News & Media


NeurAegis Announces Formation of Scientific-Medical Advisory Board

SOUTHBOROUGH, Mass.Dec. 10, 2020 /PRNewswire/ — NeurAegis, Inc., a neuropharmaceutical company developing breakthrough treatments for neurological disorders, today announced the inaugural members of its Scientific-Medical Advisory Board who will help advance the Company’s preclinical and clinical development activities and product pipeline. Members include Drs. Michel BaudryImad Najm and Barry Jordan, all internationally recognized experts in their respective fields of neurological disorders.

NeurAegis Announces Publication of Preclinical Animal Data Supporting Calpain-2 as a Promising Therapeutic Target for Concussion

SOUTHBOROUGH, Mass., July 1, 2020 /PRNewswire/ — NeurAegis, Inc., a neuropharmaceutical company pioneering the development of breakthrough treatments for neurological disorders, today announced the publication of a paper titled “Calpain-2 as a therapeutic target in repeated concussion-induced neuropathy and behavioral impairment” in Science Advances. The studies reported in the publication were performed in the laboratory of NeurAegis’ scientific founder, Dr. Michel Baudry, at Western University of Health Sciences, Pomona, CA, where the neurodegenerative role of the protease calpain-2 in repeated concussions was investigated. These studies lend further scientific rationale for the Company’s focus on developing novel calpain-2 inhibitors as therapeutic agents for concussion.

NeurAegis Scientific Founder Michel Baudry Awarded $3.8M Grant from the Department of Defense to Advance Product Candidate for Treating Traumatic Brain Injury and Concussion

SOUTHBOROUGH, Mass., Sept. 5, 2019 /PRNewswire/ — NeurAegis, Inc., a privately held pharmaceutical company pioneering the development of breakthrough treatments for neurological disorders, announced today that its scientific founder, Dr. Michel Baudry, has been awarded a multi-year, $3.8 million grant from the Department of Defense’s Combat Casualty Care Research Program. This project is focused on optimizing a neuroprotective drug candidate for traumatic brain injury (TBI) and concussion and the DOD funds will support medicinal chemistry and preclinical studies in preparation for a first-in-human Phase I clinical trial.


Calpain-2 activation in mouse hippocampus plays a critical role in seizure-induced neuropathology

Epilepsy is the most prevalent neurological disease after migraines. Almost 50 million people are affected worldwide, with 1% of the population expected to develop epilepsy by age 20 (http://www.epilep Like most neurological diseases, epilepsy exists in multiple forms and exhibits a complex and multifactorial pathology, which implicates alterations in many molecular/cellular mechanisms. Currently, there is no cure for this complex disease. While several antiepileptic drugs (AEDs) have been introduced over the last 40 years to address the symptoms, a large number of patients are resistant to these drugs, and many undesirable side-effects are associated with the current AEDs (Asconap´e, 2010; Loring et al., 2007; Sarco and Bourgeois, 2010; Schmidt, 2009).

Prolonged calpain-2 activation in hippocampus plays a critical role in seizure-induced neuropathology

Calpain has been proposed to play a critical role in the development of epilepsy, since this calcium-dependent protease is activated after seizures and is involved in neurodegeneration. In the present study we used conditional calpain-2 knock-out mice and a selective calpain-2 inhibitor to analyze the role of calpain-2 in epilepsy using the kainic acid model of epilepsy elicited by repeated injections of low doses of kainic acid. Neurodegeneration was evident in various hippocampal subfields, and in particular in the hilus of the dentate gyrus 7 days after KA-induced seizures.

Differential Activation of Calpain-1 and Calpain-2 following Kainate-Induced Seizure Activity in Rats and Mice.

Systemic injection of kainate produces repetitive seizure activity in both rats and mice. It also results in short-term synaptic modifications aswell as delayed neurodegeneration. The signaling cascades involved in both short-term and delayed responses are not clearly defined. The calcium-dependent protease calpain is activated in various brain structures following systemic kainate injection, although the precise involvement of the two major brain calpain isoforms, calpain-1 and calpain-2, remains to be defined. 

Calpain-2 as a therapeutic target for acute neuronal injury.

While calcium-activated neutral proteases (CANP) were discovered in 1964 by Guroff [1], the terms calpain and calpastatin, its endogenous inhibitor, were introduced in the 1980s [2]. Since then, many studies have been directed at understanding the physiological as well as the pathological function(s) of this family of proteases in the brain and other organs. We initially proposed in 1984 that calpain played a critical role in synaptic plasticity and learning and memory [3], and this hypothesis was recently confirmed by studies performed in calpain-1 knock-out (KO) mice [4,5].

Protection against TBI-Induced Neuronal Death with Post-Treatment with a Selective Calpain-2 Inhibitor in Mice.

Traumatic brain injury (TBI) is a significant public health problem in the United States. In 2010 alone, an estimated 2.5 million TBI patients presented for treatment, and it is likely that many more cases are never reported. The financial burden for the society is enormous, as many patients with TBI completely lose the ability to be self-sufficient and require long-term medical and rehabilitative care. Among the different types of TBI, penetrating TBI produces the worst outcomes and highest morality rates.

Calpain-1 and Calpain-2: The Yin and Yang of Synaptic Plasticity and Neurodegeneration.

Many signaling pathways participate in both synaptic plasticity and neuronal degeneration. While calpains participate in these phenomena, very few studies have evaluated the respective roles of the two major calpain isoforms in the brain, calpain-1 and calpain-2. We review recent studies indicating that calpain-1 and calpain-2 exhibit opposite functions in both synaptic plasticity and neurodegeneration. Calpain-1 activation is required for the induction of long-term potentiation (LTP) and is generally neuroprotective, while calpain-2 activation limits the extent of potentiation and is neurodegenerative.