Around 26 million people are affected by Alzheimer's disease worldwide, of which more than the half is entitled to seven major pharmaceutical markets (USA, Japan, Germany, UK, France, Italy and Spain). It is calculated that the number of AD sufferers worldwide will triple by the year 2050. The increase of the prevalence is a result of the progressive rise in life expectancy, the improvement in health care and diagnosis techniques.
Noscira, a company of Zeltia group devoted to the research and development of innovative drugs for the treatment of diseases of the nervous system, has received the approval of the Austrian health authorities and the Ethics Committee for the initiation of the first Phase II study with NP-12 for the treatment of Alzheimer's disease. NP-12, the first compound of Noscira's product pipeline, is an innovative drug of a new family of compounds. NP12 acts on the two main cellular processes that cause Alzheimer's disease, tau hyperphosphorylation and β-amyloid aggregation. Both in Alzheimer's disease and other neurodegenerative diseases, NP-12 may have a modifier and clinically relevant effect.
In Phase II clinical trials, NP12 will be administered to patients with Alzheimer's disease. Noscira is the only company in the world to have reached the clinical development stage with a compound for Alzheimer's disease, designed to inhibit the GSK3 enzyme. "This milestone reached by Noscira shows our progress in the search for new treatments, not only against cancer, through PharmaMar research activities, but also against other socially relevant diseases such as Alzheimer's disease" said Jose Maria Fernandez Sousa-Faro, President of Zeltia Group.
In words of Teodoro del Ser, Director of Clinical Development at Noscira, "We are pleased with the outcome of our work and with the efforts made at Noscira and we are confident that Phase II clinical trials results of NP12 will support our clinical expectations"
In animal models of Alzheimer's disease, it was demonstrated that NP12 improves cognitive performance and reduces amyloid deposits, hyperphosphorylation and tau aggregation, neuroinflammation and, most importantly, neuron loss, the ultimate cause of the clinical profile of progressive and widespread deterioration. Consistency of these findings supports the expectation that the compound may have a modifying effect of Alzheimer's disease when administered to patients. http://www.medicalnewstoday.com
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