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Biogen Idec buys neurodegenerative disease rights

admin — Sat, 01 Jan 2011 06:12:08 +0000

Biogen Idec has acquired a subsidiary of Swiss biotech company Neurimmune, and the rights to three pre-clinical immunotherapy drugs.

The three R&D programmes are focused on the discovery and development of new human antibodies to treat neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease and amyotrophic lateral sclerosis (ALS).

Biogen will make an initial payment of $32.5 million and up to $395 million in contingent payments.

This acquisition builds on a 2007 agreement between the two companies to explore human antibodies against beta-amyloid for the treatment and prevention of Alzheimer’s disease. The drugs are designed to hit three central nervous system (CNS) targets: alpha-synuclein, tau and TDP-43.

The mis-folding of these three neurotoxic proteins is thought to be the cause of many neurodegenerative diseases.

Biogen Idec will oversee development of the pre-clinical candidates and the commercialisation of all products. Neurimmune will be responsible for additional scientific activities with respect to the lead candidates as well as the discovery of back-up candidates, utilising its proprietary ‘Reverse Translational Medicine’ technology platform. Neurimmune retains the right to use its platform for creating therapeutic antibody products outside the scope of its agreement with Biogen Idec.

“Biogen Idec is committed to becoming the global leader in the development of innovative therapies for neurodegenerative diseases,” said Alfred Sandrock, senior vice president, Neurology Research and Development, Biogen Idec.

“Neurimmune continues to impress us with their ability to translate scientific insights into innovative antibodies for the potential treatment and prevention of many neurodegenerative diseases. The unmet medical need among patients suffering from devastating neurodegenerative diseases is high, and we are excited to be moving these three promising programs forward.”

“We are pleased that Biogen Idec decided to acquire these candidate therapeutics for neurodegenerative diseases,” said Roger Nitsch, founder and director of Neurimmune. “With its world-class expertise in the development, manufacturing and marketing of therapeutic antibodies for neurological diseases, Biogen Idec is the perfect strategic fit to drive the successful development of Neurimmune’s antibodies.”

“We are proud of what our team has achieved in proving once again the power of our human antibody discovery platform to generate highly valuable candidates for the development of immunotherapies for CNS indications,” said Jan Grimm, founder and CSO of Neurimmune.

Research into Alzheimer’s and other neurodegenerative diseases is being pursued by many different pharma and biotech companies, but the field has been beset by setbacks.

Three drugs are currently in late stage development – Pfizer/Medivation’s Dimebon, J&J/Pfizer’s bapineuzumab, and Lilly’s solanezumab.

http://www.inpharm.com/news/101221/biogen-idec-neurodegenerative-disease-neurimmune

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Roche, reMYND in Pact to Develop PD, AD Drugs

admin — Sat, 02 Oct 2010 08:33:58 +0000

Roche AG and reMYND will join forces to develop two classes of compounds against Parkinson’s disease and Alzheimer’s disease. The total deal is worth as much as $637 million to reMYND as milestones are met.

The Parkinson’s compounds target alpha-synuclein, while the Alzheimer’s compounds zero in on tau.

Roche, of Basel, Switzerland, will provide expertise in chemistry, lead-optimization and preclinical development while Leuven, Belgium-based reMYND continues nonclinical pharmacology studies and the elucidation of the mechanism. Roche has licensed worldwide commercialization rights for both programs.

“For us as a company, it’s almost a dream come true,” reMYND Managing Director Koen De Witte told BioWorld International.

The company had conversations with 15 of the top 20 pharmaceutical companies before shaking hands with Roche. De Witte cited Roche’s emphasis on first-in-class products and biomarker development as qualities that make it a good partner for reMYND.

reMYND’s technology platform analyzes diseases of protein misfolding and aggregation. The company has four CNS compounds in its pipeline for Alzheimer’s and two for Parkinson’s disease, and its lead compounds for each disease have been advanced to the IND stage.

De Witte called the preclinical results in animal models “very convincing.” In the case of the Parkinson’s mouse model, the lead Parkinson’s compound, ReS9-S, prevented degeneration for an eight-week period. Such results convinced reMYND’s scientists that the compounds in their pipeline were true disease-modifying agents.

Recent clinical trial disappointments, such as Eli Lilly and Co.’s semagacestat in Phase III trials, the failure of Medivation Inc.’s Dimebon and the 2008 cancellation of Flurizan by Myriad Genetics Inc., have created a vacuum into which a number of biotech companies are hoping to move.

There is intense competition to become the first disease-modifying treatment for Alzheimer’s. Joining reMYND and Roche in a bid for that title are biotech companies such as Elan Pharmaceuticals plc, BioChromix Pharma AB, Senex Biotechnology Inc., Alectos Therapeutics Inc. and many others.

The ultimate winner will be determined largely by which company makes the right guess as to the cause of Alzheimer’s disease. Some companies are hedging their bets with more than one target. Others are putting all of their eggs in one basket.

Elan is developing small-molecule and antibody therapeutics against beta amyloid, beta secretase, gamma secretase and a p75 ligand.

Prior to its Phase I disappointment with an Alzheimer’s vaccine, Elan had discouraging results in Phase II trials of bapineuzumab, its humanized monoclonal antibody targeted at beta amyloid. BioChromix is developing small-molecule compounds targeted at beta amyloid, and Senex is working on a mechanism involving cellular aging.

In a deal mirroring Roche’s acquisition of rights to reMYND’s compounds, Merck licensed compounds targeted against tau from Alectos for up to $289 million.

A majority of researchers still favor the beta amyloid hypothesis, but like many smaller companies, reMYND takes a minority position. ReMYND has focused its efforts on tau protein since 2002, which De Witte called “definitely underresearched.”

reMYND supports beta amyloid and tau as relevant targets. “ABeta is the initiator, and tau is the executioner. Hence, one could see a combo treatment in the future where the tau treatment would have the more direct effect, and the aBeta treatment would ensure that almost no additional toxicity is initiated,” De Witte explained.

The focus on tau, however, caused the company early difficulties in selling its approach to potential partners. “It was a very tough sell, because everyone was so focused on aBeta, and it’s only since the International Conference on Alzheimer’s Disease meeting in the summer of 2008 that there’s gradually been an interest in tau,” De Witte noted.

Roche is clearly convinced. “The work they’ve done so far is absolutely compelling,” said Shafique Virani, global head of CNS Partnering at Roche. “We have true belief that these compounds will act as diseases modifiers.”

reMYND’s Parkinson’s and Alzheimer’s compounds will round out Roche’s CNS pipeline, joining two Phase I antibody programs against beta amyloid, and a small-molecule compound for Alzheimer’s and schizophrenia targeted at the nicotinic alpha-7 receptor.

reMYND will be using its largesse to advance its program in diabetes and pursue orphan indications such as ALS, Huntington’s disease and multiple system atrophy, which are all diseases compatible with its platform for screening diseases of protein misfolding and aggregation.

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Alzheimer's drug Dimebon helps Huntington's: study

admin — Thu, 01 Apr 2010 13:54:20 +0000

(Reuters) – Dimebon, a pill being developed for Alzheimer’s disease, helped people with Huntington’s disease improve their thinking, learning and memory skills, U.S. researchers said on Monday.

Dimebon, made by Medivation Inc. under the generic name latrepirdine, appears to be safe for Huntington’s patients and has minimal side effects, the researchers reported in the journal Archives of Neurology.

Dr. Karl Kieburtz of the University of Rochester in New York said his team chose to study Dimebon because it appeared to have an impact both on cognition and aging.

“In diseases like Huntington’s disease where there is degeneration of the brain, one thing we look for is compounds that might favorably influence that and sometimes those compounds come out of things that can slow natural aging,” Kieburtz said in a telephone interview.

He said the independent study, involving 91 patients, was sponsored by Medivation. A new follow-up trial with 350 patients is being conducted to see whether the initial findings can be confirmed, Kieburtz said.

San Francisco-based Medivation has partnered with Pfizer Inc. to develop and commercialize latrepirdine for the treatment of Alzheimer’s. The drug was first sold in Russia as an antihistamine.

Medivation chief executive David Hung said on Monday the company plans relatively soon to begin trials of altered forms of Dimebon, called analogues, that may have potential against an array of disorders, including Parkinson’s disease, stroke and heart failure.

There is no cure for Huntington’s disease, a highly disabling disorder in which brain cells are damaged. People who inherit the genetic mutation that causes Huntington’s have a 100 percent chance of developing the fatal disease.

One drug, tetrabenazine, sold under the brand name Xenazine, can help manage some of Huntington’s symptoms but does not prevent the physical and cognitive decline. Danish pharmaceuticals group Lundbeck owns the rights to Xenazine, which the company says has a sales potential of $250 million in the United States alone.

Kieburtz and colleagues studied people with mild to moderate Huntington’s disease at 16 sites in the United States and one in Britain from July 2007 to July 2008.

Over 90 days, 46 of the volunteers were given 20 milligrams of latrepirdine three times a day. The other 45 patients took a placebo.

The researchers said Dimebon appears to stabilize and improve the functioning of cells damaged by the disease. It may act specifically on the mitochondria, powerhouses inside the cells that have their own unique DNA.

Side effects from the drug included headaches, falls and dizziness.

The patients who took Dimebon showed improvement in average scores on tests measuring cognitive function. The average scores of people in the placebo group remained steady, the report said.

“Huntington’s disease is usually thought of as kind of a movement disorder, but the thinking and behavior problems are as, if not, more important than the motor problems of that disease,” Kieburtz said.

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History of Head Trauma in Alzheimer's Disease

admin — Wed, 18 Mar 2009 04:24:12 +0000

It turns out generally that whether a history of head trauma or injury is a cause of Alzheimer’s disease of the symptoms of Alzheimer’s disease is not certain or indeed uncertain by itself.

It can be pointed out that some published studies of repute suggest that head trauma that results in what may or should be considered a loss of consciousness is a definite risk factor and factors into the risks of a patient developing Alzheimer’s disease.

Thus people who expose themselves to repeated head trauma or injury , such as you might find in the classic cases of boxers such as Muhammed Ali, who developed serious Parkinson’s disease – perhaps as a result of his boxing career, or football players can be said to be , as a result , at a higher risk of developing Alzheimer’s disease as opposed to if they had not followed their chosen career path or paths. Regardless of whether or not actual Alzheimer’s disease progresses as a result of the specific person’s health and mental and memory cognitive skill levels- many such people who are continually exposed to head trauma and head trauma injuries do go later to more often than the general population , have incidences of difficulties of memory , concentration, speech and other brain function difficulties higher than the general population overall .

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