BridgeBio’s Acoramidis Cuts sTTR Variability to 9.5% and Reduces Hospitalizations 34%
BBIO•Acoramidis cut intra-individual sTTR variability to 9.5% versus 12.8% on placebo (p<0.001), with lower variability linked to a 44% reduction in all-cause mortality risk (HR 0.56; p=0.014). Indirect comparison showed 34% fewer cardiovascular hospitalizations versus tafamidis (RRR 0.66; 95% CI 0.46–0.95) and 41% lower outpatient heart failure risk (HR 0.59; p<0.0001).
1. sTTR Variability and Mortality Benefits
Acoramidis increased serum transthyretin levels early and significantly reduced intra-individual sTTR variability to 9.5% versus 12.8% on placebo (p<0.001). Lower variability and higher achieved sTTR were each independently associated with reduced all-cause mortality risk (HR 0.56; p=0.014 and HR 0.46; p=0.014 respectively).
2. Outpatient Worsening Heart Failure Reduction
The treatment drove a 41% reduction in outpatient worsening heart failure (HR 0.59; 95% CI 0.46–0.75; p<0.0001), with Kaplan–Meier curves separating within 30 days and sustained through 30 months. Outpatient episodes were a strong predictor of mortality and cardiovascular hospitalizations, and acoramidis retained benefit after adjustment.
3. Cardiovascular Hospitalizations vs Tafamidis
In an anchored matching‐adjusted indirect comparison against tafamidis, acoramidis demonstrated a 34% relative reduction in cardiovascular hospitalizations (RRR 0.66; 95% CI 0.46–0.95) and showed a favorable 28% hazard reduction trend in all‐cause mortality, while maintaining a comparable safety profile.
4. Biomarker and Quality-of-Life Improvements
Additional analyses showed acoramidis attenuated NT-proBNP rise by approximately 50% across subgroups over 30 months and significantly maintained or improved Kansas City Cardiomyopathy Questionnaire Overall Summary Scores versus placebo, indicating robust biomarker and patient health status benefits.
