Lab Tests Show Molecule Appears to Spur Cell Death in Inflammation

Developed by Duke Health researchers, a new drug-like molecule appears to trigger cell death in tumors. The molecule, known as Takinib, works by reacting to a cell-signaling protein called tumor necrosis factor alpha.

Taikinib, a new drug like molecule, reacts to tumor necrosis factor alpha and appears to trigger cell death in tumor. In a study it was found that in order to develop hepatitis mice that were developed ended up developing precancerous lesions and when the TNF molecule was turned off these lesions did not develop into full malignancy state. In another group, the TNG activity was blocked by neutralizing antibody and prevented its attraction to liver cells thus cell death was triggered. In another study it was found that in order to develop colon cancer the mice that were modified ended up shutting down inflammatory activity. Thus it was seen that tumor development was managed and prevented by prohibiting NF-KB activity.

In a finding it was shown that in the growth of specific tumor chronic inflammation plays a significant role and to disrupt inflammatory response of autoimmune disease what preventative measures can be taken.  Takinib was developed by Duke Health researchers.

The research was led by Timothy Haystead. In the department of pharmacology and cancer biology he is a professor. The research was also led by Emily Derbyshire. In the Department of Chemistry she is an assistant professor.  In order to understand how the cell death in tumor is impacted by the new drug like molecule, many experiments were performed. For ensuring cell death or survival in the TNF alpha cell signalling process, an enzyme known as TAK-1 is responsible. Taikinb slows down the action of this enzyme. There is often a disruption in the delicate balance of death and survival. This process is targeted by the molecule. By only targeting tumor or inflammatory cells potentially the positive parts of TNF-alpha could be enhanced by this compound. In certain cancer cases to prevent tumor growth and expansion, TNF-alpha is injected.  In an autoimmune disease, inflammation is controlled by TNF alpha antibodies however during chronic treatment their benefits are limited.

To interfere with the TNF signalling process, over the past few years many drugs have been developed. However side effects or resistance are often developed. In reducing the inflammatory pathway of the same process this new drug like molecule if taken in small doses appears to be effective. To test Takinib in animals several studies are ongoing. Before it can be used in other diseases, the main focus is on rheumatoid arthritis. In inducing cell death in cancer and autoimmune diseases, Takinib appears to be a promising starting point.

Focusing on slowing inflammatory activity is the goal of current therapies.  In cancerous cells in preventing the inflammatory response, clinical studies for solid tumors and blood cancers are showing great promise. Formation of solid tumors that is triggered by inflammation can be prevented by a drug Rituxan.  In autoimmune diseases it suppresses B cells. It is a genetically modified antibody.

To reduce inflammatory activity scientists are working on various ways thus making cancer to flourish difficult. By altering molecular mechanisms they are finding in which ways new generation molecules can help. Enzymes that regulate NF-KB activity is being investigated by several pharmaceutical laboratories.  Hopefully this will inhibit inflammation. This new drug has a long way to go but efforts are being made towards findings that will encourage in tumors, the process of cell death.