Herceptin, BT2111 & Texas Tech As investors, understanding what we own will be vital going forward. That might seem a rather obvious statement, but it will certainly determine where you "get off the bus". Bioasis has presented us with a rare opportunity to make many multiples on our investment and one doesn't want to be selling themselves short during the process. They say knowledge is power, but it is wisdom that will carry the day for us as we apply our knowledge.
Understanding how to interpret results that will come from the Texas Tech experiments will be crucial for us. This involves knowing how Herceptin works. Herceptin is a Monoclonal Antibody that binds to the human growth factor receptor (HER2) on the surface of some cancer cells, most notably breast cancer. Herceptin binds to the HER2 receptor interfering with the process of the cancer cell reproducing. Herceptin's primary purpose is not to kill cancer cells, but it is to stop the explosive growth of the cancer cells. Normally, the body has another protein that binds to the HER2 receptor causing the normal cell division/replication, but in the case of HER2+ cancer cells, it causes explosive growth because of the proliferation of HER2 receptors.
In most of the literature on Herceptin, it is usually prescribed in conjunction with some sort of chemotherapy agent (doxorubicin and it's derivatives), to kill the cancer cells. Most literature on Herceptin states that it may stimulate the immune system to target the bound cell for destruction, but that is not Herceptin's primary purpose. In fact, no-one is quite sure how the immune system is activated by Herceptin to kill the cancer cell. They just see the effect that it does sometimes do this.
In our BT2111 experiments, the unexpected result was that we have a much higher cancer killing rate of the bound cells than Herceptin alone. This is what yielded the unexpected result and the ability to file the NCE (New Chemical Entity). Obviously, p97 was a factor in motivating the immune system to kill the cancer cell. The fact that this happened using a Monoclonal Antibody (BT2111) is a most elegant solution, because we only target the cancer cell itself. Side affects of this are minimal and the outcome is phenomenal. Imagine if we engineered a Monoclonal Antibody that also had as it's payload a component of doxorubicin! This would indeed be a powerful weapon in the arsenal of combatting one of the most deadly forms of breast cancer.
What makes BT2111 such an elegant solution, is that we essentially have a bispecific Monoclonal Antibody that binds to the HER2 receptor on the tumour and to the p97 receptor on the BBB. Since the p97 receptor is found almost exclusively on the BBB, we don't need to worry about binding on other sites throughout the body. We deliver the MAB across the BBB into the brain, it binds to the HER2 receptor on the intracranial tumour and hopefully we have the same killing rate that we experienced invitro.
Alright, why is all this important? It is important to understand that Texas Tech might say that they experienced no greater cancer cell kill rate than Herceptin alone. If they tell us that the intracranial tumour growth was arrested, that would be a complete success. It would mean that we delivered the payload and Herceptin did it's job. If we experience the same BT2111 kill rate invivo as we did invitro on the peripheral tumours, that would be a huge success and this will be a blockbuster drug. If we experience the same BT2111 kill rate invivo on the intracranial tumours, we will indeed have a drug that will displace Herceptin. It's one of these situations where you could wake up one day and the share price might have jumped to $10, you would immediately sell only to have it advance multiples from there.
In addition, you also need to understand that many of the other MAB's out there for treating brain cancer work on the same principal as Herceptin. Conjugates are easy to do and it's not unreasonable to expect similar results as BT2111.
Like Retiredcop said in one of his earlier posts: "It's pucker time". Make sure you understand what you own and make sure you make informed decisions on when to "get off the bus".