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Changing the way the world treats chronic diseases 

Genetic based therapies for type II diabetes and metabolic disorders 


How it works

Our approach can be broken down into three basic parts: our delivery vehicle, our gene interfering technology, and our targets.

Virus Based Delivery

Stark Therapeutics uses a special type of non-pathogenic virus known as Adeno-Associated Virus (AAV) to deliver DNA to specific tissues in the body. The DNA delivered by AAV contains the genetic information to edit cell function on a molecular level. It also takes on a form (episomal DNA) much like the host cell's which allows it to persist for years. This offers the potential for single administration treatments with long term benefits. In addition to its stellar safety profile, AAV continues to be the go to choice for genetic therapies and has seen great success in clinical trials.


Targeting Metabolic Regulators

The core of any therapy is its targets. Stark Therapeutics has two proprietary targets that serve as a type of regulator that influences cellular growth and metabolism. This leads to a direct impact on energy expenditure and insulin sensitivity— two key areas of focus in type II diabetes. While the targets we are using are proprietary, they share downstream targets of current diabetic drugs such as biguanides (ex. metformin) and thiazolidinediones (ex. pioglitazone). While these drugs can be effective if taken in an ideal setting, they lack the ability and specificity to prevent the progression of or reverse Type II diabetes.

Genetic Interference

Stark Therapeutics employs interference RNA (RNAi) to “silence” or turn off the production of specific genes. RNAi is a natural biological process that regulates the level of gene expression by “interfering” with messenger RNA (mRNA), which carries DNA’s instructions for making new proteins. We mimic this process using our AAV vectors to deliver DNA coding for RNAi molecules that bind to and degrade the mRNA of our target genes.

By working on the genetic level, RNAi benefits from specificity and translatability not found in other classes of medicines, such as small molecules and monoclonal antibodies. Unlike other genetic tools such as CRISPR Cas 9 and TALEN, RNAi avoids the potential for mutations by leaving the host DNA intact.

Advancing Technology

Moving beyond the cutting edge


Versatile Vector Development

Low virus yield and neutralizing antibodies are some of the problems that conventional AAV vectors face. We're developing chimeric capsids that overcome these problems while refining tissue specificity.

Enhanced RNAi

RNAi depends on precise design to be effective. Stark Therapeutics is applying novel development and composition techniques to enhance RNAi potency and reduce off target interactions.

Longterm Results

Current standard of care medications fail to prevent diabetic progression which often leads to more intense therapy and suffering for patients. Treatments with long term efficacy may prevent the progression of T2DM. 

Rapid Innovation

Inability to screen and evaluate drug candidates efficiently greatly increases lead time for new drugs. Stark Therapeutics has conducted three preclinical studies in less than a year with more planned in the coming months.


Target Validation
Early Preclinical
Late Preclinical
BLA Application
Phase I Clinical Trials
Target Identification


Type II Diabetes




ROS Inhibitor

STK-AVi3 Type II Diabetes Mellitus

Our lead candidate being evaluated for the treatment of Type II Diabetes (T2DM).

STK-AVi11 Sarcopenia

Preserving muscle mass is a key goal in staving off the effects of aging. Using the same platform for our T2DM therapy, Stark Therapeutics is working to prevent the loss of both the quality and quantity of skeletal muscle in patients over the age of 55. 


STK-AVi13 ROS Inhibitor


In parallel to our work on Type II diabetes and Sarcopenia, Stark Therapeutics is exploring the use of our approach in preventing radical oxygen species generation in skeletal muscle which has potential to improve on metabolic and physical function. We hope to further investigate this in the context of metabolic disorders involving mitochondrial dysfunction.


Who we work with

University of Michigan


Get in Touch

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