Inspired by nature. Designed with purpose.

Why Stabilize TTR?

• TTR is a naturally ocurring protein that is
  synthesized in the liver. It performs its function only when present and stable^1,2

• In ATTR-CM, aging or genetic variants can cause
  TTR to destabilize and break apart
  into monomers
  that aggregate into toxic amyloid fibrils^3-5

More on Mechanism of Disease

Attruby was designed to mimic the properties of the protective T119M mutation

T119M is a naturally ocurring stabilizing variant of TTR that has been associated with reduced disease severity.^9,10

More on T119M

Attruby delivers near-complete in vitro TTR stabilization^6,9

Attruby is the only FDA-approved treatment described as achieving near-complete (>90%) in vitro TTR stabilization in its label — no other product label includes this distinction.

More on Near-Complete
TTR Stabilization

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Watch >90%
Stabilization in Action

Low rates of discontinuations due to adverse drug reactions and convenient dosing with Attruby^6,7

See Dosing + Safety

ATTR-CM=transthyretin amyloid cardiomyopathy; TTR=transthyretin.

References: 1. Liz MA, Coelho T, Bellotti V, Fernandez-Arias MI, Mallaina P, Obici L. A narrative review of the role of transthyretin in health and disease. Neurol Ther. 2020;9(2):395-402. doi:10.1007/s40120-020-00217-0 2. Vieira M, Saraiva MJ. Transthyretin: a multifaceted protein. Biomol Concepts. 2014;5(1):45-54. doi:10.1515/bmc-2013-0038 3. Ruberg FL, Grogan M, Hanna M, Kelly JW, Maurer MS. Transthyretin amyloid cardiomyopathy: JACC state-of-the-art review. J Am Coll Cardiol. 2019;73(22):2872-2891. doi:10.1016/j.jacc.2019.04.003 4. Kittleson MM, Maurer MS, Ambardekar AV, et al. Cardiac amyloidosis: evolving diagnosis and management: a scientific statement from the American Heart Association. Circulation. 2020;142(1):e7-e22. doi:10.1161/CIR.0000000000000792 5. Witteles RM, Bokhari S, Damy T, et al. Screening for transthyretin amyloid cardiomyopathy in everyday practice. JACC Heart Fail. 2019;7(8):709-716. doi:10.1016/j.jchf.2019.04.010 6. Attruby. Prescribing information. BridgeBio Pharma, Inc.; 2024. 7. Gillmore JD, Judge DP, Cappelli F, et al. Efficacy and safety of acoramidis in transthyretin amyloid cardiomyopathy. N Engl J Med. 2024;390(2)(Suppl 1):1-34. doi:10.1056/NEJMoa2305434 8. Gertz MA, Benson MD, Dyck PJ, et al. Diagnosis, prognosis, and therapy of transthyretin amyloidosis. J Am Coll Cardiol. 2015;66(21):2451-2466. doi:10.1016/j.jacc.2015.09.075 9. Gillmore JD, Judge DP, Cappelli F, et al. Efficacy and safety of acoramidis in transthyretin amyloid cardiomyopathy. N Engl J Med. 2024;390(2):132-142. doi:10.1056/NEJMoa2305434 10. Hammarström P, Jiang X, Hurshman AR, Powers ET, Kelly JW. Sequence-dependent denaturation energetics: a major determinant in amyloid disease diversity. Proc Natl Acad Sci USA. 2002;99(suppl 4):16427-16432. doi:10.1073/pnas.202495199 11. Almeida ZL, Vaz DC, Brito RMM. Transthyretin mutagenesis: impact on amyloidogenesis and disease. Crit Rev Clin Lab Sci. 2024;61(7):616-640. doi:10.1080/10408363.2024.2350379 12. Hornstrup LS, Frikke-Schmidt R, Nordestgaard BG, Tybjaerg-Hansen A. Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy. Arterioscler Thromb Vasc Biol. 2013;33(6):1441-1447. doi:10.1161/ATVBAHA.113.301273 13. Judge DP, Heitner SB, Falk RH, et al. Transthyretin stabilization by AG10 in symptomatic transthyretin amyloid cardiomyopathy. J Am Coll Cardiol. 2019;74(3):285-295. doi:10.1016/j.jacc.2019.03.012 14. Maurer MS, Judge DP, Gillmore JD, et al. Early increase in serum transthyretin by acoramidis independently predicts improved survival in TTR amyloid cardiomyopathy. J Am Coll Cardiol. 2025;85(20):1911-1923. doi:10.1016/j.jacc.2025.03.542 15. Sarswat N, Ambardekar A, Taubel J, et al. Acoramidis-mediated early increase in serum transthyretin is associated with lower cardiovascular-related hospitalizations and mortality: insights from the ATTRibute-CM study. Poster presented at: American College of Cardiology Annual Scientific Meeting; March 29-31, 2025; Chicago, IL. 16. Data on file. BridgeBio, Inc.; 2024-2025.

T119M is a naturally occurring stabilizing variant of TTR

In TTR VARIANT CARRIERS¹¹

• The V30M mutation can induce structural alterations that lead to amyloid deposition. Researchers found that the T119M mutation may mitigate the pathogenic effects of the V30M mutation
• Carriers of T119M had higher levels of serum TTR due to slower clearance of the protein from serum, as assessed by clearance studies

In the general population¹²

Carriers of T119M are reported to have:

20% higher levels of serum TTR

5-10 years longer life expectancy

ATTR-CM=transthyretin amyloid cardiomyopathy; TTR=transthyretin.

How ATTR-CM Develops

TTR is a key transport protein that binds to and transports vitamin A and thyroxine throughout the body, and it performs its function when it's present and stable.^1,2

In ATTR-CM, aging or genetic variants can cause TTR to destabilize and break apart into monomers, which misfold and accumulate as toxic amyloid fibrils throughout the body, including in the myocardium.^3-5

By preserving TTR structure and slowing toxic amyloid fibril formation, TTR stabilizers may help alter the natural course of the disease.⁸

ATTR-CM=transthyretin amyloid cardiomyopathy; TTR=transthyretin.

It's a marker you can measure. And data you can
stand behind.

Early increase in serum TTR within
28 days of starting Attruby⁹

Change From Baseline in Serum TTR Level*

Levels of serum TTR, also known as prealbumin, are a measure of TTR stability¹³

IN 2 SEPARATE POST HOC EXPLORATORY ANALYSES

Early increases in serum TTR were associated with improved outcomes

Based on logistic
model prediction^14†

Based on Cox proportional hazards model^15‡

Based on Cox proportional
hazards model^15‡

These exploratory analyses are based on participants from the ATTRibute-CM phase 3 clinical trial for whom serum TTR levels were available at both baseline and Day 28 and may not fully reflect the broader patient population. Additionally, this effect may not be generalizable to other TTR stabilizers.

^*Per standard protocol, any missing values were imputed as placebo values.¹⁶

^†Independent study in 557 patients with ATTR-CM from the ATTRibute-CM study. Univariate analyses in both the overall population and the Attruby-treated population; change in serum TTR remained an independent predictor of ACM even after adjusting for baseline demographic variables, diuretic use, NYHA class, baseline serum TTR, TTR variant or wild-type status, and National Amyloidosis Centre stage.¹⁴

^‡Analysis of the mITT population of ATTRibute-CM. Combined outcomes of serum TTR CFB to Day 28 and Month 30, and first CVH or cardiovascular mortality, excluding those events that occurred prior to Day 28. Patient stratification was based on treatment group, baseline TTR (<20 or ≥20 mg/dL), and original randomization factors of TTR genotype (wild-type vs variant), NT-proBNP (≤3000 or >3000 pg/mL), and eGFR (<45 or ≥45 mL/min/1.73 m2).¹⁵

ACM=all-cause mortality; CFB=change from baseline; CVH=cardiovascular-related hospitalization; CVM=cardiovascular-related mortality; eGFR=estimated glomerular filtration rate; LS mean=least-squares mean; mITT=modified intent-to-treat; NT-proBNP=N-terminal pro–B-type natriuretic peptide; NYHA=New York Heart Association; RR=risk reduction; TTR=transthyretin.