Rizatriptan benzoate 是 5-HT1激动剂，通过选择性结合并激活血清素 (5-HT) 1B 受体和 5-HT 1D 受体，从而缓解偏头痛。

Rizatriptan benzoate selectively binds to and activates serotonin (5-HT) 1B receptors and 5-HT 1D receptors providing relief of migraine headaches.

Rizatriptan blocks neurogenic vasodilation via an action on 5-HT(1D) receptors located on perivascular trigeminal nerves to inhibit CGRP release in anaesthetized guinea-pigs. Rizatriptan evokes a transient reduction in dural blood vessel diameter which recovered to baseline values within 10?min in anaesthetized guinea-pigs. [1] Rizatriptan significantly inhibits dural plasma protein extravasation produced by high intensity electrical stimulation of the trigeminal ganglion. Rizatriptan significantly reduces electrically stimulated dural vasodilation in anaesthetised rats. [2] Rizatriptan Benzoate significantly reduced SP mRNA levels in the midbrains of normal and model group rats, indicating that Rizatriptan Benzoate can downregulate SP gene expression in the rat midbrain. Rizatriptan Benzoate significantly reduces midbrain PENK mRNA expression, decreasing the levels of midbrain met-enkephalin and leu-enkephalin, and thereby weakening the analgesic effects of the endogenous pain modulatory system in rat model of migraine. [3] Rizatriptan Benzoate leads to the number of Fos-like immunoreactive neurons decreased in the spinal trigeminal nucleus caudal partand raphe magnus nucleus, increased the number of Fos-like immunoreactive neurons in the periaqueductal gray and remained unchanged in the ventromedial hypothalamic nucleus and mediodorsal thalamus nucleus in conscious rats. [4] Rizatriptan Benzoate markedly reduces the number of head-flicks in the rats. Rizatriptan Benzoate also significantly reduces the duration of grooming behavior by nearly 2-fold when compared with that without treatment. [5]

145202-66-0

C22H25N5O2

391.475

苯甲酸利扎曲坦;MK-462 Benzoate

DMSO:19.6 mg/mL (50 mM)
H2O:39.2 mg/mL (100 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years