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 (816 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
Organic compounds containing the -co-nh2 radical. Amides are derived from acids by replacement of -OH by -NH2 or from ammonia by the replacement of H by an acyl group. (From Grant and Hackh's Chemical Dictionary, 5th ed)
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: Amide.
Where it fits in the MeSH classification
- Broader topics
- Organic Chemicals
- Narrower topics
- Acetamides; Acrylamides; Afatinib; Anilides; Benzamides; Benzoylarginine-2-Naphthylamide; Bimatoprost; Ceramides; Cerulenin; Dibucaine; Formamides; Lactams; Polyunsaturated Alkamides; Salicylamides
Related concepts
- Co-Nh2
Research landscape
PubMed indexes 659,019 records tagged with the MeSH heading “Amides” (counts retrieved 2026-10-31). 101,486 of them (15.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 280,047 records.
Reviews account for 43,263 records (6.6%) and meta-analyses for 4,192. Randomized controlled trials number 41,320 (6.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 280,047 |
| 2000-2009 | 122,076 |
| 2010-2019 | 155,410 |
| 2020 onward | 101,486 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 43,263 | 6.6% |
| Meta-analyses | 4,192 | 0.6% |
| Randomized controlled trials | 41,320 | 6.3% |
Method: PubMed query "Amides"[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 |
|---|---|---|---|---|
| Conformational asymmetry of human immunodeficiency virus-1 protease flaps increases along the darunavir drug resistance pathway | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42554278 · DOI · PMC13439748 |
| Resistance development in KPC-producing Klebsiella pneumoniae under ceftazidime/avibactam-meropenem pressure: KPC-2 Ω-loop mutations attenuate avibactam efficacy | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42545018 · DOI · PMC13532191 |
| Novel transposon Tn8026 contributes to the global spread of transmissible linezolid resistance in Enterococcus via a linear plasmid | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42522682 · DOI · PMC13417996 |
Conformational asymmetry of human immunodeficiency virus-1 protease flaps increases along the darunavir drug resistance pathway [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Under selective drug pressure, the structure and dynamics of HIV-1 protease (PR) evolve to confer resistance to the drug.
- Closing excerpt
- These observations indicate that drug-resistance mutations increase the asymmetry between the two flaps in the PR-inhibitor interaction in the inhibitor-bound forms.
- 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 (214 words)
Under selective drug pressure, the structure and dynamics of HIV-1 protease (PR) evolve to confer resistance to the drug. Here, we report on the conformational changes in PR flaps for drug-resistance mutations using 19F nuclear magnetic resonance (NMR) spectroscopy. We prepared wild-type (wt) PR and its three mutant variants containing 4, 10, or 11 mutations, namely 4Mut, 10Mut, and 11Mut, that were previously found in a viral passage study against darunavir (DRV). The proteins were uniformly labeled with 15N and with 19F amino-acid specifically in the 5-indole positions of two conserved tryptophan residues, W6 and W42, which are located near the dimer interface and at the edge of the flap region of PR, respectively. In solution, 19F NMR spectra of these proteins in the inhibitor-free forms showed a downfield shift of the W42 resonance as the number of mutations increased. In the DRV-bound form, the W42 resonance again shifted with increasing number of mutations and, importantly, split into two peaks, reflecting different local electronic environments of the two flaps of the dimer. Solid-state 19F magic angle spinning (MAS) NMR spectra of wt-PR and 10Mut also exhibited two W42 resonances in DRV-bound crystalline forms. These observations indicate that drug-resistance mutations increase the asymmetry between the two flaps in the PR-inhibitor interaction in the inhibitor-bound forms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42554278 · DOI · PMC13439748
Resistance development in KPC-producing Klebsiella pneumoniae under ceftazidime/avibactam-meropenem pressure: KPC-2 Ω-loop mutations attenuate avibactam efficacy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The ceftazidime/avibactam (CAZ-AVI, CZA) combination is a potent agent against KPC-producing Klebsiella pneumoniae (KPC-Kp) infections, but resistance readily emerges via KPC mutations that restore carbapenem susceptibility.
- Closing excerpt
- These findings offer critical insights for optimizing combination therapies and monitoring resistance mechanisms during treatment of KPC-Kp infections.
- 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 (335 words)
The ceftazidime/avibactam (CAZ-AVI, CZA) combination is a potent agent against KPC-producing Klebsiella pneumoniae (KPC-Kp) infections, but resistance readily emerges via KPC mutations that restore carbapenem susceptibility. Previous studies have shown that the CZA-meropenem (MEM) combination exhibits favorable therapeutic efficacy by exploiting this collateral sensitivity. Here, we investigated in vitro how this adjunctive combination impacts resistance evolution in KPC-Kp and delineated the underlying molecular mechanisms. Resistance evolution in 26 KPC-Kp isolates was selected by multipassaging under dual CZA-MEM pressure. The underlying resistant mechanisms were systematically dissected by integrating MICs, enzyme kinetics, molecular docking, and molecular dynamics simulations. In contrast to CZA alone, the CZA-MEM combination significantly suppressed resistance development, but five strains still adapted. Under dual-drug selection, mutations arose solely within KPC but were restricted to the Ω loop. Kinetic analysis showed that these mutations drive CZA resistance (R164S variants chiefly by increasing ceftazidime hydrolysis, R164L variants by weakening AVI inhibition, and D179Y by both mechanisms) while simultaneously restoring MEM susceptibility (all variants reduced MEM hydrolysis). Importantly, every mutant elevated the AVI IC50, suggesting this is the optimal evolutionary path for KPC-Kp under CZA-MEM pressure. Mechanistic studies reveal that R164L/T243S mutations destabilize the Ω loop to reposition Ser70 at the active site and confer AVI resistance by impairing acylation, destabilizing the enzyme-inhibitor complex, and potentially accelerating deacylation. Our study provides actionable clues for positioning and deploying different β-lactam agents in the treatment of KPC-Kp infections.IMPORTANCEThe global rise of KPC-producing Klebsiella pneumoniae (KPC-Kp) severely limits available therapeutic options, underscoring the urgent need for strategies that curb resistance evolution. The ceftazidime/avibactam-meropenem combination exploits collateral sensitivity to suppress resistance development, yet adaptive mutations still emerge. However, the mechanisms underlying resistance development under dual-drug pressure remain unclear. This study focused on Ω-loop mutations in KPC under dual-drug pressure, revealing that these mutations concurrently enhance avibactam resistance and restore carbapenem susceptibility, although the potential contribution of additional genetic alterations cannot be fully excluded. These findings offer critical insights for optimizing combination therapies and monitoring resistance mechanisms during treatment of KPC-Kp infections.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42545018 · DOI · PMC13532191
Novel transposon Tn8026 contributes to the global spread of transmissible linezolid resistance in Enterococcus via a linear plasmid [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Linezolid is a critical last-resort antimicrobial for multidrug-resistant Enterococcus faecium, particularly against vancomycin-resistant lineages where therapeutic options are severely limited.
- Closing excerpt
- These findings emphasize the need for detailed long-read-based surveillance of mobile genetic elements, with a particular focus on identifying linear plasmids that are often overlooked.
- 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 (267 words)
Linezolid is a critical last-resort antimicrobial for multidrug-resistant Enterococcus faecium, particularly against vancomycin-resistant lineages where therapeutic options are severely limited. While resistance has historically arisen through de novo chromosomal mutations, the global emergence of transferable resistance mechanisms threatens to render more infections untreatable. Here, we characterize a recent (2023-2024) hospital-associated outbreak of linezolid-resistant E. faecium in Queensland, Australia. Although the cohort comprised a variety of sequence types, the outbreak was primarily driven by the clonal expansion of an ST80 lineage carrying the plasmid-borne poxtA gene. Standard short-read genomic surveillance failed to resolve the genetic context of the resistance determinant. However, long-read sequencing revealed that poxtA was carried within a novel transposon, Tn8026, situated on a linear plasmid. Structural analysis defined Tn8026 as a unique element flanked by IS1678 and the novel insertion sequence ISEfa26. Furthermore, we identified an instance of Tn8026 integration into the chromosome, providing functional evidence of its mobility and capacity for stabilization within the genome. Global genomic screening demonstrated that Tn8026 significantly predates the local outbreak, identified in a historical Norwegian isolate from 2012, indicating a long-standing yet unrecognized global reservoir. Phylogenomic analysis provided strong evidence that the linear plasmid was imported from the Indian subcontinent, initiating a chain of silent dissemination in eastern Australia where the lineage circulated undetected prior to clinical recognition. Crucially, we also confirmed the presence of the linear plasmid in Enterococcus gallinarum, demonstrating its capacity to mobilize transmissible linezolid resistance across enterococcal species boundaries. These findings emphasize the need for detailed long-read-based surveillance of mobile genetic elements, with a particular focus on identifying linear plasmids that are often overlooked.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42522682 · DOI · PMC13417996
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 Treatment of Helicobacter pylori with potassium competitive acid blockers: A systematic review and meta-analysis [4]
- Research article Efficacy and safety of transarterial chemoembolization combined with lenvatinib and PD-1 inhibitor in the treatment of advanced hepatocellular carcinoma: A meta-analysis [5]
- Research article Reaction Risk to Direct Penicillin Challenges: A Systematic Review and Meta-Analysis [6]
- Research article The global prevalence of reported penicillin allergy: A systematic review and meta-analysis [7]
- Research article Cefiderocol either in monotherapy or combination versus best available therapy in the treatment of carbapenem-resistant Acinetobacter baumannii infections: A systematic review and meta-analysis [8]
- Research article The urea-to-creatinine ratio as an emerging biomarker in critical care: a scoping review and meta-analysis [9]
References
- Guerrero M, Zadorozhnyi R, Lin G, Quinn CM, Calero G, Kurt-Yilmaz N, et al.. Conformational asymmetry of human immunodeficiency virus-1 protease flaps increases along the darunavir drug resistance pathway. . 2026. PMID 42554278 · DOI · PMC13439748
- Li F-H, Zheng M, Zhong G-M, He X-M, Hu M-Z, Kuang X, et al.. Resistance development in KPC-producing Klebsiella pneumoniae under ceftazidime/avibactam-meropenem pressure: KPC-2 Ω-loop mutations attenuate avibactam efficacy. . 2026. PMID 42545018 · DOI · PMC13532191
- Hall MB, Xue Y, Lee TSE, Herring E, Hume J, Wick RR, et al.. Novel transposon Tn8026 contributes to the global spread of transmissible linezolid resistance in Enterococcus via a linear plasmid. . 2026. PMID 42522682 · DOI · PMC13417996
- Kanu JE, Soldera J. Treatment of Helicobacter pylori with potassium competitive acid blockers: A systematic review and meta-analysis. World J Gastroenterol. 2024. PMID 38577188 · DOI · PMC10989498
- Wang L, Lin L, Zhou W. Efficacy and safety of transarterial chemoembolization combined with lenvatinib and PD-1 inhibitor in the treatment of advanced hepatocellular carcinoma: A meta-analysis. Pharmacol Ther. 2024. PMID 38499069 · DOI
- Blumenthal KG, Smith LR, Mann JTS, Salciccioli I, Accarino JJO, Shah RJ, et al.. Reaction Risk to Direct Penicillin Challenges: A Systematic Review and Meta-Analysis. JAMA Intern Med. 2024. PMID 39283610 · DOI · PMC11406457
- Luintel A, Healy J, Blank M, Luintel A, Dryden S, Das A, et al.. The global prevalence of reported penicillin allergy: A systematic review and meta-analysis. J Infect. 2025. PMID 39874990 · DOI
- Onorato L, de Luca I, Monari C, Coppola N. Cefiderocol either in monotherapy or combination versus best available therapy in the treatment of carbapenem-resistant Acinetobacter baumannii infections: A systematic review and meta-analysis. J Infect. 2024. PMID 38331328 · DOI
- Paulus MC, Melchers M, van Es A, Kouw IWK, van Zanten ARH. The urea-to-creatinine ratio as an emerging biomarker in critical care: a scoping review and meta-analysis. Crit Care. 2025. PMID 40317012 · DOI · PMC12046807
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.