National MS Society Invests in Clinical Development of Human Antibody for Progressive Forms of MS
Fast Forward, a nonprofit subsidiary of the National Multiple Sclerosis Society, will invest up to $330,000 to advance the clinical development of an antibody that was shown to lessen inflammation and nerve cell damage in a multiple sclerosis (MS) mouse model.
The funding will help develop the antibody (a protein the immune system uses to neutralize pathogens such as bacteria and viruses) in order to have properties more similar to those found in humans (a humanized antibody), and to test its therapeutic potential in people with MS.
Therapies able to protect the nervous system are needed, especially by those with progressive forms of MS, an area in particular need of therapeutic strategies to halt the damage to the nervous system triggered by chronic neuroinflammation.
The antibody, being developed by MedaRed, follows the early work of the company’s co-founder Katerina Akassoglou, PhD, at the Gladstone Institutes and the University of California San Francisco.
“We are excited to see the development of this antibody accelerate toward a breakthrough for progressive MS,” Mark Allegretta, PhD, vice president of research at the National MS Society, said in a press release. “This funding will help MedaRed take a key step for translating their important findings toward a clinical trial in people with progressive MS.”
Akassoglou’s team developed an antibody that targets a blood-clotting factor, called fibrin, previously shown to trigger inflammation in the brain. Fibrin has been detected in active and chronic brain lesions of MS patients.
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They designed their antibody to selectively target a specific region within the fibrin protein known to activate the immune response. This assured that the protein’s region responsible for the blood-clotting effect remained intact.
Using a mouse model of MS, researchers showed that treatment with their newly-developed antibody halted activation of inflammation and oxidative stress, two potential sources of toxic chemicals that may contribute to nerve cell death. The same was seen in a mouse model of Alzheimer’s disease.
Moreover, the antibody reduced the activation and accumulation of inflammatory cells in the spinal cord, and lessened nerve cell damage and demyelination (loss of myelin) of nerve fibers, a hallmark of MS.
These preclinical data were reported in an article titled “Fibrin-targeting immunotherapy protects against neuroinflammation and neurodegeneration,” published in the journal Nature Immunology.
“The funding from the National MS Society accelerates the transition of this important research discovery into the clinic” said Edward Spack, PhD, president of MedaRed. “We look forward to accomplishing this key step in drug development through the support of the Society, and improving the health of people with MS.”