Biotech Values

[iwfal]

ESPR ISIS AMRN

You contend that statins likely work via a mechanism other than LDL, but the hard evidence you say regulators should require for any hypothesis involving CV biomarkers is lacking for the posited alternative MoA.

FWIW I agree I overstated my position a little when talking about other bio markers changes effected by statins. I think it is best said that the other biomarker effects of statins (lower CRP, higher HDL, specific LDL types) are gaining more and more credence as other potential, equally plausible, MOA. I.e. There is now a cloud of fog around the concept that LDL is the primary beneficial MOA of statins. And the cardiology community has been badly stung repeatedly by other highly touted bio markers that failed (repeatedly) in trials and is now backing off on all of them. Including LDL. E.g. The change in treatment guidelines in 2012/2013 (which removed HDL targets AND LDL targets largely for these reasons)