With reference to your second para, the rationale of CETP inhibition was always controversial among the scientists. The scientific community was divided, because although inhibiting CETP raises HDL cholesterol, it does so by blocking the movement of cholesterol from HDLs to other lipoproteins like LDLs, producing "bloated" overloaded HDL particles. Anacetrapib was the most potent CETP inhibitor, so potent that it also produced a big decrease in LDL cholesterol. This was why Merck continued with it when trials of other CETP inhibitors had already failed. The company was hoping the reduction of LDL cholesterol would do what the increase in HDL cholesterol was no longer expected to achieve. And it did. There was a small reduction of CVD incidence in the treated group. But the reduction in CVD was smaller than you would expect from the size of the LDL reduction. So the company dropped the drug.

Another factor was probably the knowledge that anacetrapib is so fat soluble that it is soaked up by adipose tissue (fat cells). If treatment is then stopped it leaks back into the blood so slowly that it can take years before the body gets rid of it - a huge problem if you've stopped it because of a serious adverse effect.