ArticleBlood cancer journal2011
Pacritinib (SB1518), a JAK2/FLT3 inhibitor for the treatment of acute myeloid leukemia.
Article in Blood cancer journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 106 citations in OpenAlex.
- Phase 1/2 study of pacritinib, a next generation JAK2/FLT3 inhibitor, in myelofibrosis or other myeloid malignancies.Journal of hematology & oncology · 2016Trial
- Targeting FLT3 in Acute Myeloid Leukemia: Structural Insights and Key Challenges.ACS bio & med chem Au · 2026Review
- Review
- Dual-Targeting Strategy in Cancer Therapy: The Emerging Role of Pyrrolopyrimidine Scaffolds.Chemistry & biodiversity · 2026Review
- Counter-Therapeutic Strategies for Resistance of FLT3 Inhibitors in Acute Myeloid Leukemia.Cells · 2025Review
- Molecular chameleons adaptability in target binding.Structural dynamics (Melville, N.Y.) · 2025Article
- Insights into the cellular function and mechanism of action of quinone reductase 2 (NQO2).The Biochemical journal · 2025Review
- Dual inhibition of the TrkA and JAK2 pathways using entrectinib and pacritinib suppresses the growth and metastasis of HER2-positive and triple-negative breast cancers.Cancer letters · 2024Article
- Recent Advances in IRAK1: Pharmacological and Therapeutic Aspects.Molecules (Basel, Switzerland) · 2024Review
- Review
- Pacritinib inhibits proliferation of primary effusion lymphoma cells and production of viral interleukin-6 induced cytokines.Scientific reports · 2024Article
- Design and synthesis of phenylthiophosphoryl dichloride derivatives and evaluation of their antitumour and anti-inflammatory activities.Frontiers in chemistry · 2024Article
- Developments of Fms-like Tyrosine Kinase 3 Inhibitors as Anticancer Agents for AML Treatment.Current medicinal chemistry · 2024Review
- MicroED as a Powerful Tool for Structure Determination of Macrocyclic Drug Compounds Directly from Their Powder Formulations.ACS chemical biology · 2023Article
- Rigid Scaffolds Are Promising for Designing Macrocyclic Kinase Inhibitors.ACS pharmacology & translational science · 2023Article
- MicroED as a powerful tool for structure determination of macrocyclic drug compounds directly from their powder formulations.bioRxiv : the preprint server for biology · 2023Article
- Review
- Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research.International journal of molecular sciences · 2023Review
- Pacritinib inhibits glucose consumption in squamous cell lung cancer cells by targeting FLT3.Scientific reports · 2023Article
- Potential applications of JAK inhibitors, clinically approved drugs against autoimmune diseases, in cancer therapy.Frontiers in pharmacology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FMS-like tyrosine kinase 3 (FLT3) is the most commonly mutated gene found in acute myeloid leukemia (AML) patients and its activating mutations have been proven to be a negative prognostic marker for clinical outcome. Pacritinib (SB1518) is a tyrosine kinase inhibitor (TKI) with equipotent activity against FLT3 (IC(50)=22 n) and Janus kinase 2 (JAK2, IC(50)=23 n). Pacritinib inhibits FLT3 phosphorylation and downstream STAT, MAPK and PI3 K signaling in FLT3-internal-tandem duplication (ITD), FLT3-wt cells and primary AML blast cells. Oral administration of pacritinib in murine models of FLT3-ITD-driven AML led to significant inhibition of primary tumor growth and lung metastasis. Upregulation of JAK2 in FLT3-TKI-resistant AML cells was identified as a potential mechanism of resistance to selective FLT3 inhibition. This resistance could be overcome by the combined FLT3 and JAK2 activities of pacritinib in this cellular model. Our findings provide a rationale for the clinical evaluation of pacritinib in AML including patients resistant to FLT3-TKI therapy.
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.