Bach is dedicated to developing drugs that modulate fundamental pathways regulating redox status and oxidative injury, thus normalizing the cellular redox environment and suppressing cell dysfunction and death. GVT, the lead compound, is distinct from classic "antioxidant" strategies by its ability to recycle itself, changing toxic reactive oxygen species into light, and to protect mitochondria and cross the blood-brain barrier. These properties should enable GVT to effectively address untreatable, fatal neurodegenerative disorders.

Oxidative stress occurs in cells when production of reactive oxygen species, for example in pathologically activated inflammatory processes, exceeds the level of protective cellular antioxidant enzymes. The result is oxidative injury to cellular macromolecules and, especially, to the mitochondria. Such damage is implicated in numerous serious diseases or environmental toxicities, targeting a variety of organ systems. These diseases include fatal, poorly addressed neurodegenerative disorders such as ALS, Alzheimer’s and Parkinson's diseases, Friedreich's ataxia and ataxia-telangectasia.

In preclinical studies, GVT was protective in several animal models for neurodegenerative disorders, involving mitochondrial injury, neuronal death and motor neuron dysfunction. GVT treatment attenuated mitochondrial dysfunction and cell death, normalized motor neuron function and prolonged survival. GVT is orally bioavailable, crosses the blood/brain barrier and normalizes gene expression in the brain, affecting key pathways induced in oxidative injury. Based on its compelling, multifunctional mechanism of action, GVT acts in a neuroprotective fashion, preserving neurons. In comparison, currently approved treatments are focused, instead, on lessening symptoms. Bach plans its first U.S. clinical program, to study neuroprotective effectiveness of GVT in ALS patients.

The following book has been published by researchers working with Bach Pharma's products and serving on our scientific advisory report:

Neurodegeneration Theory, Disorders, and Treatments

By: Alexander S. Mcneill, Nova Publications. (2011)

Carrì, Maria Teresa, et al. "Oxidative stress and mitochondrial damage: importance in non-SOD1 ALS." Frontiers in cellular neuroscience 9 (2015): 41.

 Carrì, Maria Teresa, et al. "Oxidative stress and mitochondrial damage: importance in non-SOD1 ALS." Frontiers in cellular neuroscience 9 (2015): 41.