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 (587 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 mixture of polymyxins B1 and B2, obtained from bacillus polymyxa strains. They are basic polypeptides of about eight amino acids and have cationic detergent action on cell membranes. Polymyxin B is used for treatment of infections with gram-negative bacteria, but may be neurotoxic and nephrotoxic.
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: Polymyxin B Sulfate; Aerosporin.
Where it fits in the MeSH classification
- Broader topics
- Polymyxins
Related concepts
- Bacillus Polymyxa
Research landscape
PubMed indexes 4,029 records tagged with the MeSH heading “Polymyxin B” (counts retrieved 2026-10-31). 783 of them (19.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,635 records.
Reviews account for 160 records (4.0%) and meta-analyses for 16. Randomized controlled trials number 133 (3.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,635 |
| 2000-2009 | 712 |
| 2010-2019 | 899 |
| 2020 onward | 783 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 160 | 4.0% |
| Meta-analyses | 16 | 0.4% |
| Randomized controlled trials | 133 | 3.3% |
Method: PubMed query "Polymyxin B"[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 |
|---|---|---|---|---|
| Antibiotics in neonatal life increase murine susceptibility to experimental psoriasis | 2015 | Research article Design not recorded in structured metadata | 141 | cc by PMID 26416167 · DOI · PMC4598725 |
| A synthetic lipopeptide targeting top-priority multidrug-resistant Gram-negative pathogens | 2022 | Research article Design not recorded in structured metadata | 125 | cc by PMID 35338128 · DOI · PMC8956739 |
| Evolution and dynamics of regulatory architectures controlling polymyxin B resistance in enteric bacteria | 2008 | Research article Design not recorded in structured metadata | 86 | cc by PMID 18949034 · DOI · PMC2565834 |
| Polymyxin B lethality requires energy-dependent outer membrane disruption | 2025 | Research article Design not recorded in structured metadata | 30 | cc by PMID 41023239 · DOI · PMC12578643 |
Antibiotics in neonatal life increase murine susceptibility to experimental psoriasis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Psoriasis is an inflammatory skin disease affecting ∼2% of the world's population, but the aetiology remains incompletely understood.
- Closing excerpt
- This link between neonatal antibiotic-mediated imbalance in microbiota and development of experimental psoriasis provides precedence for further investigation of its specific aetiology as it relates to human psoriasis.
- 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 (149 words)
Psoriasis is an inflammatory skin disease affecting ∼2% of the world's population, but the aetiology remains incompletely understood. Recently, microbiota have been shown to differentially regulate the development of autoimmune diseases, but their influence on psoriasis is incompletely understood. We show here that adult mice treated with antibiotics that target Gram-negative and Gram-positive bacteria develop ameliorated psoriasiform dermatitis induced by imiquimod, with decreased pro-inflammatory IL-17- and IL-22-producing T cells. Surprisingly, mice treated neonatally with these antibiotics develop exacerbated psoriasis induced by imiquimod or recombinant IL-23 injection when challenged as adults, with increased IL-22-producing γδ(+) T cells. 16S rRNA gene compositional analysis reveals that neonatal antibiotic-treatment dysregulates gut and skin microbiota in adults, which is associated with increased susceptibility to experimental psoriasis. This link between neonatal antibiotic-mediated imbalance in microbiota and development of experimental psoriasis provides precedence for further investigation of its specific aetiology as it relates to human psoriasis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26416167 · DOI · PMC4598725
A synthetic lipopeptide targeting top-priority multidrug-resistant Gram-negative pathogens [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The emergence of multidrug-resistant (MDR) Gram-negative pathogens is an urgent global medical challenge.
- Closing excerpt
- This resulted in the clinical candidate F365 (QPX9003) with superior safety and efficacy against lung infections caused by top-priority MDR pathogens Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae.
- 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 (146 words)
The emergence of multidrug-resistant (MDR) Gram-negative pathogens is an urgent global medical challenge. The old polymyxin lipopeptide antibiotics (polymyxin B and colistin) are often the only therapeutic option due to resistance to all other classes of antibiotics and the lean antibiotic drug development pipeline. However, polymyxin B and colistin suffer from major issues in safety (dose-limiting nephrotoxicity, acute toxicity), pharmacokinetics (poor exposure in the lungs) and efficacy (negligible activity against pulmonary infections) that have severely limited their clinical utility. Here we employ chemical biology to systematically optimize multiple non-conserved positions in the polymyxin scaffold, and successfully disconnect the therapeutic efficacy from the toxicity to develop a new synthetic lipopeptide, structurally and pharmacologically distinct from polymyxin B and colistin. This resulted in the clinical candidate F365 (QPX9003) with superior safety and efficacy against lung infections caused by top-priority MDR pathogens Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35338128 · DOI · PMC8956739
Evolution and dynamics of regulatory architectures controlling polymyxin B resistance in enteric bacteria [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Complex genetic networks consist of structural modules that determine the levels and timing of a cellular response.
- Closing excerpt
- Our results suggest that, both functionally and evolutionarily, the feedforward connector loop is the transitional stage between direct transcriptional control and indirect regulation.
- 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 (147 words)
Complex genetic networks consist of structural modules that determine the levels and timing of a cellular response. While the functional properties of the regulatory architectures that make up these modules have been extensively studied, the evolutionary history of regulatory architectures has remained largely unexplored. Here, we investigate the transition between direct and indirect regulatory pathways governing inducible resistance to the antibiotic polymyxin B in enteric bacteria. We identify a novel regulatory architecture -- designated feedforward connector loop -- that relies on a regulatory protein that connects signal transduction systems post-translationally, allowing one system to respond to a signal activating another system. The feedforward connector loop is characterized by rapid activation, slow deactivation, and elevated mRNA expression levels in comparison with the direct regulation circuit. Our results suggest that, both functionally and evolutionarily, the feedforward connector loop is the transitional stage between direct transcriptional control and indirect regulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 18949034 · DOI · PMC2565834
Polymyxin B lethality requires energy-dependent outer membrane disruption [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Polymyxin antibiotics target lipopolysaccharides (LPSs) in both membranes of the bacterial cell envelope, leading to bacterial killing through a poorly defined mechanism.
- Closing excerpt
- This work reveals how metabolic inactivity confers tolerance of an important, membrane-targeting antibiotic.
- 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)
Polymyxin antibiotics target lipopolysaccharides (LPSs) in both membranes of the bacterial cell envelope, leading to bacterial killing through a poorly defined mechanism. Here we demonstrate that metabolic activity is essential for the lethality of clinically relevant doses of polymyxin B (PmB) and leverage this insight to determine its mode of action. PmB killed exponential-phase Escherichia coli but did not eliminate stationary-phase cells unless a carbon source was available. Antibiotic lethality correlated with surface protrusions visible by atomic force microscopy and LPS loss from the outer membrane via processes that required LPS synthesis and transport but that were blocked by the MCR-1 polymyxin resistance determinant. While energy-dependent outer-membrane disruption was not directly lethal, it facilitated PmB access to the inner membrane, which the antibiotic permeabilized in an energy-independent manner, leading to cell death. This work reveals how metabolic inactivity confers tolerance of an important, membrane-targeting antibiotic.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41023239 · DOI · PMC12578643
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 International Consensus Guidelines for the Optimal Use of the Polymyxins: Endorsed by the American College of Clinical Pharmacy (ACCP), European Society of Clinical Microbiology and Infectious Diseases (ESCMID), Infectious Diseases Society of America (IDSA), International Society for Anti-infective Pharmacology (ISAP), Society of Critical Care Medicine (SCCM), and Society of Infectious Diseases Pharmacists (SIDP) [5]
- Research article Polymyxin B for the treatment of multidrug-resistant pathogens: a critical review [6]
- Research article Polymyxin B sulfate and colistin: old antibiotics for emerging multiresistant gram-negative bacteria [7]
- Research article Colistin and polymyxin B: peas in a pod, or chalk and cheese? [8]
- Research article Effectiveness of polymyxin B-immobilized fiber column in sepsis: a systematic review [9]
- Research article Nephrotoxicity of Polymyxins: Is There Any Difference between Colistimethate and Polymyxin B? [10]
References
- Zanvit P, Konkel JE, Jiao X, Kasagi S, Zhang D, Wu R, et al.. Antibiotics in neonatal life increase murine susceptibility to experimental psoriasis. . 2015. PMID 26416167 · DOI · PMC4598725
- Roberts KD, Zhu Y, Azad MAK, Han ML, Wang J, Wang L, et al.. A synthetic lipopeptide targeting top-priority multidrug-resistant Gram-negative pathogens. . 2022. PMID 35338128 · DOI · PMC8956739
- Mitrophanov AY, Jewett MW, Hadley TJ, Groisman EA. Evolution and dynamics of regulatory architectures controlling polymyxin B resistance in enteric bacteria. . 2008. PMID 18949034 · DOI · PMC2565834
- Borrelli C, Douglas EJA, Riley SMA, Lemonidi AE, Larrouy-Maumus G, Lu WJ, et al.. Polymyxin B lethality requires energy-dependent outer membrane disruption. . 2025. PMID 41023239 · DOI · PMC12578643
- Tsuji BT, Pogue JM, Zavascki AP, Paul M, Daikos GL, Forrest A, et al.. International Consensus Guidelines for the Optimal Use of the Polymyxins: Endorsed by the American College of Clinical Pharmacy (ACCP), European Society of Clinical Microbiology and Infectious Diseases (ESCMID), Infectious Diseases Society of America (IDSA), International Society for Anti-infective Pharmacology (ISAP), Society of Critical Care Medicine (SCCM), and Society of Infectious Diseases Pharmacists (SIDP). Pharmacotherapy. 2019. PMID 30710469 · DOI · PMC7437259
- Zavascki AP, Goldani LZ, Li J, Nation RL. Polymyxin B for the treatment of multidrug-resistant pathogens: a critical review. J Antimicrob Chemother. 2007. PMID 17878146 · DOI
- Evans ME, Feola DJ, Rapp RP. Polymyxin B sulfate and colistin: old antibiotics for emerging multiresistant gram-negative bacteria. Ann Pharmacother. 1999. PMID 10492501 · DOI
- Nation RL, Velkov T, Li J. Colistin and polymyxin B: peas in a pod, or chalk and cheese?. Clin Infect Dis. 2014. PMID 24700659 · DOI · PMC4305129
- Cruz DN, Perazella MA, Bellomo R, de Cal M, Polanco N, Corradi V, et al.. Effectiveness of polymyxin B-immobilized fiber column in sepsis: a systematic review. Crit Care. 2007. PMID 17448226 · DOI · PMC2206475
- Zavascki AP, Nation RL. Nephrotoxicity of Polymyxins: Is There Any Difference between Colistimethate and Polymyxin B?. Antimicrob Agents Chemother. 2017. PMID 27993859 · DOI · PMC5328560
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
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