Physicians' Academy for Cardiovascular Education

HDL-C mimetic did not induce plaque regression in post-ACS patients

Effect of Serial Infusions of CER-001, a Pre-Beta High-Density Lipoprotein Mimetic on Coronary Atherosclerosis: Results of the CARAT Study

Presented at ACC.17 by Stephen J Nicholls

News - Mar. 18, 2017


HDL-C is known for its protective effects against CAD and stroke. Therefore, it was hypothesised that increasing HDL-C levels with the infusion of CER-001, a reconstituted Pre-Beta HDL Mimetic, would lead to a reduction of arterial plaque, and would positively influence the risk of MI and stroke.

The negatively charged HDL mimetic contains apoA-I and sphingomyelin and has favourable effects on measures of lipid transport. Early studies demonstrated potential coronary plaque regression upon infusing low dose CER-001 in high plaque burden ACS patients.

In this CARAT study, 301 patients with a recent ACS and high plaque burden were randomised to receive either 10 weekly infusions of CER-100, or placebo, on top of standard therapy. At baseline, patients had at least one coronary artery stenosis with a percent atheroma volume (PAV) >30% in the proximal 10 mm of the target vessel, based on IVUS.

Main results


In post-ACS patients with at least one site of stenosis with PAV >30% in the proximal 10 mm of the target vessel, the administration of CER-001 did not lead to a significant PAV or TAV reduction. These findings suggest that short-term therapy with this dose of CER-001 is not a promising strategy in ACS patients.

Thusfar, disappointing results have been obtained when studying HDL-modifying agents; no CV benefit has been observed with attempts to raise HDL. During the press conference, Dr. Nicholls mentioned that HDL mimetics “continues to be an unfulfilled promise”. During the discussion, he was asked why he still believed this was an avenue to follow and when the moment will come to accept that it does not work. He said he walks various avenues, but the progressive failure of HDL-targeted therapies in the context of statins over the past years, shows that targeting HDL is more complicated than LDL. We know very little about HDL, and how to target it. Nicholls did acknowledge that “with every negative trial, it gets harder to believe in it”. That might mean we should look at other risk factors, or even better compliance with therapies known to work.


Our coverage of ACC.17 is based on the information provided during the congress.

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