ArticleJournal of medicinal chemistry2014
3-Substituted-N-(4-hydroxynaphthalen-1-yl)arylsulfonamides as a novel class of selective Mcl-1 inhibitors: structure-based design, synthesis, SAR, and biological evaluation.
Article in Journal of medicinal chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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Who cites it
33 citing papers in PubMed, 78 citations in OpenAlex.
- Histidine-Covalent Stapled Alpha-Helical Peptides Targeting hMcl-1.Journal of medicinal chemistry · 2024Article
- Discovery ofRSC medicinal chemistry · 2023Article
- Design, Synthesis, and Structural Characterization of Lysine Covalent BH3 Peptides Targeting Mcl-1.Journal of medicinal chemistry · 2021Article
- Binding of 2-(Triazolylthio)acetamides to Metallo-β-lactamase CcrA Determined with NMR.ACS omega · 2020Article
- Discovery and Characterization of 2,5-Substituted Benzoic Acid Dual Inhibitors of the Anti-apoptotic Mcl-1 and Bfl-1 Proteins.Journal of medicinal chemistry · 2020Article
- HCMV modulation of cellular PI3K/AKT/mTOR signaling: New opportunities for therapeutic intervention?Antiviral research · 2019Review
- Mcl-1 Phosphorylation without Degradation Mediates Sensitivity to HDAC Inhibitors by Liberating BH3-Only Proteins.Cancer research · 2018Article
- Discovery of Mcl-1 inhibitors from integrated high throughput and virtual screening.Scientific reports · 2018Article
- ICBS 2017 in Shanghai-Illuminating Life with Chemical Innovation.ACS chemical biology · 2018Article
- Discovery of N-(Naphtho[1,2-b]Furan-5-Yl) Benzenesulfonamides as Novel Selective Inhibitors of Triple-Negative Breast Cancer (TNBC).Molecules (Basel, Switzerland) · 2018Article
- Article
- Emerging molecular therapeutic targets for cholangiocarcinoma.Journal of hepatology · 2017Review
- Pathways and mechanisms of venetoclax resistance.Leukemia & lymphoma · 2017Review
- Mcl-1 Degradation Is Required for Targeted Therapeutics to Eradicate Colon Cancer Cells.Cancer research · 2017Article
- hBfl-1/hNOXA Interaction Studies Provide New Insights on the Role of Bfl-1 in Cancer Cell Resistance and for the Design of Novel Anticancer Agents.ACS chemical biology · 2017Article
- Mcl-1 small-molecule inhibitors encapsulated into nanoparticles exhibit increased killing efficacy towards HCMV-infected monocytes.Antiviral research · 2017Article
- DRP-1 is required for BH3 mimetic-mediated mitochondrial fragmentation and apoptosis.Cell death & disease · 2017Article
- Discovery and biological characterization of potent myeloid cell leukemia-1 inhibitors.FEBS letters · 2017Article
- Attacking cancer's Achilles heel: antagonism of anti-apoptotic BCL-2 family members.The FEBS journal · 2016Review
- Structure-based design of N-substituted 1-hydroxy-4-sulfamoyl-2-naphthoates as selective inhibitors of the Mcl-1 oncoprotein.European journal of medicinal chemistry · 2016Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Mcl-1, an antiapoptotic member of the Bcl-2 family of proteins, is a validated and attractive target for cancer therapy. Overexpression of Mcl-1 in many cancers results in disease progression and resistance to current chemotherapeutics. Utilizing high-throughput screening, compound 1 was identified as a selective Mcl-1 inhibitor and its binding to the BH3 binding groove of Mcl-1 was confirmed by several different, but complementary, biochemical and biophysical assays. Guided by structure-based drug design and supported by NMR experiments, comprehensive SAR studies were undertaken and a potent and selective inhibitor, compound 21, was designed which binds to Mcl-1 with a Ki of 180 nM. Biological characterization of 21 showed that it disrupts the interaction of endogenous Mcl-1 and biotinylated Noxa-BH3 peptide, causes cell death through a Bak/Bax-dependent mechanism, and selectively sensitizes Eμ-myc lymphomas overexpressing Mcl-1, but not Eμ-myc lymphoma cells overexpressing Bcl-2. Treatment of human leukemic cell lines with compound 21 resulted in cell death through activation of caspase-3 and induction of apoptosis.
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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.