top of page

Explore the Science Behind our Novel Therapeutics

Targeting Central Regulators of Neuronal Homeostasis

image.png

Explore the Biology of Key Disease Indications Below

Neurodegenerative Diseases
Alzheimer's Disease, Parkinson's Disease, and ALS
Applicable Therapeutics - ASHA-091 & ASHA-624

Neurodegenerative diseases represent one of the most poorly defined therapeutic areas with respect to the availability of disease modifying medicines... our goal is to change that. At Asha we are exploring disease-associated pathways to restore normal cellular function and mitigate pathology.

AD

Alzheimer's Disease (AD)
A Comprehensive Approach to Solving AD Pathology

image.png

At Asha we are taking a multifaceted approach to therapeutic intervention in AD. This includes addressing key metabolic pathways and mitochondrial dysfunction as well as targeting leading genetic risk factors for AD including ApoE4. 

A key feature of most neurodegenerative diseases including AD is the hyper-fragmentation of mitochondria. This promotes neuroinflammation, neuronal dysfunction, and ultimately neurodegeneration.  Protein aggregates including amyloid beta are key activators of DRP1 and fragmentation. We have developed a first-in-class highly specific inhibitor of mitochondrial fragmentation that restores normal cellular function, ASHA-091.

image.png

Parkinson's Disease (PD)
Targeting Dysfunctional Mitochondria

Mitochondrial hyper-fragmentation and dysfunction is the key pathological driver of PD. By restoring normal mitochondrial dynamics and function, curative outcomes are now a probable reality.

image.png
image.png

As a multi-indication therapeutics, ASHA-091 has demonstrated robust efficacy in preclinical models of PD by restoring normal mitochondrial homeostasis, limiting neurodegeneration, and bolstering dopamine levels.

PD

Amyotrophic Lateral Sclerosis (ALS)
Preventing Axonal Degeneration

image.png

ALS pathology is driven by the dysfunction and ultimate loss of motor neurons. Axonal degeneration is a key driving mechanism of ALS and other neuropathies and motor function disorders.

SARM1 is the primary regulator of

axon degeneration and is activated in ALS.

Using our novel intra-molecular glue technology and the PRISM™ platform, we have developed a robust SARM1 inhibitor, ASHA-624 that ameliorates ALS pathology in preclinical models in not only an effective but more importantly safe manner.

ALS

Infectious Disease & Post-Infection Illnesses
ME/CFS, Post-viral Illness, and Pathogen Resistance
Applicable Therapeutics - ASHA-091 & Undisclosed

ME

Millions of people live with chronic post-infection illnesses with currently no therapeutic interventions. Furthermore, anti-microbial and anti-bacterial resistant pathogens are ever increasing with only marginal future therapies on the horizon. These two aspects of infectious disease are at the heart of Asha's efforts to enable health security and provide hope to millions dealing with chronic post-infection illness. 

image.png
image.png

Post-viral Illness (Long COVID & ME/CFS)
Mitochondrial Fragmentation is the Commonality 

Post-viral illnesses are a set of chronic pathologies with multiple symptomatic profiles including ME/CFS and Long COVID. To date no cures, let alone effective therapies exist.

As observed in the neurodegenerative diseases described above, mitochondrial hyper-fragmentation has been identified as a driving component to post-viral illness. 

​

Similar to approaches for AD and PD, ASHA-091 intervention in preclinical models of post-viral illness is proving efficacious. Interestingly, ASHA-091 was designed specifically as the first targeted therapy for ME/CFS and post-viral illness and has since proven to have a host of other therapeutic indications including AD and PD as highlighted above. 

CRC
bottom of page