More from the new publication.  Read it!  Its a relatively easy ready. 

"Apabetalone is the only clinic-ready BETi candidate for treating chronic diseases and has a favorable safety profile [29], [30], [31], [33]. Mechanistically, apabetalone preferentially binds to the BD2 domain of BET proteins over their BD1 domain, which disrupts the occupancy of BET proteins in regulatory regions controlling target genes and reduces maladaptive inflammatory gene expression while maintaining BET protein-regulated cell homeostasis [28]. However, given that apabetalone prevents SARS-CoV-2 infection by reducing ACE2 expression [42], [43], it is important to consider whether treatment could affect normal physiology. ACE2 enzymatic activity converts angiotensin II (Ang II), a hormone that increases blood pressure, into angiotensin (1–7), which is a vasodilator that lowers blood pressure [63]. Apabetalone-mediated downregulation of ACE2 could therefore increase circulating Ang II and promote hypertension. In clinical trials, CVD patients who received apabetalone treatment for over 2000 patient years did not experience alterations in blood pressure [29], [30], [31]. Further, up to 3-years of apabetalone treatment had no impact on the incidence of infections or infestations in diabetic patients with high CVD risk on top of standard of care [29]. Therefore, apabetalone is unlikely to suppress constitutive anti-viral immune function to the point where immunity is compromised. "