"How large a differential in average event rates by statin type might you think necessary to infer that previously noted superiority of Crestor sub group is being seen in BOM as well ?"

Apologies for the delayed response. Busy afternoon. I don't have a good answer for your question. All I know is that the post-hoc analysis of ASSURE and the data presented in the patent was very impressive to me as evidence of synergy. Most of the data in the patent is related to the reductions in the percent atheroma volume (PAV); apabetalone+rosuvastatin elicited a 1.43% to 2.04% reduction in PAV  (depending on rosuvastatin dose) in just 6 months in those patients with below median HDL-C (<39 mg/dL), whereas rosuvastatin alone elicited only ~0.6% reduction. That's impressive!

In BETonMACE, all patients will be low-HDL and according to the BETonMACE design poster have a median of 33 mg/dL. The key apabetalone responder group seems to be low-HDL and rosuvastatin, with better plaque reduction seen in the higher rosuvastatin doses. High-dose statin thereapy is standard of care for these acute ACS patients in BETonMACE. 46% of BETonMACE patients will be on high dose rosuvastatin (20 mg or 40 mg per day rosuvastatin) according to the BETonMACE design poster.  

There is some MACE data in the patent (Figures 6 and 7), but as I've mentioned before this is 5-point MACE, most of the events tallied were not the hard 3-point MACE, and this is all based upon a pretty small number of event observations. So lots of caveats. But that graph in Figure 7 showing the 17.4% (rosuvastatin, low-HDL-C) vs. 1.6% (rosuvastatin+apabetalone, low-HDL-C) cumulative MACE event rate is quite sweet to think about potentially replicating in BETonMACE for 3-point MACE!

BearDownAZ