Swiss drugmaker GeNeuro has signed an agreement with the National Institute of Neurological Disorders and Stroke (NINDS) — part of the U.S. National Institutes of Health (NIH) — to advance studies of its novel therapeutic antibodies for the treatment of amyotrophic lateral sclerosis (ALS).
Under the Cooperative Research and Development Agreement, GeNeuro will provide antibodies designed to block the activity of HERV-K envelope protein — a virus of the family of Human Endogenous Retroviruses (HERVs) — which NINDS will then test in cellular and animal models. The aim is to get preclinical evidence that this approach against the virus could potentially become a valid therapeutic avenue to fight ALS.
“This agreement truly combines the strengths of both parties; the pioneering work done by GeNeuro in the HERV field, especially in the development of antibodies able to neutralize HERV-encoded proteins in associated diseases, and the excellent NIH research on the involvement of HERV-K in sporadic ALS led by Dr. Avindra Nath and his group,” Hervé Perron, GeNeuro’s chief scientific officer, said in a press release. “With this partnership, we aim to show that blocking this pathogenic HERV protein could lead to a novel ALS treatment and, in time, expand the GeNeuro clinical pipeline into additional neurological disorders.”
Nath, clinical director at NINDS, added: “We are excited about this collaboration as an initial step towards developing a therapeutic approach for altering the course of the disease for patients with ALS.”
Several viral sequences are present in the human genome but remain silent. Under pathological circumstances, however, this can change and these viruses can be expressed.
Nath and his research group recently found that the HERV-K is expressed in neurons of patients with ALS. In the study, “Human endogenous retrovirus-K contributes to motor neuron disease,” published in the journal Science Translational Medicine, the research group shows that the envelope protein of this virus causes degeneration of neurons. In addition, animals expressing this protein developed an ALS-like syndrome due to motor neuron dysfunction.
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