Japan-Flag Korea-Flag China-Simplified-Flag China-Traditional-Flag  

Conference Menu

Day 1
Day 2
Download Brochure
Hotel & Travel
Sponsor & Exhibit
Request Brochure
Exhibit Contract

Book Offer!

Be one of the first ten registrants and receive a free copy of "The Science of Fitness," co-authored by legendary cyclist, three time Tour de France champion, and Mitochondrial Myopathy sufferer Greg LeMond and Mark Horn, MD.


Media Partners: 

Bentham Science Logo 

Bio-IT World Large 

Clinical Informatics News 


Genomeweb Logo 

Insight Pharma Reports 




Science AAAS 

The Scientist 

Friday, March 20

Day 1 | Day 2 | Brochure  

8:00 Morning Coffee


8:25 Chairperson’s Remarks

Johannes Ehinger, M.D., Mitochondrial Medicine, Lund University

8:30 Adaptive Metabolic Targeting of BPM 31510 for the Treatment of Cancer

Michael Kiebish, Ph.D., Director, Integrative Systems Medicine, Diagnostics, Berg

Mitochondrial dysfunction has long been recognized as a hallmark of cancer, yet there is a paucity of biointelligently designed therapeutics that effectively and selectively reengineer cancer metabolism to effectuate a viable therapeutic strategy. Here, we utilized an adaptive Omic, phenotypic, and biophysical stratification approach to deconstruct the mechanism of action of BPM 31510, a proprietary CoQ10 containing formulation that demonstrates pleotropic effects on diverse cancers. Targeting cancer from a biological, biophysical, physiological, and bioenergetic direction is a prodigious challenge, yet initiating this process from a systems medicine approach allows for therapeutic streamlining toward positive therapeutic effects. Thus, by reengineering the Warburg effect in cancer with strategically designed therapeutics with a multiplicity of downstream effects rather than a single target, we overcome numerous barriers that define the current dogma of targeted therapeutics engaging a systems medicine approach.

9:00 Correcting Abnormal Mitochondrial Dynamics and Mitophagy in Neurodegenerative Diseases

Daria Mochly-Rosen, Ph.D., Professor, Chemical and Systems Biology, Stanford University School of Medicine

Many neurodegenerative conditions are associated with excessive mitochondrial fission and inhibition of mitophagy. However, it is not clear whether these abnormalities in mitochondrial dynamics and removal are the cause of or the result of the pathology. Using a variety of pharmacological tools that we developed rationally, we find that inhibition of mitochondrial fission inhibits neurodegeneration in several models of Parkinson’s and Huntington’s. A critical role from mitophagy was also identified. The molecular basis for protection from neurodegeneration and the potential utility of our novel pharmacological tools as leads for drug development will be the topic of our presentation.

9:30 Targeting Mitochondrial Dysfunction in Burn Injury

A. Aria Tzika, Ph.D., Director, NMR Surgical Laboratory, Department of Surgery, Massachusetts General Hospital and Shriners Burns Institute

Burn injury represents a significant public health problem in roughly 500,000 people per year in the USA. We probe mitochondrial skeletal muscle dysfunction that occurs in response to burn injury in a preclinical mouse burn model using novel methods. Our studies have the potential for strong clinical relevance with respect to the recovery and management of individuals with burn trauma.

10:00 Coffee Break with Exhibit & Poster Viewing

10:30 Supporting Mitochondrial Function in Cells with Complex I Dysfunction using Cell-Permeable Complex II Substrates: A Potential Novel Therapy for Complex I-Linked Mitochondrial Disease

Johannes Ehinger, M.D., Mitochondrial Medicine, Lund University

Chemically modified mitochondrial complex II substrates with increased cell membrane permeability can support mitochondrial respiration, increase ATP production and uphold mitochondrial membrane potential in cells with deficiencies in complex I-linked mitochondrial metabolism. This new compound class introduces the possibility to pharmacologically support patients with metabolic decompensation due to mitochondrial complex I deficiency, such as children with inborn errors of metabolism.

11:00 The Mitigation of Cytotoxic and Genotoxic Effects of Drugs on Mitochondrial DNA 

Adam E. Osborne, Ph.D., Biology Department, Brandeis University

Millions of TB and HIV patients are treated with drugs that have toxic side effects. AZT, an inexpensive nucleotide reverse transcriptase inhibitor used in highly active anti-retroviral therapy T, is associated with mitochondrial oxidative stress and DNA damage. Isoniazid (INH), a first line antibiotic used to treat or prevent tuberculosis, alters liver function in ~20% of patients and is fatal in 1%-2%. Toxic intermediates of INH in the liver deplete glutathione and oxygen radical scavenging enzymes. The resulting increase in free radicals can irreversibly damage mitochondria and mitochondrial DNA (mtDNA). We are investigating AZT and INH dependent mtDNA damage in cultured human liver cells, as well as whether palm fruit juice (PFJ), an extract rich in polyphenols from the fruit of the oil palm (Elaeis guineensis), mitigates such damage

11:30 Sponsored Presentation (Opportunity Available)

12:00 Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on Your Own


1:50 Chairperson’s Remarks

Padma K. Narayanan, Ph.D., Director, Pre-Clinical, Toxicology, Amgen

2:00 A Systematic Assessment of Mitochondrial Function Identified Novel Signatures for Drug-Induced Mitochondrial Disruption in Cells

Padma K. Narayanan, Ph.D., Director, Pre-Clinical, Toxicology, Amgen

Mitochondrial perturbation has been recognized as a contributing factor to various drug-induced organ toxicities. To address this issue, we developed a high-throughput flow cytometry-based mitochondrial signaling assay to systematically investigate mitochondrial/cellular parameters known to be directly impacted by mitochondrial dysfunction: mitochondrial membrane potential (MMP), mitochondrial reactive oxygen species (ROS), intracellular reduced glutathione (GSH) level, and cell viability. Disruptors of mitochondrial function depolarized MMP at concentrations lower than those that caused loss of cell viability, especially in cells cultured in GSM; cellular GSH levels correlated more closely to loss of viability in vitro. Subsequent classification of compounds based on ratios of IC50s of cell viability:MMP determined that this parameter is the most critical indicator of mitochondrial health in cells and provides a powerful tool to predict whether novel small molecule entities possess this liability.

2:30 Screening Small Molecules for Mitofunctional Effects: Implications for Mitochondrial Therapeutics and Mitotoxins

Gino Cortopassi, Ph.D., Professor, Molecular Biosciences, University of California, Davis; CEO, Ixchel PharmA

Mitochondrial disease is a rare/orphan indication, with no approved or effective therapy. Thus screening known FDA-approved drugs for effects on mitochondrial function is a rational approach to shorten the usual time for clinical therapeutic development. Using 4 high-throughput assays we have identified a subset of FDA-approved drugs that target mitochondria. In addition, we have used these assays to screen potential toxicants, and identify known and novel toxicants.

3:00 Targeting Disease-Causing Defects of the Mitochondrial Genome with Engineered Mitochondrial Nucleases

Carlos T. Moraes, Ph.D., Professor, Neurology and Cell Biology, University of Miami

Mutations in the mtDNA have been associated with several degenerative disorders. In most cases, mtDNA mutations are heteroplasmic, co-existing with the wild-type mtDNA. Because high levels of mutant mitochondrial genomes are required to trigger a defective phenotype, we have sought approaches to decrease the mutant mtDNA load. We found that mitochondrial-targeted restriction endonucleases could specifically reduce the levels of mutant mtDNA. This approach has been extended to any mtDNA mutation by the use of new gene editing techniques, such as mitochondrial-targeted TALENs.

3:30 Inhibitors of Mitochondrial Fission as a Therapeutic Strategy for Diseases with Oxidative Stress and Mitochondrial Dysfunction

P. Hemachandra Reddy, Ph.D., Executive Director and Chief Scientific Officer, Garrison Institute on Aging; Professor of Cell Biology & Biochemistry, Neuroscience & Pharmacology and Neurology Departments, Texas Tech University Health Science Center

Research into mitochondria and cell function has revealed that mitochondrial dynamics is impaired in a large number of aging and neurodegenerative diseases, and in several inherited mitochondrial diseases, and that this impairment involves excessive mitochondrial fission, resulting in mitochondrial structural changes and dysfunction, and cell damage. Attempts have been made to develop molecules to reduce mitochondrial fission while maintaining normal mitochondrial fusion and function in those diseases that involve excessive mitochondrial fission.

4:00 Use of Multiparametric Assays on Isolated Liver Mitochondria and HepaRG Cells to predict DILI

Annie Borgne-Sanchez, Ph.D., CEO/CSO, Mitologics

We combined mitochondrial and cellular assays to predict drug-induced mitochondrial dysfunction in liver. Extensive screening of reference compounds on isolated liver mitochondria revealed a highly significant relationship between acute mitochondrial toxicity detected by this system and DILI occurrence in human. We next showed that human HepaRG differentiated cells is a pertinent and complementary model allowing detection of long-term and/or metabolites mitochondrial toxicity.

4:30 Close of Conference

Day 1 | Day 2 | Brochure