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Affiris struck a deal with GlaxoSmithKline to develop two Alzheimer's treatments. As part of the agreement, GSK gains a fancy protein technology that could be a boon for future molecules.
GlaxoSmithKline, last week, signed a development and commercialization deal with Austrian biotech Affiris to gain access to two therapeutic Alzheimer’s vaccines and the proprietary technology to potentially develop more.
The deal will cost GSK about $29 million in cash upfront, and Affiris stands to gain up to $550 million more if the treatments achieve certain milestones. GSK, in exchange, can add two more potential vaccines to its growing portfolio of Alzheimer’s disease and dementia products in development.
Alzheimer’s is one of the fastest-growing markets in the pharmaceutical industry. With an estimated 26.6 million people worldwide diagnosed with Alzheimer’s and four times that number projected by 2050, most of the big pharmas either have their own Alzheimer’s R&D programs or are quickly buying up biotechs the specialize in the largely untreatable disease.
GSK also gains access to the Affiris Affitope technology, a protein designer that, according to GSK, features “specific binding characteristics that are ideally suited for the development of vaccines against disease-causing `rogue’ human proteins, such as beta-amyloid which is central to the pathology of Alzheimer’s disease.”
The leading hypothesis about the cause of Alzheimer’s is that deposits of amyloid beta accumulate throughout the brain. But because a correlation between the formation of these plaques and the loss of neurons has not been proved, the beta-amyloid hypothesis remains somewhat controversial.
One promising experimental vaccine has already gone bust after human trials showed that it successfully decreased the amount of plaque without effecting symptoms of the disease.
GSK spokesperson Sarah Alspach emailed Pharm Exec with a short lesson on what makes the vaccine candidates produced by the Affitope technology better bets.
“These vaccines aim to induce only antibodies to bind the A peptides reducing deposition of the A protein and clear the amyloid plaques,” Alspach wrote. “This approach is different because although AD01 and AD02 have different amino acid sequences to the naturally occurring A sequence, these induce antibody responses which specifically recognize the beta-amyloid protein in amyloid plaque.
In preclinical trials, the treatment showed a sizeable decrease in amyloid plaque in mice and showed zero T-cell inflammation or toxicity.
Alspach also said that these therapeutic vaccines “align well with our focus on vaccines and novel adjuvant systems.”