inverseon

SAN FRANCISCO, Jan. 12, 2012 /PRNewswire/ -- Inverseon, Inc., a pharmaceutical company developing drug therapies for the treatment of pulmonary disorders, announced that while it anticipates that its asthma program will advance with non-dilutive grants, it is focused on smoking cessation as the initial indication for INV102.

William J. Garner, MD, Chairman, said, "The prioritization of smoking cessation, and also an inhaled COPD program, makes sense for Inverseon given the regulatory hurdles in key markets. We credit Dr. Glass for this refinement of our priorities. Mitchell Glass's extensive drug development background, relationships with the respiratory community, and experience with the strategic development and commercialization of therapeutics will be a major asset for Inverseon as the company advances its lead product (INV102) towards commercialization."

"Inverseon has provided critical support for the use of beta-adrenergic receptor inverse agonists for treating respiratory diseases. The founder's basic scientific breakthroughs provide a rational explanation for our previous success in developing carvedilol for heart failure while I was at SmithKline Beecham and provide a rationale for using INV102 for treating COPD. Two Phase II asthma trials are supportive of further development for chronic pulmonary diseases," said Dr. Glass. "We are now collaborating with granting agencies for further development of INV102 in asthma and preparing for expanded internal Phase II clinical trials demonstrating safety and efficacy of INV102 as a treatment to aid smoking cessation and chronic bronchitis.


Inverseon’s Founder and SAB Member Published in PNAS
San Francisco, Calif., Feb. 19, 2009 (BUSINESS WIRE) -- Inverseon, Inc. (www.inverseon.com)
announces the publication in the February 17, 2009 issue of the Proceedings of the National Academy
of Sciences (PNAS) entitled, “Beta2-adrenoceptor signaling is required for the development of an
asthma phenotype in a murine model.” The article was edited by Robert Lefkowitz, The James B. Duke
Professor of Medicine at Duke University and there is an accompanying supportive commentary on this
essential asthma signaling pathway by Raymond Penn of the University of Maryland School of Medicine.
"This work using knockout mice confirms prior results from Bond and collaborators using inverse
agonists, a subset of beta blockers, in mice and patients (Callaerts-Vegh PNAS 2004; Nguyen AJRCMB
2008; Hanania 2008) that a reduction in Beta2-adrenoceptor signaling attenuates the asthma
phenotype. The current work extends the prior observations by ruling out the possibility that the effects
of inverse agonists are exerted via biased agonism. Together, these are a remarkable set of
observations that point the way towards a possible therapeutic strategy based upon the use of drugs
that had previously been considered contraindicated in asthma. The precise mechanism by which
Beta2-adrenoceptor signaling exacerbates the asthma phenotype is not yet known, but is an active area
of study. Fully understanding this phenomenon and exploiting it therapeutically will be of tremendous
interest to the asthma community," commented Burton F. Dickey, MD, Professor & Chair, Dept. of
Pulmonary Medicine, M.D. Anderson Cancer Center and Inverseon Scientific Advisory Board member.