Fremanezumab, a humanized monoclonal antibody, cuts the frequency of migraine headaches, a study of the new long-acting drug showed. The phase III HALO clinical trial evaluated the efficacy, safety and tolerability of two subcutaneous dose regimens of fremanezumab for the preventive treatment of chronic migraine.

Teva Pharmaceutical Industries, the company developing the drug, hopes for US FDA approval in 2018. Fremanezumab targets the Calcitonin gene-related peptide (CGRP) pathway, a well-validated target in migraine. Amgen, Novartis, Eli Lilly and Co. and Alder Biopharmaceuticals also are testing similar drugs.

“We are very proud that the fremanezumab chronic migraine results are the first Phase III CM anti-CGRP therapy data published, especially in such a prestigious and well-renowned peer-reviewed journal. In this article, we are pleased to share with the medical community data from what we believe is a differentiated, patient-centric clinical development program, and to advance understanding of the potential of fremanezumab as a preventive treatment option for the millions of people suffering from migraine,”

said Ernesto Aycardi, M.D., Vice President & Therapeutic Area Head, R&D, Migraine and Headache at Teva.

About 1,000 patients were given monthly shots for three months. One third got the drug each time, another third got the drug the first time and then dummy shots the next two times, and the rest got dummy shots each time.

Monthly headache days dropped by four to five in the groups given the drug and by two to three for those given dummy treatments.

Increased levels of CGRP have been reported in migraine and temporomandibular joint disorder patients as well as a variety of other diseases such as cardiac failure, hypertension, and sepsis.

Preclinical evidence suggests that, during a migraine, activated primary sensory neurons (meningeal nociceptors) in the trigeminal ganglion release CGRP from their peripherally projecting nerve endings located within the meninges. This CGRP then binds to and activates CGRP receptors located around meningeal vessels, causing vasodilation, mast cell degranulation, and plasma extravasation.

Human observations have further implicated the role of CGRP in the pathophysiology of migraine. Activation of primary sensory neurons in the trigeminal vascular system in humans can cause the release of CGRP.

During some migraine attacks, increased concentrations of CGRP can be found in both saliva and plasma drawn from the external jugular vein. Furthermore, intravenous administration of alpha-CGRP is able to induce headache in individuals susceptible to migraine.

Burden Of Illness

Migraines plague more than a billion people worldwide, more than 38 million in the U.S. alone.

They’re more severe than an ordinary headache - throbbing, squeezing pain and pressure, often accompanied by vision problems, sensitivity to light, noise or smells, and nausea. They can leave people unable to work or do simple things like cooking or even hold a conversation.

“The burden of illness faced by those with migraine is immense and can negatively impact every facet of their lives underscoring a significant unmet need for new preventive treatment options.

Results from the Phase III study of fremanezumab for the preventive treatment of chronic migraine highlight the importance of therapies targeting CGRP as a potential significant advancement in the treatment of patients suffering from debilitating symptoms,”

said Stephen D. Silberstein, M.D., Principal Investigator of the HALO trial, Professor of Neurology and Director of the Jefferson Headache Center at Thomas Jefferson University Hospital and lead author of the publication.

Stephen D. Silberstein, M.D., David W. Dodick, M.D., Marcelo E. Bigal, M.D., Ph.D., Paul P. Yeung, M.D., M.P.H., Peter J. Goadsby, M.D., Ph.D., Tricia Blankenbiller, M.A., Melissa Grozinski-Wolff, B.S., Ronghua Yang, Ph.D., Yuju Ma, M.S., and Ernesto Aycardi, M.D. Fremanezumab for the Preventive Treatment of Chronic Migraine N Engl J Med 2017; 377:2113-2122November 30, 2017DOI: 10.1056/NEJMoa1709038

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