Genentech is also a deep pocket company so it should be able to finance the extremely expensive, tortuously long and Byzantinely complex Food and Drug Administration required clinical trial ordeal. (FDA rhymes with delay.) Many potential cures for autoimmune and allergic diseases have been lost to patients by the "valley of death" caused by these immoral barricades the FDA puts between laboratory discovered potential cures and patients. Some of these delays seem to have to do with politics of Big Pharma and their real goal of profits, profits, profits. Delays that increase profits for Big Pharma are good delays. Since FDA derives significant funding from Big Pharma whatever Big Pharma wants, Big Pharma gets. But Genentech is a member of Big Pharma. As such their treatment might actually get through. Let's hope so.
Of course we have all been disappointed by past promises for good allergy treatments, Xolair comes to mind. I hope that Genentech is being truthful with their announcement in the prestigious Journal of Clinical Investigations. Some companies seem to over hype announcements like this--say for instance Osiris' Prochymal. So who knows? But I do believe there is real hope that our children may have truly effective treatments for allergies and asthma. Base on the article below, this Genentech breakthrough appears to be one likely candidate.
If this works for allergy and asthma, similar selective monoclonals might work for autoimmune disease as well. If we could only turn off the "bad" B cells that are making the auto antibodies which keep the autoimmune disease pot boiling, then the symptoms of the autoimmune disease would end. Go new science discoveries!
Eliminating the Source of Asthma Causing Immune Molecules
But now, a team of researchers, at Genentech Inc.,
IgE-producing B cells express on their surface an IgE molecule that is slightly different to the IgE molecules that they secrete. The team, led by Lawren Wu, generated a therapeutic molecule known as a monoclonal antibody that targets the portion of human IgE that is contained in IgE molecules on the surface of B cells but not in IgE molecules in the blood. When mice expressing human IgE were treated with this monoclonal antibody, their levels of IgE in the blood decreased substantially as did their numbers of IgE-producing B cells.
As the monoclonal antibody provided mice with protection in a model of allergic asthma, the authors suggest that targeting IgE-producing B cells using monoclonal antibodies similar to those described in this study might be of benefit to individuals with asthma and other allergic diseases.
The research appears in the Journal of Clinical Investigation.