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Article on New Drug

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  • Cynthia Rausch
    Hi Everyone, Off the http://www.prnewswire.com New Drug Could Improve Heart Function by Removing Free Radicals, According to Researchers at Wake Forest
    Message 1 of 1 , Apr 28, 2001
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      Hi Everyone,

      Off the http://www.prnewswire.com


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

      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.

      Administered prior 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.

      Cynthia, Taffy, Samuel
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