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New Drug Being Tested for Pancreatic Cancer

Lab findings show potential for use alone or in combination, scientist says,,

WEDNESDAY, April 15 (HealthDay News) -- An experimental drug appeared to reduce pancreatic cancer growth in laboratory tests, according to researchers from the drug's maker, Amgen.

Called AMG 479, the drug is designed to inhibit the activity of insulin-like growth factors IGF-1 and IGF-2.

"We know that insulin-like growth factors play a role in cancer development, particularly in mediating cell survival," Pedro J. Beltran, a principal scientist in oncology research at Amgen, said in a news release from the American Association for Cancer Research. "This is the first drug that specifically targets the receptor for these growth factors without cross-reacting with the closely related insulin receptor."

Beltran and his fellow researchers found that AMG 479 bound to IGF-1R and blocked both IGF-1 and IGF-2 binding factors 1 and 2. The drug also completely inhibited ligand-induced activation in some growth factors, resulting in decreased pancreatic cell viability. The drug achieved an 80 percent inhibition rate of tumor growth and receptor expression, according to the researchers.

The findings appear in the current issue of Molecular Cancer Therapies.

"These data clearly show that AMG 479 is a clinical candidate for pancreatic cancer therapy, either alone or in combination with gemcitabine," Beltran said.

Gemcitabine is the only available treatment for pancreatic cancer, but the researchers said that it has yet to show a survival benefit.

AMG 479 is now being tested in nine separate phase II studies of various cancer types.

An estimated 200,000 people are diagnosed each year with pancreatic cancer, according to background information in the news release. Less than 4 percent live more than five years, it said, making pancreatic cancer one of the deadliest cancers.

More information

The American Cancer Society has more about pancreatic cancer.

-- Robert Preidt

SOURCE: Amgen, news release, April 14, 2009

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