Abstract
Introduction
The notion that raising HDL cholesterol levels can reduce the risk of coronary
heart disease is not a new one, yet drug developers have been continually
foiled in their attempts to capitalize on this fi nding-as illustrated by Pfi
zer' s discontinuation of the once highly promising agent torcetrapib. Several
new drugs with novel mechanisms of action are in development, and although
they are promising, barriers to entry are high, and they face long-term
outcomes trials before being able to secure approval and comfort among
physicians.
Get the Answers You Need to Shape Your Strategy
- The notion that raising HDL-C can lower cardiovascular risk has been
around for a long time, yet drug developers have had trouble capitalizing on
this fact. What are the barriers in this potentially highly lucrative
market?
- Pfi zer abruptly halted development of the once-promising CETP inhibitor
torcetrapib. What are the implications for Pfi zer as well as for other
drug developers of CETP inhibitors?
- The uncertainty around CETP inhibition and HDL-C raising in general has
caused some drug developers to create new drugs using decades-old concepts.
Which agents and mechanisms of action are being tested and how do they
differ from current therapies? What is the commercial potential for these
drugs?
Scope
- HDL metabolism and how it relates to atherosclerosis: Overview of
HDL metabolism and proposed atheroprotective mechanisms, including reverse
cholesterol transport.
- Torcetrapib' s failure and outlook for other CETP inhibitors: A look
at what went wrong with Pfi zer' s torcetrapib and what developers can do to
avoid a similar fate.
- Implications of the ILLUMINATE trial: Implications for CETP
inhibitors and their manufacturers.
- Old concepts get new life: Abbott and Merck are developing new
versions of older but safe HDL modulators.
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