Atara Biotherapeutics recently published an update of the company’s quarterly financial results and operational highlights, including the advancement of its T-cell based immunotherapy strategies for multiple sclerosis (MS) and cancer. One of the investigational therapies featured in the report is ATA188, a potential treatment for MS.
According to the announcement, the company completed patient recruitment for an ongoing Phase 1 study testing ATA188 for progressive MS.
Therapeutic options for patients with progressive MS, a phase of the disease characterized by the continuous worsening of symptoms and physical disability over time, are currently limited.
ATA188 is a next-generation T-cell immunotherapy for autoimmune diseases, including MS, and was designed to selectively target and eliminate immune cells infected by the Epstein-Barr virus (EBV). Linked to several cancers and autoimmune conditions, EBV infection promotes autoimmune responses and is thought to participate in the onset and development of MS.
ATA188 works by re-educating a patient’s own T-cells — which are vital cells for the body’s immune system — to identify, attack, and eliminate the EBV-infected B-cells and plasma cells that are present at the central nervous system and increase the likelihood of autoimmunity.
Previous interim results from the ongoing Phase 1 trial with ATA188 showed that patients treated with four escalating doses of the drug experienced clinical improvements in MS symptoms. These positive results correlated with ATA188’s activity against EBV.
Atara will present updated trial results at two conferences, the 7th Joint Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), Oct. 25-28 in Paris, and the 3rd Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) meeting, Feb. 1-3, 2018 in San Diego, California.
During their presentations, researchers will discuss the latest results from the Phase 1 study of ATA188 in progressive MS and the company’s successful characterization of the molecular signature of EBV in MS brain lesions.
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