Guilford Pharmaceuticals Presents New NAALADase Inhibitor Data in Chemotherapy-Induced Neuropathy at ASCO
18 Mai 2005 - 9:00PM
PR Newswire (US)
Guilford Pharmaceuticals Presents New NAALADase Inhibitor Data in
Chemotherapy-Induced Neuropathy at ASCO BALTIMORE, May 18
/PRNewswire-FirstCall/ -- Guilford Pharmaceuticals Inc.
(NASDAQ:GLFD) today announced that new data from its NAALADase
inhibitor program were presented at the American Society of
Clinical Oncology Annual Meeting, the premier scientific event for
oncology professionals. The preclinical results suggest that the
Company's proprietary NAALADase inhibitors may have utility in
preventing and reversing chemotherapy-induced neuropathy in animal
models. "Exploring chemotherapy-induced neuropathy is a novel focus
of research for our NAALADase program, and presents an exciting
opportunity for continued investigation," commented Barbara
Slusher, Ph.D., Senior Vice President, Research. "Guilford
scientists and our academic collaborators have previously
demonstrated in multiple animal models that NAALADase inhibition
can prevent and reverse neuropathic pain and diabetic peripheral
neuropathy. To our knowledge, the data we presented at ASCO are the
first to show evidence that enzymatic inhibition of NAALADase can
ameliorate chemotherapy-induced neuropathy, a severe dose-limiting
toxicity associated with chemotherapy treatment, and believed to
affect more than 1.2 million Americans with cancer each year.
Currently, there are no drugs available that can treat this
condition." In the study, mice received cumulative doses of either
25 mg/kg taxol (five 5 mg/kg doses in two weeks) or 100 mg/kg taxol
(four 25 mg/kg doses in two weeks) in addition to orally
administered daily doses of a potent and selective NAALADase
inhibitor (2-MPPA) or placebo. Chemotherapy-induced neuropathy was
assessed by measuring sensory nerve conduction velocity (SNCV)
prior to and following treatment. The results demonstrated that
2-MPPA significantly prevented the deficit in sensory nerve
conduction velocity induced by both the 5 and 25 mg/kg taxol
regimen by 96% and 98%, respectively, (p
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