ArticleBlood advances2020
Fedratinib in myelofibrosis.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 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
51 citing papers in PubMed, 82 citations in OpenAlex.
- Primary Myelofibrosis (PMF)-The German ONKOPEDIA Guideline 2025.International journal of cancer · 2026Review
- Review
- Practical Guide for Managing Philadelphia-Negative Myeloproliferative Neoplasms in Patients with Organ Dysfunction.Oncology · 2026Review
- Rovadicitinib, a first-in-class JAK/ROCK inhibitor, in patients with myelofibrosis: a preclinical and phase I study.Blood cancer journal · 2026Article
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- [Myelofibrosis: watch and wait or treat?]Innere Medizin (Heidelberg, Germany) · 2026Review
- The Intricate Dance Between Inflammation and Myeloproliferative Neoplasms: From Origins to Outcomes.Current hematologic malignancy reports · 2026Review
- When, which and how to switch: Navigating JAK inhibitors in myelofibrosis.British journal of haematology · 2026Review
- Fedratinib treatment correlates with suppressed STAT3/AKT/calpain-1 signaling and inhibits hepatocellular carcinoma progression.Translational gastroenterology and hepatology · 2026Article
- Indirect treatment comparison of momelotinib vs fedratinib safety in patients with myelofibrosis.Future oncology (London, England) · 2025Article
- Recent advances and future perspectives in small molecule JAK2 inhibitors.Future medicinal chemistry · 2025Review
- Fedratinib in 2025 and beyond: indications and future applications.Blood advances · 2025Review
- Article
- Real-world treatment patterns and health care resource use for patients with myelofibrosis: results from the METER study.Blood advances · 2025Observational
- Article
- Identification of key modules and hub genes for sepsis-induced myopathy using weighted gene co-expression network analysis.Frontiers in genetics · 2025Article
- Non-kinase off-target inhibitory activities of clinically-relevant kinase inhibitors.European journal of medicinal chemistry · 2024Review
- The prospect of substrate-based kinase inhibitors to improve target selectivity and overcome drug resistance.Chemical science · 2024Review
- Advances in Myelofibrosis Management: New Janus Kinase Inhibitors Beyond Ruxolitinib.Journal of the advanced practitioner in oncology · 2024Article
- Drug repurposing screening and mechanism analysis based on human colorectal cancer organoids.Protein & cell · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Following the discovery of the JAK2V617F mutation in myeloproliferative neoplasms in 2005, fedratinib was developed as a small molecular inhibitor of JAK2. It was optimized to yield low-nanomolar activity against JAK2 (50% inhibitory concentration = 3 nM) and was identified to be selective for JAK2 relative to other JAK family members (eg, JAK1, JAK3, and TYK2). It quickly moved into clinical development with a phase 1 clinical trial opening in 2008, where a favorable impact on spleen and myelofibrosis (MF) symptom responses was reported. A phase 3 trial in JAK2 inhibitor treatment-naive MF patients followed in 2011 (JAKARTA); a phase 2 trial in MF patients resistant or intolerant to ruxolitinib followed in 2012 (JAKARTA-2). Clinical development suffered a major setback between 2013 and 2017 when the US Food and Drug Administration (FDA) placed fedratinib on clinical hold due to the development of symptoms concerning for Wernicke encephalopathy (WE) in 8 of 608 subjects (1.3%) who had received the drug. It was ultimately concluded that there was no evidence that fedratinib directly induces WE, but clear risk factors (eg, poor nutrition, uncontrolled gastrointestinal toxicity) were identified. In August 2019, the FDA approved fedratinib for the treatment of adults with intermediate-2 or high-risk MF. Notably, approval includes a "black box warning" on the risk of serious and fatal encephalopathy, including WE. FDA approval was granted on the basis of the JAKARTA studies in which the primary end points (ie, spleen and MF symptom responses) were met in ∼35% to 40% of patients (JAKARTA) and 25% to 30% of patients (JAKARTA-2), respectively.
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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.