CHICAGO, Nov 18 (Reuters) - The highest dose of an

experimental pill developed by Eli Lilly ( LLY ) dramatically

lowered an inherited form of high cholesterol in a mid-stage

trial, according to data presented at a medical meeting on

Monday.

The drug, muvalaplin, reduced levels of lipoprotein(a), or

Lp(a), by 70% using a traditional blood test and by nearly 86%

based on a more specific test developed by the company,

researchers reported at the American Heart Association 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

individuals globally.

Unlike low-density lipoprotein, or LDL, the so-called bad

cholesterol that can be treated with diet and statins, there are

no approved treatments for Lp(a) and few individuals even know

they have it.

Elevated Lp(a) can significantly increase the risk of heart

attack, stroke, narrowing of the aortic valve, and peripheral

artery disease, a buildup of fatty plaques in the arteries.

Individuals of African and South Asian ancestry are at highest

risk.

The trial compared three daily doses of muvalaplin - 10, 60

and 240 milligrams - with a placebo in 233 adults with high

levels of Lp(a). Researchers tested Lp(a) levels using a

traditional blood test and a new method that measures 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% on 240 mg as measured by the intact blood test versus

placebo. It was reduced by 40.4%, 70.0%, and 68.9%,

respectively, as measured by the traditional test.

Adverse events were similar in both the muvalaplin and

placebo groups.

Ruth Gimeno, Lilly's group vice president for diabetes and

metabolic research, said the company is weighing next steps for

advancing to late-stage trials.

"We'll have to have discussions with regulators, but we're

very excited," she said in an interview.

She noted that while the drug has reduced a cardiovascular

risk factor, large trials are needed to prove lowering Lp(a)

actually cuts heart attacks and other adverse cardiovascular

events.

At the same meeting, London-based Silence Therapeutics ( SLN )

reported 60-week results of a 180-patient Phase 2

trial of zerlasiran, which works by dampening the activity of

the LPA gene that leads to high levels of Lp(a) using a

technology known as short interfering RNA, or siRNA.

A 300 mg or 450 mg injection of zerlasiran given every 16 or

24 weeks reduced Lp(a) by 80% to 85% during 36 to 60 weeks of

follow up, with no major safety issues.

"We saw profound knockdown, as we saw in the Phase one," Dr.

Curtis Rambaran, the company's chief medical officer, said in an

interview. Silence will test the 300 mg dose in a late-stage

trial set to start in the middle of next year, he said.

Results of both studies were published in JAMA.

Other injectable Lp(a) treatments in clinical testing

include Lilly's lepodisiran, Amgen's ( AMGN ) olpasiran and

pelacarsen from Novartis.