ArticleJournal of thrombosis and haemostasis : JTH2022
The Btk inhibitor AB-95-LH34 potently inhibits atherosclerotic plaque-induced thrombus formation and platelet procoagulant activity.
Article in Journal of thrombosis and haemostasis : JTH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Selective degradation of platelet BTK by PROTAC NX-5948 provides antithrombotic benefits without affecting hemostasis.Blood advances · 2026Article
- Advances in targeted and cellular therapies for relapsed/refractory mantle cell lymphoma: immunotherapeutic strategies and challenges.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Hemostasis-Sparing Antiplatelet Therapy: Current Concepts and Emerging Targets in Arterial Thrombosis.Biomolecules & therapeutics · 2026Review
- Clinical application of the HALP score for predicting early neurological deterioration in older patients with acute cerebral infarction.Biomedical reports · 2026Article
- Bioinformatics analyses reveal the autophagy-related feature biomarkers in dilated cardiomyopathy with heart failure.Frontiers in cardiovascular medicine · 2025Article
- Selective Btk inhibition by PRN1008/PRN473 blocks human CLEC-2, and PRN473 reduces venous thrombosis formation in mice.Blood advances · 2024Article
- GPVI inhibition: Advancing antithrombotic therapy in cardiovascular disease.European heart journal. Cardiovascular pharmacotherapy · 2024Review
- Impact of antiplatelet therapy on microvascular thrombosis during ST-elevation myocardial infarction.Frontiers in molecular biosciences · 2024Review
- Current concepts and novel targets for antiplatelet therapy.Nature reviews. Cardiology · 2023Review
- The Btk inhibitor AB-95-LH34 potently inhibits atherosclerotic plaque-induced thrombus formation and platelet procoagulant activity.Journal of thrombosis and haemostasis : JTH · 2022Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundNew antithrombotic therapies with less effect on bleeding are needed for coronary artery disease. The Btk inhibitor ibrutinib blocks atherosclerotic plaque-mediated thrombus formation. However, it is associated with increased bleeding, possibly due to non-Btk-mediated effects. Btk-deficient patients do not have bleeding issues, suggesting selective Btk inhibition as a promising antithrombotic strategy.
objectivesTo compare the antithrombotic effects of the highly selective Btk inhibitor AB-95-LH34 (LH34) with ibrutinib.
methodsGlycoprotein VI and G-protein coupled receptor-mediated platelet function and signaling were analyzed in healthy human donor platelets by lumi-aggregometry, flow adhesion, and western blot following 1 h treatment with inhibitors in vitro.
resultsLH34 showed similar inhibition of Btk-Y223 phosphorylation as ibrutinib, but had no off-target inhibition of Src-Y418 phosphorylation. Similar dose-dependent inhibition of aggregation to atherosclerotic plaque material was observed for both. However, in response to Horm collagen, which also binds integrin α2β1, LH34 exhibited less marked inhibition than ibrutinib. Both LH34 and ibrutinib inhibited platelet adhesion and aggregation to plaque material at arterial shear. Ibrutinib demonstrated the most potent effect, with complete blockade at high concentrations. Platelet activation (P-selectin) and procoagulant activity (phosphatidylserine exposure) in thrombi were inhibited by LH34 and completely blocked by ibrutinib at high concentrations. Furthermore, plaque-induced thrombin generation was reduced by higher concentrations of LH34 and ibrutinib.
conclusionsLH34 potently inhibits atherosclerotic plaque-induced thrombus formation and procoagulant platelet activity in vitro, with less off-target inhibition of Src than ibrutinib, suggesting it is a promising antiplatelet therapy with the potential for reduced bleeding side effects.
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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.