The highest dose of an experimental pill developed by Eli Lilly dramatically reduced an inherited form of high cholesterol in a mid-stage trial, according to data presented at a medical meeting on Monday.

Researchers at the American Heart Association reported that the drug, muvalaplin, reduced lipoprotein(a), or Lp(a), levels by 70% using a conventional blood test and by about 86% based on a more specific test developed by the company. Meeting in Chicago.

Lilly’s drug is the only oral treatment in a field of several injectable therapies being tested to treat high Lp(a), a risk factor for heart disease that affects one in five people globally.

Unlike low-density lipoprotein, or LDL, so-called bad cholesterol, which can be treated with diet and statins, there is no approved treatment for Lp(a) and few individuals even know they have it. .

Increased Lp(a) can significantly increase the risk of heart attack, stroke, narrowing of the aortic valve, and peripheral artery disease, a build-up of fatty plaque in the arteries. People of African and South Asian descent are at greatest risk.

The trial compared three daily doses of muvalaplin – 10, 60 and 240 mg – with placebo in 233 adults with high levels of Lp(a). The researchers tested Lp(a) levels using traditional blood tests and a new method that measures the levels of intact Lp(a) particles in the blood.

Muvalaplin reduced Lp(a) by 47.6% at 10 mg, 81.7% at 60 mg, and 85.8% at 240 mg, as measured by intact blood test versus placebo. According to the conventional test it was reduced by 40.4%, 70.0% and 68.9% respectively.

Adverse events were similar in both the muvalaplin and placebo groups.

Ruth Gimeno, Lilly’s group vice president for diabetes and metabolism research, said the company is considering next steps to advance late-stage trials.

“We will have to discuss with regulators, but we are very excited,” he said in an interview.

He said that although the drug reduced cardiovascular risk factors, larger trials were needed to prove that reducing Lp(a) would actually reduce heart attacks and other adverse cardiovascular events. Is.

At the same meeting, London-based Cylance Therapeutics (SLNCF.PK) reported 60-week results from a 180-patient Phase 2 trial of zarlasiran, which works by reducing the activity of the LPA gene that leads to high levels of Is. LP(A) using a technique called short interfering RNA or siRNA.

300 mg or 450 mg injections of zarlesiran given every 16 or 24 weeks reduced Lp(a) by 80% to 85% during 36 to 60 weeks of follow-up, without any major safety problems.

“We saw a deep decline, similar to what we saw in Phase 1,” Dr. Curtis Rambaran, the company’s chief medical officer, said in an interview. He said Cylance will test the 300 mg dose in a late-stage trial starting in the middle of next year.

The results of both studies were published in JAMA.

Other injectable Lp(a) treatments in clinical trials include Lilly’s lepodisiran, Amgen’s (AMGN.O) opens new tab olpasiran and pelasiran from Novartis.