BioWorld International Correspondent
Borean Pharma A/S added a preclinical atherosclerosis drug to its pipeline by acquiring Proteopharma A/S for an undisclosed amount of stock. The compound, a trimerized form of Apolipoprotein A-I (ApoA-I), has attracted the attention of several major pharmaceutical companies, CEO Riku Rautsola told BioWorld International, and discussions are under way with a number of parties.
"I would not exclude anything between licensing and selling the whole company," he said.
The drug is based on one of Borean's platform technologies. It is the result of a long-standing collaboration between Borean's founders Hans Th gersen and Michael Etzerodt and its inventor, S ren Moestrup, CEO of Proteopharma, of Aarhus, Denmark, and professor of medical biochemistry at the University of Aarhus.
"About one year ago, when I came in, we decided we should get the rights to that substance because I saw the commercial potential to it," Rautsola said, who joined Borean from Cosmix Molecular Biologicals GmbH, of Braunschweig, Germany.
Esperion Therapeutics Inc., of Ann Arbor, Mich., reported Phase II results in November for ETC-216, a dimeric version of ApoA-I based on the so-called Milano mutation of the protein. Those results validated the strategy, he said. Esperion's data created a stir as they provided evidence that ETC-216 appeared to reverse atherosclerosis by reducing plaque size in coronary arteries. Pfizer Inc., of New York, recently closed a $1.3 billion cash takeover of Esperion based largely on the strength of those data.
Borean's drug candidate is based on the wild type form of ApoA-I, the major protein component of high-density lipoprotein (HDL), which is involved in the removal of cholesterol and other lipids from arterial walls. It has been trimerized using a peptide derived from the C-type lectin protein tetranectin. That, said Borean's head of research, Thor Holtet, increases its circulatory half-life as it slows excretion of the protein. It also enhances the normal HDL anti-inflammatory action that occurs within plaque complexes. "It inhibits the release of some of the key cytokines," he said.
The product has, Rautsola said, shown increased efficacy in mouse models of atherosclerosis and inflammation as compared with the monomeric, naturally occurring form of ApoA-I. As yet, however, it has not been administered to humans. The company hopes to file an investigational new drug in 2006 and commence human trials the year after, he said.
Borean, also of Aarhus, is taking a similar approach to prolonging the half-life of several other therapeutic substances, including human growth hormone. The company has two other platform technologies, an antibody analogue library based on reprogramming lectin-binding sites and a proprietary in vitro method of enhancing optimal protein conformation based on using a denaturation and renaturation step to "correct" the folding of proteins that are kinetically trapped in the wrong conformation. It currently is seeking €15 million in second-round financing, which it aims to close in the third quarter.