JL, Loriaux DL (March 1979). "Cimetidine is an antiandrogen in the rat". Gastroenterology. 76 (3): 504–8. PMID 428705.
^ Sivelle PC, Underwood AH, Jelly JA (March 1982). "The effects of histamine H2 receptor antagonists on androgen action in vivo and dihydrotestosterone binding to the rat prostate androgen receptor in vitro". Biochemical Pharmacology. 31 (5): 677–84. PMID 6123322. doi:10.1016/0006-2952(82)90449-X.
^ Galbraith RA, Michnovicz JJ (August 1989). "The effects of cimetidine on the oxidative metabolism of estradiol". The New England Journal of Medicine. 321 (5): 269–74. PMID 2747769. doi:10.1056/NEJM198908033210501.
^ Michnovicz JJ, Galbraith RA (February 1991). "Cimetidine inhibits catechol estrogen metabolism in women". Metabolism. 40 (2): 170–4. PMID 1988774. doi:10.1016/0026-0495(91)90169-W.
^ Pescovitz OH, Walvoord EC (6 June 2007). When Puberty is Precocious: Scientific and Clinical Aspects. Springer Science & Business Media. pp. 203–. ISBN 978-1-59745-499-5.
^ Cuhaci N, Polat SB, Evranos B, Ersoy R, Cakir B (March 2014). "Gynecomastia: Clinical evaluation and management". Indian Journal of Endocrinology and Metabolism. 18 (2): 150–8. PMC 3987263 . PMID 24741509. doi:10.4103/2230-8210.129104.
^ Rendic S, Di Carlo FJ (2010). "Human cytochrome P450 enzymes: a status report summarizing their reactions, substrates, inducers, and inhibitors". Drug Metabolism Reviews. 29 (1-2): 413–580. PMID 9187528. doi:10.3109/03602539709037591.
^ Galbraith RA, Michnovicz JJ (August 1989). "The effects of cimetidine on the oxidative metabolism of estradiol". The New England Journal of Medicine. 321 (5): 269–74. PMID 2747769. doi:10.1056/NEJM198908033210501.
^ Deepinder F, Braunstein GD (September 2012). "Drug-induced gynecomastia: an evidence-based review". Expert Opinion on Drug Safety. 11 (5): 779–95. PMID 22862307. doi:10.1517/14740338.2012.712109.
^ Cashman JR (September 2000). "Human flavin-containing monooxygenase: substrate specificity and role in drug metabolism". Curr. Drug Metab. 1 (2): 181–191. PMID 11465082. doi:10.2174/1389200003339135. Human FMO3 N-oxygenates primary, secondary and tertiary amines whereas human FMO1 is only highly efficient at N-oxygenating tertiary amines. Both human FMO1 and FMO3 S-oxygenate a number of nucleophilic sulfur-containing substrates and in some cases, does so with great stereoselectivity. ... For amines with smaller aromatic substituents such as phenethylamines, often these compounds are efficiently N-oxygenated by human FMO3. ... (S)-Nicotine N-1'-oxide formation can also be used as a highly stereoselective probe of human FMO3 function for adult humans that smoke cigarettes. Finally, cimetidine S-oxygenation or ranitidine N-oxidation can also be used as a functional probe of human FMO3. With the recent observation of human FMO3 genetic polymorphism and poor metabolism phenotype in certain human populations, variant human FMO3 may contribute to adverse drug reactions or exaggerated clinical response to certain medications.
^ ^a ^b ^c ^d ^e Lemke TL, Williams DA (2008). Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. pp. 273–. ISBN 978-0-7817-6879-5.
^ ^a ^b Karalliedde LD, Clarke SF, Collignon U, Karalliedde J (29 January 2010). Adverse Drug Interactions: A Handbook for Prescribers. CRC Press. pp. 633–. ISBN 978-0-340-92769-4.
^ Priskorn M, Larsen F, Segonzac A, Moulin M (1997). "Pharmacokinetic interaction study of citalopram and cimetidine in healthy subjects". European Journal of Clinical Pharmacology. 52 (3): 241–2. PMID 9218934. doi:10.1007/s002280050282.
^ Martínez C, Albet C, Agúndez JA, Herrero E, Carrillo JA, Márquez M, Benítez J, Ortiz JA (April 1999). "Comparative in vitro and in vivo inhibition of cytochrome P450 CYP1A2, CYP2D6, and CYP3A by H2-receptor antagonists". Clinical Pharmacology and Therapeutics. 65 (4): 369–76. PMID 10223772. doi:10.1016/S0009-9236(99)70129-3.
^ Delafuente JC (November 2003). "Understanding and preventing drug interactions in elderly patients". Critical Reviews in Oncology/Hematology. 48 (2): 133–43. PMID 14607376. doi:10.1016/j.critrevonc.2003.04.004.
^ ^a ^b Cairns D (2012). Essentials of Pharmaceutical Chemistry. Pharmaceutical Press. pp. 110–. ISBN 978-0-85369-979-8. Drugs interacting in this way with CYP450 include the histamine H2-receptor antagonist cimetidine, [...] Reversible inhibitors, such as cimetidine, which interact with the complexed iron at the active site of the enzyme to inhibit oxidation of other drugs. The inhibition occurs before any oxidation of the inhibitor occurs and is reversible once the inhibitor is removed.
^ Liska DJ (June 1998). "The detoxification enzyme systems". Alternative Medicine Review. 3 (3): 187–98. PMID 9630736. Cimetidine is an example of a compound that can bind directly to the heme iron of the cytochrome P450 reactive site to inhibit all cytochrome-dependent Phase I enzyme activities.13
^ Scheinfeld N (March 2003). "Cimetidine: a review of the recent developments and reports in cutaneous medicine". Dermatology Online Journal. 9 (2): 4. PMID 12639457.
^ ^a ^b ^c "Tagamet^®: Discovery of Histamine H₂-receptor Antagonists". National Historic Chemical Landmarks. American Chemical Society. Archived from the original on December 9, 2012. Retrieved June 25, 2012.
^ ^a ^b Fremantle M. "Tagamet". Chemical and Engineering news. Retrieved 1 July 2013.
^ Whitney J (February 2006). "Pharmaceutical Sales 101: Me-Too Drugs". Guernica. Archived from the original on 2008-08-07. Retrieved 2008-07-31.
^ Ranii D (21 December 2011). "GSK sells BC, Goody's and other brands". News & Observer. Archived from the original on 2012-04-15.

External links

Tagamet^®: Discovery of Histamine H₂-receptor Antagonists from American Chemical Society National Historic Chemical Landmarks

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Related Pictures

★リンクテーブル★

リンク元	「シメチジン」「H2受容体拮抗薬」「Tagamet」

「シメチジン」

Cimetidine
Clinical data
Pronunciation	/sɪˈmɛtɪdiːn/ or /saɪˈmɛtɪdiːn/
Trade names	Tagamet
Synonyms	cimetidine hydrochloride; SKF-92334
AHFS/Drugs.com	Monograph
MedlinePlus	a682256
License data	US FDA: Cimetidine;
Pregnancy; category	AU: B1; US: B (No risk in non-human studies); ;
Routes of; administration	Oral, parenteral
ATC code	A02BA01 (WHO);
Legal status
Legal status	AU: S4 (Prescription only); UK: POM (Prescription only); US: ℞-only (although 200 mg is OTC);
Pharmacokinetic data
Bioavailability	60–70%
Protein binding	15–20%
Metabolism	Hepatic
Onset of action	30 minutes
Biological half-life	2 hours
Duration of action	4–5 hours
Excretion	Renal
Identifiers
	IUPAC name 1-cyano-2-methyl-3-[2-[(5-methyl-1H-imidazol-4-yl)methylsulfanyl]ethyl]guanidine;
CAS Number	51481-61-9 ;
PubChem CID	2756;
IUPHAR/BPS	1231;
DrugBank	DB00501 ;
ChemSpider	2654 ;
UNII	80061L1WGD;
KEGG	D00295 ;
ChEBI	CHEBI:3699 ;
ChEMBL	CHEMBL30 ;
ECHA InfoCard	100.052.012
Chemical and physical data
Formula	C10H16N6S
Molar mass	252.34 g/mol
3D model (JSmol)	Interactive image;
	SMILES N#CN=C(NC)NCCSCc1nc[nH]c1CN#CN\C(=N/C)NCCSCc1nc[nH]c1C ;
	InChI InChI=1S/C10H16N6S/c1-8-9(16-7-15-8)5-17-4-3-13-10(12-2)14-6-11/h7H,3-5H2,1-2H3,(H,15,16)(H2,12,13,14) ; Key:AQIXAKUUQRKLND-UHFFFAOYSA-N ;
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　　[★]

英: cimetidine
商: アルキオーネ、イクロール、エスメラルダ、カイロック、シメチパール、シメチラン、シルカーゼット、ストマチジン、タカミジン、タガメット Tagamet、ダンスール、チーカプト、チスタメット、ファルジン
関: ヒスタミン受容体

消化性潰瘍治療薬

攻撃因子抑制剤

H₂ブロッカー = ヒスタミンH₂受容体選択的阻害薬

薬効薬理

シメチジン錠200mg「タナベ」／**シメチジン錠400mg「タナベ」／**シメチジン細粒20％「タナベ」

シメチジンは胃酸分泌抑制作用を示す．その作用機序は，胃粘膜細胞のヒスタミンのＨ2受容体に対する競合的拮抗作用による．ガストリン刺激，インスリン刺激及び食事刺激による胃酸分泌も抑制する．また，ペプシン分泌抑制作用も示す3）．

効能又は効果

シメチジン錠200mg「タナベ」／**シメチジン錠400mg「タナベ」／**シメチジン細粒20％「タナベ」

胃潰瘍，十二指腸潰瘍，吻合部潰瘍，Zollinger-Ellison症候群，逆流性食道炎，上部消化管出血（消化性潰瘍，急性ストレス潰瘍，出血性胃炎による）
下記疾患の胃粘膜病変（びらん，出血，発赤，浮腫）の改善

急性胃炎，慢性胃炎の急性増悪期

禁忌

シメチジン錠200mg「タナベ」／**シメチジン錠400mg「タナベ」／**シメチジン細粒20％「タナベ」

シメチジンに対し過敏症の既往歴のある患者

副作用

CYP2D6, CYP3A4阻害作用。これらはシメチジンとの相互作用が強い。多くの薬物代謝が影響を受ける。すなわち、副作用につながる
肝障害
抗アンドロゲン作用(女性化乳房、乳汁分泌)

相互作用

シメチジン（消化性潰瘍治療薬）→ビタミンB12の吸収低下？(根拠となる文献不明)
http://www2s.biglobe.ne.jp/~coop-dr/sougosayou.htm

添付文書

シメチジン錠200mg「タナベ」／**シメチジン錠400mg「タナベ」／**シメチジン細粒20％「タナベ」

http://www.info.pmda.go.jp/go/pack/2325001C1126_1_01/2325001C1126_1_01?view=body

「H2受容体拮抗薬」

　　[★]

英: H2 blocker H2-blockers
同: H2受容体ブロッカー H2 receptor blocker、H2受容体拮抗薬 H2 receptor antagonist H2RA、ヒスタミンH2受容体遮断薬ヒスタミンH2受容体拮抗薬 histamine H2-receptor antagonists histamine H2 receptor antagonist histamine H2 antagonist、H2拮抗薬 H2 antagonist H2-antagonist、H2遮断薬、H2ブロッカー
関: 抗ヒスタミン薬

[show details]

H2受容体拮抗薬 : 約 249,000 件
H2受容体遮断薬 : 約 24,400 件

GOO.chapter36 p.971

消化性潰瘍治療薬
命名法は" -tidine"
特徴

十二指腸潰瘍の治癒率を向上する (⇔プロトンポンプ阻害薬)

H2受容体拮抗薬

シメチジン cimetidine
ラニチジン ranitidine
ファモチジン famotidine　ガスター
ニザチジン nizatidine
ロキサチジン roxitidine
ラフチジン lafutidine　プロテカジン防御因子増強作用を有する。肝代謝なので腎機能障害があっても使用可能

構造

イミダゾール環をもち、ヒスタミンに似る

作用機序

H1受容体にはほとんど作用しない
H2受容体に可逆的、競合的に結合してヒスタミンを阻害する。
胃粘膜の局所の肥満細胞、ECL細胞

histamine→H2R→Csα→AC→cAMP↑→PKA→H+,K+-ATPase
histamine→H2R→[Ca2+]i↑→H+,K+-ATPase　　　←補助的pathway

H2RとMRとGRは相互作用しており、胃酸を分泌する。

注意

副作用5%↓
薬剤耐性
リバウンド

中止すると再発率が高い。そのため半年かけて漸減させゆっくり離脱

胃粘膜が減弱している

薬物相互作用

副作用

副作用5%↓
汎血球減少症、無顆粒球症
肝障害、抗アンドロゲン作用(女性化乳房、乳汁分泌)
中止すると再発率が高い。そのため半年かけて漸減させゆっくり離脱

胃粘膜が減弱しているから

相互作用

シメチジン：CYP2D6, CYP3A4阻害作用。 CYPs(CYP1A2,CYP2C9,CYP2D6)の阻害 (GOO.972)
ラニチジン：CYPs。しかし、シメチジンの10%程度
ファモチジン、ニザチジン：なし

「Tagamet」

　　[★]

タガメット

関: cimetidine

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[FischerGanellin2010-6] Fischer J, Ganellin CR (24 August 2010). Analogue-based Drug Discovery II. John Wiley & Sons. p. 4. ISBN 978-3-527-63212-1.

[7] Fischer, Janos; Ganellin, C. Robin (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 444. ISBN 9783527607495.

[8] Fit KE, Williams PC (July 2007). "Use of histamine2-antagonists for the treatment of verruca vulgaris". The Annals of Pharmacotherapy. 41 (7): 1222–6. PMID 17535844. doi:10.1345/aph.1H616.

[9] Glass AT, Solomon BA (June 1996). "Cimetidine therapy for recalcitrant warts in adults". Archives of Dermatology. 132 (6): 680–2. PMID 8651718. doi:10.1001/archderm.1996.03890300108014.

[10] Karabulut AA, Sahin S, Ekşioglu M (April 1997). "Is cimetidine effective for nongenital warts: a double-blind, placebo-controlled study". Archives of Dermatology. 133 (4): 533–4. PMID 9126017. doi:10.1001/archderm.133.4.533.

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[16] Sabesin SM (1993). "Safety issues relating to long-term treatment with histamine H2-receptor antagonists". Alimentary Pharmacology & Therapeutics. 7 Suppl 2: 35–40. PMID 8103374. doi:10.1111/j.1365-2036.1993.tb00597.x.

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[Rodrigues2008-22] Rodrigues AD (8 February 2008). Drug-Drug Interactions, Second Edition. CRC Press. pp. 277, 294. ISBN 978-0-8493-7594-1.

[Zhou2016-23] Shufeng Zhou (6 April 2016). Cytochrome P450 2D6: Structure, Function, Regulation and Polymorphism. CRC Press. pp. 299–. ISBN 978-1-4665-9788-4.

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[FullerSajatovic2005-25] Fuller MA, Sajatovic M (2005). Drug Information Handbook for Psychiatry. Lexi-Comp. p. 285.

[CameronFeuer2012-26] Cameron R, Feuer G, de la Iglesias F (6 December 2012). Drug-Induced Hepatotoxicity. Springer Science & Business Media. pp. 140–. ISBN 978-3-642-61013-4.

[pmid6317740-27] Richards DA (1983). "Comparative pharmacodynamics and pharmacokinetics of cimetidine and ranitidine". Journal of Clinical Gastroenterology. 5 Suppl 1: 81–90. PMID 6317740. doi:10.1097/00004836-198312001-00008.

[Becker2001-28] Becker KL (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 1196–. ISBN 978-0-7817-1750-2.

[pmid6150641-29] Jensen RT, Collen MJ, McArthur KE, Howard JM, Maton PN, Cherner JA, Gardner JD (November 1984). "Comparison of the effectiveness of ranitidine and cimetidine in inhibiting acid secretion in patients with gastric hypersecretory states". The American Journal of Medicine. 77 (5B): 90–105. PMID 6150641.

[pmid3921876-30] Biagi P, Milani G (March 1985). "[Dysfunction of the hypothalamo-hypophyseal-gonadal axis induced by histamine H2 antagonists. Review of the literature and personal observations]". Minerva Medica (in Italian). 76 (12): 579–86. PMID 3921876.

[pmid428705-31] Winters SJ, Banks JL, Loriaux DL (March 1979). "Cimetidine is an antiandrogen in the rat". Gastroenterology. 76 (3): 504–8. PMID 428705.

[pmid6123322-32] Sivelle PC, Underwood AH, Jelly JA (March 1982). "The effects of histamine H2 receptor antagonists on androgen action in vivo and dihydrotestosterone binding to the rat prostate androgen receptor in vitro". Biochemical Pharmacology. 31 (5): 677–84. PMID 6123322. doi:10.1016/0006-2952(82)90449-X.

[pmid2747769-33] Galbraith RA, Michnovicz JJ (August 1989). "The effects of cimetidine on the oxidative metabolism of estradiol". The New England Journal of Medicine. 321 (5): 269–74. PMID 2747769. doi:10.1056/NEJM198908033210501.

[pmid1988774-34] Michnovicz JJ, Galbraith RA (February 1991). "Cimetidine inhibits catechol estrogen metabolism in women". Metabolism. 40 (2): 170–4. PMID 1988774. doi:10.1016/0026-0495(91)90169-W.

[PescovitzWalvoord2007-35] Pescovitz OH, Walvoord EC (6 June 2007). When Puberty is Precocious: Scientific and Clinical Aspects. Springer Science & Business Media. pp. 203–. ISBN 978-1-59745-499-5.

[PolatCuhaci2014-36] Cuhaci N, Polat SB, Evranos B, Ersoy R, Cakir B (March 2014). "Gynecomastia: Clinical evaluation and management". Indian Journal of Endocrinology and Metabolism. 18 (2): 150–8. PMC 3987263 . PMID 24741509. doi:10.4103/2230-8210.129104.

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[GalbraithMichnovicz1989-38] Galbraith RA, Michnovicz JJ (August 1989). "The effects of cimetidine on the oxidative metabolism of estradiol". The New England Journal of Medicine. 321 (5): 269–74. PMID 2747769. doi:10.1056/NEJM198908033210501.

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[FMO3_2000_review-40] Cashman JR (September 2000). "Human flavin-containing monooxygenase: substrate specificity and role in drug metabolism". Curr. Drug Metab. 1 (2): 181–191. PMID 11465082. doi:10.2174/1389200003339135. Human FMO3 N-oxygenates primary, secondary and tertiary amines whereas human FMO1 is only highly efficient at N-oxygenating tertiary amines. Both human FMO1 and FMO3 S-oxygenate a number of nucleophilic sulfur-containing substrates and in some cases, does so with great stereoselectivity. ... For amines with smaller aromatic substituents such as phenethylamines, often these compounds are efficiently N-oxygenated by human FMO3. ... (S)-Nicotine N-1'-oxide formation can also be used as a highly stereoselective probe of human FMO3 function for adult humans that smoke cigarettes. Finally, cimetidine S-oxygenation or ranitidine N-oxidation can also be used as a functional probe of human FMO3. With the recent observation of human FMO3 genetic polymorphism and poor metabolism phenotype in certain human populations, variant human FMO3 may contribute to adverse drug reactions or exaggerated clinical response to certain medications.

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v t e Drugs for peptic ulcer and GERD/GORD (A02B)
H₂ antagonists ("-tidine")	Cimetidine Famotidine Lafutidine Lavoltidine (loxtidine) Niperotidine Nizatidine Ranitidine Roxatidine
Prostaglandins (E)/analogues ("-prost-")	Misoprostol Enprostil
Proton-pump inhibitors ("-prazole")	Dexlansoprazole Esomeprazole Ilaprazole Lansoprazole Omeprazole Pantoprazole Picoprazole Rabeprazole Tenatoprazole Timoprazole
Potassium-competitive acid blockers ("-prazan")	Linaprazan Revaprazan Soraprazan Vonoprazan
Others	Aceglutamide aluminum Acetoxolone Alginic acid Arbaclofen placarbil Carbenoxolone Cetraxate Gefarnate Lesogaberan Pirenzepine Proglumide Rebamipide Sucralfate Sulglicotide Telenzepine Teprenone Troxipide Zinc L-carnosine Zolimidine
Combinations	Bismuth subcitrate/metronidazole/tetracycline
See also: Helicobacter pylori* eradication protocols*

v t e Histamine receptor modulators
H₁	Agonists: 2-Pyridylethylamine Betahistine Histamine HTMT L-Histidine UR-AK49 Antagonists: First-generation: 4-Methyldiphenhydramine Alimemazine Antazoline Azatadine Bamipine Benzatropine (benztropine) Bepotastine Bromazine Brompheniramine Buclizine Captodiame Carbinoxamine Chlorcyclizine Chloropyramine Chlorothen Chlorphenamine Chlorphenoxamine Cinnarizine Clemastine Clobenzepam Clocinizine Cloperastine Cyclizine Cyproheptadine Dacemazine Decloxizine Deptropine Dexbrompheniramine Dexchlorpheniramine Dimenhydrinate Dimetindene Diphenhydramine Diphenylpyraline Doxylamine Embramine Etodroxizine Etybenzatropine (ethylbenztropine) Etymemazine Fenethazine Flunarizine Histapyrrodine Homochlorcyclizine Hydroxyethylpromethazine Hydroxyzine Isopromethazine Isothipendyl Meclozine Medrylamine Mepyramine (pyrilamine) Mequitazine Methafurylene Methapyrilene Methdilazine Moxastine Orphenadrine Oxatomide Oxomemazine Phenindamine Pheniramine Phenyltoloxamine Pimethixene Piperoxan Pipoxizine Promethazine Propiomazine Pyrrobutamine Talastine Thenalidine Thenyldiamine Thiazinamium Thonzylamine Tolpropamine Tripelennamine Triprolidine Second/third-generation: Acrivastine Alinastine Astemizole Azelastine Bamirastine Barmastine Bepiastine Bepotastine Bilastine Cabastinen Carebastine Cetirizine Clemastine Clemizole Clobenztropine Desloratadine Dorastine Ebastine Efletirizine Emedastine Epinastine Fexofenadine Flezelastine Ketotifen Latrepirdine Levocabastine Levocetirizine Linetastine Loratadine Mapinastine Mebhydrolin Mizolastine Moxastine Noberastine Octastine Olopatadine Perastine Pibaxizine Piclopastine Quifenadine (phencarol) Rocastine Rupatadine Setastine Sequifenadine (bicarphen) Talastine Temelastine Terfenadine Vapitadine Zepastine Others: Atypical antipsychotics (e.g., aripiprazole, asenapine, brexpiprazole, clozapine, iloperidone, olanzapine, paliperidone, quetiapine, risperidone, RP-5063, ziprasidone, zotepine) Tetracyclic antidepressants (e.g., amoxapine, loxapine, maprotiline, mianserin, mirtazapine, oxaprotiline) Tricyclic antidepressants (e.g., amitriptyline, butriptyline, clomipramine, desipramine, dosulepin (dothiepin), doxepin, imipramine, iprindole, lofepramine, nortriptyline, protriptyline, trimipramine) Typical antipsychotics (e.g., chlorpromazine, flupenthixol, fluphenazine, loxapine, perphenazine, prochlorperazine, thioridazine, thiothixene) Unknown/unsorted: Belarizine Elbanizine Flotrenizine Napactadine Tagorizine Trelnarizine Trenizine
H₂	Agonists: Amthamine Betazole Dimaprit Histamine HTMT Impromidine L-Histidine UR-AK49 Antagonists: Bisfentidine Burimamide Cimetidine Dalcotidine Donetidine Ebrotidine Etintidine Famotidine Isolamtidine Lafutidine Lamtidine Lavoltidine (loxtidine) Lupitidine Metiamide Mifentidine Niperotidine Nizatidine Osutidine Oxmetidine Pibutidine Quisultazine (quisultidine) Ramixotidine Ranitidine Roxatidine Sufotidine Tiotidine Tuvatidine Venritidine Xaltidine Zolantidine
H₃	Agonists: α-Methylhistamine Cipralisant Histamine Imetit Immepip Immethridine L-Histidine Methimepip Proxyfan Antagonists: A-349,821 A-423,579 ABT-239 ABT-652 AZD5213 Betahistine Burimamide Ciproxifan Clobenpropit Conessine Enerisant GSK-189,254 Impentamine Iodophenpropit Irdabisant JNJ-5207852 MK-0249 NNC 38-1049 PF-03654746 Pitolisant SCH-79687 Thioperamide VUF-5681
H₄	Agonists: 4-Methylhistamine α-Methylhistamine Histamine L-Histidine OUP-16 VUF-8430 Antagonists: JNJ-7777120 Mianserin Thioperamide Toreforant VUF-6002
See also: Receptor/signaling modulators • Monoamine metabolism modulators • Monoamine reuptake inhibitors

匿名

検索

案内

cimetidine

WordNet

Wikipedia preview

wiki en

Contents

Medical uses

Other uses

Side effects

Overdose

Interactions

Pharmacology

Pharmacodynamics

Histamine H2 receptor antagonism

Antiandrogenic and estrogenic effects

Pharmacokinetics

Metabolism

Enzyme inhibition

History

References

External links

UpToDate Contents

English Journal

Japanese Journal

Related Links

Related Pictures

★リンクテーブル★

「シメチジン」

薬効薬理

効能又は効果

禁忌

副作用

相互作用

添付文書

「H2受容体拮抗薬」

H2受容体拮抗薬

構造

作用機序

注意

副作用

相互作用

「Tagamet」