Evidence map›Paper›PMID 32198525›Full record

ReviewAnnals of hematology2020

Management of myelofibrosis after ruxolitinib failure.

Claire N Harrison, Nicolaas Schaap, Ruben A Mesa

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Annals of hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07750574 (A Randomized, Phase 2 Study to Evaluate the Safety, Pharmacokinetics, Pharmacodynamics, and Efficacy of Oral Flonoltinib Maleate in Patients With JAK Inhibitor Treatment-Naïve or Resistant Myelofibrosis), which is not on this map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
8.1field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

NCT07750574 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

A Randomized, Phase 2 Study to Evaluate the Safety, Pharmacokinetics, Pharmacodynamics, and Efficacy of Oral Flonoltinib Maleate in Patients With JAK Inhibitor Treatment-Naïve or Resistant Myelofibrosis

TypeinterventionalSponsorChengdu Zenitar Biomedical Technology Co., LtdRan2026 to 2028Enrolled105ConditionsMyelofibrosis, Myelofibrosis Due to and Following Polycythemia Vera, Myelofibrosis Transformation in Essential Thrombocythemia, Myelofibrosis With High Molecular Risk MutationsArmsFlonoltinib Maleate orally
3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 95 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 3 countries.

Claire N HarrisonGuy's and St Thomas' Hospital Foundation Trust, Westminster Bridge Rd, London, SE1 7EH, UK. claire.harrison@gstt.nhs.uk.
Nicolaas SchaapRadboud University Medical Centre, Nijmegen, Netherlands.
Ruben A MesaUniversity of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Guy's and St Thomas' NHS Foundation Trust · GBRadboud University Medical Center · NLThe University of Texas Health Science Center at San Antonio · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
NCI NIH HHS P30 CA054174
6 · The paper itself

Abstract

Myelofibrosis is a BCR-ABL1-negative myeloproliferative neoplasm characterized by anemia, progressive splenomegaly, extramedullary hematopoiesis, bone marrow fibrosis, constitutional symptoms, leukemic progression, and shortened survival. Constitutive activation of the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathway, and other cellular pathways downstream, leads to myeloproliferation, proinflammatory cytokine expression, and bone marrow remodeling. Transplant is the only curative option for myelofibrosis, but high rates of morbidity and mortality limit eligibility. Several prognostic models have been developed to facilitate treatment decisions. Until the recent approval of fedratinib, a JAK2 inhibitor, ruxolitinib was the only available JAK inhibitor for treatment of intermediate- or high-risk myelofibrosis. Ruxolitinib reduces splenomegaly to some degree in almost all treated patients; however, many patients cannot tolerate ruxolitinib due to dose-dependent drug-related cytopenias, and even patients with a good initial response often develop resistance to ruxolitinib after 2-3 years of therapy. Currently, there is no consensus definition of ruxolitinib failure. Until fedratinib approval, strategies to overcome ruxolitinib resistance or intolerance were mainly different approaches to continued ruxolitinib therapy, including dosing modifications and ruxolitinib rechallenge. Fedratinib and two other JAK2 inhibitors in later stages of clinical development, pacritinib and momelotinib, have been shown to induce clinical responses and improve symptoms in patients previously treated with ruxolitinib. Fedratinib induces robust spleen responses, and pacritinib and momelotinib may have preferential activity in patients with severe cytopenias. Reviewed here are strategies to ameliorate ruxolitinib resistance or intolerance, and outcomes of clinical trials in patients with myelofibrosis receiving second-line JAK inhibitors after ruxolitinib treatment.

Indexed as

Disease ManagementBenzenesulfonamidesClinical Trials as TopicHumansJanus KinasesNitrilesPrimary MyelofibrosisPyrazolesPyrimidinesPyrrolidinesSulfonamidesTreatment FailureBenzenesulfonamidesfedratinibJanus KinasesNitrilesPyrazolesPyrimidinesPyrrolidinesruxolitinibSulfonamidesFedratinibMomelotinibMyelofibrosisPacritinibRuxolitinib

Identifiers

PMID32198525
PMCPMC7237516
OpenAlexW3012454590

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.