Teva, Active Biotech Partner To Develop Laquinimod For Huntington’s Disease
Active Biotech, a Sweden-based biopharmaceutical company that is developing therapies for autoimmune diseases, inflammatory diseases, and cancers, recently announced that it is partnering with Teva Pharmaceutical Industries Ltd. to develop a new, experimental drug for treating Huntington’s disease. The two companies will work together to launch a new phase 2 clinical trial in order to evaluate whether the use of oral laquinimod in the treatment of Huntington’s is both safe and effective.
The trial, entitled, “A Clinical Study in Subjects With Huntington’s Disease to Assess the Efficacy and Safety of Three Oral Doses of Laquinimod,” is posted on the clinical trials.gov website, but has yet to begin enrollment.
Laquinimod is seen as a promising therapy for a wide range of diseases. Acting as a CNS-active immunomodulator, it is typically administered as a once-daily oral drug, and features a novel mechanism of action that is primarily being developed primarily in order to treat the relapsing-remitting form of Multiple Sclerosis. Currently, Teva is recruiting for an RRMS trial utilizing Laquinimod, entitled, “The Efficacy and Safety and Tolerability of Laquinimod in Subjects With Relapsing Remitting Multiple Sclerosis,” which is recruiting patients for 280 different study locations across the United States and Europe. To date, the company reports that laquinimod has been shown to work both as an anti-inflammatory and neuroprotective therapy, providing positive results for participants involved in extensive non-clinical and clinical studies.
In addition, Active Biotech is also developing tasquinimod, currently in a pivotal study phase, as a treatment for prostate cancer, and has also finished a Phase II development of Laquinimod for Crohn’s and Lupus.
Huntington’s disease is a genetic neurodegenerative disorder that impacts muscle coordination and eventually leads to cognitive decline and behavioral symptoms. Mitochondrial DNA damage is associated with reduced mitochondrial bioenergetics in Huntington’s disease.