Chinese name: Atogepam
CAS No:1374248-81-3
Molecular formula :C29H23F6N5O3
Boiling point :693.9±55.0 °C(Predicted)
Flash point :373.5±31.5 °C
Refractive index :1.624
Density :1.54± 0.1g /cm3(Predicted)
Migraine is the most common recurrent neurovascular disease worldwide, affecting more than 1 billion people worldwide, of which approximately 39 million people in the United States alone are among the leading causes of disability in people younger than 50 years of age. Migraine attacks occur 4 to 72 hours per month and are usually pulsating and unilateral, accompanied by nausea, vomiting and sound/photosensitivity. Moderate to severe intensity can be very severe, incapacitating the patient and having a substantial impact on life. In 2016, the Global Burdenof Disease Study Group (GBD) ranked it as the second most disabling disease in the world, as one of the parameters of the "years living with disability" (YLDs),<50 Ranked first in the age group. Preventive treatment goals for migraine include reducing the frequency and intensity of attacks, shortening the duration of attacks, and improving functional capacity and quality of life. B-adrenergic receptor blockers, antagonistic antidepressants, and antiepileptics are currently prescribed clinically to reduce the number of migraine attacks. Unfortunately, many oral prophylactic treatments are not effective and are associated with potential adverse events or contraindications that may interfere with concurrent disease and treatment.
Atogi is a CGRP receptor antagonist, one of the currently accepted theories of migraine pathophysiology, which believes that migraine is caused by the dysfunction of the central nervous system, especially the dysfunction of the trigeminal ganglion. Activation of the trigeminal ganglion triggers stimulation of the trigeminal afferent nerve, which projects to the spinal cord and synapses on various intracranial and extracranial pain structures, such as the dura. Pain signals are then further transmitted via second-order ascending neurons to the brainstem, hypothalamus, and thalamic nucleus, and from there to several cortical regions (such as the auditory visual motor cortex) where the trigeminal ganglion appears to amplify and sustain migraine by activating perivascular fibers and releasing molecules involved in pain production, such as CGRP. The O-subtype of CGRP, which is expressed in primary sensory neurons, is an effective vasodilator and has been implicated in the pathogenesis of migraine, CCRP levels rise sharply during migraine attacks, return to normal after triptan treatment, and intravenous CGRP has been shown to trigger migraine-like headaches in migraine patients. In addition to its vasodilatory properties,CGRP appears to be a pain-stimulating factor that modulates neuronal excitability to promote pain response. Atoghian is an antagonist of CGRP receptors and competes with CGRP for occupancy of these receptors, preventing the effects of CGRP and its ability to induce and persist migraines
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