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Beyonttra▼(Acoramidis)
Mode of Action (MOA)
Maximising TTR stabilisation is essential to helping towards slowing disease progression for patients with ATTR-CM.
ATTR-CM is a disease of Transthyretin (TTR) destabilisation, leading to a build up of amyloid fibrils in the heart. TTR stabilisation prevents the formation of amyloid fibrils, reducing further toxic amyloid deposition and preserving cardiac function.
TTR, or prealbumin, is essential for everyday health and function.
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How does Beyonttra (Acoramidis) work?
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Beyonttra▼(Acoramidis) has been specifically designed to maximise TTR stabilisation, and is the only stabiliser with near-complete(≥90%) TTR stabilisation in the label
- T119M is a rare protective genetic variant TTR Mutation*that kinetically and thermodynamically stabilises the tetramer
- Beyonttra mimics the structure of the protective T119M mutation, thereby limiting the formation and deposition of amyloid fibrils
- A mechanism of action that is applicable to both variant or wild-type ATTR-CM
- Beyonttra provides>90% TTR stabilisation in vitro, providing maximum stabilisation.
*Most variants of TTR increase the amyloidogenic potential of the protein by destabilising the tetramers, but there are a few variants (like T119M) that have been shown to increase stabilisation of TTR tetramers and thereby prevent amyloidogenesis
PP-BEY-GB-0004, November 2025
- Referencesexpand_less
- 1UK Summary of Product Characteristics for BEYONTTRA (acoramidis)
- 2Ruberg FL, et al. J Am Coll Cardiol. 2019;73(22):2872–2891.
- 3Morfino P, et al. Pharmaceutics.2023:15(1129):1-18.
- 4Liz MA, et al. Neurol Ther. 2020;9(2):395–402;
- 5Miller M, et al. J Med Chem. 2018;61(17):7862–7876
- 6Penchala SC, et al. Proc Natl Acad Sci USA. 2013;110(24):9992–9997

