Nonalcoholic fatty liver disease (NAFLD) has an increasing prevalence worldwide. 
At present, no specific pharmacotherapy is approved for NAFLD. Simple steatosis 
and nonalcoholic steatohepatitis (NASH) can progress to liver fibrosis that is 
associated with mortality in NAFLD. The recruitment of inflammatory monocytes 
and macrophages via chemokine receptor CCR2 as well as of lymphocytes and 
hepatic stellate cells via CCR5 promote the progression of NASH to fibrosis. 
Areas covered: I summarize preclinical and clinical data on the efficacy and 
safety of the dual CCR2/CCR5 inhibitor cenicriviroc (CVC, also TBR-652 or 
TAK-652) for the treatment of NASH and fibrosis. In animal models of liver 
diseases, CVC potently inhibits macrophage accumulation in the liver and 
ameliorates fibrosis. In a phase 2b clinical trial (CENTAUR) on 289 patients 
with NASH and fibrosis, CVC consistently demonstrated liver fibrosis improvement 
after 1 year of therapy and had an excellent safety profile, leading to the 
implementation of a phase 3 trial (AURORA). Expert opinion: Preclinical and 
clinical data support the development of CVC as a safe and potent antifibrotic 
agent. However, open questions around CVC are the durability of antifibrotic 
responses, divergent effects on NASH versus fibrosis, potential long-term 
concerns and the expected path to approval.