Technology | X Tosis

Innovating Mitochondrial Protection Against Neurodegeneration

Advancing Disease-Modifying Mitochondrial Medicine

X-tosis is developing first-in-class therapeutics that address the upstream biology driving neurodegenerative diseases. Our approach centers on restoring mitochondrial stability and preventing neuronal death—an essential step toward true disease modification in conditions such as Alzheimer’s, Parkinson’s, ALS, and other disorders marked by mitochondrial dysfunction and chronic inflammation.

Targeting VDAC1 to Halt the Neurodegeneration
Cascade

Mitochondrial dysfunction is one of the earliest and most consistent features of neurodegenerative disease. XTS compounds selectively inhibit oligomerization of VDAC1, a mitochondrial pore protein whose aggregation leads to:

loss of mitochondrial membrane potential
excessive reactive oxygen species (ROS)
release of apoptotic factors
inflammatory activation

By stabilizing VDAC1 in its healthy state, XTS compounds restore mitochondrial function, protect neurons, and interrupt the pathways that drive progressive neurodegeneration.

Compelling Preclinical Efficacy Across Neurodegenerative Models

XTS compounds have demonstrated strong disease-modifying potential in multiple preclinical models, including Alzheimer’s and Parkinson’s disease. Key findings include:

preserved neuronal structure and reduced cell death
improved learning and memory performance
restored mitochondrial function and ATP production
reduced amyloid-beta burden
decreased neuroinflammation
glial shift toward neuroprotective phenotypes

These results support VDAC1 modulation as a powerful upstream therapeutic strategy.

A Pathway Implicated
Across More Than
18 Diseases

VDAC1 overexpression and mitochondrial dysfunction are implicated in more than 18 neurological and systemic disorders. By intervening at this fundamental point of failure, XTS compounds hold potential for broad therapeutic application across diseases characterized by neuronal stress, metabolic imbalance, and inflammation.

How XTS001 Works

XTS001 targets the root cause of mitochondrial collapse by preventing VDAC1 oligomerization. In neurodegenerative disease:

VDAC1 becomes overexpressed
VDAC1 oligomerizes, forming toxic pores
Mitochondria lose membrane potential and energy production
Apoptotic factors leak into the cytosol
Neurons die; inflammation accelerates degeneration

XTS001 blocks this cascade, restoring mitochondrial integrity and reducing neuronal loss. This mechanism is supported by more than 20 years of academic research and independent validation.