So yes, you know how pharmaceutical pricing works. The first drug company sets the price, which has been done. And then you can adjust the pricing based on whether you’re better. We think if we do meet our clinical goal of stabilizing cognitive decline that allows us for premium pricing. And I would expect that premium pricing would come well within that $82,000 bracket, although don’t hold me to that, we’re a little ways off from that decision. But the bottom line is the current drugs are difficult to use. They’re complicated. I think their uptake is going to be somewhat — will be slow because of that sophistication needed for managing those patients and the resources, such as MRI scans, which are going to be needed for those managing those patients.
As far as the more recent events with major depressive disorder, we found that very interesting and actually quite validating about how we do our CNS drug development. Clearly, although I’ve not seen the data, I’m not going to comment on it, we are very sensitive to the fact that particularly in depression, but in all central nervous system diseases, placebo effects always are what captured you by surprise. And the way to eliminate surprises on the placebo side is to better control your patient enrollment criteria using enrichment factors. The oncologist learned this, 20 years ago. The CNS drug developers have not yet learned it. We take this seriously. And in our Alzheimer’s trials, these patients all have neuroinflammation and actually in the trial that we planned in treatment-resistant depression, they will all have neuroinflammation.
We believe by using that kind of, shall we say, discipline and enrollment, it will prevent surprises on the placebo end or the placebo response and allow you to really accurately assess the drug’s effect on the disease.
Unidentified Analyst: Great. Thank you.
Operator: At this time, there are no further questions. And now I would like to turn the floor back over to RJ for any closing comments.
RJ Tesi: Yes. Thank you. So just in summary, XPro is a unique asset in the Alzheimer’s therapeutics space. And this became particularly clear when at AAIC this year, where there are a lot of companies have jumped on the anti-inflammatory bandwagon for Alzheimer’s. But as many of you know, CJ, as CJ likes to say, CJ is our VP of CNS Drug Development. For those of you who don’t know CJ. It’s not treating neuroinflammation that’s important. It’s how you treat neuroinflammation. Many of the anti-inflammatory strategies are what we call glial suppressive. Another is they turn off glial cells, both astroglia or microglia cells. And while that may prevent production of destructive inflammatory cytokines, it doesn’t fix the problem because glial cells play a very, very important and active role in the remodeling and repair needed to control and reverse CNS diseases, including Alzheimer’s disease.
So turning off a dysfunctional glial cell is not a winning strategy. Converting a dysfunctional, destructive glial cell into functioning — normally functioning glial cells, the Phagocytize Mylan debris promotes synaptic plasticity and improved neurons function is needed for success. So far, we have evidence that XPro plays this role well. And as far as we know, we’re the only drug that plays this role. And finally, why is the NK cell base so confusing. We believe it’s a pretty simple reason. Everybody has assumed NK cells are like T cells. When in fact, the how and why of NK cells in oncology is a separate and distinct scientific discipline. INKmune is a therapy that solves the three major problems facing today’s NK therapies. INKmune therapy leverages the patient’s own NK cells to treat their disease.
