ArticlePloS one2011
Structure-based development of small molecule PFKFB3 inhibitors: a framework for potential cancer therapeutic agents targeting the Warburg effect.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 78 citations in OpenAlex.
- First-in-Class Covalent Inhibitors of PFKFB3: Discovery and Characterization in PDAC Models.Journal of medicinal chemistry · 2026Article
- Energy Metabolism and Cancer Pain: A Pathway to Innovative Treatment Strategies.Current topics in medicinal chemistry · 2026Review
- Metabolism in the tumor microenvironment: implications for pathogenesis and therapeutics.Frontiers in immunology · 2025Review
- Targeting Glycolysis for Treatment of Breast Cancer Resistance: Current Progress and Future Prospects.International journal of biological sciences · 2025Review
- Targeting the Warburg effect: A revisited perspective from molecular mechanisms to traditional and innovative therapeutic strategies in cancer.Acta pharmaceutica Sinica. B · 2024Review
- A high-throughput screening campaign against PFKFB3 identified potential inhibitors with novel scaffolds.Acta pharmacologica Sinica · 2023Article
- Targeting Glucose Metabolism Enzymes in Cancer Treatment: Current and Emerging Strategies.Cancers · 2022Review
- Treatment against glucose-dependent cancers through metabolic PFKFB3 targeting of glycolytic flux.Cancer metastasis reviews · 2022Review
- Energy Metabolism on Mitochondrial Maturation and Its Effects on Cardiomyocyte Cell Fate.Frontiers in cell and developmental biology · 2022Review
- Review
- Mir-488 alleviates chemoresistance and glycolysis of colorectal cancer by targeting PFKFB3.Journal of clinical laboratory analysis · 2021Article
- Glycolysis-Independent Glucose Metabolism Distinguishes TE from ICM Fate during Mammalian Embryogenesis.Developmental cell · 2020Article
- Article
- Tuning PFKFB3 Bisphosphatase Activity Through Allosteric Interference.Scientific reports · 2019Article
- PFKFB3-mediated endothelial glycolysis promotes pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Synergistic Effect of Colistin Combined with PFK-158 against Colistin-Resistant Enterobacteriaceae.Antimicrobial agents and chemotherapy · 2019Article
- Tumorigenicity assay essential for facilitating safety studies of hiPSC-derived cardiomyocytes for clinical application.Scientific reports · 2019Article
- 6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 and 4: A pair of valves for fine-tuning of glucose metabolism in human cancer.Molecular metabolism · 2019Review
- Regulation of Nephron Progenitor Cell Self-Renewal by Intermediary Metabolism.Journal of the American Society of Nephrology : JASN · 2017Article
- PFKFB3 Control of Cancer Growth by Responding to Circadian Clock Outputs.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer cells adopt glycolysis as the major source of metabolic energy production for fast cell growth. The HIF-1-induced PFKFB3 plays a key role in this adaptation by elevating the concentration of Fru-2,6-BP, the most potent glycolysis stimulator. As this metabolic conversion has been suggested to be a hallmark of cancer, PFKFB3 has emerged as a novel target for cancer chemotherapy. Here, we report that a small molecular inhibitor, N4A, was identified as an initial lead compound for PFKFB3 inhibitor with therapeutic potential. In an attempt to improve its potency, we determined the crystal structure of the PFKFB3•N4A complex to 2.4 Å resolution and, exploiting the resulting molecular information, attained the more potent YN1. When tested on cultured cancer cells, both N4A and YN1 inhibited PFKFB3, suppressing the Fru-2,6-BP level, which in turn suppressed glycolysis and, ultimately, led to cell death. This study validates PFKFB3 as a target for new cancer therapies and provides a framework for future development efforts.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.