雅思阅读模拟题:Why did a promising heart drug fail?

雅思阅读模拟题:Why did a promising heart drug fail?


2024年4月12日发(作者:)

雅思阅读模拟题:Why did a promising heart

drug fail?

Why did a promising heart drug fail?

Doomed drug highlights complications of meddling with

cholesterol.

1. The failure of a high-profile cholesterol drug has

thrown a spotlight on

the complicated machinery that regulates cholesterol levels.

But many

researchers remain confident that drugs to boost levels of

'good' cholesterol

are still one of the most promising means to combat

spiralling heart

disease.

2. Drug company Pfizer announced on 2 December that it

was cancelling all

clinical trials of torcetrapib, a drug designed to raise

heart-protective

high-density lipoproteins (HDLs). In a trial of 15000

patients, a safety board

found that more people died or suffered cardiovascular

problems after taking the

drug plus a cholesterol-lowering statin than those in a

control group who took

the statin alone.

3. The news came as a kick in the teeth to many

cardiologists because

earlier tests in animals and people suggested it would lower

rates of

cardiovascular disease. "There have been no red flags to my

knowledge," says

John Chapman, a specialist in lipoproteins and

atherosclerosis at the National

Institute for Health and Medical Research (INSERM) in Paris

who has also studied

torcetrapib. "This cancellation came as a complete shock."

4. Torcetrapib is one of the most advanced of a new

breed of drugs designed

to raise levels of HDLs, which ferry cholesterol out of

artery-clogging plaques

to the liver for removal from the body. Specifically,

torcetrapib blocks a

protein called cholesterol ester transfer protein (CETP),

which normally

transfers the cholesterol from high-density lipoproteins to

low density,

plaque-promoting ones. Statins, in contrast, mainly work by

lowering the 'bad'

low-density lipoproteins.

Under pressure

5. Researchers are now trying to work out why and how

the drug backfired,

something that will not become clear until the clinical

details are released by

Pfizer. One hint lies in evidence from earlier trials that it

slightly raises

blood pressure in some patients. It was thought that this

mild problem would be

offset by the heart benefits of the drug. But it is possible

that it actually

proved fatal in some patients who already suffered high blood

pressure. If blood

pressure is the explanation, it would actually be good news

for drug developers

because it suggests that the problems are specific to this

compound. Other

prototype drugs that are being developed to block CETP work

in a slightly

different way and might not suffer the same downfall.

6. But it is also possible that the whole idea of

blocking CETP is flawed,


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