Imtesty,

I believe that is the abstract from a presentation - poster? - that was given at the recent EDTA-ERA meeting.  Interesting to note that:

Consistent with phase 2, BETonMACE saw serum ALP reduced by 6.8 U/L with apabetalone (n=1082) vs placebo (n=1070; p<0.001) at 24 weeks. 

and

BET-dependent epigenetic modulation of ALP by apabetalone can affect several pathogenetic processes, and thereby improve cardiovascular outcomes. This study provides insights to the CVD event reductions observed in the CKD subpopulation in the BETonMACE Phase 3 trial.

If RVX can link the reduction in ALP closely enough to the marked reduction in MACE in the CKD group (i.e. support a likely causal relationship of lowered ALP leading to reduced MACE) and if ALP levels show a significant drop within 24 weeks of treatment, then there is the possibility that a reduction in ALP levels could be a quickly achieved endpoint in the BoM2 trial.  We know from BoM1 that the reduced level of MACE in the apabetalone group started almost from the beginning of the trial - that certainly supports the idea that apabetalone starts modulating important physiological parameters very quickly once treatment is initiated. 

Jupe