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A Novel Treatment for the Reduction of Obesity by Inhibiting c-Abl Kinase Activity

Technology Number: 

1770
Summary 

Obesity is reaching epidemic proportions throughout the western world and is also now becoming a problem in a number of countries in the developing world. This is primarily due to the over-consumption of high-calorie foods compounded with the lethargic lifestyles that are becoming common place.

The issue of obesity is that it is linked to the development of many other diseases such as diabetes, heart disease, and cancer. Consquently numerous countries healthcare systems are being put under enormous strain from the increase and severity of obesity related diseases. Additionally the financial strain is being compounded by the requirement for special equipment in hospitals that are larger and reinforced to handle the more extreme cases that are becoming common. Therefore there is a clear need for a treatment that can reduce obesity in a cost-effective manner and that is simple for individuals to follow.

The present technology from the laboratory of Prof. Yosef Shaul offers a novel target in reducing obesity by inhibiting c-Abl kinase, which has the added benefit of being a well-known and clinically tested drug target. Subsequently the technology offers a new method in reducing obesity using a well understood molecular target that has already been tested for other diseases. 

Applications


?  Generating therapeutics towards reducing obesity.


Advantages


·         Specific – the technology targets c-Abl kinase to reduce obesity.

·         Well Studied – c-Abl has been studied and targeted for other indications.

·         Clinically tested – small molecule c-Abl inhibitors such as Imantinib (Gleevec) have been clinically approved for treating cancer, possibly simplifying future clinical trials.

·         Numerous therapeutic options – A variety of small molecule inihibitors already exist along with other options such as RNAi to target c-Abl.


Technology's Essence


The invention is the inhibition of the Abelson murine leukemia viral oncogene homolog 1 (c-Abl) for the purpose of reducing obesity. The inhibition of the c-Abl kinase activity has the effect of lowering the amount of peroxisome proliferator-activator receptor gamma 2 (PPAR?2), which is known as a master regulator in the development of adipocytes (fat accumulating cells). The mechanism works by reducing the stability of the PPAR?2 and leading to its to depletion. Subsequently it has been shown that inhibiting c-Abl leads to reduced fat accumulation in cells and lowering of body mass in multiple mouse models.  

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