Asha Therapeutics presented exciting new data for their lead Parkinson's Disease therapeutic ASHA-091 in one of its secondary indications for the drug this past week at The 12th International Biomedical Research into ME Colloquium at the Wellcome Sanger Institute in the United Kingdom.
"Targeting mitochondrial dynamics is a promising therapeutic avenue to treating post-viral illnesses including ME/CFS. ASHA-091 is the perfect compound to do just this and we are excited to continue developing it as a potential cure for Parkinson's Disease, ME/CFS and many other mito fragmentation-linked diseases" - Bradlee Heckmann, Ph.D., Chief Scientific Officer.
*Select data from the presentation is included below.
Mice with induced ME/CFS and chronic fatigue (labeled here as ME/Fatigue) were treated with ASHA-091 for a period of two weeks folllowing onset of symptoms and fatigue. ME/Fatigue mice treated with a control compound (Video 1) were sedentary and displayed reduced activity. ME/Fatigue mice treated with ASHA-091 for two weeks had a robust improvement in their overall activity and reduced fatigue (Video 2).
VIDEO 1: Vehicle Treated ME/Fatigue Mice
VIDEO 2: ASHA-091 Treated ME/Fatigue Mice
***Videos are 4x original speed.
A DEEPER DIVE: ME/CFS & TARGETING MITOCHONDRIA USING ASHA-091
Myalgic encephalomyelitis/chronic fatigue syndrome (ME of ME/CFS) is a devestating and debilitating post-infectious illness that is characterized by a multitude of symptoms including chronic fatigue and post-exertional malaise, brain fog, nerve pain, motor dysfunction, and many others. There is no cure for ME/CFS and relatively few treatment options beyond lifestyle and dietary changes and symptomatic therapies which are typically not robustly successful.
Mitochondrial hyper-fragmentation is a centric driver of pathology across many diseases, not only Parkinson's Disease.
Although the etiology of ME/CFS and other post-infection illnesses including Long COVID is poorly understood and heterogenous in nature, multiple studies have now implicated mitochondrial dysfunction and mitochondrial fragmentation as a key contributor to ME/CFS pathology. Interestingly, the majority of ME/CFS symptoms can be attributed and/or linked to changes in mitochondrial function as shown below.
ARE VIRUSES THE PRIMARY CULPRIT?
Post-viral ME/CFS is by far the most common form of the illness. A variety of viruses including the human herpes virus family, especially HHV-6 and SARS-CoV2 are highly associated with ME/CFS. Viruses including HHV-6 can directly induce mitochondrial fragmentation through DRP1, the protein target of ASHA-091.
Moreover, reactivation of viruses in patients has been linked to the onset of ME/CFS symptoms. These viral reactivation events can further induce mitochondrial fragmentation as shown below with HHV-6 and work from Bhupesh Prusty.
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Based on all of the emerging evidence implicating mitochondrial dysfunction and fragmentation in ME/CFS pathology, its our mission at Asha Therapeutics to utilize our novel compounds including ASHA-091 to address as many diseases as possible. Although early in its development in the context of ME/CFS, we believe ASHA-091 represents a potential breakthrough therapy for treating this debilitating and life altering illness.
At Asha we are committed and driven to create world chaning, disease modifying medicines. We are dedicated to the cure of diseases including ME/CFS and are excited to see the development of ASHA-091 towards this goal.
If you'd like to run a trial involving people with ME/CFS then contacting the Open Medicine Foundation would be a good start.
How do you induce ME/CFS in mice?