TAU Therapeutics LLC
A New Way of Treating Cancer
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The Next Generation: TAU’s Cytostatic Checkpoint Therapy TM – A Common Pathway to Controlling Cellular Proliferation The different philosophical approaches embodied in anti-angiogenic and cytotoxic chemotherapy has spawned a new generation of research activity. At Tau, we are studying the molecular signaling events associated with cell proliferation with a focus on the movement of calcium ions across the cell membrane. The entry of calcium ions into the cell at specific times in the cell cycle is universally accepted as essential for the proliferation of cancer cells. The most widely accepted mechanism for calcium entry is through an ion channel, but recent human genome analysis indicates that there are 406 ion channels—10-20% of which could be considered “calcium channels." Thus, the race has been to determine which calcium ion channel is involved and the universality of that channel for all types of cancer cells. Our studies led to the identification of a universal, developmentally regulated, proliferation-producing mechanism dependent on a particular calcium T channel, a protein also known as Cav3.2. This finding was surprising because T channels are known to be voltage gated, but proliferation does not depend upon cellular voltage changes. However, Cav3.2 has been shown to modulate growth in cultured cancer cells, antibodies to Cav3.2 inhibit cell growth of virtually all cancer cells studied, and synthetic molecules known to inhibit T channels almost universally block cancer cell growth. Clearly, T channels must have multiple functions and multiple regulatory mechanisms—an observation that is increasingly realized as we unravel the functions of this proteome. Cytostatic Checkpoint Therapy TM Studies by Tau’s scientific founders led to the identification of a universal, developmentally regulated, proliferation-producing mechanism dependent on a particular calcium T channel, a protein also known as Cav3.2. Tau’s founders have identified three FDA approved drugs that block this important point and have named it, Cytostatic Checkpoint Therapy TM. This finding, is surprising because T channels are known to be voltage gated, but proliferation does not depend upon cellular voltage changes. However, Cav3.2 has been shown to modulate growth in cultured cancer cells and in animal models of human cancer. In addition, antibodies to Cav3.2 inhibit cell growth of virtually all cancer cells studied, and Tau’s lead T-channel inhibitors almost universally block cancer cell growth in vitro (60 from the NCI)and in experimental animal models of prostate, breast and colon cancer. For example, Tau’s lead compound, TTL-1177, has shown an impressive 144% increase in life span (ILS) in an animal model of human colon cancer (HCT 116) xenograft model. Additional studies show that these compounds hold promise for the treatment of cancers of the lung, ovary, pancreas and other tissues. Importantly, the blockade of Cav3.2 does not result in cell death, but only in the halting of growth. We have also shown that cancer cells treated with our compounds do not develop resistance to them, which is extremely common following therapy with cytotoxic drugs. Reference: Cell Calcium: Dec. 2004, The Role of Voltagegated T-type Ca2 + Channel isoforms in mediating “capacitative” Ca2 + in Cancer Cells: Gray, Perez-Reyes et. al. |
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