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 (664 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
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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: Inhibitors, Enzyme; Enzyme Inhibitor; Inhibitor, Enzyme.
Where it fits in the MeSH classification
- Broader topics
- Molecular Mechanisms of Pharmacological Action
- Narrower topics
- 5-Lipoxygenase-Activating Protein Inhibitors; Acetaldehyde Dehydrogenase Inhibitors; Adenosine Deaminase Inhibitors; Adenylyl Cyclase Inhibitors; Aromatic Amino Acid Decarboxylase Inhibitors; beta-Lactamase Inhibitors; Calcineurin Inhibitors; Carbonic Anhydrase Inhibitors; Catechol O-Methyltransferase Inhibitors; Cholinesterase Inhibitors; Cyclooxygenase Inhibitors; Cytochrome P-450 Enzyme Inhibitors; Folic Acid Antagonists; Gamma Secretase Inhibitors and Modulators
Research landscape
PubMed indexes 572,134 records tagged with the MeSH heading “Enzyme Inhibitors” (counts retrieved 2026-10-29). 99,121 of them (17.3%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 179,759 records.
Reviews account for 83,318 records (14.6%) and meta-analyses for 6,402. Randomized controlled trials number 22,069 (3.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 119,014 |
| 2000-2009 | 174,240 |
| 2010-2019 | 179,759 |
| 2020 onward | 99,121 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 83,318 | 14.6% |
| Meta-analyses | 6,402 | 1.1% |
| Randomized controlled trials | 22,069 | 3.9% |
Method: PubMed query "Enzyme Inhibitors"[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 |
|---|---|---|---|---|
| Nerandomilast is Associated With Altered Alveolar Epithelial Cell State Dynamics While Attenuating Fibrotic Remodeling in Pulmonary Fibrosis | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42827411 · DOI · PMC13633504 |
| CDK7, CDK9, or CDK11 inhibition reduces neutrophil-driven inflammation and tissue damage in experimental autoimmune models | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42823736 · DOI · PMC13628873 |
| The enzyme inhibitory activity of helminth-derived serine protease inhibitor rapidly establishes immune tolerance to ameliorate allergic diseases | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42702014 · DOI · PMC13556981 |
Nerandomilast is Associated With Altered Alveolar Epithelial Cell State Dynamics While Attenuating Fibrotic Remodeling in Pulmonary Fibrosis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Pulmonary fibrosis is a progressive and life-threatening lung disorder characterized by excessive fibrogenesis and impaired respiratory function.
- Closing excerpt
- Collectively, our findings suggest that nerandomilast attenuates fibrotic remodeling while modulating alveolar epithelial cell state dynamics, which may provide a possible cellular explanation for its clinical efficacy in patients with pulmonary fibrosis.
- 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 (170 words)
Pulmonary fibrosis is a progressive and life-threatening lung disorder characterized by excessive fibrogenesis and impaired respiratory function. Nerandomilast, a preferential phosphodiesterase 4B inhibitor, is currently approved for the treatment of idiopathic pulmonary fibrosis and progressive pulmonary fibrosis in several countries following its demonstrated clinical efficacy in Phase III trials. However, its cellular mechanisms of action remain incompletely understood. In this study, we investigated the effects of nerandomilast on a bleomycin-induced mouse model of lung fibrosis. Nerandomilast treatment attenuates fibrotic remodeling and preserves alveolar epithelial architecture. Single-cell transcriptomic analyses revealed altered alveolar epithelial cell state dynamics accompanied by increased cell cycle-associated pathways in alveolar type 2 cells and an increased relative abundance of alveolar type 2 cells. Consistent with the single-cell findings, nerandomilast was associated with an increased SFTPC-positive area and the preservation of alveolar epithelial architecture in vivo. Collectively, our findings suggest that nerandomilast attenuates fibrotic remodeling while modulating alveolar epithelial cell state dynamics, which may provide a possible cellular explanation for its clinical efficacy in patients with pulmonary fibrosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42827411 · DOI · PMC13633504
CDK7, CDK9, or CDK11 inhibition reduces neutrophil-driven inflammation and tissue damage in experimental autoimmune models [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundCyclin-dependent kinases (CDKs) are involved in basic cellular processes like regulation of cell-cycle progression and transcription.
- Closing excerpt
- ConclusionsCDK7, CDK11, and especially CDK9 inhibition show therapeutic potential in IC-driven neutrophil-mediated diseases such as inflammatory arthritis and EBA.
- 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 (278 words)
BackgroundCyclin-dependent kinases (CDKs) are involved in basic cellular processes like regulation of cell-cycle progression and transcription. However, recent data also indicate a specific role in terminally differentiated neutrophils by promoting reactive oxygen species (ROS) release, degranulation, neutrophil extracellular trap formation, or apoptosis. Since these mechanisms are implicated in multiple autoimmune diseases, we aimed to delineate the role of CDKs in immune complex (IC)-mediated autoimmune diseases both in vitro and in vivo.MethodsWe analyzed CDK activity and gene expression in unstimulated and IC-stimulated neutrophils. Subsequently, we investigated the effect of pharmacological CDK inhibition on IC-activated neutrophil functions. To analyze the inhibitors in a more translational approach, we proceeded with the systemic and topical application of the effective inhibitors in a murine antibody transfer-induced local epidermolysis bullosa acquisita (EBA) model. The most effective inhibitor, MC180295, was validated in two other IC-mediated models of autoimmune disease: KBxN serum-transfer arthritis (KBxN STA), which also, but not exclusively, depends on neutrophils and immune thrombocytopenia (ITP), which is considered less neutrophil-dependent.ResultsWe found 14 CDKs expressed in unstimulated cells, while the IC-stimulation showed an upregulation of CDK2 and CDK4 expression. Inhibitors selectively targeting CDK1, CDK2, CDK4/6, CDK7, CDK9, CDK11, and CDK12 showed effects on different neutrophil functions (surface activation marker expression, ROS release, adhesion, apoptosis) in vitro. In the predominantly neutrophil-driven EBA model, we observed a reduction of disease severity upon treatment with CDK7, CDK9, or CDK11 inhibitors. Inhibiting these CDKs with topical THZ2, MC180295, or OTS964, respectively, also improved the clinical phenotype. In line with our hypothesis, MC180295 impaired the development of KBxN STA, but not ITP.ConclusionsCDK7, CDK11, and especially CDK9 inhibition show therapeutic potential in IC-driven neutrophil-mediated diseases such as inflammatory arthritis and EBA.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42823736 · DOI · PMC13628873
The enzyme inhibitory activity of helminth-derived serine protease inhibitor rapidly establishes immune tolerance to ameliorate allergic diseases [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Allergic diseases are a class of important immune imbalance diseases that lack effective cures.
- Closing excerpt
- These findings suggest that the rapid regulatory properties of enzymatic reactions have great potential in the prevention and treatment of allergic inflammation.
- 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 (216 words)
Allergic diseases are a class of important immune imbalance diseases that lack effective cures. Helminth-derived serine protease inhibitors (serpins) exert immunoregulatory effects similar to those of helminth, are controllable, have few side effects, and have great application potential in correcting unbalanced immune responses. However, the immune regulatory effects and mechanisms mediated by the enzyme inhibitory activity of helminth-derived serpins have not been investigated or clarified in previous studies. We obtained mutant serpin proteins with significantly reduced enzyme inhibitory activity by predicting and mutating the single key amino acid. The therapeutic effect of immunoregulation mediated by enzyme inhibitory activity of serpin on allergic inflammation was investigated based on an acute allergy model constructed in OVA-specific T-cell receptor transgenic C57BL/6 mice. Unlike the Trichinella spiralis-derived serpin (Ts-serpin), the mutant proteins showed significantly reduced inhibitory activity against the chymotrypsin and elastase. Meanwhile, the immunosuppressive ability of the mutant proteins was weakened and mutant protein intervention groups showed more severe allergic inflammation in the lungs. Additionally, enzyme inhibitory activity regulates the differentiation of macrophages and Treg cells to establish immune tolerance, which is the key to rapidly improving lung injury at the challenge and treatment stages of allergy. These findings suggest that the rapid regulatory properties of enzymatic reactions have great potential in the prevention and treatment of allergic inflammation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42702014 · DOI · PMC13556981
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 Age and Sex Differences in Efficacy of Treatments for Type 2 Diabetes: A Network Meta-Analysis [4]
- Research article Assessment of adverse effects attributed to statin therapy in product labels: a meta-analysis of double-blind randomised controlled trials [5]
- Research article Impact of statins as immune-modulatory agents on inflammatory markers in adults with chronic diseases: A systematic review and meta-analysis [6]
- Research article Impact of Lipid-Lowering Combination Therapy With Statins and Ezetimibe vs Statin Monotherapy on the Reduction of Cardiovascular Outcomes: A Meta-analysis [7]
- Research article PARP Inhibitor Maintenance After First-Line Chemotherapy in Advanced-Stage Epithelial Ovarian Cancer: A Systematic Review and Meta-Analysis [8]
- Research article Early treatment versus expectant management of hemodynamically significant patent ductus arteriosus for preterm infants [9]
References
- Hamada N, Hayashi Y, Motooka D, Kuwahara A, Akira S, Fukushima K. Nerandomilast is Associated With Altered Alveolar Epithelial Cell State Dynamics While Attenuating Fibrotic Remodeling in Pulmonary Fibrosis. . 2026. PMID 42827411 · DOI · PMC13633504
- Schlotfeldt M, Voss L, Mansini AP, Mehlberg D, Johannisson S, Radziewitz M, et al.. CDK7, CDK9, or CDK11 inhibition reduces neutrophil-driven inflammation and tissue damage in experimental autoimmune models. . 2026. PMID 42823736 · DOI · PMC13628873
- Shi W, Xu N, Liu Y, Bai X, Liu X, Xu N, et al.. The enzyme inhibitory activity of helminth-derived serine protease inhibitor rapidly establishes immune tolerance to ameliorate allergic diseases. . 2026. PMID 42702014 · DOI · PMC13556981
- Hanlon P, Butterly E, Wei L, Wightman H, Almazam SAM, Alsallumi K, et al.. Age and Sex Differences in Efficacy of Treatments for Type 2 Diabetes: A Network Meta-Analysis. JAMA. 2025. PMID 39899304 · DOI · PMC11791772
- Cholesterol Treatment Trialists' (CTT) Collaboration. Electronic address: ctt@ndph.ox.ac.uk, Cholesterol Treatment Trialists' (CTT) Collaboration. Assessment of adverse effects attributed to statin therapy in product labels: a meta-analysis of double-blind randomised controlled trials. Lancet. 2026. PMID 41655587 · DOI · PMC7619005
- Sabeel S, Motaung B, Nguyen KA, Ozturk M, Mukasa SL, Wolmarans K, et al.. Impact of statins as immune-modulatory agents on inflammatory markers in adults with chronic diseases: A systematic review and meta-analysis. PLoS One. 2025. PMID 40440323 · DOI · PMC12121830
- Banach M, Jaiswal V, Ang SP, Sawhney A, Deb N, Amarenco P, et al.. Impact of Lipid-Lowering Combination Therapy With Statins and Ezetimibe vs Statin Monotherapy on the Reduction of Cardiovascular Outcomes: A Meta-analysis. Mayo Clin Proc. 2025. PMID 40126455 · DOI
- Petousis S, Kahramanoglu I, Appenzeller-Herzog C, Angeles MA, Margioula-Siarkou C, Kacperczyk-Bartnik J, et al.. PARP Inhibitor Maintenance After First-Line Chemotherapy in Advanced-Stage Epithelial Ovarian Cancer: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2025. PMID 41191357 · DOI · PMC12590296
- Mitra S, Scrivens A, Fiander M, Disher T, Weisz DE. Early treatment versus expectant management of hemodynamically significant patent ductus arteriosus for preterm infants. Cochrane Database Syst Rev. 2025. PMID 40548426 · DOI · PMC12183776
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.
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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.