Key result
E5555 (atopaxar) did not significantly reduce major cardiovascular adverse events compared to placebo in patients with ACS (5.0% vs 6.6%, P=0.73) or CAD (1.0% vs 4.5%, P=0.066).
Why the study?
Does the PAR-1 antagonist E5555 (atopaxar) added to standard therapy increase bleeding or improve cardiovascular outcomes in Japanese patients with ACS or high-risk CAD?
RCT (n=504)
double-blind
randomized
Yes
Does the PAR-1 antagonist E5555 (atopaxar) added to standard therapy increase bleeding or improve cardiovascular outcomes in Japanese patients with ACS or high-risk CAD?
Absolute Event Rate: 5% vs 6.6%
p-value: p=0.73
In Japanese patients with ACS or high-risk CAD, the PAR-1 antagonist atopaxar achieved significant platelet inhibition without increasing clinically significant bleeding, though it caused dose-dependent increases in liver function abnormalities and QTcF.
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Atopaxar adds no MACE benefit in ACS or CAD; challenges PAR-1 antagonism as an effective antiplatelet strategy.
Goto et al. (2010) conducted an RCT in Acute coronary syndrome or high-risk coronary artery disease (n=504). E5555 (atopaxar) vs. placebo was evaluated on Major cardiovascular adverse events (ACS cohort) (p=0.73). E5555 (atopaxar) did not significantly reduce major cardiovascular adverse events compared to placebo in patients with ACS (5.0% vs 6.6%, P=0.73) or CAD (1.0% vs 4.5%, P=0.066).
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