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LEADING RESEARCHERS PRESENT PRECLINICAL RESULTS WITH THE LIPOSOME COMPANY'S TCL C-53

 LEADING RESEARCHERS PRESENT PRECLINICAL RESULTS
 WITH THE LIPOSOME COMPANY'S TCL C-53
 PRINCETON, N.J., May 4 /PRNewswire/ -- A new drug under development by The Liposome Company, Inc. (NASDAQ: LIPO) appears to be active in preclinical models of Adult Respiratory Distress Syndrome (ARDS) and Acute Myocardial Infarction (AMI), more commonly referred to as heart attack, according to investigators who presented experimental results this weekend at the annual meeting of the American Society of Clinical Investigation and the American Federation for Clinical Research.
 The drug, TLC C-53, consists of liposome-encapsulated prostaglandin E1 (PGE1) (Note: 1 is subscript). Because of its postulated unique mechanism of action, it may have utility in a broad range of inflammatory and vaso-occlusive diseases. The data presented this weekend provide the first hard evidence in preclinical models that TLC C-53 is performing as expected.
 Investigators from the Webb-Waring Institute of the University of Colorado, one of the country's leading ARDS research and teaching centers, presented findings from their ARDS experiments with TLC C-53, and researchers from the University of Texas Medical School, a prestigious heart research center, reported results from experiments with the drug in models of heart attacks. In these tests, TLC C-53 was highly effective in treating both disease conditions. Specifically, TLC C-53 was able to reduce neutrophilmediated lung injury, a key component of ARDS, and it was also able to reduce the amount of heart damage following a simulated heart attack.
 TLC C-53 is believed to be able to inactivate neutrophils, platelets, and endothelial cells, and to prevent them from adhering or sticking together. Neutrophils and platelets are cells that circulate in the blood. Endothelial cells line the walls of the blood vessels, including veins and arteries. When neutrophils and endothelial cells become activated and adhere to each other, a series of cellular and biochemical reactions is triggered, which can lead to tissue and organ damage, known as inflammation. This type of inflammation is thought to be one of the prime culprits in many serious illnesses, including ARDS.
 ARDS is a condition stemming from a variety of insults, including trauma, burns, sepsis, aspiration, and hyperoxia, that appears to be mediated by the activation of neutrophils. It is characterized by the lungs' filling with fluid that leaks out of injured capillaries. Once the lungs fill with fluid, breathing becomes difficult, and 50 percent to 60 percent of patients die. There are currently no effective drugs for this condition, which kills more than 100,000 people each year in the United States. It has been hypothesized that by preventing neutrophil activation and migration, it may be possible to reduce ARDS lung injury.
 A heart attack is caused by a blood clot blocking an artery carrying blood to the heart muscle. When the clot dissolves or dislodges, either on its own or through the use of drugs such as tissue plasminogen activator (tPA) or streptokinase, blood flow is restored to the oxygen- deprived region of the heart. This is called reperfusion. Reperfusion can activate neutrophils, leading to inflammation and further injury to heart muscle, known as reperfusion injury. In addition, platelets may also be activated. Activated platelets tend to stick to each other in a process known as platelet aggregation. Platelet aggregation can prevent blood from reaching oxygen-starved tissue, causing what is known as the "No-Reflow Phenomenon." By preventing activation of platelets, as well as neutrophils and endothelial cells, TLC C-53 may be able to both reduce reperfusion injury and prevent the no-reflow phenomenon.
 In the Webb-Waring study, researchers compared the effectiveness of TLC C-53 -- a liposome-encapsulated prostaglandin E1 (PGE1) -- to free PGE1 in decreasing the neutrophil activation and migration that appear to cause ARDS. Rats given interleukin-1 (IL-1), a chemical that activates neutrophils, showed increased numbers of lung lavage neutrophils and increased lung leak, signs of ARDS. When TLC C-53 was subsequently injected, lung leak was reduced by 70 percent to 86 percent. Free PGE1, or empty liposomes produced no effect.
 In addition, those rats treated with TLC C-53 after administration of IL-1 had neutrophil levels in lung lavage reduced by 57 percent, compared to rats given IL-1 alone.
 In the University of Texas study, researchers looked at the effect TLC C-53 had on an animal model of a simulated heart attack. Compared to an inactive control, TLC C-53 significantly reduced the amount of heart tissue that remained oxygen-deprived, and it significantly decreased the extent of heart damage caused by the infarct. The investigators concluded that TLC C-53 salvaged viable heart tissue, reduced heart damage and abolished the no-reflow phenomenon.
 "While free PGE1, has been effective in some animal models, it has proved disappointing in patients with ARDS," said John Repine, M.D., director of the Webb-Waring Lung Institute and professor of medicine at the University of Colorado. "Our study demonstrates that liposomal PGE1, works much better than free PGE1 to decrease neutrophil-mediated lung injury. We have hypothesized that this may be because liposomal PGE1 has an affinity for neutrophils."
 "There is considerable evidence that activated neutrophils are involved in the development of ARDS," said Repine. "They also may be the culprit in a number of serious inflammatory conditions, including reperfusion injury after heart attacks and other disorders. Accordingly, an agent that could inactivate many of the functions of neutrophils has the potential for limiting the development or extent of these diseases."
 "We found that not only did liposome-encapsulated PGE1, inhibit neutrophil activation, it also appears to inhibit platelet aggregation," said principal investigator Richard W. Smalling, M.D., Ph.D., professor of medicine, Division of Cardiology, University of Texas Medical School at Houston. "This combination may be synergistic in treating heart attacks."
 "Most of the therapeutic efforts to date have focused on dissolving the blood clots that cause heart attacks," said Smalling. "However, when the blood clot is dissolved, the blood that rushes in can cause further damage. While this reperfusion injury has been demonstrated in animals the effects in man have not been evaluated. Our experiment shows that liposome-encapsulated PGE1, when infused during heart attacks, reduces the amount of heart damage by 50 percent compared to restoration of the blood flow alone. If these animal results apply to humans, this suggests that liposome-encapsulated PGE1 may significantly limit the heart damage over and above that achieved by clot-busting drugs currently."
 TLC C-53, a cell adhesion antagonist, is under investigation in the treatment of a variety of inflammatory and vaso-occlusive disease conditions, including ARDS, sepsis/trauma syndrome, and reperfusion injury following acute myocardial infarction, as well as for the prevention of restenosis after angioplasty.
 The Liposome Company expects to file and IND (Investigational New Drug) application with the U.S. Food and Drug Administration and begin clinical trials later in 1992.
 A leading company dedicated exclusively to the development of liposome and lipid-based pharmaceuticals, The Liposome Company selectively develops proprietary parenteral pharmaceuticals for the treatment, prevention and diagnosis of life-threatening illnesses.
 -0- 5/4/92
 /CONTACT: Anne Van Lent, senior vice president of The Liposome Company, 609-452-7060, or Steven Marks of Bozell, 312-988-2348, for The Liposome Company/
 (LIPO) CO: Liposome Company, Inc. ST: New Jersey IN: MTC SU: PDT


CK-LR -- NY011 -- 5806 05/04/92 08:02 EDT
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