# Cimetidine

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Medication

Pharmaceutical compound

Cimetidine Clinical data Pronunciation /sɪˈmɛtɪdiːn/ or /saɪˈmɛtɪdiːn/ Trade names Tagamet, others Other names SKF-92334[1] AHFS/Drugs.com Monograph MedlinePlus a682256 License data US DailyMed: Cimetidine Pregnancy category AU: B1 Routes of administration By mouth, intramuscular injection, intravenous infusion[2] ATC code A02BA01 (WHO) Legal status Legal status AU: S4 (Prescription only) UK: POM (Prescription only) US: ℞-only / OTC[3][4] Pharmacokinetic data Bioavailability 60–70%[5][6] Protein binding 13–25%[6][7] Metabolism Liver[6] Metabolites • Cimetidine sulfoxide[6] • Hydroxycimetidine[6] • Guanyl urea cimetidine[6] Onset of action 30 minutes[8] Elimination half-life 123 minutes (~2 hours)[7] Duration of action 4–8 hours[2] Excretion Urine[7] Identifiers IUPAC name 1-cyano-2-methyl-3-[2-[(5-methyl-1H-imidazol-4-yl)methylsulfanyl]ethyl]guanidine CAS Number 51481-61-9 Y PubChem CID 2756 IUPHAR/BPS 1231 DrugBank DB00501 Y ChemSpider 2654 Y UNII 80061L1WGD KEGG D00295 Y ChEBI CHEBI:3699 Y ChEMBL ChEMBL30 Y CompTox Dashboard (EPA) DTXSID4020329 ECHA InfoCard 100.052.012 Chemical and physical data Formula C10H16N6S Molar mass 252.34 g·mol−1 3D model (JSmol) Interactive image SMILES CC1=C(N=CN1)CSCCNC(=NC)NC#N 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) Y Key:AQIXAKUUQRKLND-UHFFFAOYSA-N Y (verify)

**Cimetidine**, sold under the brand name **Tagamet** among others, is a [histamine](/source/Histamine) [H2 receptor antagonist](/source/H2-receptor_antagonist) that inhibits [stomach acid](/source/Stomach_acid) production.[1][9][10] It is mainly used in the treatment of [heartburn](/source/Heartburn) and [peptic ulcers](/source/Peptic_ulcer).[1][10][11]

With the development of [proton pump inhibitors](/source/Proton_pump_inhibitor), such as [omeprazole](/source/Omeprazole), approved for the same indications, cimetidine is available as an over-the-counter formulation to prevent heartburn or acid indigestion, along with the other H2-receptor antagonists.[12]

Cimetidine was developed in 1971 and came into commercial use in 1977.[13][14] Cimetidine was approved in the United Kingdom in 1976,[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*] and was approved in the United States by the [Food and Drug Administration](/source/Food_and_Drug_Administration) in 1979.[15]

## Medical uses

Main article: [H2 antagonist](/source/H2_antagonist)

Cimetidine is indicated for the treatment of [duodenal ulcers](/source/Duodenal_ulcer), [gastric ulcers](/source/Gastric_ulcer), [gastroesophageal reflux disease](/source/Gastroesophageal_reflux_disease), and pathological hypersecretory conditions.[3] Cimetidine is also used to relieve or prevent heartburn.[4]

## Side effects

Reported [side effects](/source/Side_effect) of cimetidine include [diarrhea](/source/Diarrhea), [rashes](/source/Rash), [dizziness](/source/Dizziness), [fatigue](/source/Fatigue_(medical)), [constipation](/source/Constipation), and [muscle pain](/source/Myalgia), all of which are usually mild and transient.[16] It has been reported that [mental confusion](/source/Mental_confusion) may occur in the elderly.[16] Because of its hormonal effects, cimetidine rarely may cause [sexual dysfunction](/source/Sexual_dysfunction) including loss of [libido](/source/Libido) and [erectile dysfunction](/source/Erectile_dysfunction) and [gynecomastia](/source/Gynecomastia) (0.1–0.2%) in males during long-term treatment.[16][17][18] Rarely, [interstitial nephritis](/source/Interstitial_nephritis), [urticaria](/source/Urticaria), and [angioedema](/source/Angioedema) have been reported with cimetidine treatment.[16] Cimetidine is also commonly associated with transient raised [aminotransferase](/source/Aminotransferase) activity; [hepatotoxicity](/source/Hepatotoxicity) is rare.[19]

## Overdose

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

## Interactions

Due to its non-selective [inhibition](/source/Enzyme_inhibition) of [cytochrome P450](/source/Cytochrome_P450) [enzymes](/source/Enzyme), cimetidine has numerous [drug interactions](/source/Drug_interaction). Examples of specific interactions include, but are not limited to, the following:

- Cimetidine affects the metabolism of [methadone](/source/Methadone), sometimes resulting in higher blood levels and a higher incidence of side effects, and may interact with the [antimalarial](/source/Antimalarial) medication [hydroxychloroquine](/source/Hydroxychloroquine).[21]

- Cimetidine can also interact with a number of psychoactive medications, including [tricyclic antidepressants](/source/Tricyclic_antidepressant) and [selective serotonin reuptake inhibitors](/source/Selective_serotonin_reuptake_inhibitor), causing increased blood levels of these drugs and the potential of subsequent toxicity.[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

- Following administration of cimetidine, the elimination half-life and [area-under-curve](/source/Area_under_the_curve_(pharmacokinetics)) of [zolmitriptan](/source/Zolmitriptan) and its [active metabolites](/source/Active_metabolite) were roughly doubled.[22]

- Cimetidine is a potent inhibitor of tubular [creatinine](/source/Creatinine) secretion. Creatinine is a metabolic byproduct of [creatine](/source/Creatine) breakdown. Accumulation of creatinine is associated with [uremia](/source/Uremia), but the symptoms of creatinine accumulation are unknown, as they are hard to separate from other nitrogenous waste buildups.[23]

- Like several other medications (e.g., [erythromycin](/source/Erythromycin)), cimetidine interferes with the body's metabolization of [sildenafil](/source/Sildenafil), causing its strength and duration to increase and making its side effects more likely and prominent.[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

- Clinically significant drug interactions with the CYP1A2 substrate [theophylline](/source/Theophylline), the CYP2C9 substrate [tolbutamide](/source/Tolbutamide), the CYP2D6 substrate [desipramine](/source/Desipramine), and the CYP3A4 substrate [triazolam](/source/Triazolam) have all been demonstrated with cimetidine, and interactions with other substrates of these enzymes are likely as well.[24]

- Cimetidine has been shown clinically to reduce the clearance of [mirtazapine](/source/Mirtazapine), [imipramine](/source/Imipramine), [timolol](/source/Timolol), [nebivolol](/source/Nebivolol), [sparteine](/source/Sparteine), [loratadine](/source/Loratadine), [nortriptyline](/source/Nortriptyline), [gabapentin](/source/Gabapentin), and [desipramine](/source/Desipramine) in humans.[25]

- Cimetidine inhibits the [renal](/source/Renal) [excretion](/source/Excretion) of [metformin](/source/Metformin) and [procainamide](/source/Procainamide), resulting in increased circulating levels of these drugs.[16]

- Interactions of potential clinical importance with cimetidine include [warfarin](/source/Warfarin), [theophylline](/source/Theophylline), [phenytoin](/source/Phenytoin), [carbamazepine](/source/Carbamazepine), [pethidine](/source/Pethidine) and other [opioid](/source/Opioid) [analgesics](/source/Analgesic), [tricyclic antidepressants](/source/Tricyclic_antidepressant), [lidocaine](/source/Lidocaine), [terfenadine](/source/Terfenadine), [amiodarone](/source/Amiodarone), [flecainide](/source/Flecainide), [quinidine](/source/Quinidine), [fluorouracil](/source/Fluorouracil), and [benzodiazepines](/source/Benzodiazepine).[16][26]

- Cimetidine may decrease the effects of CYP2D6 substrates that are [prodrugs](/source/Prodrug), such as [codeine](/source/Codeine), [tramadol](/source/Tramadol), and [tamoxifen](/source/Tamoxifen).[27]

- Cimetidine reduces the [absorption](/source/Absorption_(pharmacokinetics)) of [ketoconazole](/source/Ketoconazole) and [itraconazole](/source/Itraconazole) (which require a low [pH](/source/PH)).[16]

- Cimetidine has a theoretical but unproven benefit in [paracetamol toxicity](/source/Paracetamol_toxicity).[19] This is because [N-acetyl-p-benzoquinone imine](/source/N-acetyl-p-benzoquinone_imine) (NAPQI), a [metabolite](/source/Metabolite) of [paracetamol](/source/Paracetamol) (acetaminophen) that is responsible for its [hepatotoxicity](/source/Hepatotoxicity), is formed from it by the cytochrome P450 system (specifically, CYP1A2, CYP2E1, and CYP3A4).[28]

- Cimetidine is used in cancer metastasis research as a blocker of E-selectin.[29]

- Cimetidine may significantly increase the blood levels of [loperamide](/source/Loperamide), which can lead to serious and potentially fatal complications such as cardiac arrhythmias and cardiac arrest, especially if loperamide is taken in excessive doses.[30]

## Pharmacology

### Pharmacodynamics

#### Histamine H2 receptor antagonism

The [mechanism of action](/source/Mechanism_of_action) of cimetidine as an [antacid](/source/Antacid) is as a [histamine](/source/Histamine) [H2 receptor](/source/H2_receptor) [antagonist](/source/Receptor_antagonist).[31] It has been found to bind to the H2 receptor with a Kd of 42 nM.[32]

#### Cytochrome P450 inhibition

Cimetidine is a [potent](/source/Potency_(pharmacology)) [inhibitor](/source/Enzyme_inhibitor) of certain [cytochrome P450](/source/Cytochrome_P450) (CYP) [enzymes](/source/Enzyme),[20][33] including [CYP1A2](/source/CYP1A2), [CYP2C9](/source/CYP2C9), [CYP2C19](/source/CYP2C19), [CYP2D6](/source/CYP2D6), [CYP2E1](/source/CYP2E1), and [CYP3A4](/source/CYP3A4).[20][33][34] The drug appears to primarily inhibit CYP1A2, CYP2D6, and CYP3A4,[35] of which it is described as a moderate inhibitor.[8] This is notable since these three CYP [isoenzymes](/source/Isoenzyme) are involved in CYP-mediated drug [biotransformations](/source/Biotransformation);[36] however, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 are also involved in the oxidative [metabolism](/source/Metabolism) of many commonly used drugs.[37] As a result, cimetidine has the potential for a large number of [pharmacokinetic interactions](/source/Pharmacokinetic_interactions).[20][33][34]

Cimetidine is reported to be a [competitive](/source/Competitive_inhibition) and [reversible inhibitor](/source/Enzyme_inhibitor#Reversible_inhibitors) of several CYP enzymes,[19][26][33][38] although [mechanism-based](/source/Suicide_inhibition) (suicide) [irreversible inhibition](/source/Enzyme_inhibitor#Irreversible_inhibitors) has also been identified for cimetidine's inhibition of CYP2D6.[25] It reversibly inhibits CYP enzymes by binding directly with the complexed [heme](/source/Heme)-[iron](/source/Iron) of the [active site](/source/Active_site) via one of its [imidazole](/source/Imidazole) [ring](/source/Ring_(chemistry)) [nitrogen](/source/Nitrogen) [atoms](/source/Atom), thereby blocking the oxidation of other drugs.[33][38][39]

#### Antiandrogenic and estrogenic effects

Cimetidine has been found to possess weak [antiandrogenic](/source/Antiandrogen) activity at high doses.[31][40][41][42] It directly and [competitively](/source/Competitive_antagonist) [antagonizes](/source/Receptor_antagonist) the [androgen receptor](/source/Androgen_receptor) (AR), the [biological target](/source/Biological_target) of [androgens](/source/Androgen) like [testosterone](/source/Testosterone) and [dihydrotestosterone](/source/Dihydrotestosterone) (DHT).[43][44] However, the [affinity](/source/Affinity_(pharmacology)) of cimetidine for the AR is very weak; in one study, it showed only 0.00084% of the [affinity](/source/Affinity_(pharmacology)) of the [anabolic steroid](/source/Anabolic_steroid) [metribolone](/source/Metribolone) (100%) for the human AR (Ki = 140 μM and 1.18 nM, respectively).[45] In any case, at sufficiently high doses, cimetidine has demonstrated weak but significant antiandrogenic effects in animals, including antiandrogenic effects in the rat [ventral prostate](/source/Ventral_prostate) and mouse [kidney](/source/Kidney), reductions in the weights of the [male accessory glands](/source/Male_accessory_gland) like the [prostate gland](/source/Prostate_gland) and [seminal vesicles](/source/Seminal_vesicle) in rats, and elevated [gonadotropin](/source/Gonadotropin) levels in male rats (due to reduced [negative feedback](/source/Negative_feedback) on the [HPG axis](/source/Hypothalamic%E2%80%93pituitary%E2%80%93gonadal_axis) by androgens).[46][47] In addition to AR antagonism, cimetidine has been found to inhibit the 2-[hydroxylation](/source/Hydroxylation) of [estradiol](/source/Estradiol) (via inhibition of CYP450 enzymes, which are involved in the metabolic inactivation of estradiol), resulting in increased [estrogen](/source/Estrogen) levels.[48][49][50][51][52] The medication has also been reported to reduce testosterone [biosynthesis](/source/Biosynthesis) and increase [prolactin](/source/Prolactin) levels in individual [case reports](/source/Case_report), effects which might be secondary to increased estrogen levels.[53]

At typical therapeutic levels, cimetidine has either no effect on or causes small increases in circulating testosterone concentrations in men.[46] Any increases in testosterone levels with cimetidine have been attributed to the loss of negative feedback on the HPG axis that results due to AR antagonism.[46][47] At typical clinical dosages, such as those used to treat peptic ulcer disease, the incidence of [gynecomastia](/source/Gynecomastia) (breast development) with cimetidine is very low at less than 1%.[54][46] In one survey of over 9,000 patients taking cimetidine, gynecomastia was the most frequent [endocrine](/source/Endocrine_system)-related complaint but was reported in only 0.2% of patients.[46] At high doses however, such as those used to treat [Zollinger–Ellison syndrome](/source/Zollinger%E2%80%93Ellison_syndrome), there may be a higher incidence of gynecomastia with cimetidine.[54] In one small study, a 20% incidence of gynecomastia was observed in 25 male patients with duodenal ulcers who were treated with 1,600 mg/day cimetidine.[53] The symptoms appeared after 4 months of treatment and regressed within a month following discontinuation of cimetidine.[53] In another small study, cimetidine was reported to have induced [breast](/source/Breast) changes and [erectile dysfunction](/source/Erectile_dysfunction) in 60% of 22 men treated with it.[53] These adverse effects completely resolved in all cases when the men were switched from cimetidine to [ranitidine](/source/Ranitidine).[53] A study of the [United Kingdom](/source/United_Kingdom) [General Practice Research Database](/source/Clinical_Practice_Research_Datalink#General_Practice_Research_Database), which contains over 80,000 men, found that the [relative risk](/source/Relative_risk) of gynecomastia in cimetidine users was 7.2 relative to non-users.[53] People taking a dosage of cimetidine of greater than or equal to 1,000 mg showed more than 40 times the risk of gynecomastia than non-users.[53] The risk was highest during the period of time of 7 to 12 months after starting cimetidine.[53] The gynecomastia associated with cimetidine is thought to be due to blockade of ARs in the breasts, which results in estrogen action unopposed by androgens in this [tissue](/source/Tissue_(biology)), although increased levels of estrogens due to inhibition of estrogen metabolism is another possible mechanism.[53] Cimetidine has also been associated with [oligospermia](/source/Oligospermia) (decreased [sperm count](/source/Sperm_count)) and [sexual dysfunction](/source/Sexual_dysfunction) (e.g., [decreased libido](/source/Decreased_libido), erectile dysfunction) in men in some research, which are hormonally related similarly.[47][46][53]

In accordance with the very weak nature of its AR antagonistic activity, cimetidine has shown minimal effectiveness in the treatment of [androgen-dependent conditions](/source/Androgen-dependent_condition) such as [acne](/source/Acne), [hirsutism](/source/Hirsutism) (excessive hair growth), and [hyperandrogenism](/source/Hyperandrogenism) (high androgen levels) in women.[55][56][54][57] As such, its use for such indications is not recommended.[56][57]

### Pharmacokinetics

Cimetidine is rapidly [absorbed](/source/Absorption_(pharmacokinetics)) regardless of [route of administration](/source/Route_of_administration).[7] The [oral](/source/Oral_administration) [bioavailability](/source/Bioavailability) of cimetidine is 60 to 70%.[5][6] The [onset of action](/source/Onset_of_action) of cimetidine when taken orally is 30 minutes,[8] and [peak levels](/source/Cmax_(pharmacology)) occur within 1 to 3 hours.[5] Cimetidine is widely [distributed](/source/Distribution_(pharmacology)) throughout all [tissues](/source/Tissue_(biology)).[7] It is able to cross the [blood–brain barrier](/source/Blood%E2%80%93brain_barrier) and can produce effects in the [central nervous system](/source/Central_nervous_system) (e.g., [headaches](/source/Headache), [dizziness](/source/Dizziness), [somnolence](/source/Somnolence)).[2] The [volume of distribution](/source/Volume_of_distribution) of cimetidine is 0.8 L/kg in adults and 1.2 to 2.1 L/kg in children.[6] Its [plasma protein binding](/source/Plasma_protein_binding) is 13 to 25% and is said to be without pharmacological significance.[6][7] Cimetidine undergoes relatively little [metabolism](/source/Metabolism), with 56 to 85% [excreted](/source/Excretion) unchanged.[7] It is metabolized in the [liver](/source/Liver) into cimetidine sulfoxide, hydroxycimetidine, and guanyl urea cimetidine.[6] The major [metabolite](/source/Metabolite) of cimetidine is the [sulfoxide](/source/Sulfoxide), which accounts for about 30% of excreted material.[7] Cimetidine is rapidly [eliminated](/source/Elimination_(pharmacology)), with an [elimination half-life](/source/Elimination_half-life) of 123 minutes, or about 2 hours.[7] It has been said to have a [duration of action](/source/Duration_of_action) of 4 to 8 hours.[2] The medication is mainly [eliminated](/source/Elimination_(pharmacology)) in [urine](/source/Urine).[7]

## History

Cimetidine, approved by the FDA for inhibition of gastric acid secretion, has been advocated for a number of dermatological diseases.[58] Cimetidine was the prototypical histamine [H2 receptor antagonist](/source/H2-receptor_antagonist) from which the later members of the class were developed. Cimetidine was the culmination of a project at [Smith, Kline & French](/source/Smith%2C_Kline_%26_French) (SKF) Laboratories in Welwyn Garden City (now part of [GlaxoSmithKline](/source/GlaxoSmithKline)) by [James W. Black](/source/James_W._Black), [C. Robin Ganellin](/source/C._Robin_Ganellin), and others to develop a [histamine receptor](/source/Histamine_receptor) [antagonist](/source/Receptor_antagonist) to suppress stomach acid secretion.[59] This was one of the first drugs discovered using a [rational drug design](/source/Rational_drug_design) approach. Sir James W. Black shared the 1988 Nobel Prize in Physiology or Medicine for the discovery of [propranolol](/source/Propranolol) and also is credited for the discovery of cimetidine.

At the time (1964), [histamine](/source/Histamine) was known to stimulate the secretion of stomach acid, but also that traditional [antihistamines](/source/Antihistamine) 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 *Nα*-guanylhistamine, a partial H2 receptor antagonist. From this lead, the receptor model was further refined and eventually led to the development of [burimamide](/source/Burimamide), the first H2 receptor antagonist. Burimamide, a specific [competitive antagonist](/source/Competitive_antagonist) at the H2 receptor, 100 times more potent than *Nα*-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](/source/PKa) of the compound, led to the development of [metiamide](/source/Metiamide). Metiamide was an effective agent; it was associated, however, with unacceptable [nephrotoxicity](/source/Nephrotoxicity) and [agranulocytosis](/source/Agranulocytosis).[59] The toxicity was proposed to arise from the [thiourea](/source/Thiourea) group, and similar [guanidine](/source/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.[60]

The commercial name "Tagamet" was decided upon by fusing the two words "an**tag**onist" and "ci**met**idine".[59] Subsequent to the introduction onto the U.S. drug market, two other H2 receptor antagonists were approved, [ranitidine](/source/Ranitidine) (Zantac, Glaxo Labs) and [famotidine](/source/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](/source/Pharmaceutical_drug#Blockbuster_drug).[61]

Tagamet has been largely replaced by proton pump inhibitors for treating peptic ulcers, but is available as an over-the-counter medicine for heartburn in many countries.[60]

## Lawsuit

On 21 August 1989, Danlex Research Laboratories, Inc. filed a petition with the Filipino Bureau of Patents, Trademarks and Technology Transfer (BPTTT) for a compulsory license to manufacture, use, and sell Cimetidine, citing the provisions of the Patent Law (R.A. 165) for medicinal products. Pre-1995, the Bureau of Patents, Trademarks and Technology Transfer (BPTTT) ruled in favor of Danlex and granted the compulsory license, subject to Danlex paying a royalty of 2.5% of net sales to Smith, Kline & French. On 27 January 1995, Smith, Kline & French appealed to the Court of Appeals, but the CA affirmed the BPTTT's decision, upholding the grant of the compulsory license to Danlex. On 25 July 1995, the Court of Appeals denied Smith, Kline & French's Motion for Reconsideration. On 15 September 1995, Smith, Kline & French filed a Petition for Review on Certiorari with the Supreme Court of the Philippines, challenging the CA's decision. On 23 October 2001, the Supreme Court (G.R. No. 121267) rendered its decision, affirming the Court of Appeals and upholding the grant of the compulsory license to Danlex. This marked the final judicial resolution of the case.[62]

## Research

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.[63][64][65]

Tentative evidence supports a beneficial role as add-on therapy in colorectal cancer.[66]

Cimetidine inhibits [ALA synthase](/source/ALA_synthase) activity and hence may have some therapeutic value in preventing and treating [acute porphyria](/source/Acute_porphyria) attacks.[67][68]

There is some evidence supporting the use of cimetidine in the treatment of [PFAPA](/source/Periodic_fever%2C_aphthous_stomatitis%2C_pharyngitis_and_adenitis).[69]

## Veterinary use

In dogs, cimetidine is used as an [antiemetic](/source/Antiemetic) when treating chronic [gastritis](/source/Gastritis).[70]

## References

1. ^ [***a***](#cite_ref-Elks2014_1-0) [***b***](#cite_ref-Elks2014_1-1) [***c***](#cite_ref-Elks2014_1-2) Elks J (14 November 2014). [*The Dictionary of Drugs: Chemical Data: Chemical Data, Bibliographies*](https://books.google.com/books?id=0vXTBwAAQBAJ&pg=PA275). Springer. pp. 275–. [ISBN](/source/ISBN_(identifier)) [978-1-4757-2085-3](https://en.wikipedia.org/wiki/Special:BookSources/978-1-4757-2085-3).

1. ^ [***a***](#cite_ref-GuptaSingh-Radcliff2013_2-0) [***b***](#cite_ref-GuptaSingh-Radcliff2013_2-1) [***c***](#cite_ref-GuptaSingh-Radcliff2013_2-2) [***d***](#cite_ref-GuptaSingh-Radcliff2013_2-3) Gupta A, Singh-Radcliff N (12 March 2013). [*Pharmacology in Anesthesia Practice*](https://books.google.com/books?id=a85oAgAAQBAJ&pg=PT177). Oxford University Press. pp. 177–. [ISBN](/source/ISBN_(identifier)) [978-0-19-934399-7](https://en.wikipedia.org/wiki/Special:BookSources/978-0-19-934399-7).

1. ^ [***a***](#cite_ref-Cimetidine_FDA_label_3-0) [***b***](#cite_ref-Cimetidine_FDA_label_3-1) ["Cimetidine tablet, film coated"](https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=496e258d-a5fd-42da-9a86-73afc8be359b). *DailyMed*. 30 November 2022. Retrieved 24 June 2024.

1. ^ [***a***](#cite_ref-Tagamet_FDA_label_4-0) [***b***](#cite_ref-Tagamet_FDA_label_4-1) ["Tagamet - cimetidine tablet"](https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e6401e0a-8612-42e8-bf89-2d67243f28dc). *DailyMed*. 10 June 2024. Retrieved 24 June 2024.

1. ^ [***a***](#cite_ref-DowdJohnson2016_5-0) [***b***](#cite_ref-DowdJohnson2016_5-1) [***c***](#cite_ref-DowdJohnson2016_5-2) Dowd FJ, Johnson B, Mariotti A (3 September 2016). [*Pharmacology and Therapeutics for Dentistry - E-Book*](https://books.google.com/books?id=6xT7DAAAQBAJ&pg=PA406). Elsevier Health Sciences. pp. 406–. [ISBN](/source/ISBN_(identifier)) [978-0-323-44595-5](https://en.wikipedia.org/wiki/Special:BookSources/978-0-323-44595-5).

1. ^ [***a***](#cite_ref-LeikinPaloucek1995_6-0) [***b***](#cite_ref-LeikinPaloucek1995_6-1) [***c***](#cite_ref-LeikinPaloucek1995_6-2) [***d***](#cite_ref-LeikinPaloucek1995_6-3) [***e***](#cite_ref-LeikinPaloucek1995_6-4) [***f***](#cite_ref-LeikinPaloucek1995_6-5) [***g***](#cite_ref-LeikinPaloucek1995_6-6) [***h***](#cite_ref-LeikinPaloucek1995_6-7) [***i***](#cite_ref-LeikinPaloucek1995_6-8) [***j***](#cite_ref-LeikinPaloucek1995_6-9) Leikin JB, Paloucek FP (1995). [*Poisoning & Toxicology Handbook, 1995-1996*](https://books.google.com/books?id=JpZrAAAAMAAJ). Lexi-Comp, Incorporated. p. 184. [ISBN](/source/ISBN_(identifier)) [978-0-916589-08-0](https://en.wikipedia.org/wiki/Special:BookSources/978-0-916589-08-0).

1. ^ [***a***](#cite_ref-AcademicPress1984_7-0) [***b***](#cite_ref-AcademicPress1984_7-1) [***c***](#cite_ref-AcademicPress1984_7-2) [***d***](#cite_ref-AcademicPress1984_7-3) [***e***](#cite_ref-AcademicPress1984_7-4) [***f***](#cite_ref-AcademicPress1984_7-5) [***g***](#cite_ref-AcademicPress1984_7-6) [***h***](#cite_ref-AcademicPress1984_7-7) [***i***](#cite_ref-AcademicPress1984_7-8) [***j***](#cite_ref-AcademicPress1984_7-9) [*Profiles of Drug Substances, Excipients and Related Methodology*](https://books.google.com/books?id=Fz6X-GmS-GgC&pg=PA176). Academic Press. 24 October 1984. pp. 176–. [ISBN](/source/ISBN_(identifier)) [978-0-08-086108-1](https://en.wikipedia.org/wiki/Special:BookSources/978-0-08-086108-1).

1. ^ [***a***](#cite_ref-VallerandSanoski2016_8-0) [***b***](#cite_ref-VallerandSanoski2016_8-1) [***c***](#cite_ref-VallerandSanoski2016_8-2) Vallerand AH, Sanoski CA, Deglin JH (25 May 2016). [*Davis's Drug Guide for Nurses*](https://books.google.com/books?id=ORa1DAAAQBAJ&pg=PA636). F.A. Davis. pp. 636–. [ISBN](/source/ISBN_(identifier)) [978-0-8036-5779-3](https://en.wikipedia.org/wiki/Special:BookSources/978-0-8036-5779-3).

1. **[^](#cite_ref-IndexNominum2000_9-0)** [*Index Nominum 2000: International Drug Directory*](https://books.google.com/books?id=5GpcTQD_L2oC&pg=PA234). Taylor & Francis. January 2000. pp. 234–. [ISBN](/source/ISBN_(identifier)) [978-3-88763-075-1](https://en.wikipedia.org/wiki/Special:BookSources/978-3-88763-075-1).

1. ^ [***a***](#cite_ref-MortonMorton1999_10-0) [***b***](#cite_ref-MortonMorton1999_10-1) Morton I, Morton IK, Hall JM (31 October 1999). [*Concise Dictionary of Pharmacological Agents: Properties and Synonyms*](https://books.google.com/books?id=mqaOMOtk61IC&pg=PA77). Springer Science & Business Media. pp. 77–. [ISBN](/source/ISBN_(identifier)) [978-0-7514-0499-9](https://en.wikipedia.org/wiki/Special:BookSources/978-0-7514-0499-9).

1. **[^](#cite_ref-BurchumRosenthal2014_11-0)** Jacqueline B, Rosenthal L (2 December 2014). ["Drugs for Peptic Ulcer Disease"](https://books.google.com/books?id=C7_NBQAAQBAJ&pg=PA952). *Lehne's Pharmacology for Nursing Care*. Elsevier Health Sciences. pp. 952–. [ISBN](/source/ISBN_(identifier)) [978-0-323-34026-7](https://en.wikipedia.org/wiki/Special:BookSources/978-0-323-34026-7).

1. **[^](#cite_ref-12)** Pino MA, Azer SA (March 2023). ["Cimetidine"](https://www.ncbi.nlm.nih.gov/books/NBK544255/). *StatPearls [Internet]*. Treasure Island (FL): StatPearls Publishing. [PMID](/source/PMID_(identifier)) [31334975](https://pubmed.ncbi.nlm.nih.gov/31334975). Bookshelf ID: NBK544255. Retrieved 6 November 2023 – via U.S. National Library of Medicine.

1. **[^](#cite_ref-FischerGanellin2010_13-0)** Fischer J, Ganellin CR (24 August 2010). [*Analogue-based Drug Discovery II*](https://books.google.com/books?id=h2Kd8ci4Ln8C&pg=PA4). John Wiley & Sons. p. 4. [ISBN](/source/ISBN_(identifier)) [978-3-527-63212-1](https://en.wikipedia.org/wiki/Special:BookSources/978-3-527-63212-1).

1. **[^](#cite_ref-14)** Alapi EM, Fischer J (2006). ["Table of Selected Analogue Classes"](https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA444). In Fischer J, Ganellin CR (eds.). *Analogue-based Drug Discovery*. John Wiley & Sons. p. 444. [ISBN](/source/ISBN_(identifier)) [978-3-527-60749-5](https://en.wikipedia.org/wiki/Special:BookSources/978-3-527-60749-5).

1. **[^](#cite_ref-15)** ["Tagamet: FDA-Approved Drugs"](https://web.archive.org/web/20170430220843/https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=017939). *U.S. [Food and Drug Administration](/source/Food_and_Drug_Administration) (FDA)*. Archived from [the original](https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=017939) on 30 April 2017. Retrieved 9 November 2023.

1. ^ [***a***](#cite_ref-RitterLewis2008_16-0) [***b***](#cite_ref-RitterLewis2008_16-1) [***c***](#cite_ref-RitterLewis2008_16-2) [***d***](#cite_ref-RitterLewis2008_16-3) [***e***](#cite_ref-RitterLewis2008_16-4) [***f***](#cite_ref-RitterLewis2008_16-5) [***g***](#cite_ref-RitterLewis2008_16-6) Ritter J, Lewis L, Mant T, Ferro A (25 April 2008). ["Alimenary System and Liver"](https://books.google.com/books?id=TD59BgAAQBAJ&pg=PA250). *A Textbook of Clinical Pharmacology and Therapeutics* (5th ed.). CRC Press. pp. 250–. [ISBN](/source/ISBN_(identifier)) [978-1-4441-1300-6](https://en.wikipedia.org/wiki/Special:BookSources/978-1-4441-1300-6).

1. **[^](#cite_ref-17)** Sawyer D, Conner CS, Scalley R (February 1981). "Cimetidine: adverse reactions and acute toxicity". *American Journal of Hospital Pharmacy*. **38** (2): 188–197. [PMID](/source/PMID_(identifier)) [7011006](https://pubmed.ncbi.nlm.nih.gov/7011006).

1. **[^](#cite_ref-18)** Sabesin SM (1993). "Safety issues relating to long-term treatment with histamine H2-receptor antagonists". *Alimentary Pharmacology & Therapeutics*. **7** (Suppl 2): 35–40. [doi](/source/Doi_(identifier)):[10.1111/j.1365-2036.1993.tb00597.x](https://doi.org/10.1111%2Fj.1365-2036.1993.tb00597.x). [PMID](/source/PMID_(identifier)) [8103374](https://pubmed.ncbi.nlm.nih.gov/8103374). [S2CID](/source/S2CID_(identifier)) [42564864](https://api.semanticscholar.org/CorpusID:42564864).

1. ^ [***a***](#cite_ref-Kelly2009_19-0) [***b***](#cite_ref-Kelly2009_19-1) [***c***](#cite_ref-Kelly2009_19-2) Murray KF (26 January 2009). ["Drug-Induced Liver Disease"](https://books.google.com/books?id=z7nO3OrNXckC&pg=PA224). In Kelly D (ed.). *Diseases of the Liver and Biliary System in Children*. John Wiley & Sons. pp. 224–. [ISBN](/source/ISBN_(identifier)) [978-1-4443-0054-3](https://en.wikipedia.org/wiki/Special:BookSources/978-1-4443-0054-3).

1. ^ [***a***](#cite_ref-Dart2004_20-0) [***b***](#cite_ref-Dart2004_20-1) [***c***](#cite_ref-Dart2004_20-2) [***d***](#cite_ref-Dart2004_20-3) Whyte IM (2004). ["Histaminde H2 Antagonists"](https://books.google.com/books?id=BfdighlyGiwC&pg=PA402). In Dart RC (ed.). *Medical Toxicology*. Lippincott Williams & Wilkins. pp. 402–. [ISBN](/source/ISBN_(identifier)) [978-0-7817-2845-4](https://en.wikipedia.org/wiki/Special:BookSources/978-0-7817-2845-4).

1. **[^](#cite_ref-21)** Furst DE (June 1996). "Pharmacokinetics of hydroxychloroquine and chloroquine during treatment of rheumatic diseases". *Lupus*. **5** (Suppl 1): S11–S15. [doi](/source/Doi_(identifier)):[10.1177/096120339600500104](https://doi.org/10.1177%2F096120339600500104). [PMID](/source/PMID_(identifier)) [8803904](https://pubmed.ncbi.nlm.nih.gov/8803904). [S2CID](/source/S2CID_(identifier)) [44999237](https://api.semanticscholar.org/CorpusID:44999237).

1. **[^](#cite_ref-22)** See complete drug interactions for Zomig (zolmitriptan succinate used for migraine relief) in package insert: ["Highlights of Zomig Prescribing Information"](https://web.archive.org/web/20150218190357/http://www1.astrazeneca-us.com/pi/Zomig.pdf) (PDF). AstraZeneca. Archived from [the original](http://www1.astrazeneca-us.com/pi/Zomig.pdf) (PDF) on 18 February 2015. Retrieved 28 January 2010.

1. **[^](#cite_ref-23)** 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"](https://doi.org/10.2133%2Fdmpk.20.200). *Drug Metabolism and Pharmacokinetics*. **20** (3): 200–205. [doi](/source/Doi_(identifier)):[10.2133/dmpk.20.200](https://doi.org/10.2133%2Fdmpk.20.200). [PMID](/source/PMID_(identifier)) [15988122](https://pubmed.ncbi.nlm.nih.gov/15988122). [S2CID](/source/S2CID_(identifier)) [13857940](https://api.semanticscholar.org/CorpusID:13857940).

1. **[^](#cite_ref-Rodrigues2008_24-0)** Ogilvie BW, Usuki E, Yerino P, Parkinson A (8 February 2008). ["In vitro approaches for studying the inhibition of drug-metabolizing enzymes and identifying the drug-metabolizing enzymes responsible for the metabolism of drugs (reaction phenotyping) with emphasis on cytochrome P450"](https://books.google.com/books?id=rmCGQ8qAv8AC&pg=PA294). In Rodrigues DA (ed.). *Drug-Drug Interactions* (Second ed.). CRC Press. pp. 277, 294. [ISBN](/source/ISBN_(identifier)) [978-0-8493-7594-1](https://en.wikipedia.org/wiki/Special:BookSources/978-0-8493-7594-1).

1. ^ [***a***](#cite_ref-Zhou2016_25-0) [***b***](#cite_ref-Zhou2016_25-1) Zhou S (6 April 2016). ["Inhibitors of Human CYP2D6"](https://books.google.com/books?id=UJqmCwAAQBAJ&pg=PA299). *Cytochrome P450 2D6: Structure, Function, Regulation and Polymorphism*. CRC Press. pp. 299–. [ISBN](/source/ISBN_(identifier)) [978-1-4665-9788-4](https://en.wikipedia.org/wiki/Special:BookSources/978-1-4665-9788-4).

1. ^ [***a***](#cite_ref-RosenfeldLoose2007_26-0) [***b***](#cite_ref-RosenfeldLoose2007_26-1) Rosenfeld GC, Loose DS (2007). [*Pharmacology*](https://books.google.com/books?id=fm8kmMDjdiAC&pg=PA202). Lippincott Williams & Wilkins. pp. 202–. [ISBN](/source/ISBN_(identifier)) [978-0-7817-8074-2](https://en.wikipedia.org/wiki/Special:BookSources/978-0-7817-8074-2).

1. **[^](#cite_ref-FullerSajatovic2005_27-0)** Fuller MA, Sajatovic M (2005). [*Drug Information Handbook for Psychiatry*](https://books.google.com/books?id=LzBtAAAAMAAJ). Lexi-Comp. p. 285. [ISBN](/source/ISBN_(identifier)) [978-1-59195-114-8](https://en.wikipedia.org/wiki/Special:BookSources/978-1-59195-114-8).

1. **[^](#cite_ref-CameronFeuer2012_28-0)** Leeder JS, Okey AB (6 December 2012). ["Cytochrome P450 and Liver injury"](https://books.google.com/books?id=xZf-CAAAQBAJ&pg=PA140). In Cameron R, Feuer G, de la Iglesias F (eds.). *Drug-Induced Hepatotoxicity*. Springer Science & Business Media. pp. 140–. [ISBN](/source/ISBN_(identifier)) [978-3-642-61013-4](https://en.wikipedia.org/wiki/Special:BookSources/978-3-642-61013-4).

1. **[^](#cite_ref-29)** Coppo R, Orso F, Virga F, Dalmasso A, Baruffaldi D, Nie L, et al. (July 2021). ["ESDN inhibits melanoma progression by blocking E-selectin expression in endothelial cells via STAT3"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8581997). *Cancer Letters*. **510**: 13–23. [doi](/source/Doi_(identifier)):[10.1016/j.canlet.2021.04.005](https://doi.org/10.1016%2Fj.canlet.2021.04.005). [hdl](/source/Hdl_(identifier)):[2318/1791282](https://hdl.handle.net/2318%2F1791282). [PMC](/source/PMC_(identifier)) [8581997](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8581997). [PMID](/source/PMID_(identifier)) [33862151](https://pubmed.ncbi.nlm.nih.gov/33862151).

1. **[^](#cite_ref-30)** [https://www.drugs.com/drug-interactions/cimetidine-with-loperamide-669-0-1482-0.html](https://www.drugs.com/drug-interactions/cimetidine-with-loperamide-669-0-1482-0.html)

1. ^ [***a***](#cite_ref-pmid6317740_31-0) [***b***](#cite_ref-pmid6317740_31-1) Richards DA (1983). "Comparative pharmacodynamics and pharmacokinetics of cimetidine and ranitidine". *Journal of Clinical Gastroenterology*. **5** (Suppl 1): 81–90. [doi](/source/Doi_(identifier)):[10.1097/00004836-198312001-00008](https://doi.org/10.1097%2F00004836-198312001-00008). [PMID](/source/PMID_(identifier)) [6317740](https://pubmed.ncbi.nlm.nih.gov/6317740). [S2CID](/source/S2CID_(identifier)) [24909853](https://api.semanticscholar.org/CorpusID:24909853).

1. **[^](#cite_ref-Osborne2013_32-0)** Taylor JE (22 October 2013). Osborne NN (ed.). ["Neurochemical and neuropharmacological aspects of histamine receptors"](https://books.google.com/books?id=ldnWAgAAQBAJ&pg=PA297). *Neurochemistry International*. **4** (2–3). Elsevier Science: 89–96. [doi](/source/Doi_(identifier)):[10.1016/0197-0186(82)90001-8](https://doi.org/10.1016%2F0197-0186%2882%2990001-8). [ISBN](/source/ISBN_(identifier)) [978-1-4832-8635-8](https://en.wikipedia.org/wiki/Special:BookSources/978-1-4832-8635-8). [PMID](/source/PMID_(identifier)) [20487855](https://pubmed.ncbi.nlm.nih.gov/20487855). [S2CID](/source/S2CID_(identifier)) [40069290](https://api.semanticscholar.org/CorpusID:40069290).

1. ^ [***a***](#cite_ref-LemkeWilliams2008_33-0) [***b***](#cite_ref-LemkeWilliams2008_33-1) [***c***](#cite_ref-LemkeWilliams2008_33-2) [***d***](#cite_ref-LemkeWilliams2008_33-3) [***e***](#cite_ref-LemkeWilliams2008_33-4) Williams DA (2008). ["Drug Metabolism"](https://books.google.com/books?id=R0W1ErpsQpkC&pg=PA273). In Lemke TL, Williams DA (eds.). *Foye's Principles of Medicinal Chemistry*. Lippincott Williams & Wilkins. pp. 273–. [ISBN](/source/ISBN_(identifier)) [978-0-7817-6879-5](https://en.wikipedia.org/wiki/Special:BookSources/978-0-7817-6879-5).

1. ^ [***a***](#cite_ref-KarallieddeClarke2010_34-0) [***b***](#cite_ref-KarallieddeClarke2010_34-1) Karalliedde LD, Clarke SF, Collignon U, Karalliedde J (29 January 2010). ["Drugs Acting on the Gastrointestinal Track"](https://books.google.com/books?id=B2YwH371uzYC&pg=PA633). *Adverse Drug Interactions: A Handbook for Prescribers*. CRC Press. pp. 633–. [ISBN](/source/ISBN_(identifier)) [978-0-340-92769-4](https://en.wikipedia.org/wiki/Special:BookSources/978-0-340-92769-4).

1. **[^](#cite_ref-PriskornLarsen1997_35-0)** 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): 241–242. [doi](/source/Doi_(identifier)):[10.1007/s002280050282](https://doi.org/10.1007%2Fs002280050282). [PMID](/source/PMID_(identifier)) [9218934](https://pubmed.ncbi.nlm.nih.gov/9218934). [S2CID](/source/S2CID_(identifier)) [22540140](https://api.semanticscholar.org/CorpusID:22540140).

1. **[^](#cite_ref-MartinezAlbet1999_36-0)** Martínez C, Albet C, Agúndez JA, Herrero E, Carrillo JA, Márquez M, et al. (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): 369–376. [doi](/source/Doi_(identifier)):[10.1016/S0009-9236(99)70129-3](https://doi.org/10.1016%2FS0009-9236%2899%2970129-3). [PMID](/source/PMID_(identifier)) [10223772](https://pubmed.ncbi.nlm.nih.gov/10223772). [S2CID](/source/S2CID_(identifier)) [25151710](https://api.semanticscholar.org/CorpusID:25151710).

1. **[^](#cite_ref-Delafuente2003_37-0)** Delafuente JC (November 2003). "Understanding and preventing drug interactions in elderly patients". *Critical Reviews in Oncology/Hematology*. **48** (2): 133–143. [doi](/source/Doi_(identifier)):[10.1016/j.critrevonc.2003.04.004](https://doi.org/10.1016%2Fj.critrevonc.2003.04.004). [PMID](/source/PMID_(identifier)) [14607376](https://pubmed.ncbi.nlm.nih.gov/14607376).

1. ^ [***a***](#cite_ref-Cairns2012_38-0) [***b***](#cite_ref-Cairns2012_38-1) Cairns D (2012). ["Drug Metabolism: Drug Conjugating Reactions (Phase 2)"](https://books.google.com/books?id=gNliFkwHYgEC&pg=PA110). *Essentials of Pharmaceutical Chemistry*. Pharmaceutical Press. pp. 110–. [ISBN](/source/ISBN_(identifier)) [978-0-85369-979-8](https://en.wikipedia.org/wiki/Special:BookSources/978-0-85369-979-8). Drugs interacting in this way with CYP 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.

1. **[^](#cite_ref-pmid9630736_39-0)** Liska DJ (June 1998). "The detoxification enzyme systems". *Alternative Medicine Review*. **3** (3): 187–198. [PMID](/source/PMID_(identifier)) [9630736](https://pubmed.ncbi.nlm.nih.gov/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

1. **[^](#cite_ref-Becker2001_40-0)** Matsumoto AM (2001). ["Clinical Use and Abuse of Androgens and Antiandrogens"](https://books.google.com/books?id=FVfzRvaucq8C&pg=PA1196). In Becker KL (ed.). *Principles and Practice of Endocrinology and Metabolism*. Lippincott Williams & Wilkins. pp. 1196–. [ISBN](/source/ISBN_(identifier)) [978-0-7817-1750-2](https://en.wikipedia.org/wiki/Special:BookSources/978-0-7817-1750-2).

1. **[^](#cite_ref-pmid6150641_41-0)** Jensen RT, Collen MJ, McArthur KE, Howard JM, Maton PN, Cherner JA, et al. (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](/source/PMID_(identifier)) [6150641](https://pubmed.ncbi.nlm.nih.gov/6150641).

1. **[^](#cite_ref-pmid3921876_42-0)** 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): 579–586. [PMID](/source/PMID_(identifier)) [3921876](https://pubmed.ncbi.nlm.nih.gov/3921876).

1. **[^](#cite_ref-pmid428705_43-0)** Winters SJ, Banks JL, Loriaux DL (March 1979). ["Cimetidine is an antiandrogen in the rat"](https://doi.org/10.1016%2FS0016-5085%2879%2980217-6). *Gastroenterology*. **76** (3): 504–508. [doi](/source/Doi_(identifier)):[10.1016/S0016-5085(79)80217-6](https://doi.org/10.1016%2FS0016-5085%2879%2980217-6). [PMID](/source/PMID_(identifier)) [428705](https://pubmed.ncbi.nlm.nih.gov/428705).

1. **[^](#cite_ref-pmid6123322_44-0)** 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): 677–684. [doi](/source/Doi_(identifier)):[10.1016/0006-2952(82)90449-X](https://doi.org/10.1016%2F0006-2952%2882%2990449-X). [PMID](/source/PMID_(identifier)) [6123322](https://pubmed.ncbi.nlm.nih.gov/6123322).

1. **[^](#cite_ref-pmid6725525_b_45-0)** Eil C, Edelson SK (July 1984). "The use of human skin fibroblasts to obtain potency estimates of drug binding to androgen receptors". *The Journal of Clinical Endocrinology and Metabolism*. **59** (1): 51–55. [doi](/source/Doi_(identifier)):[10.1210/jcem-59-1-51](https://doi.org/10.1210%2Fjcem-59-1-51). [PMID](/source/PMID_(identifier)) [6725525](https://pubmed.ncbi.nlm.nih.gov/6725525).

1. ^ [***a***](#cite_ref-GerallMoltz2013_46-0) [***b***](#cite_ref-GerallMoltz2013_46-1) [***c***](#cite_ref-GerallMoltz2013_46-2) [***d***](#cite_ref-GerallMoltz2013_46-3) [***e***](#cite_ref-GerallMoltz2013_46-4) [***f***](#cite_ref-GerallMoltz2013_46-5) Ward OB (11 November 2013). ["Fetal drug exposure and sexual differentiation of males."](https://books.google.com/books?id=4nb1BwAAQBAJ&pg=PA207). In Gerall AA, Moltz H, Ward EL (eds.). *Sexual Differentiation*. Springer Science & Business Media. pp. 207–. [ISBN](/source/ISBN_(identifier)) [978-1-4899-2453-7](https://en.wikipedia.org/wiki/Special:BookSources/978-1-4899-2453-7). In high concentrations cimetidine acts as a weak antiandrogen by competitively binding to cytosol androgen receptors, as has been demonstrated in rat ventral prostate (Foldesy, Vanderhoof, & Hahn, 1985; Sivelle, Underwood, & Jelly, 1982) and mouse kidney tissue (Funder & Mercer, 1979). In vivo, cimetidine, in high dose levels, causes reductions in prostate and seminal vesicle weights in male rats (Foldesy et al., 1985; Leslie & Walker, 1977; Sivelle et al., 1982). After 6 weeks of daily cimetidine administration to male rats, reduced weights of accessory sexual organs were accompanied by elevated gonadotropin levels (Baba, Paul, Pollow, Janetschek, & Jacobi, 1981). At therapeutic levels in men, cimetidine either has no effect on plasma T levels (Spona et al., 1987; Stubbs et al., 1983) or causes small increases in T (Peden, Boyd, Browning, Saunders, & Wormsley, 1981; Van Thiel, Gavaler, Smith, & Paul, 1979; Wang, Lai, Lam, & Yeung, 1982). The increases in T have been attributed to cimetidine's antagonism of the normal negative feedback that androgens exert on gonadotropin secretion (Peden, Cargill, Browning, Saunders, & Wormsley, 1979). Gynecomastia and even loss of libido that progressed to impotence have occasionally been reported in men taking cimetidine (Peden et al., 1979; Spence & Celestin, 1979), but the occurrence of these disorders is very rare (Gifford, Aeugle, Myerson, & Tannenbaum, 1980). In one survey, gynecomastia, the most frequent endocrine-related complaint, was reported in only 0.2% of over 9,000 patients taking cimetidine (Gifford et al., 1980).

1. ^ [***a***](#cite_ref-PlessisAgarwal2014_47-0) [***b***](#cite_ref-PlessisAgarwal2014_47-1) [***c***](#cite_ref-PlessisAgarwal2014_47-2) Barazani Y, Sabanegh Jr ES (26 July 2014). ["Risks from Medical and Therapeutic Treatments"](https://books.google.com/books?id=-I4kBAAAQBAJ&pg=PA233). In du Plessis SS, Agarwal A, Sabanegh Jr ES (eds.). *Male Infertility: A Complete Guide to Lifestyle and Environmental Factors*. Springer. pp. 233–. [ISBN](/source/ISBN_(identifier)) [978-1-4939-1040-3](https://en.wikipedia.org/wiki/Special:BookSources/978-1-4939-1040-3). Like other antiandrogens, [cimetidine] leads to elevated gonadotropin levels by antagonizing the negative feedback control of gonadotropin secretion by testosterone [1, 34]. Cimetidine has been reported to have antiandrogenic effects ranging from gynecomastia to oligospermia [4]. In one clinical study, men administered cimetidine exhibited a significant reduction in sperm concentration compared to placebo-treated controls [35]. In another study of men receiving cimetidine for chronic duodenal ulcers, testosterone and FSH were elevated during treatment with cimetidine compared to both pre- and posttreatment levels. Moreover, these hormonal effects were associated with a reduction in mean sperm count compared to the period after drug withdrawal [34].

1. **[^](#cite_ref-GalbraithMichnovicz1989_48-0)** Galbraith RA, Michnovicz JJ (August 1989). "The effects of cimetidine on the oxidative metabolism of estradiol". *The New England Journal of Medicine*. **321** (5): 269–274. [doi](/source/Doi_(identifier)):[10.1056/NEJM198908033210501](https://doi.org/10.1056%2FNEJM198908033210501). [PMID](/source/PMID_(identifier)) [2747769](https://pubmed.ncbi.nlm.nih.gov/2747769).

1. **[^](#cite_ref-pmid1988774_49-0)** Michnovicz JJ, Galbraith RA (February 1991). "Cimetidine inhibits catechol estrogen metabolism in women". *Metabolism*. **40** (2): 170–174. [doi](/source/Doi_(identifier)):[10.1016/0026-0495(91)90169-W](https://doi.org/10.1016%2F0026-0495%2891%2990169-W). [PMID](/source/PMID_(identifier)) [1988774](https://pubmed.ncbi.nlm.nih.gov/1988774).

1. **[^](#cite_ref-PescovitzWalvoord2007_50-0)** Pescovitz OH, Walvoord EC (6 June 2007). [*When Puberty is Precocious: Scientific and Clinical Aspects*](https://books.google.com/books?id=seYO1f1JgzYC&pg=PA203). Springer Science & Business Media. pp. 203–. [ISBN](/source/ISBN_(identifier)) [978-1-59745-499-5](https://en.wikipedia.org/wiki/Special:BookSources/978-1-59745-499-5).

1. **[^](#cite_ref-PolatCuhaci2014_51-0)** Cuhaci N, Polat SB, Evranos B, Ersoy R, Cakir B (March 2014). ["Gynecomastia: Clinical evaluation and management"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987263). *Indian Journal of Endocrinology and Metabolism*. **18** (2): 150–158. [doi](/source/Doi_(identifier)):[10.4103/2230-8210.129104](https://doi.org/10.4103%2F2230-8210.129104). [PMC](/source/PMC_(identifier)) [3987263](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987263). [PMID](/source/PMID_(identifier)) [24741509](https://pubmed.ncbi.nlm.nih.gov/24741509).

1. **[^](#cite_ref-RendicCarlo2010_52-0)** 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. [doi](/source/Doi_(identifier)):[10.3109/03602539709037591](https://doi.org/10.3109%2F03602539709037591). [PMID](/source/PMID_(identifier)) [9187528](https://pubmed.ncbi.nlm.nih.gov/9187528).

1. ^ [***a***](#cite_ref-pmid22862307_53-0) [***b***](#cite_ref-pmid22862307_53-1) [***c***](#cite_ref-pmid22862307_53-2) [***d***](#cite_ref-pmid22862307_53-3) [***e***](#cite_ref-pmid22862307_53-4) [***f***](#cite_ref-pmid22862307_53-5) [***g***](#cite_ref-pmid22862307_53-6) [***h***](#cite_ref-pmid22862307_53-7) [***i***](#cite_ref-pmid22862307_53-8) [***j***](#cite_ref-pmid22862307_53-9) Deepinder F, Braunstein GD (September 2012). "Drug-induced gynecomastia: an evidence-based review". *Expert Opinion on Drug Safety*. **11** (5): 779–795. [doi](/source/Doi_(identifier)):[10.1517/14740338.2012.712109](https://doi.org/10.1517%2F14740338.2012.712109). [PMID](/source/PMID_(identifier)) [22862307](https://pubmed.ncbi.nlm.nih.gov/22862307). [S2CID](/source/S2CID_(identifier)) [22938364](https://api.semanticscholar.org/CorpusID:22938364). Cimetidine. Spence and Celestin reported a 20% incidence of gynecomastia in a prospective study of 25 male duodenal ulcer patients treated with cimetidine 1.6 g/day [13]. Symptoms developed after 4 months of treatment and regressed within a month of stopping therapy. In another prospective cohort study involving 22 patients, cimetidine caused breast changes and erectile dysfunction in 60% of men which resolved completely in all cases when switched to ranitidine [14]. In the UK general practice database of over 80,000 men, the relative risk (RR) of gynecomastia among cimetidine users was 7.2 (95% confidence interval (CI 4.5 -- 11.3)) as compared with the non-users. Users with a daily dose ‡ 1000 mg had more than 40 times the risk of developing gynecomastia than the non-users. The period of highest risk was 7 -- 12 months after starting cimetidine treatment [15]. Cimetidine blocks the androgen receptors in the breast leading to decreased androgen action causing the growth of breast tissue because of 'unopposed' estrogen action [16]. Another possible mechanism includes decreased 2-hydroxylation of estrogen leading to elevated serum estrogen levels [17]. There also are reports of cimetidine blocking testosterone biosynthesis and causing elevated prolactin levels in individual cases [18].

1. ^ [***a***](#cite_ref-WattsFaingold2009_54-0) [***b***](#cite_ref-WattsFaingold2009_54-1) [***c***](#cite_ref-WattsFaingold2009_54-2) Dunaway G (1 April 2009). ["Androgens and Antiandrogens"](https://books.google.com/books?id=kfsrz_-OrMQC&pg=PA472). In Watts S, Faingold C, Dunaway G, Crespo L (eds.). *Brody's Human Pharmacology - E-Book*. Elsevier Health Sciences. pp. 472–. [ISBN](/source/ISBN_(identifier)) [978-0-323-07575-6](https://en.wikipedia.org/wiki/Special:BookSources/978-0-323-07575-6). The histamine receptor antagonist cimetidine, used to decrease gastric acid secretion in treatment of peptic ulcer disease and esophagitis (see Chapter 14), also acts as an antiandrogen. Thus it has been reported to produce gynecomastia when given in large doses, such as those used in the treatment of patients with Zollinger-Ellison syndrome. Gynecomastia occurs in less than 1% of patients treated with the doses used in peptic ulcer disease. Cimetidine interacts with ARs approximately 0.01% as effectively as testosterone and has been used with limited effectiveness to treat hirsutism in women.

1. **[^](#cite_ref-AltchekDeligdisch2003_55-0)** Copperman AB, Mukherjee T, Kase NG (4 September 2003). ["Polycystic Ovarian Syndrome"](https://books.google.com/books?id=vds_TQpTIhoC&pg=PA351). In Altchek A, Deligdisch L, Kase N (eds.). *Diagnosis and Management of Ovarian Disorders*. Academic Press. pp. 351–. [ISBN](/source/ISBN_(identifier)) [978-0-08-049451-7](https://en.wikipedia.org/wiki/Special:BookSources/978-0-08-049451-7). Cimetidine is a weak androgen receptor antagonist. A controlled clinical study has not found cimetidine to be effective in the treatment of hyperandrogenism.[123, 124] 5.

1. ^ [***a***](#cite_ref-PreglerDeCherney2002_56-0) [***b***](#cite_ref-PreglerDeCherney2002_56-1) Pregler JP, DeCherney AH (2002). ["Approach to the Patient with Hirsutism"](https://books.google.com/books?id=zC99_it1C5YC&pg=PA595). *Women's Health: Principles and Clinical Practice*. PMPH-USA. pp. 595–. [ISBN](/source/ISBN_(identifier)) [978-1-55009-170-0](https://en.wikipedia.org/wiki/Special:BookSources/978-1-55009-170-0). Cimetidine is a histamine type 2 blocker, which also binds to the androgen receptor to inhibit its function." However, this antiandrogen activity of cimetidine is weak, and the clinical benefit of its use in women with hirsutism is minimal. Thus, this drug is not recommended for the treatment of hyperandrogenism.

1. ^ [***a***](#cite_ref-pmid20082945_57-0) [***b***](#cite_ref-pmid20082945_57-1) Katsambas AD, Dessinioti C (2010). "Hormonal therapy for acne: why not as first line therapy? facts and controversies". *Clinics in Dermatology*. **28** (1): 17–23. [doi](/source/Doi_(identifier)):[10.1016/j.clindermatol.2009.03.006](https://doi.org/10.1016%2Fj.clindermatol.2009.03.006). [PMID](/source/PMID_(identifier)) [20082945](https://pubmed.ncbi.nlm.nih.gov/20082945).

1. **[^](#cite_ref-58)** Scheinfeld N (March 2003). "Cimetidine: a review of the recent developments and reports in cutaneous medicine". *Dermatology Online Journal*. **9** (2): 4. [doi](/source/Doi_(identifier)):[10.5070/D33S15Q645](https://doi.org/10.5070%2FD33S15Q645). [PMID](/source/PMID_(identifier)) [12639457](https://pubmed.ncbi.nlm.nih.gov/12639457).

1. ^ [***a***](#cite_ref-ACS_Landmarks_59-0) [***b***](#cite_ref-ACS_Landmarks_59-1) [***c***](#cite_ref-ACS_Landmarks_59-2) ["Tagamet: Discovery of Histamine H2-receptor Antagonists"](http://portal.acs.org/portal/PublicWebSite/education/whatischemistry/landmarks/cimetidinetagamet/). *National Historic Chemical Landmarks*. American Chemical Society. Retrieved 25 June 2012.{{[cite web](https://en.wikipedia.org/wiki/Template:Cite_web)}}: CS1 maint: deprecated archival service ([link](https://en.wikipedia.org/wiki/Category:CS1_maint:_deprecated_archival_service))

1. ^ [***a***](#cite_ref-Freemantle_60-0) [***b***](#cite_ref-Freemantle_60-1) Fremantle M. ["Tagamet"](http://pubs.acs.org/cen/coverstory/83/8325/8325tagamet.html). *Chemical and Engineering news*. Retrieved 1 July 2013.

1. **[^](#cite_ref-Broome_1996_61-0)** Broome H (29 September 1996). ["Drug Story"](https://www.latimes.com/archives/la-xpm-1996-09-29-tm-48916-story.html). *Los Angeles Times*. Retrieved 11 February 2026.

1. **[^](#cite_ref-62)** ["G.R. No. 121267 October 23, 2001 - SMITH KLINE & FRENCH LABORATORIES v. COURT OF APPEALS, ET AL.:"](https://www.chanrobles.com/cralaw/2001octoberdecisions.php?id=1097).

1. **[^](#cite_ref-63)** Fit KE, Williams PC (July 2007). "Use of histamine2-antagonists for the treatment of verruca vulgaris". *The Annals of Pharmacotherapy*. **41** (7): 1222–1226. [doi](/source/Doi_(identifier)):[10.1345/aph.1H616](https://doi.org/10.1345%2Faph.1H616). [PMID](/source/PMID_(identifier)) [17535844](https://pubmed.ncbi.nlm.nih.gov/17535844). [S2CID](/source/S2CID_(identifier)) [19769702](https://api.semanticscholar.org/CorpusID:19769702).

1. **[^](#cite_ref-64)** Glass AT, Solomon BA (June 1996). "Cimetidine therapy for recalcitrant warts in adults". *Archives of Dermatology*. **132** (6): 680–682. [doi](/source/Doi_(identifier)):[10.1001/archderm.1996.03890300108014](https://doi.org/10.1001%2Farchderm.1996.03890300108014). [PMID](/source/PMID_(identifier)) [8651718](https://pubmed.ncbi.nlm.nih.gov/8651718).

1. **[^](#cite_ref-65)** 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): 533–534. [doi](/source/Doi_(identifier)):[10.1001/archderm.133.4.533](https://doi.org/10.1001%2Farchderm.133.4.533). [PMID](/source/PMID_(identifier)) [9126017](https://pubmed.ncbi.nlm.nih.gov/9126017).

1. **[^](#cite_ref-66)** Deva S, Jameson M (August 2012). ["Histamine type 2 receptor antagonists as adjuvant treatment for resected colorectal cancer"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11627143). *The Cochrane Database of Systematic Reviews*. **2012** (8) CD007814. [doi](/source/Doi_(identifier)):[10.1002/14651858.CD007814.pub2](https://doi.org/10.1002%2F14651858.CD007814.pub2). [PMC](/source/PMC_(identifier)) [11627143](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11627143). [PMID](/source/PMID_(identifier)) [22895966](https://pubmed.ncbi.nlm.nih.gov/22895966).

1. **[^](#cite_ref-67)** Whatley SD, Badminton MN (2013). Adam MP, Everman DB, Mirzaa GM, Pagon RA, Wallace SE, Bean LJ, Gripp KW, Amemiya A, Bird TD, Ledbetter N, Mefford HC, Smith RJ, Stephens K (eds.). [*Acute Intermittent Porphyria*](https://www.ncbi.nlm.nih.gov/books/NBK1193/). University of Washington, Seattle. [PMID](/source/PMID_(identifier)) [20301372](https://pubmed.ncbi.nlm.nih.gov/20301372).

1. **[^](#cite_ref-68)** Schug SA, Palmer GM, Scott DA, Halliwell R, Trinca J, et al. (APM:SE Working Group of the Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine) (2015). [*Acute Pain Management: Scientific Evidence*](https://web.archive.org/web/20190731120330/http://fpm.anzca.edu.au/documents/apmse4_2015_final) (4th ed.). Melbourne, Australia: Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. p. 316. [ISBN](/source/ISBN_(identifier)) [978-0-9873236-6-8](https://en.wikipedia.org/wiki/Special:BookSources/978-0-9873236-6-8). Archived from [the original](http://fpm.anzca.edu.au/documents/apmse4_2015_final) (PDF) on 31 July 2019. Retrieved 7 September 2017.

1. **[^](#cite_ref-ped-rheum_69-0)** Vanoni F, Theodoropoulou K, Hofer M (June 2016). ["PFAPA syndrome: a review on treatment and outcome"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4924332). *Pediatric Rheumatology Online Journal*. **14** (1) 38. [doi](/source/Doi_(identifier)):[10.1186/s12969-016-0101-9](https://doi.org/10.1186%2Fs12969-016-0101-9). [PMC](/source/PMC_(identifier)) [4924332](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4924332). [PMID](/source/PMID_(identifier)) [27349388](https://pubmed.ncbi.nlm.nih.gov/27349388).

1. **[^](#cite_ref-70)** Le Traon G, Burgaud S, Horspool LJ (June 2009). "Pharmacokinetics of cimetidine in dogs after oral administration of cimetidine tablets". *Journal of Veterinary Pharmacology and Therapeutics*. **32** (3): 213–218. [doi](/source/Doi_(identifier)):[10.1111/j.1365-2885.2008.01026.x](https://doi.org/10.1111%2Fj.1365-2885.2008.01026.x). [PMID](/source/PMID_(identifier)) [19646084](https://pubmed.ncbi.nlm.nih.gov/19646084).

## External links

- Media related to [Cimetidine](https://commons.wikimedia.org/wiki/Category:Cimetidine) at Wikimedia Commons

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") Anaprazole Azeloprazole Dexlansoprazole Dexrabeprazole Esomeprazole Ilaprazole Lansoprazole Omeprazole# Pantoprazole Picoprazole Rabeprazole Tenatoprazole Timoprazole Potassium-competitive acid blockers ("-prazan") Fexuprazan Keverprazan Linaprazan Revaprazan Soraprazan Tegoprazan Vonoprazan Zastaprazan Others Aceglutamide aluminum Acetoxolone Alginic acid Arbaclofen placarbil Bismuth subcitrate Carbenoxolone Cetraxate Gefarnate Irsogladine Lesogaberan Pirenzepine Proglumide Rebamipide Sucralfate Sulglicotide Telenzepine Teprenone Troxipide Zinc L-carnosine Zolimidine Combinations Bismuth subcitrate/metronidazole/tetracycline Omeprazole/amoxicillin/rifabutin Vonoprazan/amoxicillin Vonoprazan/amoxicillin/clarithromycin See also: Helicobacter pylori eradication protocols #WHO-EM ‡Withdrawn from market Clinical trials: †Phase III §Never to phase III

v t e Histamine receptor modulators H1 Agonists 2-Pyridylethylamine Betahistine Histamine HTMT L-Histidine UR-AK49 Antagonists First-generation (sedating): 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 LY-2624803 (HY-10275) Meclozine Medrylamine Mepyramine (pyrilamine) Mequitazine Methafurylene Methapyrilene Methdilazine Moxastine NBI-75043 Orphenadrine Oxatomide Oxomemazine Perlapine Phenindamine Pheniramine Phenyltoloxamine Pimethixene Piperoxan Pipoxizine Promethazine Propiomazine Pyrrobutamine Talastine Thenalidine Thenyldiamine Thiazinamium Thonzylamine Tolpropamine Tripelennamine Triprolidine Second/third-generation (non-sedating): 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, brilaroxazine, clozapine, iloperidone, olanzapine, paliperidone, quetiapine, risperidone, ziprasidone, zotepine) Phenylpiperazine antidepressants (e.g., hydroxynefazodone, nefazodone, trazodone, triazoledione) 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: Azanator Belarizine Elbanizine Flotrenizine GSK1004723 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 BP 2.94 Cipralisant (GT-2331) GT-2203 (VUF-5296) Histamine Imetit Immepip Immethridine (BP-1-5375) L-Histidine Methimepip Proxyfan SCH-50971 VUF-5297 Antagonists A-349821 A-423579 ABT-239 ABT-652 ALTO-203 AZD5213 Bavisant Betahistine Burimamide Ciproxifan Clobenpropit Conessine Contilisant Enerisant GSK-189254 Impentamine Iodophenpropit Irdabisant JNJ-5207852 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 Seliforant Thioperamide Toreforant VUF-6002 See also Receptor/signaling modulators Monoamine metabolism modulators Monoamine reuptake inhibitors

v t e Androgen receptor modulators ARTooltip Androgen receptor Agonists Testosterone derivatives: 4-Androstenediol 4-Dehydroepiandrosterone (4-DHEA) 4-Hydroxytestosterone 4,17α-Dimethyltestosterone 5-Androstenedione 11-Ketotestosterone 11β-Hydroxyandrostenedione Adrenosterone (11-ketoandrostenedione, 11-oxoandrostenedione) Androstenediol (5-androstenediol) Androstenediol 3β-acetate Androstenediol 17β-acetate Androstenediol diacetate Androstenediol dipropionate Androstenedione (4-androstenedione) Atamestane Boldenone Boldenone undecylenate Boldione (1,4-androstadienedione) Clostebol Clostebol acetate Clostebol caproate Clostebol propionate Cloxotestosterone Cloxotestosterone acetate Dehydroandrosterone DHEA (androstenolone, prasterone; 5-DHEA) DHEA enanthate (prasterone enanthate) DHEA sulfate Exemestane Formestane Plomestane Quinbolone Silandrone Testosterone# (+dutasteride) Testosterone esters Polytestosterone phloretin phosphate 5α-Dihydrotestosterone derivatives: 1-Androstenediol 1-Androstenedione 1-Androsterone (1-andro, 1-DHEA) 1-Testosterone 3α-Androstanediol 5α-Androst-2-en-17-one 7β-Hydroxyepiandrosterone 11-Ketodihydrotestosterone Androsterone Bolazine Bolazine capronate Dihydroethyltestosterone Dihydrofluoxymesterone Dihydromethylandrostenediol Dihydrotestosterone (DHT) (androstanolone, stanolone) Dihydrotestosterone esters Drostanolone Drostanolone propionate Epiandrosterone Epitiostanol Mepitiostane Mesabolone Mesterolone Mesterolone cipionate Methyldiazinol Nisterime Nisterime acetate Prostanozol Stenbolone Stenbolone acetate Testifenon (testiphenon, testiphenone) 19-Nortestosterone derivatives: 7α-Methyl-19-norandrostenedione (MENT dione, trestione) 11β-Methyl-19-nortestosterone 11β-Methyl-19-nortestosterone dodecylcarbonate 19-Nor-5-androstenediol 19-Nor-5-androstenedione 19-Nordehydroepiandrosterone Bolandiol Bolandiol dipropionate Bolandione (19-nor-4-androstenedione) Bolmantalate (nandrolone adamantoate) Dienedione Dienolone Dimethandrolone Dimethandrolone buciclate Dimethandrolone dodecylcarbonate Dimethandrolone undecanoate LS-1727 (nandrolone 17β-N-(2-chloroethyl)-N-nitrosocarbamate) Methoxydienone (methoxygonadiene) Nandrolone Nandrolone esters Norclostebol Norclostebol acetate Normethandrone (methylestrenolone, normethisterone) Oxabolone Oxabolone cipionate (oxabolone cypionate) Trenbolone Trenbolone acetate Trenbolone enanthate Trenbolone hexahydrobenzylcarbonate Trenbolone undecanoate Trendione Trestolone (MENT) Trestolone acetate Trestolone enanthate 5α-Dihydro-19-nortestosterone derivatives: 5α-Dihydronandrolone 5α-Dihydrotrestolone 19-Norandrosterone 17α-Alkylated testosterone derivatives: Bolasterone Calusterone Chlorodehydromethylandrostenediol (CDMA) Chlorodehydromethyltestosterone (CDMT) Chloromethylandrostenediol (CMA) Enestebol Ethyltestosterone Fluoxymesterone Formebolone Hydroxystenozole Metandienone (methandrostenolone) Methandriol (methylandrostenediol) Methandriol bisenanthoyl acetate Methandriol diacetate Methandriol dipropionate Methandriol propionate Methylclostebol (chloromethyltestosterone) Methyltestosterone (+esterified estrogens) Methyltestosterone 3-hexyl ether Oxymesterone Penmesterol Tiomesterone 17α-Alkylated 5α-dihydrotestosterone derivatives: Androisoxazole Desoxymethyltestosterone Furazabol Mebolazine (dimethazine) Mestanolone Metenolone Metenolone acetate Metenolone enanthate Methasterone Methyl-1-testosterone Methylepitiostanol Methylstenbolone Oxandrolone Oxymetholone Stanozolol 17α-Alkylated 19-nortestosterone derivatives: Bolenol Dimethyldienolone Dimethyltrienolone Ethyldienolone Ethylestrenol Methyldienolone Methylhydroxynandrolone (MOHN, MHN) Metribolone Mibolerone Norboletone Norethandrolone Propetandrol RU-2309 Tetrahydrogestrinone 17α-Alkylated 5α-dihydro-19-nortestosterone derivatives: 5α-Dihydronorethandrolone 5α-Dihydronormethandrone 17α-Vinyltestosterone derivatives: Norvinisterone (vinylnortestosterone) 17α-Vinyl-19-nortestosterone derivatives: Vinyltestosterone 17α-Ethynyltestosterone derivatives: Danazol Ethinylandrostenediol Ethandrostate Ethisterone (ethynyltestosterone) 5α-Dihydro-17α-ethynyltestosterone derivatives: 17α-Ethynyl-3α-androstanediol 17α-Ethynyl-3β-androstanediol Dihydroethisterone 17α-Ethynyl-19-nortestosterone derivatives: Δ4-Tibolone Desogestrel Etonogestrel Etynodiol Etynodiol diacetate Gestodene Gestrinone Levonorgestrel Levonorgestrel esters (e.g., levonorgestrel butanoate) Lynestrenol Lynestrenol phenylpropionate Norethisterone Norethisterone esters (e.g., norethisterone acetate, norethisterone enanthate) Norgestrel Norgestrienone Quingestanol Quingestanol acetate Tibolone 5α-Dihydro-17α-ethynyl-19-nortestosterone derivatives: 5α-Dihydrolevonorgestrel 5α-Dihydronorethisterone Progesterone derivatives: 6α-Methylprogesterone Medroxyprogesterone acetate Megestrol acetate Others/unsorted: 3-Keto-5α-abiraterone 5α-Androstane Alternariol Cl-4AS-1 Drupanol Trilostane ZM-182345 SARMsTooltip Selective androgen receptor modulator Nonsteroidal: 198RL26 ACP-105 AC-262,536 Acetothiolutamide Acetoxolutamide Andarine (acetamidoxolutamide, androxolutamide, GTx-007, S-4) BMS-564,929 DTIB Enobosarm (ostarine, MK-2866, GTx-024, S-22) FTBU-1 GLPG-0492 GSK2881078 GSK-4336A GSK-8698 LG121071 (LGD-121071) LGD-2226 LGD-2941 (LGD-122941) LGD-3303 LGD-4033 LY305 JNJ-26146900 JNJ-28330835 JNJ-37654032 OPK-88004 (LY-2452473, TT-701) ORM-11984 PF-06260414 R-1 RU-59063 S-1 S-23 S-40503 S-101479 Vosilasarm Steroidal: EM-9017 MK-0773 S42 TFM-4AS-1 YK-11 Antagonists Steroidal: 7α-Thioprogesterone 7α-Thiospironolactone 7α-Thiomethylspironolactone 11α-Hydroxyprogesterone 15β-Hydroxycyproterone acetate Abiraterone Abiraterone acetate Allyltestosterone Benorterone BOMT Canrenoic acid Canrenone Chlormadinone acetate Clascoterone Clometerone Cyproheptadine Cyproterone Cyproterone acetate Delanterone Delmadinone acetate Dicirenone Dienogest Drospirenone DU-41165 Edogestrone EM-4350 EM-5854 EM-5855 EM-6537 Epitestosterone Galeterone Guggulsterone Ludaterone Medrogestone Megestrol acetate Mespirenone Metogest Mexrenone Mifepristone Nomegestrol acetate Nordinone Osaterone Osaterone acetate Oxendolone Potassium canrenoate Promegestone Prorenone Rosterolone RU-15328 SC-5233 (spirolactone) Spironolactone Spirorenone Spiroxasone Topterone Trimegestone Trimethyltrienolone (R-2956) Zanoterone Nonsteroidal: 5N-Bicalutamide AA560 Antarlides Arabilin Apalutamide Atraric acid AZD-3514 Bakuchiol Bavdegalutamide BAY-1024767 Bicalutamide Bisphenols (e.g., BADGE, BFDGE, bisphenol A, bisphenol F, bisphenol S) BMS-501949 BMS-570511 BMS-641988 CH5137291 Cimetidine Cioteronel Cyanonilutamide Darolutamide DDT (via metabolite p,p’-DDE) Dieldrin DIMP Endosulfan Enzalutamide EPI-001 Fenarimol Flutamide Hydroxyflutamide Inocoterone Inocoterone acetate Ketoconazole Ketodarolutamide Lavender oil LG-105 LG-120907 LGD-1331 Linuron Masofaniten Methiocarb N-Butylbenzenesulfonamide N-Desmethylapalutamide N-Desmethylenzalutamide Nilutamide ONC1-13B Pentomone PF-998425 Phenothrin Prochloraz Procymidone Proxalutamide Pyrilutamide Ralaniten (EPI-002) Ralaniten acetate (EPI-506) RD-162 Rezvilutamide Ro 2-7239 Ro 5-2537 RU-22930 RU-56187 RU-57073 RU-58642 RU-58841 Seviteronel Thalidomide Topilutamide (fluridil) Valproic acid Vinclozolin YM-580 YM-92088 YM-175735 GPRC6A Agonists Cations (incl. aluminium, calcium, gadolinium, magnesium, strontium, zinc) Dehydroandrosterone Dihydrotestosterone Estradiol L-α-Amino acids (incl. L-arginine, L-lysine, L-ornithine) Osteocalcin SHBGTooltip Sex hormone-binding globulin Testosterone See also Receptor/signaling modulators Androgens and antiandrogens Estrogen receptor modulators Progesterone receptor modulators List of androgens and anabolic steroids

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