New Drug Could Improve Heart Function by Removing Free Radicals, According to Researchers at Wake Forest University Baptist Medical Center

Apr 28, 2001, 01:00 ET from MetaPhore Pharmaceuticals, Inc.

    BALTIMORE, Md., April 28 /PRNewswire/ -- A developmental drug being
 studied at Wake Forest University Baptist Medical Center has been shown to
 improve heart function in animal models of heart attack, according to
 researchers in a study presented at the annual meeting of the Pediatric
 Academic Societies here today.
     The drug, a synthetic compound developed by MetaPhore Pharmaceuticals in
 St. Louis, removes free radicals from injured heart tissues.  Free radicals
 can cause extensive damage to the heart following a heart attack.
 Administeredprior to re-opening the blood vessels in the heart in animal
 models of heart attack, the compound, which mimics the action of a natural
 free-radical fighting enzyme, appears to protect the heart cells from further
 damage.
     In laboratory rats, the drug has been shown to be highly protective
 against injury from free radicals, according to R. Mark Payne, M.D. associate
 professor of pediatric cardiology at Wake Forest University School of
 Medicine and principal investigator of the study.
     "The applications of this research are enormous," Payne said.  "The early
 animal studies are very positive, but more animal studies need to be
 completed.  These data support our hypothesis that tissue can be protected
 during a heart attack, with potentially improved cardiac function."
     When a person has a heart attack, blood flow to the heart and other organs
 is restricted.  Doctors must quickly reestablish blood flow by opening up the
 damaged blood vessels, providing needed blood to the heart and other organs
 in the body.
     However, additional damage also typically occurs when the blood flow is
 reestablished.  The renewed inflow of blood to heart tissues produces a large
 excess of dangerous free radicals, which damage proteins and DNA in the
 cell, causing the tissue to die.  Dead tissue later results in scar tissue
 in the heart, according to Payne.
     If the drug is administered before the blood vessels in the heart have
 been re-opened -- the period in which most of the cardiac damage occurs --
 then cardiac tissue may be saved with a better long-term outlook for the
 patient.
     "Normally these cells have coping mechanisms to deal with free radicals
 that are generated within the cells in low amounts," he said.  "But when the
 heart has suffered an attack, the cells become overwhelmed and cannot cope
 with the enormous burst of free radicals that are produced when blood flow is
 reestablished to the injured regions of the heart.  As a result, the cells
 die and are replaced by scar tissue, which does not function as normal heart
 muscle."
     The enzyme mimetic compound replicates the action of the natural enzyme,
 superoxide dismutase (SOD), one of the body's primary defense mechanisms
 against free radical damage to tissues and cells.
     "This enzyme mimetic is much smaller in size than naturally occurring
 enzymes that usually remove free radicals," Payne said.  "The small size is
 very important because it allows the drug to penetrate into tissues, such as
 the brain and the heart, that larger synthetic drugs and proteins cannot
 easily penetrate."
     In other studies, the SOD enzyme mimetic also has been shown effective in
 decreasing stroke injury in laboratory animals when administered prior to
 the onset of the stroke.
     "These data are exciting because they suggest a role for these drugs in
 the early treatment of stroke, as well as heart attacks," added Payne.
     More studies need to be conducted to study the efficacy of the drug if it
 were administered after the opening of the blood vessels, instead of prior
 to opening them up.
     Researchers studied the enzyme mimetic M40403 in rat models of heart
 attack.  Half the rats were given the drug and half were used as a control
 group.  The half given the drug showed less damage to the heart than the
 control group.
     In addition to Payne, Daniela Salvemini, Ph.D., with MetaPhore
 Pharmaceuticals, participated in the study.  The National Institutes of
 Health and the Brenner Center for Child and Adolescent Health funded the
 study.
     Statements in this press release that are not strictly historical are
 "forward looking" statements as defined in the Private Securities Litigation
 Reform Act of 1995.  The actual results may differ from those projected in
 the forward looking statement due to risks and uncertainties that exist in
 the company's operations, development efforts and business environment.
 
                     MAKE YOUR OPINION COUNT -  Click Here
                http://tbutton.prnewswire.com/prn/11690X34189350
 
 

SOURCE MetaPhore Pharmaceuticals, Inc.
    BALTIMORE, Md., April 28 /PRNewswire/ -- A developmental drug being
 studied at Wake Forest University Baptist Medical Center has been shown to
 improve heart function in animal models of heart attack, according to
 researchers in a study presented at the annual meeting of the Pediatric
 Academic Societies here today.
     The drug, a synthetic compound developed by MetaPhore Pharmaceuticals in
 St. Louis, removes free radicals from injured heart tissues.  Free radicals
 can cause extensive damage to the heart following a heart attack.
 Administeredprior to re-opening the blood vessels in the heart in animal
 models of heart attack, the compound, which mimics the action of a natural
 free-radical fighting enzyme, appears to protect the heart cells from further
 damage.
     In laboratory rats, the drug has been shown to be highly protective
 against injury from free radicals, according to R. Mark Payne, M.D. associate
 professor of pediatric cardiology at Wake Forest University School of
 Medicine and principal investigator of the study.
     "The applications of this research are enormous," Payne said.  "The early
 animal studies are very positive, but more animal studies need to be
 completed.  These data support our hypothesis that tissue can be protected
 during a heart attack, with potentially improved cardiac function."
     When a person has a heart attack, blood flow to the heart and other organs
 is restricted.  Doctors must quickly reestablish blood flow by opening up the
 damaged blood vessels, providing needed blood to the heart and other organs
 in the body.
     However, additional damage also typically occurs when the blood flow is
 reestablished.  The renewed inflow of blood to heart tissues produces a large
 excess of dangerous free radicals, which damage proteins and DNA in the
 cell, causing the tissue to die.  Dead tissue later results in scar tissue
 in the heart, according to Payne.
     If the drug is administered before the blood vessels in the heart have
 been re-opened -- the period in which most of the cardiac damage occurs --
 then cardiac tissue may be saved with a better long-term outlook for the
 patient.
     "Normally these cells have coping mechanisms to deal with free radicals
 that are generated within the cells in low amounts," he said.  "But when the
 heart has suffered an attack, the cells become overwhelmed and cannot cope
 with the enormous burst of free radicals that are produced when blood flow is
 reestablished to the injured regions of the heart.  As a result, the cells
 die and are replaced by scar tissue, which does not function as normal heart
 muscle."
     The enzyme mimetic compound replicates the action of the natural enzyme,
 superoxide dismutase (SOD), one of the body's primary defense mechanisms
 against free radical damage to tissues and cells.
     "This enzyme mimetic is much smaller in size than naturally occurring
 enzymes that usually remove free radicals," Payne said.  "The small size is
 very important because it allows the drug to penetrate into tissues, such as
 the brain and the heart, that larger synthetic drugs and proteins cannot
 easily penetrate."
     In other studies, the SOD enzyme mimetic also has been shown effective in
 decreasing stroke injury in laboratory animals when administered prior to
 the onset of the stroke.
     "These data are exciting because they suggest a role for these drugs in
 the early treatment of stroke, as well as heart attacks," added Payne.
     More studies need to be conducted to study the efficacy of the drug if it
 were administered after the opening of the blood vessels, instead of prior
 to opening them up.
     Researchers studied the enzyme mimetic M40403 in rat models of heart
 attack.  Half the rats were given the drug and half were used as a control
 group.  The half given the drug showed less damage to the heart than the
 control group.
     In addition to Payne, Daniela Salvemini, Ph.D., with MetaPhore
 Pharmaceuticals, participated in the study.  The National Institutes of
 Health and the Brenner Center for Child and Adolescent Health funded the
 study.
     Statements in this press release that are not strictly historical are
 "forward looking" statements as defined in the Private Securities Litigation
 Reform Act of 1995.  The actual results may differ from those projected in
 the forward looking statement due to risks and uncertainties that exist in
 the company's operations, development efforts and business environment.
 
                     MAKE YOUR OPINION COUNT -  Click Here
                http://tbutton.prnewswire.com/prn/11690X34189350
 
 SOURCE  MetaPhore Pharmaceuticals, Inc.