"Its initial approval was based on clinical evidence that the drug lowered the bad cholesterol by about 60 percent and decreased the rate of cardiovascular events, including heart attack, heart failure leading to hospitalization and death, by approximately 50 percent."

I'm not sure where the author of that BioSpace piece is getting the ~50% decrease in rate of cardiovascular events. From the FOURIER trial data released in March 2017:

"Patients on Repatha experienced a reduction in the risk of heart attack (27 percent, nominal p<0.001), stroke (21 percent, nominal p=0.01) and coronary revascularization (22 percent, nominal p<0.001). Consistent with recent trials of more intensive LDL lowering, there was no observed effect on cardiovascular mortality. Similarly, there was no observed effect on hospitalization for unstable angina. In an exploratory analysis, the relative risk reduction for fatal and non-fatal heart attack or stroke was 19 percent in the first year (p=0.003) and 33 percent beyond the first year (p<0.00001)."

Even this latest sub-study showing Repatha significantly reduces risk of CV events in several high risk patient population (including patients with PAD) only achieved RRR in the range of 20% to 30%. Also one must keep in mind that with Repatha there was no observed effect on cardiovascular mortality. Combine that with the cost of the drug and you have an overly expensive antibody therapy with somewhat disappointing results for the price. Are there high-risk sub-groups that this can be marketed to? Sure. But will Repatha ever be a standard of care therapy? Probably not due to the cost. 

But back to apabetalone.......apabetalone doesn't modulate LDL (at least in the Phase 2 trials) and modulates entirely different risk factors (apoAI, HDL, hsCRP, ALP, etc). So apabetalone can always be added on to any LDL-lowering therapy. 

BDAZ