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Pfizer’s Torcetrapib/Atorvastatin Significantly Raised "Good" Cholesterol While Lowering "Bad" Cholesterol, New Data Show


DALLAS, November 15 -- Pfizer Inc said today that torcetrapib combined with all doses of atorvastatin (Lipitor) resulted in significant increases in patients’ “good” cholesterol (HDL) levels while also significantly decreasing their “bad” cholesterol (LDL).

Two Phase 2 studies involving the new experimental medicine and presented here at the annual meeting of the American Heart Association were designed to determine whether torcetrapib/atorvastatin therapy can effectively raise HDL-cholesterol while lowering LDL-cholesterol, a leading risk factor for heart disease.

In a study of nearly 500 patients, those who received torcetrapib (60 mg) and atorvastatin (10, 20, 40, 80 mg) had increases in HDL-cholesterol of 44 percent to 66 percent. At the same time, their LDL-cholesterol dropped between 41 percent to 60 percent.

“These results demonstrate that torcetrapib/atorvastatin can dramatically raise HDL while providing LDL-lowering benefits greater than Lipitor alone,” said Dr. Joseph Feczko, Pfizer’s chief medical officer. “These results were pivotal in our decision to move forward with a Phase 3 program, the final stage in clinical development. If this program is successful, this new approach could change the way physicians manage cholesterol and reduce further the risk of atherosclerosis in their patients.”

Numerous clinical studies have established that lowering LDL-cholesterol plays a critical role in reducing the risk of heart attacks, stroke and cardiovascular death. One of the main effects attributed to HDL-cholesterol is the ability to carry cholesterol away from cells (such as in the artery wall where it contributes to heart disease) back to the liver. Researchers believe that raising HDL-cholesterol may provide further benefits in the management of cardiovascular disease, which may have the potential to further reduce cardiovascular risk for patients.

Discovered and developed by Pfizer, torcetrapib works by blocking CETP, a protein in the blood that transfers cholesterol and triglycerides between LDL-cholesterol and HDL-cholesterol. Torcetrapib also lowers LDL cholesterol, but prior studies had shown the effect is greater and more consistent when combined with atorvastatin.

In this study, side effects of torcetrapib/atorvastatin were similar to those most commonly associated with statin therapy. Patients taking 60 mg of torcetrapib with atorvastatin also experienced an increase in systolic blood pressure of approximately 2 mm Hg, which will be further defined in ongoing Phase 3 studies.

Pfizer researchers also presented data from a separate study involving 40 patients to determine if the HDL particles in patients taking torcetrapib can maintain the ability to carry cholesterol away from the cells. Patients who received torcetrapib 120 mg had increases of 40 to 60 percent in their HDL-cholesterol levels compared to patients who received placebo.

Additionally, the raising of HDL cholesterol in torcetrapib treated patients showed an increased ability to transport cholesterol from cells—an effect seen to be functionally similar to patients with naturally occurring high levels of HDL-cholesterol.

“This study provides important information to support CETP inhibition with torcetrapib as an efficacious way to raise HDL which could offer significant cardiovascular benefits for patients,” said Dr. Feczko.

Pfizer’s torcetrapib/atorvastatin development program is the largest and most comprehensive clinical trial program the company has ever undertaken. In attempting to establish the role and benefits of HDL in heart disease, the world’s leading cause of death in adults, Pfizer is studying some 25,000 patients at hundreds of medical centers worldwide at a cost of about $800 million.

CETP (cholesterol-ester transfer protein) is a protein that regulates cholesterol and is responsible for transferring cholesterol from its “good” HDL carrier to LDL, the “bad” carrier of cholesterol that results in plaque buildup in the arteries. Scientists believe that CETP inhibition raises HDL levels because cholesterol remains attached to HDL and is unable to be transferred or attached to LDL, where it can build up in the arteries. In addition, researchers believe that blocking CETP and raising HDL may reduce the risk of heart disease and stroke.

Pfizer scientists have spent years trying to find a compound that could inhibit CETP. Preliminary work led them to their most promising compound—CP-529,414, now known as torcetrapib. Other Pfizer researchers then spent several more years improving the compound’s physical properties and understanding how torcetrapib worked before it could be administered to people in 1999.

“The torcetrapib/atorvastatin clinical program is building on the proven efficacy of Lipitor, which is the world’s most studied cholesterol-lowering medicine,” said Dr. Feczko. “As we continue into our Phase 3 studies we hope to show that this compound will provide important new information in reducing the risk of cardiovascular disease by substantially raising HDL and lowering LDL cholesterol together.”

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DISCLOSURE NOTICE: The information contained in this release is as of November 16, 2005. Pfizer assumes no obligation to update any forward-looking statements contained in this release as the result of new information or future events or developments.

This release contains forward-looking information about a product candidate and its potential benefits that involves substantial risks and uncertainties. Such risks and uncertainties include, among other things, the uncertainties inherent in research and development; decisions by regulatory authorities regarding whether and when to approve any drug applications that may be filed for the product candidate as well as their decisions regarding labeling and other matters that could affect its commercial potential; and competitive developments.

A further list and description of risks and uncertainties can be found in Pfizer’s Annual Report on Form 10-K for the fiscal year ended December 31, 2004 and in its reports on Form 10-Q and Form 8-K.


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