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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 onthe complicated machinery that regulates cholesterol levels. But manyresearchers remain confident that drugs to boost levels of 'good' cholesterolare still one of the most promising means to combat spiralling heartdisease.
2. Drug company Pfizer announced on 2 December that it was cancelling allclinical trials of torcetrapib, a drug designed to raise heart-protectivehigh-density lipoproteins (HDLs). In a trial of 15000 patients, a safety boardfound that more people died or suffered cardiovascular problems after taking thedrug plus a cholesterol-lowering statin than those in a control group who tookthe statin alone.接下来为大家介绍"述说雅思阅读模拟练习：Why did a promising heart drug fail?"
雅思阅读模拟练习：Why did a promising heart drug fail?
3. The news came as a kick in the teeth to many cardiologists becauseearlier tests in animals and people suggested it would lower rates ofcardiovascular disease. "There have been no red flags to my knowledge," saysJohn Chapman, a specialist in lipoproteins and atherosclerosis at the NationalInstitute for Health and Medical Research (INSERM) in Paris who has also studiedtorcetrapib. "This cancellation came as a complete shock."
4. Torcetrapib is one of the most advanced of a new breed of drugs designedto raise levels of HDLs, which ferry cholesterol out of artery-clogging plaquesto the liver for removal from the body. Specifically, torcetrapib blocks aprotein called cholesterol ester transfer protein (CETP), which normallytransfers the cholesterol from high-density lipoproteins to low density,plaque-promoting ones. Statins, in contrast, mainly work by lowering the 'bad'low-density lipoproteins.
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 byPfizer. One hint lies in evidence from earlier trials that it slightly raisesblood pressure in some patients. It was thought that this mild problem would beoffset by the heart benefits of the drug. But it is possible that it actuallyproved fatal in some patients who already suffered high blood pressure. If bloodpressure is the explanation, it would actually be good news for drug developersbecause it suggests that the problems are specific to this compound. Otherprototype drugs that are being developed to block CETP work in a slightlydifferent way and might not suffer the same downfall.
6. But it is also possible that the whole idea of blocking CETP is flawed,says Moti Kashyap, who directs atherosclerosis research at the VA Medical Centerin Long Beach, California. When HDLs excrete cholesterol in the liver, theyactually rely on LDLs for part of this process. So inhibiting CETP, whichprevents the transfer of cholesterol from HDL to LDL, might actually cause anabnormal and irreversible accumulation of cholesterol in the body. "You'reblocking a physiologic mechanism to eliminate cholesterol and effectivelyconstipating the pathway," says Kashyap.
7. Most researchers remain confident that elevating high densitylipoproteins levels by one means or another is one of the best routes forhelping heart disease patients. But HDLs are complex and not entirelyunderstood. One approved drug, called niacin, is known to both raise HDL andreduce cardiovascular risk but also causes an unpleasant sensation of heat andtingling. Researchers are exploring whether they can bypass this side effect andwhether niacin can lower disease risk more than statins alone. Scientists arealso working on several other means to bump up high-density lipoproteins by, forexample, introducing synthetic HDLs. "The only thing we know is dead in thewater is torcetrapib, not the whole idea of raising HDL," says Michael Miller,director of preventive cardiology at the University of Maryland Medical Center,Baltimore.
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