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 (606 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
An antibiotic compound derived from Streptomyces niveus. It has a chemical structure similar to coumarin. Novobiocin binds to DNA gyrase, and blocks adenosine triphosphatase (ATPase) activity. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p189)
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: Crystallinic Acid; Streptonivicin; Novobiocin Calcium; Calcium, Novobiocin; Novobiocin Sodium; Sodium, Novobiocin; Novobiocin, Monosodium Salt; Monosodium Salt Novobiocin.
Where it fits in the MeSH classification
- Broader topics
- Aminocoumarins; Glycosides
Research landscape
PubMed indexes 2,144 records tagged with the MeSH heading “Novobiocin” (counts retrieved 2026-10-31). 64 of them (3.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,622 records.
Reviews account for 73 records (3.4%) and meta-analyses for 1. Randomized controlled trials number 7 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,622 |
| 2000-2009 | 266 |
| 2010-2019 | 192 |
| 2020 onward | 64 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 73 | 3.4% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 7 | 0.3% |
Method: PubMed query "Novobiocin"[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 |
|---|---|---|---|---|
| Thai ethnomedicinal plants as resistant modifying agents for combating Acinetobacter baumannii infections | 2012 | Research article Design not recorded in structured metadata | 28 | cc by PMID 22536985 · DOI · PMC3416686 |
| A novel function of novobiocin: disrupting the interaction of HIF 1α and p300/CBP through direct binding to the HIF1α C-terminal activation domain | 2013 | Research article Design not recorded in structured metadata | 26 | cc by PMID 23671581 · DOI · PMC3646014 |
| Novobiocin-induced anti-proliferative and differentiating effects in melanoma B16 | 1992 | Research article Design not recorded in structured metadata | 13 | cc by PMID 1739614 · DOI · PMC1977725 |
| The evolution of heat shock protein 90 C-terminal inhibitors: From novobiocin to potential clinical candidates | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 41796637 · DOI · PMC13053691 |
Thai ethnomedicinal plants as resistant modifying agents for combating Acinetobacter baumannii infections [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundAcinetobacter baumannii is well-recognized as an important nosocomial pathogen, however, due to their intrinsic resistance to several antibiotics, treatment options are limited.
- Closing excerpt
- baumannii 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 (154 words)
BackgroundAcinetobacter baumannii is well-recognized as an important nosocomial pathogen, however, due to their intrinsic resistance to several antibiotics, treatment options are limited. Synergistic effects between antibiotics and medicinal plants, particularly their active components, have intensively been studied as alternative approaches.MethodsFifty-one ethanol extracts obtained from 44 different selected medicinal plant species were tested for resistance modifying agents (RMAs) of novobiocin against A. baumannii using growth inhibition assay.ResultsAt 250 μg/ml, Holarrhena antidysenterica, Punica granatum, Quisqualis indica, Terminalia bellirica, Terminalia chebula, and Terminalia sp. that possessed low intrinsic antibacterial activity significantly enhanced the activity of novobiocin at 1 μg/ml (1/8xminimum inhibitory concentration) against this pathogen. Holarrhena antidysenterica at 7.8 μg/ml demonstrated remarkable resistant modifying ability against A. baumannii in combination with novobiocin. The phytochemical study revealed that constituents of this medicinal plant contain alkaloids, condensed tannins, and triterpenoids.ConclusionThe use of Holarrhena antidysenterica in combination with novobiocin provides an effective alternative treatment for multidrug resistant A. baumannii infections.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 22536985 · DOI · PMC3416686
A novel function of novobiocin: disrupting the interaction of HIF 1α and p300/CBP through direct binding to the HIF1α C-terminal activation domain [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Hypoxia-inducible factor 1α (HIF1α) is an important cellular survival protein under hypoxic conditions, regulating the cellular response to low oxygen tension via recruitment of a transcriptional co-activator, p300/CBP.
- Closing excerpt
- These findings suggest a novel mechanism of action for novobiocin which has the potential for innovative therapeutic use in tumor treatment.
- 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 (181 words)
Hypoxia-inducible factor 1α (HIF1α) is an important cellular survival protein under hypoxic conditions, regulating the cellular response to low oxygen tension via recruitment of a transcriptional co-activator, p300/CBP. p300/CBP induces expression of multiple genes involved in cell survival, proliferation, angiogenesis, and tumor development. Thus, a strategy to inhibit hypoxic responses in tumors may be to target the protein-protein interaction between HIF1α and p300/CBP. Here, we document, for the first time, that the aminocoumarin antibiotic, novobiocin, directly blocks the protein-protein interaction between the HIF1α C-terminal activation domain (CTAD) and the cysteine-histidine rich (CH1) region of p300/CBP. Also, novobiocin down-regulated HIF1α-controlled gene expression, specifically CA9, which is related to tumorigenesis. In a monolayer cell culture, novobiocin inhibited cell proliferation and colony formation in the MCF-7 human breast adenocarcinoma cell line and the A549 human lung cancer cell line. Rescue experiments revealed that the recombinant CTAD fragment of HIF1α partially reversed novobiocin's inhibitory effects on cell proliferation and colony formation in MCF-7 cells. These findings suggest a novel mechanism of action for novobiocin which has the potential for innovative therapeutic use in tumor treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23671581 · DOI · PMC3646014
Novobiocin-induced anti-proliferative and differentiating effects in melanoma B16 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The antibiotic drug novobiocin was evaluated for its anti-tumour properties in B16 melanoma cells.
- Closing excerpt
- Our results support the contention further that novobiocin and other differentiating agents might be of potential value in melanoma therapy.
- 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 (162 words)
The antibiotic drug novobiocin was evaluated for its anti-tumour properties in B16 melanoma cells. Novobiocin is shown to inhibit melanoma B16 cell proliferation. The anti-proliferative effect was gradually reversible upon removal of novobiocin from the culture medium. Growth inhibition by novobiocin was accompanied by phenotypic alterations, that included morphological changes, lipid accumulation and marked increases in the activities of NADPH cytochrome c reductase and gamma glutamyl transpeptidase. In vivo administration of repeated i.p. doses of novobiocin, to mice implanted with B16 melanoma cells resulted in growth retardation. The combined treatment of the B16 melanoma cells with novobiocin and other chemical inducers of differentiation was examined in a cell growth assay. Novobiocin and sodium butyrate inhibited cell growth in a near additive manner, while combination of novobiocin with the GTP-depleting agents, tiazofurin or mycophenolic acid resulted in a synergistic decrease in cell growth. Our results support the contention further that novobiocin and other differentiating agents might be of potential value in melanoma therapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 1739614 · DOI · PMC1977725
The evolution of heat shock protein 90 C-terminal inhibitors: From novobiocin to potential clinical candidates [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Heat shock protein 90 (Hsp90) is a highly conserved molecular chaperone that regulates the maturation of various client proteins.
- Closing excerpt
- Structure-activity relationship studies are discussed, demonstrating how medicinal chemistry optimization has produced CTD modulators with selective anti-proliferative or neuroprotective activities.
- 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 (109 words)
Heat shock protein 90 (Hsp90) is a highly conserved molecular chaperone that regulates the maturation of various client proteins. Most therapeutic studies have focused on N-terminal Hsp90 inhibitors, but these are limited by dose-escalating toxicities that are caused by induction of the heat shock response. Leonard Neckers' discovery of novobiocin as a Hsp90 C-terminal inhibitor revealed an alternative mode to Hsp90 inhibition and established the C-terminal domain (CTD) as a therapeutic target. This review highlights recent advances in Hsp90 CTD inhibition and summarizes the evolution of novobiocin-based C-terminal inhibitors. Structure-activity relationship studies are discussed, demonstrating how medicinal chemistry optimization has produced CTD modulators with selective anti-proliferative or neuroprotective activities.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41796637 · DOI · PMC13053691
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 Novobiocin and additional inhibitors of the Hsp90 C-terminal nucleotide-binding pocket [5]
- Research article Inhibitors of the HSP90 molecular chaperone: current status [6]
- Research article The interaction between coumarin drugs and DNA gyrase [7]
- Research article MECHANISMS OF ANTIBIOTIC ACTION [8]
- Research article Targeting novel sites in DNA gyrase for development of anti-microbials [9]
- Research article ANTIMICROBIAL CHEMOTHERAPEUTIC AGENTS: THE NATURE OF THEIR ACTION AND SELECTIVE TOXICITY [10]
References
- Phatthalung PN, Chusri S, Voravuthikunchai SP. Thai ethnomedicinal plants as resistant modifying agents for combating Acinetobacter baumannii infections. . 2012. PMID 22536985 · DOI · PMC3416686
- Wu D, Zhang R, Zhao R, Chen G, Cai Y, Jin J. A novel function of novobiocin: disrupting the interaction of HIF 1α and p300/CBP through direct binding to the HIF1α C-terminal activation domain. . 2013. PMID 23671581 · DOI · PMC3646014
- Nordenberg J, Albukrek D, Hadar T, Fux A, Wasserman L, Novogrodsky A, et al.. Novobiocin-induced anti-proliferative and differentiating effects in melanoma B16. . 1992. PMID 1739614 · DOI · PMC1977725
- Jiang X, Blagg BSJ. The evolution of heat shock protein 90 C-terminal inhibitors: From novobiocin to potential clinical candidates. . 2026. PMID 41796637 · DOI · PMC13053691
- Donnelly A, Blagg BS. Novobiocin and additional inhibitors of the Hsp90 C-terminal nucleotide-binding pocket. Curr Med Chem. 2008. PMID 18991631 · DOI · PMC2729083
- Sharp S, Workman P. Inhibitors of the HSP90 molecular chaperone: current status. Adv Cancer Res. 2006. PMID 16860662 · DOI
- Maxwell A. The interaction between coumarin drugs and DNA gyrase. Mol Microbiol. 1993. PMID 8231802 · DOI
- GALE EF. MECHANISMS OF ANTIBIOTIC ACTION. Pharmacol Rev. 1963. PMID 14064356 · DOI
- Salman M, Sharma P, Kumar M, Ethayathulla AS, Kaur P. Targeting novel sites in DNA gyrase for development of anti-microbials. Brief Funct Genomics. 2023. PMID 36064602 · DOI
- FEINGOLD DS. ANTIMICROBIAL CHEMOTHERAPEUTIC AGENTS: THE NATURE OF THEIR ACTION AND SELECTIVE TOXICITY. N Engl J Med. 1963. PMID 14050990 · 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.