SI
SI
discoversearch

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor.  We ask that you disable ad blocking while on Silicon Investor in the best interests of our community.  If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.
Biotech / Medical : Regeneron Pharmaceuticals -- Ignore unavailable to you. Want to Upgrade?


To: Miljenko Zuanic who wrote (421)3/28/2000 10:27:00 PM
From: juneau_boy  Read Replies (1) | Respond to of 3559
 
Phase 11 initiated. Stock down. Could this AP news be the reason?

"NEW YORK (AP) -- Scientists have created strains of mice that can eat a high-fat diet without getting chubby using a single gene that might lead to a new obesity treatment for people.

In its normal form, the gene, called HMGIC, apparently helps mice make more cells to store fat when they have been eating a fatty diet, researchers said. But the mice in the experiment had a defective version of the gene.

They apparently failed to create storage cells in response to the high-fat diet, and so avoided putting on weight, the researchers said in the April issue of the journal Nature Genetics.

The finding could lead to a human obesity treatment if scientists can find a drug that interferes with the effect of the normal HMGIC gene, said Kiran Chada, a biochemistry professor at the University of Medicine and Dentistry of New Jersey and senior author of the paper. He is also president of a company formed to develop products related to the gene.

Dr. Bradford Lowell, an obesity expert at Harvard Medical School, said it will take a lot more work to find out how promising Chada's approach would be for humans.

Dr. Rudy Leibel, an obesity expert at Columbia University in New York, said if a person's supply of fat-storing cells were restricted, fat might build up in the liver instead. That could seriously interfere with liver function, he said.

Chada said he has seen no sign of fatty liver buildup in the mice.

Mice born with the genetic defect develop only about 10 percent of the normal amount of body fat but are otherwise normal, Chada said. Mutant mice that ate a high-fat diet for six months didn't put on any more weight than mutants that ate a standard diet.

Normal mice, in contrast, did become obese on the high-fat diet. All three groups of mice ate about the same amount."
________________
Question: Wouldn't it take years even with new genomic tools to get a drug to market from this discovery, and would'nt REGN have the obesity field to itself until then?
Eric