Eli Lilly and Co.’s experimental drug doubled levels of good cholesterol in a study, setting up a race with Merck & Co. and Roche Holding AG to develop a new class of medicines to lower heart risk.

Good cholesterol, or HDL, sweeps the bad form of the fatty substance, known as LDL, out of arteries, reducing clogs. The treatment being developed by Indianapolis-based Lilly, evacetrapib, boosted HDL by as much as 129 percent and lowered bad cholesterol as much as 36 percent, the research found.

The data, reported at the American Heart Association meeting Tuesday in Orlando, Fla., were similar to those seen last year with a rival from Merck & Co., called anacetrapib, researchers at the conference said. The Lilly trial is in the second of three phases of testing generally required for U.S. approval.

The Merck and Roche products are in the final stage. Both drugs are predicted to be blockbusters with more than $5 billion in annual sales if they are approved.

“We got everything we could hope for from this drug, and maybe more,” said Steven Nissen, the study’s senior author and chief of cardiology at the Cleveland Clinic in Ohio, in a telephone interview. “We are going to move evacetrapib forward as rapidly as possible” into a final-stage trial to prove it lowers heart risk.

Lilly shares were down 21 cents Tuesday morning, to $37.44 each.

All three rivals aim to avoid the toxicity seen with a previous good cholesterol drug from New York-based Pfizer Inc. that was abandoned in 2006 after it triggered deaths in a study.

Like the failed Pfizer drug, all three medicines boost good cholesterol by blocking a molecule called CETP. Unlike the Pfizer compound, Lilly’s drug didn’t raise blood pressure or levels of an adrenal hormone called aldosterone, the results show.

Lilly plans to meet with regulators “in the very near future” to discuss starting a final-stage trial as soon as possible, David Moller, a vice president for the company said. That trial would aim to show that the Lilly drug reduces heart attacks and cardiovascular deaths when given with standard cholesterol-lowering therapy.

“We feel we have a very competitive molecule,” he said. “This is a home-grown Lilly molecule that we diligently pursued under the radar of the public eye with the notion that we could get around” the problems seen with Pfizer’s torcetrapib.

The Lilly trial, in 398 patients, found that evacetrapib worked well combined with common cholesterol-lowering drugs such as Pfizer’s Lipitor, Crestor from London-based AstraZeneca Plc and simvastatin, the generic version of Merck’s Zocor.

If good cholesterol-raising treatments work, “it is going to revolutionize what we do,” said Christopher Cannon, a cardiologist at Brigham and Women’s Hospital in Boston, who has worked on Whitehouse Station, N.J.-based Merck’s compound. “If HDL means anything, these drugs should be amazing,” he said in an interview at the heart meeting.

Only giant trials in thousands of heart patients can prove if the CETP medicines really prevent heart attacks and deaths. Merck’s anacetrapib drug is in the process of being tested in a study of 30,000 heart patients.

“These could be as big as the statins were 20 years ago” if the data continues to be positive, Nissen said.

The promising Lilly results come as another marketed drug that modestly raises good cholesterol, Abbott Laboratories’ Niaspan, failed to show any benefit in reducing heart attacks and heart deaths when given with generic Zocor. The trial was stopped early by the National Institutes of Health in May because of lack of benefit and possible higher stroke risk.

Detailed results from the Niaspan research are also being presented at the heart meeting.

Patients on Niaspan, an extended release form of niacin, saw their HDL increase by 25 percent in the study versus just 9.8 percent HDL increase in those patients who received placebo. Yet the overall rate of heart attacks and several other cardiovascular events in both groups were virtually the same, the study found.

The higher number of strokes in patients who got Niaspan, a $927 million sales generator in 2010, weren’t statistically significant, said William Boden, a study investigator and professor at the University at Buffalo Schools of Medicine and Public Health.

“The clinical results were chillingly null,” wrote Robert Giugliano from Brigham and Women’s Hospital in an editorial accompanying the study in the New England Journal of Medicine.

For patients with stable heart disease whose bad cholesterol is under control, “there is no reason to prescribe niacin to raise low levels of HDL,” Boden said. Niacin still has a role in patients who can’t get their cholesterol under control with statin drugs, he said.