Rimegepant

2 Registered Brands From ৳150.00 / unit Other drugs for migraine
Brands & Prices (2) 📋 Indications & Uses Dosage & Administration⚠️ Contraindications⚡ Side Effects & Adverse Reactions🛡️ Warnings & Precautions🔬 Pharmacology & Mechanism

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📖 Official Clinical Monograph

DGDA Approved Prescribing Guidelines
📋 Indications & Uses

Apremig ODT is a calcitonin gene-related peptide receptor antagonist indicated for the acute treatment of migraine with or without aura in adults & preventive treatment of episodic migraine in adults.

Dosage & Administration

Acute Treatment of Migraine
: The recommended dose of Rimegepant is 75 mg taken orally, as needed. The maximum dose in a 24-hour period is 75 mg. The safety of using more than 18 doses in a 30-day period has not been established.
Preventive Treatment of Episodic Migraine
: The recommended dosage of Rimegepant is 75 mg taken orally every alternate day.

⚠️ Contraindications

Rimegepant is contraindicated in patients with a history of hypersensitivity reaction to rimegepant tablet or any of its components.

⚡ Side Effects & Adverse Reactions

Allergic reactions, including trouble breathing and rash, can happen after you taking Apremig ODT. The most common side effects of Apremig ODT are: nausea, stomach pain & indigestion.

🛡️ Warnings & Precautions

Hypersensitivity reactions, including dyspnea and rash, have occurred with Apremig ODT in clinical studies. Hypersensitivity reactions can occur days after administration, and delayed serious hypersensitivity has occurred. If a hypersensitivity reaction occurs, discontinue Apremig ODT and initiate appropriate therapy.

🔬 Pharmacology & Mechanism

The currently accepted theory of migraine pathophysiology considers dysfunction of the central nervous system, in particular the trigeminal ganglion, to be the root cause behind the condition. Activation of the trigeminal ganglion triggers the stimulation of trigeminal afferents that project to the spinal cord and synapse on various pain-sensing intra- and extracranial structures, such as the dura mater. Pain signals are then further transmitted via second-order ascending neurons to the brainstem, hypothalamus, and thalamic nuclei, and from there to several cortical regions (e.g. auditory, visual, motor cortices). The trigeminal ganglion appears to amplify and perpetuate the migraine headache pain through the activation of perivascular fibers and the release of molecules involved in pain generation, such as calcitonin gene-related peptide (CGRP).
The α-isoform of CGRP, expressed in primary sensory neurons, is a potent vasodilator and has been implicated in migraine pathogenesis - CGRP levels are acutely elevated during migraine attacks, return to normal following treatment with triptan medications, and intravenous infusions of CGRP have been shown to trigger migraine-like headaches in migraine patients. In addition to its vasodilatory properties, CGRP appears to be a pronociceptive factor that modulates neuronal excitability to facilitate pain responses.
Rimegepant is an antagonist of the calcitonin gene-related peptide receptor- it competes with CGRP for occupancy at these receptors, preventing the actions of CGRP and its ability to amplify and perpetuate migraine headache pain, ultimately terminating the headache.