By: BRUCE JANCIN, Clinical Neurology News Digital Network | July 23, 2015
VALENCIA, SPAIN – In the lecture halls and corridors at the International Headache Congress, far and away the dominant topic of conversation was the latest highly promising data for the CGRP (calcitonin gene–related peptide)-inhibiting monoclonal antibodies being developed for migraine prophylaxis.
“The question of efficacy, to me, has been resolved: They’re spectacularly effective. The whole reason for the phase III studies is to establish safety,” Dr. Marcelo E. Bigal, a vice president at Teva Pharmaceuticals, said in the opening plenary session.
“This is the second revolution in the history of migraine therapy,” declared another opening plenary speaker, Dr. Messoud Ashina, professor of neurology at the University of Copenhagen.
“It is a really exciting emerging field. It kind of reminds me of the triptan story,” observed Richard J. Hargreaves, Ph.D., vice president for discovery science at Biogen in Cambridge, Mass.
With a long track record of success in new drug development and having conducted research on CGRP for more than 2 decades, it fell to Dr. Hargreaves to provide an introductory overview of the CGRP inhibitors. Each of the monoclonal antibodies has a different mechanism of action. However, they share several key characteristics: They are highly specific in their mechanisms of action, they have long circulating plasma half-lives, they are largely peripherally restricted rather than acting at the level of the central nervous system, and they typically have a low toxicity profile. Indeed, in phase I and -II studies the type and frequency of adverse events was essentially indistinguishable from placebo.
Now advancing through the developmental pipeline are three CGRP ligand-neutralizing antibodies and one CGRP receptor antibody.
“The race is on. It’s estimated that 40% of migraine patients are candidates for prophylaxis. That’s 14 million U.S. patients. And preventive therapy represents a significant unmet medical need,” Dr. Hargreaves said at the meeting sponsored by the International Headache Society and the American Headache Society.
“Clearly the CGRP monoclonal antibodies aren’t going to be used for acute migraine therapy. That’s going to be the province for oral small-molecule CGRP inhibitors because of the need for rapid activity. But if the antibodies prevent well, then hopefully the need for acute medications will go down,” he continued.
A particularly impressive feature of the investigational agents is that a substantial proportion of treated patients are hyperresponders – that is, individuals who experience at least a 75% and in some cases a 100% reduction in migraine days per month.
Full article can be found on Clinical Neurology News website – http://www.clinicalneurologynews.com/specialty-focus/pain/single-article-page/growing-buzz-surrounds-cgrp-inhibitors-in-migraine/76aa5dd6c0f4fdf03fd548e038775489.html
