Merck unveiled another kind of HDL-raiser, a drug to inhibit the cholesterol ester transfer protein (CETP).
In the meantime, testing of CETP-blocking drugs at Roche and Merck is likely to be delayed.
Some studies showed that people with gene defects that caused low CETP levels had less heart disease.
In follow-up studies, it's not clear that raising HDL by blocking CETP works.
Torcetrapib does not seem to raise total cholesterol, as completely inhibiting CETP might.
When CETP is blocked, the HDL particles become larger--and they may actually become so big that they no longer function.
But Merck kept working on its CETP inhibitor anyway, in a stealth program unbeknown to Wall Street or the public.
The single biggest issue for the industry are the failed Ph3 programmes for drug classes like CETP inhibitors and anti-amyloids.
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The most promising: a pill called a CETP inhibitor, which raises good cholesterol and may reduce cardiac inflammation and heart disease.
Still, many leading investigators say that it is worth testing new CETP inhibitors--even though the process will take many more years.
However, this is the THIRD CETP inhibitor to advance to phase 3 with the Pfizer and Roche entries having failed previously.
Finally, should REGN727 have safety issues which arise on long term use (CETP inhibitors come to mind), this compound will be dead.
But we'll only know if CETP works, he says, if Merck, Roche or another company conducts further studies on a different drug.
There are still big doubts about CETP, and the new results add another burning question: could CETP inhibitors affect the immune system?
By 2004 Merck and Roche had followed with their own CETP-blocking drugs.
Although clinical trials of HDL-boosting CETP inhibitors have so far failed to produce positive results, many other avenues of HDL-related research remain active.
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The new drug, called a CETP inhibitor, works by blocking the action of a protein which lowers levels of "good" cholesterol in the body.
Researchers got excited about HDL in the late 1990s because they found a way to raise it by blocking a molecule called cholesterol ester transfer protein (CETP).
HPS2-THRIVE adds to the string of failures associated with trials of HDL-related therapies, although some hope remains for CETP inhibitors, despite the failure of two large clinical trials.
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Merck says it remains hopeful about its own CETP inhibitor now in clinical trials, but declined to discuss details of the Tredaptive study pending full publication of the results.
Both work by inhibiting an obscure molecule called the cholesterol ester transfer protein (CETP) that works indirectly to prevent HDL from being used to create low-density lipoprotein (LDL), the bad cholesterol.
For some experimental medicines, like HDL-raising drugs being developed by Merck and Eli Lilly that are known as CETP inhibitors, this result only affects how much value investors assign to those research programs.
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Pfizer says that it believes partially inhibiting CETP, as its pill does, will still produce effective HDL. A recent paper by Pfizer researchers in the journal Arteriosclerosis, Thrombosis, and Vascular Biology does seem to bolster Pfizer's case.
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