Mitergy is a late stage, mitochondrial therapeutic discovery company focused on the progressive cell death that accompanies several human diseases. Diseases with inappropriate cell loss include stroke, progressive heart failure and neurodegenerative diseases such as Parkinson's, Alzheimer's and Amyotropic Lateral Sclerosis (ALS), or Lou Gehrig's Disease. Mitergy's business strategy is predicated on a strong intellectual property position covering a novel disease-related, validated drug target and a new class of therapeutic drugs that prevent cardiomyocyte cell loss due to chemotherapy. Because of the expected involvement of Mitergy's drug target in a variety of end-stage diseases that exhibit accelerated cell loss in affected adult tissues, Mitergy is now poised to form strategic alliances to ensure translation of Mitergy's pre-clinical R&D to meeting the clinical challenge posed by the causative or contributing role premature cell loss in the pathogenesis or progression of human diseases.
Kathryn Maschhoff, MD PhD and Paul Anziano, PhD have discovered genetic-modifying etiologies and atrophic, mitochondriopathic mechanisms that progress human neurodegeneration and heart disease. Their work has provided fundamental insights into the root cause of “secondary”, non-inherited mitochondrial oxidative stress, clearly defining a novel therapeutic target and discovering a new class of non-antioxidant, mitochondrial therapeutic that have shown superior in vivo efficacy in highly translatable murine models of human disease.
Patients with terminal heart failure and dilated cardiomyopathy (DCM) or coronary artery disease (CAD) exhibit loss of heart muscle cells or cardiomyocytes.
This condition also occurs with cancer patients subjected to the severe cardiotoxic side effect of chemotherapy. The National Cancer Institute estimates that 1 of 7 or 13% of the women in this country will develop breast cancer during their lifetime and that a third of these will require a combination of chemotherapy and the new generation of anti-neoplastic, Her2 inhibitors which target the activity of the ErbB2 receptor in cancerous cells. Because of the adverse side effects of these drugs, about 2% of the women in this country will be at risk for severe, possibly fatal, heart failure during their lifetime.
Mitochondrial pathology is a key indicator of the progressive decline of nerve function and the premature loss of nerves cells that occurs in Parkinson's Disease and in Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig's Disease, caused by premature loss of nerve cells in the dopamine-producing, substantia nigra nerve center or the loss of spinal cord motor neurons, respectively.
For more information about opportunities with Mitergy, please send correspondance to the following:
Paul Q. Anziano, PhD
When a cell becomes damaged due to disease or to chemical insult, or is otherwise no longer of use to the body, the cell dismantles itself in a well-contained process termed apoptosis. Apoptosis can be triggered either by external chemical signals acting on cellular membrane receptors or by triggers within the cell itself.
In diseases characterized by premature cell death, apoptosis is induced in an otherwise healthy cell due to conditions brought on by disease. One approach to the treatment of these conditions is to disrupt the process of apoptosis and stop the detrimental depletion of cells from the affected tissues.
Mitergy's preclincial research has now characterized a superior disease-related, drug target that is activated during the development of congestive heart failure associated with chemotherapy. Mitergy's cardio protective, small molecule drugs are also now being tested in animal models of neurodegeneration due to the fundamental nature of the premature cell death pathway.
As a general rule, biopharmaceutical drug development requires that a disease-related protein is an actual drug target when tested in animal models. For the apoptotic cell death pathway, prevention of cell death has focused squarely on the caspase proteins. Unfortunately, caspases have not been shown to be viable drug targets in preclinical, animal model studies of heart failure and neurodegeneration, especially when linked to mitochondrial damage.
Even without a clear protein target for drug development, small molecule, super antioxidant drugs have been identified that partially extend the life of the neurodegenerative animal model for ALS or Lou Gehrig's Disease. Even so, end-stage pathology is only delayed in the treated animal and they will eventually mirror the precipitous decline toward paralysis as in the untreated animal.
Due to the current lack of suitable, small molecule drug targets to slow or prevent the progressive loss of cells during end-stage pathology, there is urgent, clinical need to identify a new candidate protein that will prove to be bona fide drug target to block the premature cell death pathway in diseased adult tissues.