ReviewCardiology and therapy2025
Transthyretin Kinetic Stabilizers for ATTR Amyloidosis: A Narrative Review of Mechanisms and Therapeutic Benefits.
Review in Cardiology and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Disease-Modifying Therapies for Hereditary Transthyretin Amyloidosis with Polyneuropathy: Current Status and Future Perspectives.Neurology and therapy · 2026Review
- Specific treatment of ATTR-CM in Germany-expert consensus of the German Society of Amyloid Diseases (DGAK) and German Cardiac Society (DGK).Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Impact of Tafamidis on Transthyretin Concentration and Its Relation to All-Cause Mortality in Patients with Transthyretin Amyloid Cardiomyopathy: An Analysis from ATTR-ACT.Cardiology and therapy · 2026Article
- Survival in a Contemporary, Real-World, Matched Cohort of Patients with Transthyretin Amyloid Cardiomyopathy Treated vs Not Treated with Tafamidis.Cardiology and therapy · 2026Article
- Cofactor-Free Tau Filaments Are Dynamic and Undergo Structural Evolution Driven by Thermodynamic Control.Journal of the American Chemical Society · 2026Article
- Machine Learning-Based Prediction of Transthyretin-Binding Activity and Its Application to Screening Food-Derived Compounds for ATTR Amyloidosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Clinical outcomes with vutrisiran in transthyretin amyloidosis: a systematic review and meta-analysis of randomized trials.Global cardiology science & practice · 2026Review
- The Promise and Pitfalls of TTR Stabilization Assays in ATTR-CM.JACC. CardioOncology · 2026Article
- Exploring Tafamidis Effects Through PBPK-QSP Modelling.Pharmaceutics · 2026Article
- Synthesis, Structural Characterization, and In Silico Evaluation of the Salicylidene Schiff Base 4‑{(ACS omega · 2026Article
- Phenomenological model of transthyretin stabilization.Scientific reports · 2026Article
- Beyond a gatekeeper: the non-classical signaling role of STRA6 in driving endothelial senescence and atherosclerosis.Frontiers in immunology · 2026Review
- Development and characterization of chimeric antigen receptor macrophages for amyloid clearance.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transthyretin amyloidosis (ATTR amyloidosis) is a systemic disease affecting multiple organ systems, particularly the heart and peripheral nervous system. Decades of research suggest the disease is caused by the dissociation, misfolding, and aggregation of transthyretin (TTR), resulting in extracellular deposition of amyloid fibrils in tissue and organs. If untreated, ATTR amyloidosis leads to substantial functional impairment, quality-of-life burden, and mortality. Because dissociation of the TTR tetramer is rate-limiting for aggregation and amyloid fibril formation, small molecules that bind to and stabilize the natively folded tetramer of TTR have been developed. Subunit exchange experiments demonstrated that tafamidis and acoramidis effectively slow TTR tetramer dissociation and aggregation in plasma at concentrations achieved with approved oral doses in patients with ATTR amyloidosis. In randomized controlled clinical trials, these TTR kinetic stabilizers have significantly reduced cardiomyopathy progression and improved quality of life in patients with variant or wild-type disease (tafamidis is also approved to slow polyneuropathy progression). Current availability of two kinetic stabilizers has increased interest in their pharmacological properties and clinical effects, including potential similarities and disparities. In this review, the mechanisms involved in TTR kinetic stabilization are summarized with preclinical and clinical study findings on the use of the kinetic stabilizers tafamidis and acoramidis.
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