ReviewJournal of medicinal chemistry2016
Targeting Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 (MAPKAPK2, MK2): Medicinal Chemistry Efforts To Lead Small Molecule Inhibitors to Clinical Trials.
Review in Journal of medicinal chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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
40 citing papers in PubMed, 82 citations in OpenAlex.
- A novel framework for the discovery of MAPK-activated protein kinase 2 (MAPKAPK2) inhibitors using a multi-feature deep learning ensemble.Journal of computer-aided molecular design · 2026Article
- Proteomic Analysis of Influenza.Advances in experimental medicine and biology · 2026Review
- Article
- Non-Catalytic Inhibitors of the p38/MK2 Interface: Repurposing Approved Drugs to Target Neuroinflammation in Alzheimer's Disease.Journal of medicinal chemistry · 2025Article
- Molecular Docking and Target-Specific Binding Profiles of Benzosuberane-Based Compounds.ChemMedChem · 2025Review
- MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction.Physiological reports · 2025Article
- MK2 promotes p16 negative head and neck cancer migration, invasion, and metastasis.Cancer letters · 2025Article
- Decoding STAT3: a new frontier in understanding and treating hyperoxic lung injury.Frontiers in immunology · 2025Review
- MK2-mediated AKT/MYC signaling activation promotes epithelial-mesenchymal transition in lung adenocarcinoma.Frontiers in genetics · 2025Article
- Article
- Expression profile of mRNAs and miRNAs related to mitogen-activated kinases in HaCaT cell culture treated with lipopolysaccharide a and adalimumab.Cell cycle (Georgetown, Tex.) · 2024Article
- Recent Advancements in the Treatment of Alzheimer's Disease: A Multitarget-directed Ligand Approach.Current medicinal chemistry · 2024Review
- Small molecule targeting of the p38/Mk2 stress signaling pathways to improve cancer treatment.BMC cancer · 2023Article
- Revisiting p38 Mitogen-Activated Protein Kinases (MAPK) in Inflammatory Arthritis: A Narrative of the Emergence of MAPK-Activated Protein Kinase Inhibitors (MK2i).Pharmaceuticals (Basel, Switzerland) · 2023Review
- MAPKAPK2-centric transcriptome profiling reveals its major role in governing molecular crosstalk of IGFBP2, MUC4, and PRKAR2B during HNSCC pathogenesis.Computational and structural biotechnology journal · 2023Article
- Metastasis and MAPK Pathways.International journal of molecular sciences · 2022Review
- Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.Molecular carcinogenesis · 2022Article
- Cross-species transcriptomic signatures predict response to MK2 inhibition in mouse models of chronic inflammation.iScience · 2021Article
- Development of cell-based high throughput luminescence assay for drug discovery in inhibiting OCT4/DNA-PKcs and OCT4-MK2 interactions.Biotechnology and bioengineering · 2021Article
- MK2-Deficient Mice Are Bradycardic and Display Delayed Hypertrophic Remodeling in Response to a Chronic Increase in Afterload.Journal of the American Heart Association · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The p38/MAPK-activated kinase 2 (MK2) pathway is involved in a series of pathological conditions (inflammation diseases and metastasis) and in the resistance mechanism to antitumor agents. None of the p38 inhibitors entered advanced clinical trials because of their unwanted systemic side effects. For this reason, MK2 was identified as an alternative target to block the pathway but avoiding the side effects of p38 inhibition. However, ATP-competitive MK2 inhibitors suffered from low solubility, poor cell permeability, and scarce kinase selectivity. Fortunately, non-ATP-competitive inhibitors of MK2 have been already discovered that allowed circumventing the selectivity issue. These compounds showed the additional advantage to be effective at lower concentrations in comparison to the ATP-competitive inhibitors. Therefore, although the significant difficulties encountered during the development of these inhibitors, MK2 is still considered as an attractive target to treat inflammation and related diseases to prevent tumor metastasis and to increase tumor sensitivity to chemotherapeutics.
Indexed as
Identifiers
What OpenQuestion holds
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.