Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (720 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A histamine congener, it competitively inhibits histamine binding to histamine H2 receptors. Cimetidine has a range of pharmacological actions. It inhibits gastric acid secretion, as well as pepsin and gastrin output.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: N-Cyano-N'-methyl-N''-(2-(((5-methyl-1H-imidazol-4-yl)methyl)thio)ethyl)guanidine; Altramet; Biomet; Biomet400; Tagamet; SK and F-92334; SK and F92334; SK and F 92334.
Where it fits in the MeSH classification
- Broader topics
- Guanidines; Imidazoles
Related concepts
- Histamine
- Receptors
- Gastric Acid
- Pepsin
- Gastrin
Research landscape
PubMed indexes 9,357 records tagged with the MeSH heading “Cimetidine” (counts retrieved 2026-10-31). 133 of them (1.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 8,153 records.
Reviews account for 537 records (5.7%) and meta-analyses for 24. Randomized controlled trials number 1,034 (11.1%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 8,153 |
| 2000-2009 | 744 |
| 2010-2019 | 327 |
| 2020 onward | 133 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 537 | 5.7% |
| Meta-analyses | 24 | 0.3% |
| Randomized controlled trials | 1,034 | 11.1% |
Method: PubMed query "Cimetidine"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Histamine, mast cells and tumour cell proliferation in breast cancer: does preoperative cimetidine administration have an effect? | 2000 | Randomized controlled trial Design not recorded in structured metadata | 49 | cc by PMID 10638985 · DOI · PMC2363200 |
| Ranitidine and cimetidine differ in their in vitro and in vivo effects on human colonic cancer growth | 1996 | Research article Design not recorded in structured metadata | 33 | cc by PMID 8611398 · DOI · PMC2074256 |
| Anti-neoplastic action of Cimetidine/Vitamin C on histamine and the PI3K/AKT/mTOR pathway in Ehrlich breast cancer | 2022 | Research article Design not recorded in structured metadata | 22 | cc by PMID 35798765 · DOI · PMC9262990 |
| A rare case of hyperuricemia and acute kidney injury in a kidney transplant patient | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41081896 · DOI · PMC12727850 |
Histamine, mast cells and tumour cell proliferation in breast cancer: does preoperative cimetidine administration have an effect? [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Endogenous histamine has been shown to effect growth mechanisms in experimental mammary carcinomas via H2 membrane receptors (Cricco et al, 1994).
- Closing excerpt
- Tumour cell proliferation correlated well with other prognostic indicators such as grade and differentiation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (201 words)
Endogenous histamine has been shown to effect growth mechanisms in experimental mammary carcinomas via H2 membrane receptors (Cricco et al, 1994). Both H1 and H2 binding sites are present in human mammary glands but only 75% malignant carcinomas express H2 receptors (Lemos et al, 1995). The presence of mast cells around tumour tissue raises questions concerning the source of histamine in breast tumour tissue. While cimetidine, an H2 antagonist, has been shown to influence the presence of tumour infiltrating lymphocytes (TIL) in colorectal cancer (Adams and Morris, 1994, 1997) that was not found to be the case in breast cancer (Ng et al, 1995). In recent studies tumour cell proliferation, as measured by Ki-67 antibody labelling, has been seen as an additional prognostic indicator in breast cancer (Railo et al, 1993, 1997; Ferno, 1998; Schauer et al, 1998). We investigated the possibility that cimetidine may influence tumour proliferation by blocking the growth-promoting effects of histamine. No relationship between preoperative cimetidine administration and tumour cell proliferation was seen overall. A weak correlation was seen between tissue histamine content and mast cell count which was not influenced by cimetidine. Tumour cell proliferation correlated well with other prognostic indicators such as grade and differentiation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 10638985 · DOI · PMC2363200
Ranitidine and cimetidine differ in their in vitro and in vivo effects on human colonic cancer growth [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Histamine has recently been shown to be a growth factor for some gastric and colorectal cancer cells.
- Closing excerpt
- Ranitidine had no effect on in vitro cell proliferation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (145 words)
Histamine has recently been shown to be a growth factor for some gastric and colorectal cancer cells. Previous studies have shown that cimetidine blocks in vitro and in vivo histamine-stimulated growth and cAMP release from the human colonic cancer cell line, C170. In this study, ranitidine, another H2 receptor antagonist, did not affect either basal or histamine-stimulated in vitro proliferation of C170, and failed to prevent cAMP release in vitro. Ranitidine did not inhibit in vivo growth of C170 at a dose of 1, 10, 25, 50 or 100 mg/kg, in contrast to 50 mg/kg/day cimetidine, which produced 39.3% inhibition of tumour volume (p<0.01) after 23 days' treatment. Ranitidine did not inhibit in vivo histamine-stimulated growth of C170 cells . LIM2412, another colonic cancer cell line, was significantly stimulated by both cimetidine and ranitidine in vivo. Ranitidine had no effect on in vitro cell proliferation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 8611398 · DOI · PMC2074256
Anti-neoplastic action of Cimetidine/Vitamin C on histamine and the PI3K/AKT/mTOR pathway in Ehrlich breast cancer [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The main focus of our study is to assess the anti-cancer activity of cimetidine and vitamin C via combating the tumor supportive role of mast cell mediators (histamine, VEGF, and TNF-α) within the tumor microenvironment and their effect on the protein kinase A(PKA)/insulin receptor substrate-1(IRS-1)/phosphatidylinositol-3-kinase (PI3K)/serine/threonine kinase-1 (AKT)/mammalian target of rapamycin (mTOR) cue in Ehrlich induced breast cancer in mice.
- Closing excerpt
- Finally, we concluded that the synergistic combination provided a promising anti-neoplastic effect via reducing the angiogenesis, oxidative stress, increasing apoptosis,as well as inhibiting the activation of PI3K/AKT/mTOR cue, and suggesting its use as a treatment option for breast cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (260 words)
The main focus of our study is to assess the anti-cancer activity of cimetidine and vitamin C via combating the tumor supportive role of mast cell mediators (histamine, VEGF, and TNF-α) within the tumor microenvironment and their effect on the protein kinase A(PKA)/insulin receptor substrate-1(IRS-1)/phosphatidylinositol-3-kinase (PI3K)/serine/threonine kinase-1 (AKT)/mammalian target of rapamycin (mTOR) cue in Ehrlich induced breast cancer in mice. In vitro study was carried out to evaluate the anti-proliferative activity and combination index (CI) of the combined drugs. Moreover, the Ehrlich model was induced in mice via subcutaneous injection of Ehrlich ascites carcinoma cells (EAC) in the mammary fat pad, and then they were left for 9 days to develop obvious solid breast tumor. The combination therapy possessed the best anti-proliferative effect, and a CI < 1 in the MCF7 cell line indicates a synergistic type of drug interaction. Regarding the in vivo study, the combination abated the elevation in the tumor volume, and serum tumor marker carcinoembryonic antigen (CEA) level. The serum vascular endothelial growth factor (VEGF) level and immunohistochemical staining for CD34 as markers of angiogenesis were mitigated. Additionally, it reverted the state of oxidative stress and inflammation. Meanwhile, it caused an increment in apoptosis, which prevents tumor survival. Furthermore, it tackled the elevated histamine and cyclic adenosine monophosphate (cAMP) levels, preventing the activation of the (PKA/IRS-1/PI3K/AKT/mTOR) cue. Finally, we concluded that the synergistic combination provided a promising anti-neoplastic effect via reducing the angiogenesis, oxidative stress, increasing apoptosis,as well as inhibiting the activation of PI3K/AKT/mTOR cue, and suggesting its use as a treatment option for breast cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35798765 · DOI · PMC9262990
A rare case of hyperuricemia and acute kidney injury in a kidney transplant patient [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Hyperuricemia is a common finding in kidney transplant recipients, often associated with calcineurin inhibitor or diuretic use, obesity, metabolic syndrome, dyslipidemia, high purine intake, and reduced allograft function.
- Closing excerpt
- This case highlights the significance of monitoring uric acid levels post-transplant and the importance of attention to potential drug interactions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (114 words)
Hyperuricemia is a common finding in kidney transplant recipients, often associated with calcineurin inhibitor or diuretic use, obesity, metabolic syndrome, dyslipidemia, high purine intake, and reduced allograft function. We report a unique case of hyperuricemia leading to acute kidney injury associated with the use of cimetidine for treatment of mosaic warts in a 12-year-old female pediatric kidney transplant patient. With the reduction in the patient's serum uric acid levels, there was concurrent marked improvement in her eGFR. Subsequently, her uric acid remained low, suggesting the cessation of cimetidine maintained her baseline uric acid level. This case highlights the significance of monitoring uric acid levels post-transplant and the importance of attention to potential drug interactions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41081896 · DOI · PMC12727850
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Drug interactions with cimetidine [5]
- Research article Pharmacokinetic interactions of cimetidine 1987 [6]
- Research article Clinical pharmacokinetics of cimetidine [7]
- Research article Cimetidine: a review of its pharmacological properties and therapeutic efficacy in peptic ulcer disease [8]
- Research article Drug therapy: Cimetidine [9]
- Research article Cimetidine: II. Adverse reactions and patterns of use [10]
References
- Bowrey PF, King J, Magarey C, Schwartz P, Marr P, Bolton E, et al.. Histamine, mast cells and tumour cell proliferation in breast cancer: does preoperative cimetidine administration have an effect?. . 2000. PMID 10638985 · DOI · PMC2363200
- Lawson JA, Adams WJ, Morris DL. Ranitidine and cimetidine differ in their in vitro and in vivo effects on human colonic cancer growth. . 1996. PMID 8611398 · DOI · PMC2074256
- Ibrahim SSA, El-Aal SAA, Reda AM, Achy SE, Shahine Y. Anti-neoplastic action of Cimetidine/Vitamin C on histamine and the PI3K/AKT/mTOR pathway in Ehrlich breast cancer. . 2022. PMID 35798765 · DOI · PMC9262990
- Nidhiry AS, Puliyanda D, Blifeld C, Pizzo H. A rare case of hyperuricemia and acute kidney injury in a kidney transplant patient. . 2026. PMID 41081896 · DOI · PMC12727850
- Somogyi A, Gugler R. Drug interactions with cimetidine. Clin Pharmacokinet. 1982. PMID 7042171 · DOI
- Somogyi A, Muirhead M. Pharmacokinetic interactions of cimetidine 1987. Clin Pharmacokinet. 1987. PMID 3301148 · DOI
- Somogyi A, Gugler R. Clinical pharmacokinetics of cimetidine. Clin Pharmacokinet. 1983. PMID 6418428 · DOI
- Brogden RN, Heel RC, Speight TM, Avery GS. Cimetidine: a review of its pharmacological properties and therapeutic efficacy in peptic ulcer disease. Drugs. 1978. PMID 342231 · DOI
- Finkelstein W, Isselbacher KJ. Drug therapy: Cimetidine. N Engl J Med. 1978. PMID 357977 · DOI
- Freston JW. Cimetidine: II. Adverse reactions and patterns of use. Ann Intern Med. 1982. PMID 6753681 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.