ArticleExperimental hematology & oncology2020
The SMAC mimetic LCL-161 selectively targets JAK2
Article in Experimental hematology & oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 43 citations in OpenAlex.
- Final results of a phase 2 clinical trial of LCL161, an oral SMAC mimetic for patients with myelofibrosis.Blood advances · 2021Trial
- Targeting "undruggable" cancer proteins: pharmacological challenges and emerging strategies.Translational cancer research · 2026Review
- Cytokine Landscapes, Immune Dysregulation, and Treatment Perspectives in Philadelphia-Negative Myeloproliferative Neoplasms: A Narrative Review.Journal of clinical medicine · 2025Review
- Uncovering the rewired IAP-JAK regulatory axis as an immune-dependent vulnerability of LKB1-mutant lung cancer.Nature communications · 2025Article
- Mitochondrial transfer from bone mesenchymal stem cells protects against tendinopathy both in vitro and in vivo.Stem cell research & therapy · 2023Article
- Recent advances in therapies for primary myelofibrosis.Faculty reviews · 2023Review
- Novel Therapies in Myelofibrosis: Beyond JAK Inhibitors.Current hematologic malignancy reports · 2022Review
- Novel Therapies in Myeloproliferative Neoplasms: Beyond JAK Inhibitor Monotherapy.Journal of immunotherapy and precision oncology · 2021Review
- Review
- Inflammatory Pathophysiology as a Contributor to Myeloproliferative Neoplasms.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEvasion from programmed cell death is a hallmark of cancer and can be achieved in cancer cells by overexpression of inhibitor of apoptosis proteins (IAPs). Second mitochondria-derived activator of caspases (SMAC) directly bind to IAPs and promote apoptosis; thus, SMAC mimetics have been investigated in a variety of cancer types. particularly in diseases with high inflammation and NFĸB activation. Given that elevated TNFα levels and NFĸB activation is a characteristic feature of myeloproliferative neoplasms (MPN), we investigated the effect of the SMAC mimetic LCL-161 on MPN cell survival in vitro and disease development in vivo.
methodsTo investigate the effect of the SMAC mimetic LCL-161 in vitro, we utilized murine and human cell lines to perform cell viability assays as well as primary bone marrow from mice or humans with JAK2
resultsWe found that JAK2
conclusionLCL-161 may be therapeutically useful in MPN, in particular when exogenous TNFα signaling is blocked. NFĸB activation is a characteristic feature of JAK2
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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.