Apremig ODT

The theory most widely accepted today says migraine starts with a problem in the central nervous system, in particular the trigeminal ganglion. When the trigeminal ganglion is activated, it stimulates trigeminal afferents. These project to the spinal cord and synapse on several pain-sensing structures inside and outside the skull, such as the dura mater. Second-order ascending neurons then carry the pain signals to the brainstem, hypothalamus and thalamic nuclei, and from there to several cortical regions (for example the auditory, visual and motor cortices). The trigeminal ganglion seems to amplify and prolong the migraine headache pain. It does this by activating perivascular fibers and releasing molecules involved in generating pain, such as calcitonin gene-related peptide (CGRP). The α-isoform of CGRP is expressed in primary sensory neurons and is a potent vasodilator, and it has been linked to migraine pathogenesis. CGRP levels rise sharply during migraine attacks and return to normal after treatment with triptan medications, and intravenous infusions of CGRP have triggered migraine-like headaches in people with migraine. Besides widening blood vessels, CGRP appears to be a pronociceptive factor, meaning it changes how excitable neurons are and so makes pain responses easier. Rimegepant is an antagonist of the calcitonin gene-related peptide receptor. It competes with CGRP for a place on these receptors, which stops CGRP from acting and from amplifying and prolonging the headache pain, and so the headache ends.

There aren't enough data to say whether Rimegepant carries a risk to the development of a baby when pregnant women use it. Nothing is known either about whether rimegepant or its metabolites pass into human milk, what effect rimegepant might have on a breastfed infant, or whether it changes milk production.

Pediatric Use

Safety and effectiveness of Rimegepant in children have not been established.

Geriatric Use

In pharmacokinetic studies, no clinically significant differences were seen between elderly and younger subjects. The clinical studies of Rimegepant did not include enough patients aged 65 and over to say whether they respond differently from younger patients.

Hepatic Impairment

No dosage adjustment of Rimegepant is needed in patients with mild (Child-Pugh A) or moderate (Child-Pugh B) hepatic impairment. In subjects with severe (Child-Pugh C) hepatic impairment, plasma concentrations of Rimegepant were significantly higher. Avoid using Rimegepant in patients with severe hepatic impairment.

Renal Impairment

No dosage adjustment of Rimegepant is needed in patients with mild, moderate, or severe renal impairment. It has not been studied in patients with end-stage renal disease or in patients on dialysis, so avoid using Rimegepant in patients with end-stage renal disease (CrCl<15 mL/min).

Doctors have limited clinical experience with Rimegepant overdose. If it happens, treatment is general supportive care, which means monitoring the patient's vital signs and watching their clinical status. There is no specific antidote for Rimegepant overdose. Dialysis is unlikely to remove much of the medicine, because Rimegepant binds strongly to proteins in the serum.

Store Rimegepant below 25°C, and keep it away from light and moisture. Keep it out of the reach of children.