Migraine affects more than a billion people and many cases are difficult to treat. An old acquaintance from research, substance P, is back in the spotlight. Dismissed in the 90s due to failures of drugs against a single receptor, new studies confirm its key role in migraine pain and inflammation. This reopens a therapeutic pathway with renewed prospects.
From NK1 Receptors to MRGPRX2: Precision with Monoclonal Antibodies 🔬
The drugs from the 90s failed because they only blocked the NK1 receptor of substance P. Now it is known that it also acts on other receptors, such as MRGPRX2 in immune cells, triggering inflammation that amplifies pain. Current technology allows the development of monoclonal antibodies targeted against substance P itself or its specific receptors, offering a more complete and selective blockade that could avoid the effects of previous attempts.
Substance P Pulled the Wool Over Our Eyes (And We Didn't Notice) 😅
It turns out we've been blaming the wrong receptor for years. While science wrote off substance P as dead, it was still there, laughing and sending pain signals through the back door of MRGPRX2. It's like, after closing the main entrance to a party, discovering that the problematic guests have been sneaking in through the garage for thirty years. A classic case of it wasn't the messenger, we had the address wrong.