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FASTOX Pharma and University of Padua enter a research collaboration on botulinum neurotoxins

Lausanne, 13 March 2021 – FASTOX Pharma and University of Padua today announced that they have entered into a neuroscience research collaboration aimed at identifying the mechanism of action of drugs enhancing the performance of botulinum neurotoxins. The one-year collaboration will explore how some drug candidates identified by FASTOX are able to prolong botulinum toxin duration of action.

FASTOX will leverage its unique expertise on drugs able to increase botulinum toxin performance and will benefit from the decades of expertise on neuro-muscular junction and on the cutting-edge models developed by Dr. Ornella Rossetto and her team at the Neuroparalysis and Neuroregeneration Laboratory of the University of Padua.

Dr. Mickaël Machicoane, Innovation Manager at FASTOX Pharma, said: “We are very eager to understand the science behind the ability of our drugs to significantly prolong the toxin duration, a prod

uct feature the market has been waiting for a long time. We are enthusiastic to collaborate with this highly-renowned team in the field of neuromuscular junction biology and botulinum toxin”.

Dr. Marco Pirazzini, Principal Investigator at Padua University, said: “The modulation of botulinum toxin by drugs is an exciting new research field in neurosciences. Understanding the molecular mechanism of action of FASTOX drug candidates may improve our knowledge of the neuro-muscular junction and create new therapeutic opportunities”.



Fastox Pharma is a Swiss independent pharmaceutical company specialized in designing Botulinum Neurotoxin (BoNT) enhancing drugs boosting BoNT performances. Fastox Pharma is headquartered in Lausanne, Switzerland.

About Neuroparalysis and Neuroregeneration Laboratory of the University of Padua, Italy

The laboratory, coordinated by Professor Emeritus Cesare Montecucco, studies the unique properties of regeneration of the neuromuscular junction, after degeneration or paralysis, to discover the signals exchanged among the motor axon terminal, perisynaptic Schwann cells and the muscle fiber leading to its functional recovery.


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