Monday, Eli Lilly and Co. (LLY:  News ) said it agreed to acquire cancer-drug developer ImClone Systems Inc. (IMCL:  News ) for about $6.5 billion in cash in a bid to boost its oncology pipeline. Following the news, Lilly stock was down more than 4%, while Imclone rose above 4% in the intra-day trading.

The deal is expected to broaden Lilly’s portfolio of marketed cancer therapies and boost Lilly’s oncology pipeline with up to three promising targeted therapies in Phase III in 2009.

Further, the acquisition provides an important source of growth for Lilly amid patent expirations of various drugs. The acquisition of ImClone will help Lilly meet the challenge posed by patent expirations on several currently marketed products in the middle of the next decade.

The purchase would also boost Lilly’s biotech business as the biotech drugs, which comes at a hefty price tag and don’t face generic competition, are expected to offset slowing revenues from traditional drugs.

As per the terms of the deal, Lilly would acquire ImClone through an all cash tender offer of $70.00 per share, a premium of 51% to ImClone’s closing stock price on July 30, the day before Bristol-Myers Squibb’s (BMY: News ) offer for ImClone was made public. The price also represents an 8% premium to Imclone’s October 3 closing price of $64.96.

Lilly had been touted as the secret suitor for the New York-based ImClone. When ImClone rebuffed a revised offer of $62/share from Bristol-Myers last month, it referred again to the unnamed “large pharma company” willing to buy it for $70/share. However, Lilly had not commented on the reports.

On October 2, ImClone issued a statement saying that its unnamed suitor has completed due diligence and made a proposal that is not subject to financing or further due diligence.

Lilly’s interest in ImClone mainly stems from Erbitux, which is approved as a treatment for colon and head and neck cancers. The drug, which fetched $1.3 billion in 2007 sales, would be a significant addition to Lilly’s shaky portfolio, which is facing intense generic competition. One of Lilly’s key cancer drugs – Gemzar – will run off patent in 2010. The drug fetched sales of $1.6 billion in 2007. Lilly’s top-selling schizophrenia treatment — Zyprexa, loses patent protection in 2011. Zyprexa represented about $4.76 billion or more than 25% of the company’s $18.6 billion in sales last year.

Original Article

POT of gold. Mice lacking POT1b have shortened telomeres (green) and develop a rare yet fatal premature aging syndrome called dyskeratosis congenita. (Credit: Image courtesy of Rockefeller University)

Each time a cell divides, the protective caps at the ends of chromosomes shorten — and when these caps are gone, so are we. Now, by using an unconventional strategy to shorten telomeres in mice, researchers at Rockefeller University have not only created the first faithful mouse model for studying a rare yet fatal premature aging syndrome, but they have revealed the molecular defect behind the disease.

At a time when the world seems to be age-obsessed, this research may ultimately help scientists disentangle which genes play a role in the normal aging process from those involved in age-related disease. “Our mouse model is a step forward in understanding the pathogenesis of this disease and it may help us understand how we age in general,” says Titia de Lange, head of the Laboratory of Cell Biology and Genetics and Leon Hess Professor at Rockefeller University.

Sufferers of the disease, called dyskeratosis congentia, tend to have problems in tissues in which cells multiply rapidly — skin, hair, nails, tongue, gut and bone marrow — and usually die between the ages of 16 and 50 from bone marrow failure, or the inability to replenish their blood cells. According to some estimates, dyskeratosis congenita has only been diagnosed in 70 individuals since it was first described in 1906. “But the disease is probably much more frequent than previously inferred,” says de Lange, “as it is part of a spectrum of disorders with diverse clinical manifestations, such as anemia and lung fibrosis.”

Although patients were found to have severely shortened telomeres at the time of diagnosis, perplexing findings emerged that left researchers wondering whether dyskeratosis congenita was a telomere-based disease after all. When bits of DNA are lost from telomeres during each cell division, telomeres are partially rebuilt with an enzyme called telomerase. However, when researchers genetically engineered mice that didn’t produce telomerase, the mice had very short telomeres but didn’t show any signs of the disease, particularly its hallmark: bone marrow failure.

De Lange and her former graduate student Dirk Hockemeyer, who graduated in 2007, took a different approach: They made mice that lack POT1b, a protein that protects telomeres from getting degraded. Without POT1b, mice do not show the signs and symptoms of dyskeratosis congenita, but the telomeres shorten so fast that telomerase is incapable of keeping up with the loss. But without POT1b and reduced telomerase activity, mice develop the major hallmarks of the disease and die of bone marrow failure. When the mice that lacked POT1b were bred with mice that lacked telomerase, the offspring died.

“Dirk’s mutant mouse is the first faithful mouse model for a human telomere disease” says de Lange. “Together, these results suggest that in patients suffering from dyskeratosis congenita, the enzyme telomerase can’t elongate telomeres as fast as the nucleases chew them away.”

“Clearly, the next step is to understand how telomeres are degraded in human cells,” says de Lange. “We need to identify the nucleases at work and find out how they are regulated — a problem that will have to be tackled by a next generation of graduate students.

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Gene therapy is the insertion of genes into an individual’s cells and tissues to treat a disease, and hereditary diseases in which a defective mutant allele is replaced with a functional one. Although the technology is still in its infancy, it has been used with some success. Antisense therapy is not strictly a form of gene therapy, but is a genetically-mediated therapy and is often considered together with other methods.

Gene therapy using an Adenovirus vector. A new gene is inserted into an adenovirus vector, which is used to introduce the modified DNA into a human cell. If the treatment is successful, the new gene will make a functional protein.

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