ArticleNature communications2022
Resistance to the isocitrate dehydrogenase 1 mutant inhibitor ivosidenib can be overcome by alternative dimer-interface binding inhibitors.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
34 citing papers in PubMed, 53 citations in OpenAlex.
- Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Trial
- Olutasidenib in combination with azacitidine induces durable complete remissions in patients with relapsed or refractory mIDH1 acute myeloid leukemia: a multicohort open-label phase 1/2 trial.Journal of hematology & oncology · 2025Trial
- Evolving precision: Updates in targeted therapy for cholangiocarcinoma.Hepatology (Baltimore, Md.) · 2026Review
- The new era of AML therapy: current standards and emerging targets.International journal of clinical oncology · 2026Review
- The allosteric IDH1 inhibitor ivosidenib overcomes chemoresistance in intrahepatic cholangiocarcinoma models expressing wild-type IDH1.The Journal of clinical investigation · 2026Article
- Review
- Advancements in targeted therapies for acute myeloid leukemia.Current opinion in pharmacology · 2026Review
- The Art of Domesticating Proteins: How Cancer Cells Adapt to Therapeutic and Environmental Stressors.International journal of molecular sciences · 2026Review
- Resistance to Targeted Therapy in AML: Current Challenges and Emerging Treatment Strategies.Journal of clinical medicine · 2026Review
- Mitochondrial targets in IDH1-mutated cholangiocarcinoma.Hepatology communications · 2026Review
- Metabolomics using anion-exchange chromatography mass spectrometry for the analysis of cells, tissues and biofluids.Nature protocols · 2026Review
- IDH1 mutation creates a dependency on fatty acid metabolism that underlies sensitivity to cuproptosis in acute myeloid leukemia cells.International journal of medical sciences · 2026Article
- Olutasidenib: an Achilles' heel for IDH1-mutated MDS?Blood advances · 2025Article
- Establishment and characterization of TK-DDCS1: a novel IDH1 mutated dedifferentiated chondrosarcoma cell line.Human cell · 2025Article
- Extending protein-film electrochemistry across enzymology and biological inorganic chemistry to investigate, track and control the reactions of non-redox enzymes and spectroscopically silent metals.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2025Review
- Building Localized NADP(H) Recycling Circuits to Advance Enzyme Cascadetronics.Angewandte Chemie (International ed. in English) · 2025Article
- Metal coordination and enzymatic reaction of the glioma-target R132H isocitrate dehydrogenase 1: Insights by molecular simulations.PloS one · 2025Article
- Looking Beyond the Surface: Olutasidenib and Ivosidenib for Treatment of mIDH1 Acute Myeloid Leukemia.Current treatment options in oncology · 2024Review
- Treatment of IDH-mutant glioma in the INDIGO era.NPJ precision oncology · 2024Review
- Interactive biocatalysis achieved by driving enzyme cascades inside a porous conducting material.Communications chemistry · 2024Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 4 countries.
Funding
Abstract
Ivosidenib, an inhibitor of isocitrate dehydrogenase 1 (IDH1) R132C and R132H variants, is approved for the treatment of acute myeloid leukaemia (AML). Resistance to ivosidenib due to a second site mutation of IDH1 R132C, leading to IDH1 R132C/S280F, has emerged. We describe biochemical, crystallographic, and cellular studies on the IDH1 R132C/S280F and R132H/S280F variants that inform on the mechanism of second-site resistance, which involves both modulation of inhibitor binding at the IDH1 dimer-interface and alteration of kinetic properties, which enable more efficient 2-HG production relative to IDH1 R132C and IDH1 R132H. Importantly, the biochemical and cellular results demonstrate that it should be possible to overcome S280F mediated resistance in AML patients by using alternative inhibitors, including some presently in phase 2 clinical trials.
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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.