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Yale, NFCR launch cancer drug research center
November 2006
by Jeffrey Bouley  |  Email the author
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NEW HAVEN, Conn.—A five-year, $750,000 grant from the National Foundation for Cancer Research (NFCR) is allowing for the establishment of an NFCR Center for Anti-Cancer Drug Design and Discovery at Yale University that will work to develop new beta-peptide inhibitors.

Under the leadership of Drs. Alanna Schepartz and William Jorgensen, the cen­ter will work in particular to better under­stand how beta-peptides can be designed to disrupt protein-protein interactions that transmit cell signals. Abnormally behav­ing proteins can send incorrect signals that result in uncontrolled cell growth and division, and the idea is to block transmis­sion of cellular signals that lead to cancer growth.

"[Our] focus is on cancer targets such as the complex between p53 and hDM2—hDM2 amplification is implicated in many soft tissue cancers—and between Myc and Max, as c-Myc overexpression is implicat­ed in Burkitt's lymphoma as well as can­cers of the breast, GI tract, and the pros­tate," says Schepartz.

Unlike the more commonly used small-molecule inhibitors, beta-peptides have a chemical structure very similar to that of their target proteins, allow­ing the drug to bind the target pro­teins more specifically and inhibit them more effectively. Schepartz and Jorgensen report that because beta-peptides are stable within the human body, the center's research has the potential to create a com­pletely new technology platform for more effective and long-lasting anticancer drugs.

 But while the promise is there, Schepartz also notes that signifi­cant work remains.

"At this point, beta-peptides are simply a potential option in cases where inhibition of a protein-protein interaction is needed," she says. "We are working hard to learn how to best design these molecules to balance the often competing goals of affinity, speci­ficity, bioavailability and cost."

In addition to implications for cancer, beta-peptides hold promise for other areas of drug discovery, Schepartz notes.

"We have already reported beta-peptides that block HIV cell fusion through their interactions with gp41," she says. "In theory, these molecules represent the first step towards a cheaper, more tolerable replacement for Fuseon."

 
Code: E110619

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