Hot flashes—experienced by 70%-80% of menopausal women—are physically distressing and worsen quality of life. Newer therapies, such as NK3R antagonists, leverage a non-hormonal approach to addressing these symptoms.
For example, fezolinetant is a selective NK3R antagonist that directly blocks NKB from binding to the KNDy neuron. NKB is a known trigger of vasomotor symptoms (VMS).
KNDy neurons located at the level of the hypothalamus are inhibited by estrogen and triggered by the neuropeptide NKB, thus resulting in the regulation of body temperature.
During menopause, estrogen decline interferes with this balance involving NKB. Left unopposed, NKB signaling increases KNDy neuronal activity. This process sets off heat-dissipation mechanisms, such as vasodilation and sweating (or VMS).
Thus, fezolinetant helps decrease the frequency and intensity of hot flashes and night sweats, honing in on NK3R with an affinity 450 times higher than that of NK1 or NK2 receptors.
What are your thoughts on this new mechanism of action for the treatment of VMS?
It makes a lot of like an effective treatment