ArticleOncotarget2014
Linking off-target kinase pharmacology to the differential cellular effects observed among PARP inhibitors.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Comparison of the Efficacy and Safety of PARP Inhibitors as a Monotherapy for Platinum-Sensitive Recurrent Ovarian Cancer: A Network Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Neuroinflammation and Graft Survival in Pluripotent Stem Cell-Derived Therapies for the Central Nervous System.Journal of neurochemistry · 2026Review
- Global Proteomic Determination of the Poly-Pharmacological Effects of PARP Inhibitors Following Treatment of High-Grade Serous Ovarian Cancer Cells.International journal of molecular sciences · 2025Article
- A review of diffuse hemispheric glioma, H3 G34-mutant disease development, DNA repair, microenvironment, and treatments on the horizon.NPJ precision oncology · 2025Review
- Time-Trend Analysis and Risk Factors for Niraparib-Induced Nausea and Vomiting in Ovarian Cancer: A Prospective Study.Cancer research and treatment · 2025Article
- R2eGIN: Residual Reconstruction Enhanced Graph Isomorphism Network for Accurate Prediction of Poly (ADP-Ribose) Polymerase Inhibitors.Bioinformatics and biology insights · 2025Article
- Dual Targeting of CXCancers · 2024Article
- The role of epigenetic changes in the pathology and treatment of inherited retinal diseases.Frontiers in cell and developmental biology · 2023Review
- Review
- Therapeutic Potentials of Poly (ADP-Ribose) Polymerase 1 (PARP1) Inhibition in Multiple Sclerosis and Animal Models: Concept Revisiting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- A multi-task FP-GNN framework enables accurate prediction of selective PARP inhibitors.Frontiers in pharmacology · 2022Article
- Poly(ADP)-Ribosylation Inhibition: A Promising Approach for Clear Cell Renal Cell Carcinoma Therapy.Cancers · 2021Article
- PARP Inhibitors Display Differential Efficacy in Models ofInternational journal of molecular sciences · 2021Article
- Pharmacological Poly (ADP-Ribose) Polymerase Inhibitors DecreaseFrontiers in immunology · 2021Article
- Article
- Drug repurposing studies of PARP inhibitors as a new therapy for inherited retinal degeneration.Cellular and molecular life sciences : CMLS · 2020Article
- Poly (ADP-Ribose) Polymerase Inhibitors: Talazoparib in Ovarian Cancer and Beyond.Drugs in R&D · 2020Review
- The kinase polypharmacology landscape of clinical PARP inhibitors.Scientific reports · 2020Article
- PARP Inhibitors in Ovarian Cancer: The Route to "Ithaca".Diagnostics (Basel, Switzerland) · 2019Review
- Dual Inhibitors of PARPs and ROCKs.ACS omega · 2018Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PARP inhibitors hold promise as a novel class of targeted anticancer drugs. However, their true mechanism of action is still not well understood following recent reports that show marked differences in cellular effects. Here, we demonstrate that three PARP drug candidates, namely, rucaparib, veliparib, and olaparib, have a clearly different in vitro affinity profile across a panel of diverse kinases selected using a computational approach that relates proteins by ligand similarity. In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK. In contrast, olaparib does not inhibit any of the sixteen kinases tested. In between, veliparib inhibits only two, namely, PIM1 and CDK9. The differential kinase pharmacology observed among PARP inhibitors provides a plausible explanation to their different cellular effects and offers unexplored opportunities for this drug class, but alerts also on the risk associated to transferring directly both preclinical and clinical outcomes from one PARP drug candidate to another.
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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.