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Although the exact mechanism of action is not known, one study (PMID: 16413681) proposes that tesmilifene may be an activating p-gp substrate, which enables the p-gp pump to extrude typical p-gp substrates (such as anthracyclines or taxanes) more efficiently. This process consumes ATP, since the p-gp is absolutely, and highly dependent on ATP hydrolysis. The mechanism of cell death is likely to result not from the presence of chemotherapy inside the cell (in fact the chemotherapy is extruded) but, directly or indirectly, from the enhanced consumption of ATP. The ATP may be consumed below a threshold necessary for survival, or, (more likely) the enhanced ATP production required to maintain ATP levels may result in the generation of reactive oxygen species (ROS) to an extent that overwhelms the cell’s ability to inactivate them. The result would be additional cell death, but only in the mdr+ population. The doxorubicin would continue to act on the drug sensitive remainder of the cell population, but without the help of tesmilifene.

Drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists. Classical antihistaminics block the histamine H1 receptors only.

Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.