Lasmiditan Hemisuccinate

In the past, acute migraine headaches were treated by constricting the blood vessels of the brain, because the sudden widening of these vessels seen during a migraine was thought to cause the pain. The neurogenic hypothesis of migraine pathophysiology is an alternative to this vascular hypothesis. It suggests that cerebral vasodilation is a secondary mechanism in migraine pathogenesis, and that the main contributor to the headache pain is increased pathogenic firing of the trigeminal nerve pathways. While the precise mechanism of action of lasmiditan is unclear, it likely supports this neurogenic hypothesis, with its therapeutic effects coming from potent and selective agonism of the 5-HT1F receptor. These receptors are found in both the central and peripheral nervous system (on the central and peripheral ends of trigeminal neurons), and they appear to contribute to hyperpolarization of nerve terminals and inhibition of trigeminal neuronal activity. So lasmiditan's agonism at these receptors may inhibit the firing of the trigeminal nerves responsible for migraine headache pain. Lasmiditan has virtually no affinity for other 5-HT receptor subtypes or monoamine receptors (e.g. adrenergic, dopaminergic).