SOURCE: GENSET
Publication in PNAS Shows That GENSET's Famoxin Causes Significant Weight Reduction in Animal Model of Obesity
PARIS, Feb. 5 /PRNewswire/ -- GENSET (Nasdaq: GENXY - news; Nouveau Marche: GENSET) announced today the publication of preclinical results of Famoxin, the company's lead protein in obesity, in the February 6, 2001 Early Edition of the Proceedings of the National Academy of Sciences (PNAS). The publication resulted from the collaboration between scientists led by Prof. Harvey F. Lodish of the Whitehead Institute for Biomedical Research, an affiliate of the Massachusetts Institute of Technology (MIT) and researchers under Dr. Bernard E. Bihain, vice president of functional genomics at GENSET. This group discovered that the administration of Famoxin to massively obese mice consuming high fat diets caused significant weight reductions without altering food consumption. Famoxin is a recombinant protein based on the active portion of a naturally occurring serum protein, designated Acrp30, which is exclusively expressed by adipocytes (fat cells) and found in lower than normal levels in some obese patients.
Prof. Lodish commented on the reported findings: ``The preclinical data demonstrate that Famoxin exhibits potent and novel pharmacological properties for regulation of body weight and lipid metabolism. Unlike molecules that primarily work through activation of the central nervous system, Famoxin appears to exert its effects at the peripheral level, stimulating muscle oxidation of free fatty acids (FFA) and thereby clearing free fatty acids from the bloodstream. This increase in oxidation of FFA may account for the loss in weight.''
Dr. Bihain also commented, ``In some important ways, it is interesting to note that the parent molecule of Famoxin is deficient in a great number of obese human subjects. This opens the possibility to correct this metabolic defect by supplying this naturally occurring new compound to individuals with very low levels of this molecule.* In addition, it has been an exciting scientific adventure for scientists at GENSET to collaborate on this project with the outstanding team of the Whitehead Institute led by Prof. Harvey Lodish.''
Andre Pernet, president & chief executive officer of GENSET, added, ``We are particularly proud of this work, since it demonstrates the ability of GENSET's integrated genomics platform to generate promising compounds that address important human diseases. Just as insulin regulates glucose in individuals, we see that Famoxin regulates FFA. In that way, we can see Famoxin as being the Insulin of Obesity. ''
An estimated 150 million people worldwide are affected by obesity and its complications. In the United States and Europe, it is a highly prevalent condition, with some estimates of obesity in the United States ranging between 25 and 33 percent of the population. Obesity-related diseases, including diabetes, cardiovascular diseases, and certain cancers, lead to several hundred thousand deaths per year in the United States.
Though it is widely understood that obesity results from an imbalance between food intake and energy expenditure, it remains a scientific challenge to understand the mechanisms that allow some individuals to maintain appropriate body weight while others become obese. Indeed, relatively small changes in energy balance and basal metabolic rate can translate into massive weight gain.
The discovery of a new hormone like Acrp30 allows GENSET to envisage increasing the energy expenditure of obese subjects. Based on the recently reported and other preclinical results, the company anticipates initiating clinical trials of Famoxin towards the end of this year.* |
