ArticleOncotarget2016
A method for quantification of exportin-1 (XPO1) occupancy by Selective Inhibitor of Nuclear Export (SINE) compounds.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 30 citations in OpenAlex.
- Spatial memory in Alzheimer's disease 5XFAD mice is enhanced by XPO1 inhibitor KPT-330.GeroScience · 2026Article
- Preclinical characterization of a reversible XPO1 inhibitor for cancer therapy.Nature communications · 2026Article
- Refining the role of selinexor in multiple myeloma: strategic use in a shifting treatment landscape.ESMO open · 2026Review
- Regulation of RNA-binding proteins by small biomolecules.Nature reviews. Molecular cell biology · 2026Review
- Selinexor enhances temozolomide efficacy in glioblastoma through modulation of multiple resistance-associated mechanisms.Frontiers in oncology · 2026Article
- Cysteine Alkylation in Enzymes and Transcription Factors: A Therapeutic Strategy for Cancer.Cancers · 2025Review
- Targeting the chromatin binding of exportin-1 disrupts NFAT and T cell activation.Nature chemical biology · 2024Article
- Next-Generation SINE Compound KPT-8602 Ameliorates Dystrophic Pathology in Zebrafish and Mouse Models of DMD.Biomedicines · 2022Article
- Selinexor synergizes with azacitidine to eliminate myelodysplastic syndrome cells through p53 nuclear accumulation.Investigational new drugs · 2022Article
- The selective inhibitor of nuclear export (SINE) verdinexor exhibits biologic activity against canine osteosarcoma cell lines.Veterinary and comparative oncology · 2021Article
- The SINE Compound KPT-350 Blocks Dystrophic Pathologies in DMD Zebrafish and Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Association of XPO1 Overexpression with NF-κB and Ki67 in Colorectal Cancer.Asian Pacific journal of cancer prevention : APJCP · 2019Article
- Anti-tumor efficacy of Selinexor (KPT-330) in gastric cancer is dependent on nuclear accumulation of p53 tumor suppressor.Scientific reports · 2018Article
- Article
- Inhibition of exportin-1 function results in rapid cell cycle-associated DNA damage in cancer cells.Oncotarget · 2017Article
- Inhibiting cancer cell hallmark features through nuclear export inhibition.Signal transduction and targeted therapyReview
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selective Inhibitor of Nuclear Export (SINE) compounds are a family of small-molecules that inhibit nuclear export through covalent binding to cysteine 528 (Cys528) in the cargo-binding pocket of Exportin 1 (XPO1/CRM1) and promote cancer cell death. Selinexor is the lead SINE compound currently in phase I and II clinical trials for advanced solid and hematological malignancies. In an effort to understand selinexor-XPO1 interaction and to establish whether cancer cell response is a function of drug-target engagement, we developed a quantitative XPO1 occupancy assay. Biotinylated leptomycin B (b-LMB) was utilized as a tool compound to measure SINE-free XPO1. Binding to XPO1 was quantitated from SINE compound treated adherent and suspension cells in vitro, dosed ex vivo human peripheral blood mononuclear cells (PBMCs), and PBMCs from mice dosed orally with drug in vivo. Evaluation of a panel of selinexor sensitive and resistant cell lines revealed that resistance was not attributed to XPO1 occupancy by selinexor. Administration of a single dose of selinexor bound XPO1 for minimally 72 hours both in vitro and in vivo. While XPO1 inhibition directly correlates with selinexor pharmacokinetics, the biological outcome of this inhibition depends on modulation of pathways downstream of XPO1, which ultimately determines cancer cell responsiveness.
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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.