This is why there needs to be a push to make other biomarkers such as EPA/AA and hs-CRP an acceptable surrogate endpoint to approve drugs for CV risk reduction.
Woodcock recently claimed:
“But even that fervor has caused collateral damage, Woodcock said. Health burdens such as cardiovascular illness, addiction and antimicrobial resistance are now less attractive candidates for research, even though they affect far more people.
Woodcock urged researchers to leverage big data — such as electronic health records — to study those diseases with efficient, universal protocols. She also encouraged her audience to incorporate practicing doctors in the research process.”
She also claims:
“And above all other concerns was patient access. Other industries focus on making their products cheaper. But that’s not the case with the pharmaceutical industry, where high failure rates and expensive clinical trials have led to drugs far beyond the financial reach of those in need.”
So here we have a drug that alleviates all her concerns and yet there was a last minute adcom? Why?
To answer Raf’s question: I believe the reason for the late ADCOM is the vast amount of “profound” data the FDA had to scour through (icosapent mechanisms of action) and realized they needed more time and experts in the field to go through it.
I believe this ADCOM will be about introducing other biomarkers (EPA/AA, hs-CRP) as acceptable surrogate end points to approve drugs for CVD reduction and really ushering in a new change in the way doctors deal with heart disease. This is why I also believe we will get a stand-alone label like Repatha did.
The ADCOM is going to be paradigm shifting and doctors and scientists will enjoy a thriller as Bhattman (hopefully) and Mason explain the mechanisms of action of EPA (hopefully with Evaporate images) that will change the landscape of heart disease forever.
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