ArticleMarine life science & technology2023
Identification of marine natural product Pretrichodermamide B as a STAT3 inhibitor for efficient anticancer therapy.
Article in Marine life science & technology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- Review
- MR2938 relieves DSS-induced colitis in mice through inhibiting NF-κB signaling and improving epithelial barrier.Marine life science & technology · 2025Article
- STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Novel Epidithiodiketopiperazine Derivatives in the Mutants of the Filamentous FungusJournal of fungi (Basel, Switzerland) · 2025Article
- Quinazolinone Derivative MR2938 Protects DSS-Induced Barrier Dysfunction in Mice Through Regulating Gut Microbiota.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Semisynthesis, Structure Elucidation and Anti-Marine drugs · 2024Article
- Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) regulates the expression of various critical mediators of cancer and is considered as one of the central communication nodes in cell growth and survival. Marine natural products (MNP) represent great resources for discovery of bioactive lead compounds, especially anti-cancer agents. Through the medium-throughput screening of our in-house MNP library, Pretrichodermamide B, an epidithiodiketopiperazine, was identified as a JAK/STAT3 signaling inhibitor. Further studies identified that Pretrichodermamide B directly binds to STAT3, preventing phosphorylation and thus inhibiting JAK/STAT3 signaling. Moreover, it suppressed cancer cell growth, in vitro, at low micromolar concentrations and demonstrated efficacy in vivo by decreasing tumor growth in a xenograft mouse model. In addition, it was shown that Pretrichodermamide B was able to induce cell cycle arrest and promote cell apoptosis. This study demonstrated that Pretrichodermamide B is a novel STAT3 inhibitor, which should be considered for further exploration as a promising anti-cancer therapy. Supplementary Information: The online version contains supplementary material available at 10.1007/s42995-022-00162-x.
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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.