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: 3 complete abstracts (600 words), 9 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
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
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: Antimetabolite.
Where it fits in the MeSH classification
- Broader topics
- Molecular Mechanisms of Pharmacological Action; Noxae
- Narrower topics
- Antimetabolites, Antineoplastic; Hypolipidemic Agents
Research landscape
PubMed indexes 98,815 records tagged with the MeSH heading “Antimetabolites” (counts retrieved 2026-10-29). 14,072 of them (14.2%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 34,199 records.
Reviews account for 18,205 records (18.4%) and meta-analyses for 2,097. Randomized controlled trials number 7,808 (7.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 18,958 |
| 2000-2009 | 31,586 |
| 2010-2019 | 34,199 |
| 2020 onward | 14,072 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 18,205 | 18.4% |
| Meta-analyses | 2,097 | 2.1% |
| Randomized controlled trials | 7,808 | 7.9% |
Method: PubMed query "Antimetabolites"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in pharmacology
Drug evidence builds in layers: laboratory pharmacology describes how a compound acts, pharmacokinetic studies describe how the body handles it, and randomized trials test whether it helps and what harms it causes. Post-marketing surveillance and observational studies reveal rarer adverse effects but cannot prove causation. This page is educational and is not a recommendation to start, stop or change any medicine; decisions about treatment belong with a qualified clinician.
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 |
|---|---|---|---|---|
| Synergizing hypomethylating agents with off-the-shelf CD70-targeted chimeric antigen receptor-engineered natural killer T cells for the treatment of acute myeloid leukemia | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41888396 · DOI · PMC13149322 |
| APOE genotype and the effect of statins on lipid outcomes: A meta-analysis | 2026 | Meta-analysis Design not recorded in structured metadata | 6 | cc by PMID 41702864 · DOI · PMC13122289 |
| Efficacy and Safety of Statins in MASLD and Other Chronic Liver Diseases | 2026 | Review article Design not recorded in structured metadata | 5 | cc by PMID 41718130 · DOI · PMC12922148 |
Synergizing hypomethylating agents with off-the-shelf CD70-targeted chimeric antigen receptor-engineered natural killer T cells for the treatment of acute myeloid leukemia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by the uncontrolled expansion of undifferentiated myeloid precursors in the bone marrow.
- Closing excerpt
- These findings highlight AlloCAR70-NKT cells as a safe and powerful off-the-shelf immunotherapy that can synergize with HMAs to improve treatment outcomes for patients with AML.
- 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 (193 words)
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by the uncontrolled expansion of undifferentiated myeloid precursors in the bone marrow. Hypomethylating agents (HMAs) such as azacitidine and decitabine can reverse abnormal DNA methylation, promote leukemic cell differentiation, and enhance immune recognition, yet relapse and therapeutic resistance remain major challenges. In this study, we found that long-term, low-dose HMA treatment upregulated CD70, NK receptor ligands, and CD1d on AML tumor cells, rendering them more susceptible to chimeric antigen receptor (CAR)-engineered invariant natural killer T (CAR-NKT) cell-mediated cytotoxicity. To exploit these features, we generated two types of CD70-targeting CAR-NKT cells: cord blood hematopoietic stem and progenitor cell (HSPC)-derived allogeneic CAR70-NKT (AlloCAR70-NKT) cells and peripheral blood mononuclear cell (PBMC)-derived CAR70-NKT (PBMCCAR70-NKT) cells. Both CAR70-NKT cell products exhibited potent cytotoxicity against AML cells and synergized with HMAs, while AlloCAR70-NKT cells demonstrated superior antitumor efficacy, multi-target recognition, and sustained expansion. In multiple xenograft models, AlloCAR70-NKT cells effectively killed AML tumors without inducing graft-versus-host disease, cytokine release syndrome, or long-term organ toxicity. These findings highlight AlloCAR70-NKT cells as a safe and powerful off-the-shelf immunotherapy that can synergize with HMAs to improve treatment outcomes for patients with AML.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41888396 · DOI · PMC13149322
APOE genotype and the effect of statins on lipid outcomes: A meta-analysis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- AimAPOE genotype may affect statin therapy response.
- Closing excerpt
- ConclusionOur meta-analysis shows that APOE genotype may influence statin response, emphasizing the need to incorporate known genetic factors into personalized treatment regimens.
- 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 (233 words)
AimAPOE genotype may affect statin therapy response. We conducted a meta-analysis to update and quantify this association across various outcomes.MethodsWe searched seven databases (MEDLINE, Scopus, Web of Science, the Cochrane Library, APA PsycINFO, CINAHL Plus and ClinicalTrials.gov) on 9 May 2024. Screening and data extraction were performed by two reviewers and a machine learning tool (ASReview).ResultsFrom 4352 de-duplicated records, 52 studies were included in the meta-analysis. Biomarkers analysed included low-density lipoprotein cholesterol (LDLC), total cholesterol (TC), triglycerides (TG) and high-density lipoprotein cholesterol (HDLC). Compared to ε3 carriers, ε2 carriers showed greater reductions in LDLC in response to statin treatment (mean difference in percentage change: -2.98%, 95% CI: -5.88% to -0.08%) and similar reductions in TC (-2.73%, -5.62% to 0.16%), and TG (-4.95%, -11.93% to 2.04%) with no significant difference in HDLC (-0.09%, -3.10% to 2.91%). After adjusting for publication bias, ε4 carriers showed less pronounced statin effects, with smaller reductions in LDLC (mean difference: 10.04%, 6.04% to 14.04%), TC (8.99%, 5.08% to 12.90%) and TG (8.24%, 2.15% to 14.33%), along with a smaller increase in HDLC (-10.08%, -15.30% to -4.85%) compared to ε3 carriers. Study quality was unclear, and heterogeneity (partly explained by sex and Familial hypercholesterolemia) was high, especially for the percentage changes. A stronger genotype effect was seen in males.ConclusionOur meta-analysis shows that APOE genotype may influence statin response, emphasizing the need to incorporate known genetic factors into personalized treatment regimens.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41702864 · DOI · PMC13122289
Efficacy and Safety of Statins in MASLD and Other Chronic Liver Diseases [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease worldwide, with an estimated global prevalence of 38% in adults.
- Closing excerpt
- This comprehensive review aims to explore the evidence regarding the use of statin therapy for conventional, lipid-lowering indications in patients with MASLD and its potential benefits for the treatment of MASLD and its complications.
- 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 (174 words)
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease worldwide, with an estimated global prevalence of 38% in adults. MASLD confers a significant increase in morbidity and mortality due to its association with cardiovascular disease and progressive liver disease, including cirrhosis and hepatocellular carcinoma. Current treatment paradigms for MASLD are centred around lifestyle modification and weight loss, with a need for pharmacotherapeutic options. Given the strong relationship between MASLD and cardiovascular disease, there is an interest in evaluating the efficacy and safety of cardiovascular medications such as statins in liver disease. Statins are the most commonly prescribed lipid-lowering medication in the world, with an established role in reducing cardiovascular morbidity and mortality. Statins are currently under-prescribed in the MASLD patient population, yet there is growing interest in determining whether statins could be utilised to treat MASLD itself. This comprehensive review aims to explore the evidence regarding the use of statin therapy for conventional, lipid-lowering indications in patients with MASLD and its potential benefits for the treatment of MASLD and its complications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41718130 · DOI · PMC12922148
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 Prevalence of statin intolerance: a meta-analysis [4]
- Research article Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials [5]
- Research article Statin use and risk of dementia or Alzheimer's disease: a systematic review and meta-analysis of observational studies [6]
- Research article Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis [7]
- Research article Statin therapy and lipoprotein(a) levels: a systematic review and meta-analysis [8]
- Research article Cholesteryl ester transfer protein (CETP) as a drug target for cardiovascular disease [9]
References
- Li YR, Shen X, Chen Y, Zhu Y, Huang J, Oliai C, et al.. Synergizing hypomethylating agents with off-the-shelf CD70-targeted chimeric antigen receptor-engineered natural killer T cells for the treatment of acute myeloid leukemia. . 2026. PMID 41888396 · DOI · PMC13149322
- Asiimwe IG, Gebru T, Jorgensen AL, Pirmohamed M, Multimorbidity Mechanism and Therapeutics Research Collaborative. APOE genotype and the effect of statins on lipid outcomes: A meta-analysis. . 2026. PMID 41702864 · DOI · PMC13122289
- Commins I, Clayton-Chubb D, Janko N, Majeed A, Kemp W, Roberts SK. Efficacy and Safety of Statins in MASLD and Other Chronic Liver Diseases. . 2026. PMID 41718130 · DOI · PMC12922148
- Bytyçi I, Penson PE, Mikhailidis DP, Wong ND, Hernandez AV, Sahebkar A, et al.. Prevalence of statin intolerance: a meta-analysis. Eur Heart J. 2022. PMID 35169843 · DOI · PMC9757867
- Cholesterol Treatment Trialists' Collaboration. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials. Lancet. 2022. PMID 36049498 · DOI · PMC7613583
- Olmastroni E, Molari G, De Beni N, Colpani O, Galimberti F, Gazzotti M, et al.. Statin use and risk of dementia or Alzheimer's disease: a systematic review and meta-analysis of observational studies. Eur J Prev Cardiol. 2022. PMID 34871380 · DOI
- Cholesterol Treatment Trialists’ (CTT) Collaboration. Electronic address: ctt@ndph.ox.ac.uk, Cholesterol Treatment Trialists’ (CTT) Collaboration. Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis. Lancet Diabetes Endocrinol. 2024. PMID 38554713 · DOI · PMC7615958
- de Boer LM, Oorthuys AOJ, Wiegman A, Langendam MW, Kroon J, Spijker R, et al.. Statin therapy and lipoprotein(a) levels: a systematic review and meta-analysis. Eur J Prev Cardiol. 2022. PMID 34849724 · DOI
- Schmidt AF, Hunt NB, Gordillo-Marañón M, Charoen P, Drenos F, Kivimaki M, et al.. Cholesteryl ester transfer protein (CETP) as a drug target for cardiovascular disease. Nat Commun. 2021. PMID 34561430 · DOI · PMC8463530
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 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
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.