"I’d say probably more than one-third of my patients are on combination therapy for lipid lowering," the cardiologist said.
With 553, it will also become possible to take to its logical conclusion the hypothesis that a lower LDL is better for preventing atherosclerosis.
"The average LDL in a newborn is 35 mg/dL, and they have clean vasculature. There aren’t even the lipid streaks that occur as the first step in the atherosclerotic process," he noted.
In phase III, the monoclonal antibody will be self-administered subcutaneously using a fixed-dose pen, much like the insulin-sensitizing agent exenatide (Byetta or Bydureon).
Discussant Dr. Karol E. Watson said 553 "has a lot of potential and certainly does offer up some hope." But she zeroed in on the fact that as a monoclonal antibody – even a fully human one – it has the potential for autoimmunity.
"That is something that clearly would limit the usefulness of this molecule. I’d want to see more data on that," added Dr. Watson, codirector of the University of California, Los Angeles, program in preventive cardiology.
Her fellow panelist Dr. Christie M. Ballantyne was particularly intrigued by the fact that C-reactive protein levels did not change significantly during the phase II study.
A clinical trial with 553 could settle the question of whether the clinical benefits of statin therapy are due solely to LDL lowering, or if the concomitant decrease in CRP is also essential, said Dr. Ballantyne, professor of medicine at Baylor College of Medicine, Houston.
The study was sponsored by Sanofi and Regeneron. Dr. McKenney reported that he has received research grants from both companies to conduct clinical trials of 553. He also serves as a consultant to Sanofi, which is developing 553, and to numerous other pharmaceutical companies with an interest in lipid-altering agents. Dr. Kereiakes reported having no financial conflicts.