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Monday, July 15, 2013

Compugen Announces US Patent Allowance for Idiopathic Pulmonary Fibrosis Drug Candidate Recently Presented at 2013 American Thoracic Society Meeting

Sometimes "good things" also happen in this world (http://finance.yahoo.com/news/compugen-announces-us-patent-allowance-110000411.html):

"Compugen Ltd. (NASDAQ: CGEN) announced today that the company has received an Issue Notification from the U.S. Patent and Trademark Office for a patent application covering the company's drug candidate CGEN-25009. CGEN-25009 is intended for the treatment of idiopathic pulmonary fibrosis, a devastating disease with no current effective treatment. This novel peptide agonist of the relaxin receptor was the subject of a recent presentation by Dr. Daniel Kass, from the University of Pittsburgh (“Pitt”), at the 2013 American Thoracic Society Conference.

In his presentation, Dr. Kass, Assistant Professor of Medicine at Pitt and Assistant Director for Novel Therapeutics and Translational Research at The Dorothy P. and Richard P. Simmons Center for Interstitial Lung Disease at the University of Pittsburgh Medical Center, presented experimental data demonstrating that CGEN-25009 protects mice from bleomycin-induced pulmonary fibrosis. In this model, CGEN-25009 treatment reduced lung fibrosis as determined by collagen deposition in both preventive and therapeutic administration regimens."

My involvement in this project? As noted in an October 2011 blog entry (http://jgcaesarea.blogspot.co.il/2011/10/idiopathic-pulmonary-fibrosis-and.html):

"Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by scarring of the lungs, leading to respiratory failure. Despite an improved understanding of IPF's molecular mechanisms, the prognosis is poor, with a median survival of some three years from the onset of symptoms. Other than lung transplantation, there is no known effective treatment.

Estimated to affect five million people worldwide and 128,000 persons in the US, IPF has no known cause. These numbers are small relative to the 200,000 persons diagnosed with lung cancer in the US each year, but this is of little comfort if you contract IPF. Peter Benchley, the author of Jaws, died of IPF in 2006. A member of my family also died from the disease.

Several years ago, I read about a tiny Israeli biotech company named Compugen, which models disease processes at the molecular level and aims to predict drug candidates in silico, i.e. by computer. Although larger entities have failed at what Compugen is attempting, Compugen has persisted in its lonely efforts and believes it is well along the road to success.

In February 2007, Compugen, created a platform for the predictive discovery of novel G-protein coupled receptors ("GPCRs"), and in the initial run of this platform, eight novel GPCR ligands were found. Given that some 40% of all drugs modulate GPCRs and the relative high probability of newly discovered GPCR peptide ligands ultimately becoming drugs, Compugen's announcement elicited significant recognition from the scientific community.

In March 2009, Compugen announced that one of these newly discovered ligands, CGEN-25009, was able to activate the Relaxin receptor, and studies conducted by Professor Daniele Bani, an expert in the field of relaxin and fibrotic diseases from the University of Florence, demonstrated that administration of CGEN-25009 led to robust reduction of the fibrotic tissue in the lungs of mice induced with IPF.

. . . .

In 2009, I wanted to do something that mattered. Specifically, I wanted to move CGEN-25009 ahead. I called Compugen, and was fortunate enough to be hired as an external consultant.

Next, a cold call to the Pulmonary Fibrosis Foundation in Chicago, which was sufficiently intrigued to consult, inter alia, with the University of Pittsburgh's Simmons Center for Interstitial Lung Diseases.

Last week it was announced in a press release that the Pulmonary Fibrosis Foundation will provide a grant to the Simmons Center to further establish the anti-fibrotic properties of CGEN-25009 in multiple animal models of fibrosis, to elucidate the mechanism of CGEN-25009's anti-fibrotic effects, and to prioritize potential biomarkers for the study of CGEN-25009 in patients with IPF (see: http://www.cgen.com/Content.aspx?Page=press_releases&NewsId=569)."

Needless to say, I am extremely pleased by today's press release, and I pray that CGEN-25009 will ultimately emerge as an effective treatment for idiopathic pulmonary fibrosis and alleviate the suffering of millions of persons around the globe.

[As noted in prior blog entries, I am a Compugen shareholder, this blog entry is not a recommendation to buy or sell Compugen shares, and in September 2009 I began work as a part-time external consultant to Compugen. The opinions expressed herein are mine and are based on publicly available information. This blog entry has not been authorized, approved or reviewed prior to posting by Compugen.]

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