Thursday, May 10, 2007

Blocking Immune Signals gives "Stunning Results"!!


More good news on autoimmune treatments—new treatments in phase III testing are expected to revolutionize treatment strategies for autoimmune disease.
http://www.medicalnewstoday.com/printerfriendlynews.php?newsid=62755 and
http://www.medicalnewstoday.com/medicalnews.php?newsid=62755
These new treatments are not cures or virtual cures but they are better than anything we now have. They should make as big an impact on autoimmune disease as the introduction of TNF-alpha inhibitors—Enbrel, Humira and Remicade.

These new biologics are fully human monoclonals that block two immune system chemical signals called interleukin 12 and 23. The experimental results have been so good that the two companies involved are racing to get this product through clinical trials and to market. Whoever wins is going to make a fortune. Even the runner-up should get rich with the leftovers. For stock speculators, the companies are Abbott and Centocor (Johnson and Johnson).

Right now the companies are both using plaque psoriasis autoimmune patients in clinical trials. The “wow!” factor of showing before and after pictures of patients with cleared plaque patches has won out over the lure of more patients and more potential customers that the Big Four (RA, SLE, MS, and Type 1 diabetes) have in their favor.

This is great news for my son and others with psoriasis, not so good for the rest of you. However, now that Big Pharma has figured out that a treatment for one autoimmune disease is a potential treatment for all autoimmune disease, I feel confident that this new monoclonal will be quickly tested on other autoimmune diseases.* Johnson and Johnson’s division, Centocor made too much money qualifying Remicade for just about everything while Abbott and Amgen sat on the sidelines. Abbott will not let that happen again.

This treatment while potentially revolutionary will not be the final cure we are looking for. It does block the inflammatory process farther upsteam than TNF-alpha inhibitors. This is good news. The closer to the beginning of the initiator of the autoimmune cascade, the more likely the biologic will be to have greater efficacy and fewer side effects. However, what we all want is to shut down the cascade completely. These new biologics will not do that. The cascade will still be constantly trying to re-start. These medications to block IL-12 and 23 will needed to be taken for the long term. Once they are stopped, the autoimmune disease will return.

Better still than blocking Il-12 and IL-23 will be blocking or disabling “autoimmune, antibody producing” B cells. (See my blog entry: B Cells keep the autoimmune pot boiling) There are new medications which will do that coming down the road in the next two or three years. These medications will need to be taken once a month to once every six months. They will have significant danger of infection and cancer and will not be a permanent cure. The first of these to be FDA approved for use in autoimmune disease was Rituxan. It is quite dangerous. There are better and less dangerous ones just around the corner—possibly FDA approved by about 2010. But they will not be a cure.

What we want is a permanent cure--something that turns off the cascade completely. Mice have these type of cures. We could too if we are willing to agitate and yell loud enough. Those full blown human cures to come will be with vaccines, fetal stem cells, or gene therapy manipulation of our own bone marrow. All three techniques have been successful at curing mice with autoimmune disease. Wouldn't it be nice to be cured? Wouldn't you like to be normal again? You could be if you are willing to yell as loud as AIDS patients did in the eighties.

What will you do today to get those cures to clinical trials?

*IL-23: a master regulator in Crohn disease - Nature Medicine
Indeed, several recent studies knocking out IL-12 and IL-23 subunits in animal models of inflammatory diseases such as multiple sclerosis and rheumatoid ...www.nature.com/nm/journal/v13/n1/full/nm0107-26.html

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