Hyperactivation of hypothalamic KNDy neurons—which express kisspeptin, neurokinin B, and dynorphin—drives VMS during estrogen deprivation, providing the mechanistic basis for dual NK1/NK3 receptor antagonism as a nonhormonal strategy that may also improve sleep quality.
Vasomotor symptoms affect more than 50% of patients receiving endocrine therapy for hormone receptor–positive breast cancer and can reach 90% in younger patients on ovarian function suppression, with more than 20% of affected patients discontinuing treatment—a factor directly linked to increased recurrence risk and reduced survival.
