Relenza, Tamiflu and the new class of molecules being developed, are known as neuraminidase inhibitors because they prevent the neuraminidase enzyme from working properly.
The drugs can do this because their molecular structure closely resembles the molecules the enzyme normally attaches to on the infected cell, except the drug molecules bind much tighter to the neuraminidase.
Rather than interacting with the molecules on the surface of the infected cell, the neuraminidase enzyme binds to the drug instead. The drug physically gets in the way and inhibits the action of the enzyme.
This stops the virus from spreading to new cells and helps to reduce the severity and duration of flu so that the body's own defence mechanisms, together with other medical interventions, can help aid recovery.
However, the influenza virus can develop resistance to the drugs by mutating, or changing, parts of its surface that Tamiflu and Relenza absolutely need to achieve their strong binding to the neuraminidase. When this happens, the neuraminidase is able to escape from the drug and continue its job.
The new class of molecule being developed by the University of Bath and CSIRO researchers blocks the action of the neuraminidase in a very different manner, by undergoing a chemical reaction with protein. Furthermore, this chemical reaction only takes place at one specific part of the neuraminidase, a part that is essential for the neuraminidase to carry out its natural job.
This process stops the neuraminidase enzyme in its tracks, and makes it impossible for the virus to develop resistance to the new molecule.
The researchers are currently narrowing-down the class of molecules they have discovered to identify the best candidate for developing a drug. They will then need to refine the delivery mechanisms and begin trials that will ensure its efficacy in patients.