Signal transduction inhibitor
As a signal transduction inhibitor ( STI , English signal transduction inhibitor ) refers to substances that interfere with important cellular signal transduction or inhibit this. In this context, signal transduction is the term used to describe the biochemical transfer of information or information forwarding from the cell membrane to the inside of the cell, or from one cell compartment to another.
Illustrated with an example: When an extracellular growth factor (e.g. erythropoietin ) hits the corresponding receptor on the cell surface (e.g. erythropoietin receptor), the corresponding signal is transmitted into the cell interior (the erythropoietin molecule remains outside the cell surface) Cell). This happens in such a way that the receptor changes its intracellularly located configuration and thereby activates other intracellularly located proteins (e.g. by phosphorylation ). These in turn activate other proteins, and so the signal transmission continues. An endpoint of activation can e.g. B. the activation or deactivation of a gene (e.g. in the case of erythropoietin, the activation of hemoglobin- synthesizing enzymes ).
Specific signal transduction inhibitors, especially tyrosine kinase inhibitors, are considered "drugs of the future". With many diseases, especially with many cancer diseases , we now know that they are based on disturbed signal transductions, the z. B. lead to permanent activation in tumor cells. If one succeeds in specifically inhibiting this signal transduction, one has an effective drug for treating the disease.
example
The best known example, the active ingredient is imatinib (trade name Gleevec, earlier than S ignal T ransduction I nhibitor 571, STI571 known). Imatinib is a relatively specific inhibitor for ABL tyrosine kinase. At the clinical picture of chronic myelogenous leukemia , a permanent activation of this kinase is present, by a chromosomal translocation comes about in the ABL with another gene BCR to a gene BCR-ABL fused.
Imatinib is structurally similar to an adenosine triphosphate molecule. By introducing this “synthetic” adenosine triphosphate, the BCR-ABL tyrosine kinase can no longer activate effectors and its activity can therefore be inhibited.
