"Single target single molecule...bingo...that is what most medical professionals understand. RVX208 upends that conventional wisdom...one small molecule that will achieve so many targets?  Very difficult for hard core researchers to accept that they have been doing research in CVD (not to mention renal etc) all wrong all these decades!"

The closest comparison drugs I can think of for apabetalone's mutliple genes/pathways mechanism of action are for drugs that are agonists or partial agonists of certain nuclear hormone receptors like peroxisome proliferator-activated receptors (PPARs) and farnesoid-X-receptor (FXR). Fibrate drugs (i.e. clofibrate, gemfibrozil, fenofibrate) mainly activate PPAR-alpha and thiazolidinediones (TZDs aka glitazones like rosiglitazone/Avandia) drugs mainly activate PPAR-gamma. I say mainly because some, but not all, of these can activate more than one member of the PPAR-alpha, PPAR-delta, PPAR-gamma class of nuclear hormone receptors. Newer PPAR drugs, like Kowa Research Institute's pemafibrate (K-877) are much more selective for PPARalpha, and Genfit's elafibranor is a dual PPAR-alpha/delta agonist. Here's a great review on the PPAR drugs with emphasis on K-877. Another comparison is for agonists of FXR, such as Intercept's Ocaliva (Obeticholic acid).

The reason I bring these up is because as agonists of nuclear hormone receptor transcription factor(s), they simultaneously modulate the expression of many mRNAs and biological pathways at the same time! Sound familiar? So the general concept of a drug that simultaneously modulates several genes/pathways is not new. BET bromodomain inhibitor drugs like apabetalone elicit their transcriptional changes differently than how the PPAR or FXR agonists do it. But the end result is the same: multiple mRNAs involved in multiple biological pathways altered simultaneously by one drug. 

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