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Probiodrug Funds Brigham and Women's Research into Antibody Targeting Pyroglutamated Abeta for Treatment of Alzheimer's Disease
[December 23, 2013]

Probiodrug Funds Brigham and Women's Research into Antibody Targeting Pyroglutamated Abeta for Treatment of Alzheimer's Disease


HALLE/SAALE, Germany --(Business Wire)--

Probiodrug AG (Probiodrug) announced today the decision to provide research funding to the laboratory of Cynthia Ann Lemere, Ph.D., in the Center for Neurologic Diseases at Brigham and Women's Hospital, a teaching hospital affiliated with Harvard Medical School in Boston, MA. Funded by the National Institutes of Health (NIH), Dr. Lemere is pioneering immunotherapy approaches to eliminate pyroglutamated (pGlu) Abeta, a highly toxic peptide that has been correlated with cognitive decline in individuals with Alzheimer's disease. The funding provided by Probiodrug will be used to expand this work to include additional research aimed at understanding mechanisms of clearance using several experimental anti-pGlu Abeta monoclonal antibodies (mAb) provided by Probiodrug.

Konrad Glund, Ph.D., CEO of Probiodrug commented, "The work being done in Dr. Lemere's laboratory is of the highest quality, and we believe this project shows enormous potential. By establishing this new collaboration with her team, we hope to advance the understanding of how the removal of pGlu Abeta may arrest the progression of Alzheimer's disease."

By providing funding to Dr. Lemere, Probiodrug has extended a long-standing collaboration with Brigham and Women's Hospital that began in 2008. In the initial stage of the collaboration, Probiodrug scientists and Dr. Lemere worked to characterize the deposition of pGlu Abeta in different animal models with Alzheimer's-like pathology and in the human brain. Based on this research, Probiodrug developed an anti-pGlu Abeta mAb that was shown in transgenic pre-clinical models to significantly reduce the cncentration of plaque deposits in the hippocampus and cerebellum that is characteristic of Alzheimer's disease progression. A summary of this work was published in the journals Neurodegenerative Diseases1 and American Journal of Pathology2 in 2012 and 2013, respectively. This and other anti-pGlu Abeta mAbs supplied by Probiodrug continue to be used by Dr. Lemere in her NIH-funded research.



"The work we are planning to commence with Dr. Lemere will further address the science behind the observed clearance of pGlu Abeta by the antibody," Dr. Glund added. "Our next steps include demonstrating the therapeutic potential of this antibody for treating Alzheimer's disease. By gaining a better understanding of the manner in which the antibody contributes to clearance of pGlu Abeta and reduction of Alzheimer's pathology, we will move one step closer to advancing a meaningful therapy against this terrible disease."

About Probiodrug AG


Probiodrug is a biopharmaceutical company dedicated to the discovery and development of novel therapeutic solutions to treat people with Alzheimer's disease. The Company has medical use and composition of matter patents related to the inhibition of glutaminyl cyclase, providing the Company with a dominant position in this field of research. Probiodrug is backed by institutions such as BB Biotech, Edmond de Rothschild Investment Partners, Goodvent/IBG, HBM, TVM Capital, Life Sciences Partners, Biogen Idec New Ventures, CFH Group, funds managed by Wellington Management and private investors.

Probiodrug's core capabilities are based on its long-standing expertise in the elucidation of the structure and function of enzymes which play a central role in the maturation of hormones. Probiodrug was founded in 1997 by Prof. Dr. Hans-Ulrich Demuth and Dr. Konrad Glund. For more information, please visit www.probiodrug.de.

* EDITOR NOTES:

1 Frost J.L. et al. Passive Immunization against Pyroglutamate-3 Amyloid-ß Reduces Plaque Burden in Alzheimer-Like Transgenic Mice: A Pilot Study. Neurodegenerative Dis 2012;10:265-270.

2 Frost J.L. et al. Pyroglutamate-3 amyloid-ß deposition in the brains of humans, non-human primates, canines, and Alzheimer disease-like transgenic mouse models. Am J Pathol. 2013;183:369-81


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