Great medical need but lack of innovation, until now.
This is how KAND567 works
KAND567 acts by blocking the Fractalkine receptor. Scientific studies have shown elevated levels of Fractalkine associated with cardiovascular disease, inflammatory diseases and certain forms of cancer. The receptor is an important link in the inflammatory process and a promising target for new anti-inflammatory drugs because it is primarily found on the surface of lymphocytes and monocytes (in everyday terms, white blood cells) – precisely those cells that are now understood to be central to the emergence of multiple acute and chronic diseases.
The cells are transported in the body through the blood, and the Fractalkine receptor plays a key role when the lymphocytes find the damaged tissue and initiate the inflammatory process. Since the response of the immune system can become too strong after a heart attack, the reaction quickly turns into a harmful inflammation. When KAND567 blocks the receptor, it prevents immune cells from accumulating in the tissue and hence the whole inflammatory reaction is suppressed. In this way, tissue is saved. At the same time, animal studies show that other important functions of the immune system continue to function well, despite the fact that the Fractalkine receptor is blocked. KAND567 thus has the potential to selectively and effectively counteract local inflammation without significantly affecting the body’s immune system in general.
In order for a drug to be able to counteract an acute reaction in the damaged tissue, activation must be immediate, the effect specific and one must be able to quickly influence the strength of the treatment. Here KAND567 has great advantages over an anti-inflammatory antibody. Small molecules have an excellent ability to penetrate damaged tissue with poor blood flow; in addition, the effect level is easy to control because they generally have a shorter half-life compared to an antibody. KAND567 is the only small-molecule Fractalkine inhibitor in clinical development.