Dan Carlson, TW Research (Dan)
RJ and CJ, thanks for joining us today. I’d like to start out by saying I find it very interesting how, for a small company, first with inflammation and now with biomarkers such as EMACC (Cognitive Endpoints for Early Alzheimer’s Disease Trials: Development of the Early AD/ MCI Alzheimer’s Cognitive Composite), INmune seems to be ahead of the curve on what’s going on in the CNS (Central Nervous System) arena. Perhaps we can start with what you guys see as the biggest trends in this space right now?
R.J. Tesi, INmune Bio (R.J.)
Let me start there, and then I’ll let C.J. jump in. When I look at what’s happening across biopharma in the CNS, I see a number of things. First of all, clearly, big companies are reassessing the need to be involved in CNS. I think the best example of that was Pfizer’s acquisition of Biohaven just a couple of days ago for a very large number for an epilepsy drug, quite frankly, I was surprised by the price. Although I think if you look under the hood at Biohaven, they have a lot more going on than just epilepsy.
I believe this was more of a strategic acquisition by Pfizer, a company that very noisily got out of CNS less than a decade ago. The reasons I think this is important is because, one, Pfizer is one of the companies that has a lot of dry powder. They’ve made a huge amount of profit on the COVID vaccine story. And as you know, Big Pharma changes and grows by M&A. They don’t develop anything internally.
I think that the fact that they have chosen to invest in CNS is a very important signal because it has been my bias for quite a while that although investors and companies love oncology, I think the clutter and complexity of the oncology space makes it really hard to pick winners and losers.
And this is what I tell my team and board all the time. I said, “…you can have a great idea backed with great data, both based on commercial need and scientific need when you start a development program, but five or six years later, when you get to the market, you’re completely irrelevant. Because the oncology market is so crowded and so rapidly evolving, it’s hard to look into the future.
CNS, in my opinion, because there’s less activity, less insight, quite honestly, less innovation, I think is a little more predictable. So, in fact, we believe that you have the opportunity to be patient. And I don’t mean patient, meaning long time. You don’t have a lot of time, I mean patient, more like being precise development. And when you get to the market, you’re going to be rewarded for your efforts from a commercial point of view.
So I think that the Biohaven deal with Pfizer is a bellwether, and I expect more M&A in the future. Now, what does that M&A look like? Obviously, from our perspective, our two benchmark programs in CNS are Alzheimer’s and treatment-resistant depression, both have significant unmet needs. Both have a history of failures. So I suspect that there’ll be a little more trepidation for M&A in those areas. But we are quite comfortable with the idea that once we have phase 2 data, that we will be in the conversation for partnering.
And as you know, it is our heartfelt opinion that there really are only two things that really bring value to a microcap biotech like us, and that’s positive human data and partnering. And when you really strip all that away, you don’t get into partnering discussions without having decent data. So it’s all about data.
To that end, we are moving forward with the phase 2 programs. We love our design, we love our product. We love the fact that we can do studies that are short and small, which is right-sized for a company that is our size with our resources. And we think that the delta, the potential for a significant valuation collection when we get the positive data first iin Alzheimer’s and then farther along in TRD are both very real.
We just had a company-wide meeting down in Boca and assessing our strategic priorities, and there’s no question that we got it right so far. The company’s strategic priorities are Alzheimer’s and depression.
Obviously, we believe there are uses beyond those two indications, but for now, at least in the near term, we’re going to be judged on how we execute against those two indications. But we don’t want people to forget that those are the tip of a very large iceberg in the CNS space.
I think that when we ring the bell in both Alzheimer’s and TRD, we will be able to really say with vigor that, in fact, X-Pro is a platform program for treating multiple CNS diseases.
I have been challenged on this concept, on the tip of the iceberg concept that how can you say you’re going to treat all these other diseases? You don’t have anything going on in those diseases. You’ve only announced programs in ALS, Treatment Resistant Depression (TRD) and Alzheimer’s. Well, yeah, but remember, we do have a lot going on that is not necessarily in the public’s eye, because right now we want everybody to focus on Alzheimer’s and TRD because that’s what is going to make the difference in this company.
So R.J., along those lines of your novel therapeutic, XPro-1595, being a platform across multiple diseases beyond AD and TRD, you guys did have an announcement about some data in multiple sclerosis. So maybe C.J., you can jump in and, since you have a platform for a lot of CNS indications, talk about the role of Tumor Necrosis Factor (TNF) in the CNS.
C.J. Barnum, INmune Bio (C.J.)
I like to think our Philosophy is simple. I don’t know whether that translates well to investors, but what we’re really doing is treating a single disease that manifests in a variety of different ways. We’re treating neuroinflammation, and neuroinflammation drives the pathology of a variety of different diseases.
TNF is THE master regulator of neuroinflammation. It governs the activity of all the immune cells in the brain and is upstream of every immune target currently in clinical development, including drugs that target RIPK and TREM2. You only need to look at the 70 preclinical studies that have been published with XProTM to understand the significance of targeting TNF.
Our preclinical studies are very clear- it doesn’t matter the model of CNS disease, if you neutralize solTNF (soluble TNF) with XProTM, you change the outcome. If you just look at our preclinical programs in the CNS space, you’ll see Huntington’s, you’ll see depression, you’ll see MS, you’ll see eye-related diseases, you’ll see spinal cord injury, stroke, and epilepsy, Parkinson’s, you name it. Where we’ve looked, we’ve been able to see a difference by targeting solTNF.
But, of course, your lead program being Alzheimer’s, you guys had a bunch of presentations at AD/PD in Barcelona last month. I’m in the camp that you’re not getting any real recognition in the stock market, but it seems to be that you’re getting it in the industry. Can you talk about what the industry is seeing, and what they’re doing, and trends in the space for Alzheimer’s, especially with Biogen in the picture?
Yeah. Let me jump in there because I want to make a point. There’s no question that our lead program is Alzheimer’s disease. I’ll let C.J. comment on this also. I want people to think that our lead program is really dementia, it’s really cognitive decline. Why do I say that? Obviously, the most important clinical element of dementia, of Alzheimer’s, is cognitive decline. There’s a lot of behavioral elements which complicate the care of these patients.
But let’s focus on what everybody, including the stock market and investors, are focused on. What happens with cognition? Well, it turns out that if you expand the definition of cognitive decline to include all the dementias, there’s a whole list of diseases that we think are low-hanging fruit. You have FTD (frontotemporal dementia), you have dementia associated with MS and Parkinson’s disease, you have dementia associated with a number of CNS diseases.
The advantage of a drug like X-Pro, which targets neuroinflammation, which is what drives synaptic dysfunction and nerve cell death, the hallmarks of cognitive decline. Because we target those two elements, that we can target cognitive decline and dementia across multiple disease types, everything we are learning in our Alzheimer’s program, every biomarker we utilize, every cognitive endpoint we utilize, basically is a cassette that we can plug and play in other diseases.
The Alzheimer’s disease is not only the first indication in the large subgroup of CNS diseases where neuroinflammation plays a role, which is a very large group, but it’s the first and the largest disease in the subset of diseases where neuroinflammation causes dementia or cognitive decline.
Everything that C.J. has put in place for Alzheimer’s can be used over and over and over again in these other development programs. As you know, the more often you do it, whether you’re making omelets, doing kidney transplants, or doing drug development, the better you get at it and the more efficient you become.
C.J., anything you want to add there before I answer the question about whether academia and industry are beginning to look our way?
When we have the opportunity to sit down with people and walk them through what we’re doing, they get it, they’re excited, they think the data is fantastic.
But they need to be walked through it because as you well know, we don’t do things the same way everyone else does. We do things based on what’s relevant for our clinical development program. In other words, we design our early phase studies to measure biology we expect to change with the drug, but that also has implications in Alzheimer’s disease. Right now, that’s just not how the field does it.
I was just at a neuroimmunology meeting which was highly focused on Alzheimer’s disease, and they’re still looking at amyloid and tau as endpoints. Part of the reason they’re doing that is because there is considerable debate and confusion as to how to determine target engagement of anti-inflammatory drugs. In other words, everyone is trying to figure out what the anti-inflammatory response should look like
As a result, many companies are using disease biomarkers such as amyloid and tau that may or may not have any relevance to how their drug might be working. The risk here is that you are making decisions on endpoints that may have no relevance to how your drug works or whether it will have a clinical benefit.
We’ve done the target engagement studies and we’ve shown that XProTM modulates the immune system. I use the word modulates because part of the confusion relates to the directionality of the change. We are taught that reducing immune biomarkers is good. Unfortunately, it’s not that simple. Many of the same biomarkers increase when the immune cells are active and acting in a neuroprotective way. I think the field really struggles with how to think about that. It’s extremely complicated, and in my opinion we are nowhere near being able to say a given immune biomarker is inherently “good” or “bad”. This is exactly why we need to look at the downstream consequence of modulating the immune system. Is the brain changing in a positive way? Do we see changes in biomarkers of brain function that XProTM improves in preclinical studies?
For example, our preclinical studies tell us that XProTM has a big impact on synaptic function and white matter. We have designed our studies to measure any potential change in synaptic function and white matter quality. You just don’t see that with immune therapies developed by other companies – they simply plug their drug into the old Alzheimer’s clinical development where they’re looking at amyloid and tau and maybe some cognitive measures. This is a recipe for failure.
That said, our approach is a bit too cutting edge for most companies, even the ones that are very positive on our data. It’s too novel and new for them. But they’ll get there. As R.J. likes to say, with positive clinical data in phase 2, you’ll see people embrace this.
Now, one small comment on that. The white matter MRI metrics that we’ve been using are beginning to be used by other companies. In fact, Imeka, the imaging CRO that developed these white matter techniques, has seen an uptick in business – and not just biotech, big Pharma is starting to explore these endpoints. We paved the way for that.
The same goes for the novel cognitive endpoint (EMACC) we are using in our Phase 2 studies. While we are the first to use it as a primary endpoint, Biogen has used it in previous studies and is using it in current studies. Other companies are starting to use it, too. It’s not going to be adopted overnight, but people understand that we need better metrics. We, and others, feel the EMACC is ideally suited to for measuring early AD. We think this justifies what we’re doing, not just for our program, but for Alzheimer’s more broadly.
Let me comment about what the business world is thinking, and I’m going to give you a bit of a contrarian view of someone who sat across the table in partnering discussions from Big Pharma for more than 20 years.
So first of all, I think the people that are looking for Alzheimer’s therapeutic assets are quite sophisticated. I think they recognize that we now understand the value of anti-amyloid therapies, they work but they don’t work particularly well, and I will say they’ve worked consistently. I mean, whether you look at either the Biogen drugs, the Roche drug, or the Lilly drug, their efficacy is about exactly the same: they decrease the rate of progression by a third over 18 months.
You can argue a little bit about difference in safety, I’m not going to go there because it’s complicated. They understand that although tau seems like an attractive target, anti-tau drugs haven’t worked at all, so they are actively looking at all these other strategies, of which targeting neuroinflammation is very high on the list.
But remember what you’re dealing with. You’re dealing with a business development professional and the way their reward structure is. If they bring in a blockbuster, their career is made, right? If they bring in a dud, they might as well become a plumber because they’re never going to go anywhere in BioPharma.
So when you are asking them to say, “We no longer believe in what the industry has believed in for 20 years. We want to believe in this new idea. Even though the data are great, we’re going to wait until you show us really good clinical data.” What they are thinking is, “Man, I can’t move forward on this until I’m really, really sure, because the risk to me personally is just way too high.”
They would rather be employed than be a hero! I understand it is a cynical set of comments. But in fact, it’s human nature.. If they were swashbuckling risk-takers, they’d be sitting where C.J. and I are. They’re not risk-takers because they’re sitting in big pharma. They get rewarded for success and punished for failure, but they do not get punished for missing the “next big thing”.
So to go back to CJ’s point, is they get it. They’re enthusiastic about it, but they’re still sitting on their hands because they need proof, and the level of proof when you are first in concept—I’m not saying first in class because there are other people in neuroinflammation—but nobody has rung the bell yet in a blinded, randomized trial. When you’re first in concept, people really want to see data from a blinded, randomized trial, full stop. And that’s what we’re providing them.
We’re providing them that data from a position of incredible strength because we really, really, did I say, really?, understand how our drug works. My mentor in drug development, a very talented guy, told me, “You can never understand enough about how your drug works.”
Now, I never really took that mantra to heart until XPro in CNS. And the more we learn about how XPro works, the better we get at designing trials, the better we get at de-risking the trials, and the better we understand the opportunities that are before us. I admit we’ve taken a science-heavy approach, but that translates into an AD clinical trial are 6 months and 200 patients, that costs one-fifth of what any other company is doing in Phase Two because they’re having to do four or five times the number of patients for three times as long. I often ask myself if companies doing 18 month trials with 800 patients really understand their drug or the disease they are treating?
Our approach works well for us. Knowledge provides precision. We have grown to accept that we’re not getting the attention we think we deserve by those in the field. But as CJ says, it’ll come.
RJ, you’ve talked about how well you know your drug. As you’ve gone through these programs. What about the drug have you learned that has surprised you positively and/or negatively?
I’ve always liked the idea of this idea of treating glial dysfunction and all that stuff, I thought it was great. The day that I said, “Holy shit, this is amazing!” was the day we got the Imeka studies on the white matter response on apparent fiber density.
Here you have a guy that was 65 years old. He had retired because of his dementia and then six months into treatment with XPro, he went back to work. Every three months we had scans on him where we could measure apparent fiber density. And that brain basically remodeled itself, repaired itself over those nine months under the influence of XPro.
I was taught in medical school that the brain doesn’t fix itself after adolescence. I think the people that graduate medical school today are probably taught the brain doesn’t fix itself after about age 28 or so. Here we have a 65-year-old that is repairing and remodeling their brain.
First of all, that gives hope to us old dogs. But more importantly, it shows that the brain is just as resilient as the skin, as the bone, as the liver, as being able to fix pathology if you give it a chance, give it the tools to repair and remodel. If you dig a little bit deeper, the remodeling that was going on in that 65-year-old brain looks a lot like the remodeling that occurs naturally in an eight-year-old as he becomes a 20-year-old, our brains mature.
It appears when you get rid of the pathologic pressure that’s caused by glial dysfunction, and I use the word glial dysfunction because it’s a little more complicated than just neuroinflammation, you get rid of the pressure, that degenerative pressure, the brain goes, “Hey, baby, I’m six years old again.” Let’s fix what’s broken. Let’s remodel for better performance.” Repair and remodeling of the CNS – that’s why I am very bullish about our Alzheimer’s programs, and bullish on the use of this drug in other neurodegenerative diseases.
I’m not smart enough to understand how this plays out in things like depression. That’s CJ’s turf. But for me, where my insight is more on the neurodegenerative side, that was my aha moment, that “Holy cow, we have something that’s really special here that makes the brain do something it shouldn’t do or we didn’t know it could do.” And in fact, it’s going to make a big difference in the lives of patients.
So, Dan, I’m shocked that the results were as consistent and as strong as they were in the Phase 1 study. I always believed the drug would work, but I did not think it would be that clear, especially since we had patients that spanned the spectrum of disease status – mild, moderate and severe. Irrespective of their disease status, their biomarkers improved!
The most important data for me was the proteomic report. The proteomic report was an unbiased analysis of what’s happening in the CSF of these patients. The report showed the exact same changes in humans that we saw in the animal models. The translation from animals to humans is so rare. As soon as I saw that, I knew we had a drug that was going to work.
The thing that I think really surprised me, though, was how fast it worked clinically in the patients that had mild enough disease. We saw almost double performance on cognitive tasks within six weeks. Really crazy. Now, I don’t expect that to be the norm, but I expect some percentage of patients to have a similar response.
There isn’t anything, I would say, that I’ve been disappointed by, except for the timing of COVID and not being able to have more data points. But to R.J.’s point, we know our biology. All the endpoints we chose worked, and they worked spectacularly, because we understood our biology and we had the tools available to measure that biology, like white matter.
This thing just works. I don’t know what to say, except for we were able to get enough to design a phase 2 study that will tell us that we’ve got a drug that will have a clinical benefit and further refine a registration study so that we see a very big, powerful effect.
I can tell you, as I think we mentioned on the earnings call—we may have talked about it before—the earlier we go in patients, the more we believe we’re going to show improvement. Not just slow decline, but we’re going to restore normal cognitive function in many patients. I’m just excited to get that data.
Two additions there, Dan. although C.J. is probably better prepared to comment on this as a bench scientist, let me talk to it as a translational drug developer. It is extremely rare when your preclinical models translate faithfully into the clinic. Your preclinical models are usually in rodents. They may be in non-human primates, and they never translate faithfully into the clinic.
In fact, to the point where we like to joke that the FDA (U.S. Food & Drug Administration)’s only interest in all the preclinical models is whether the drug is safe. The FDA does not emphasize the efficacy response in those preclinical models as part of their decision making of allowing you to go into humans. It’s all about safety, safety, safety.
Now we like to boast about the 70 publications we have on the website, and I think a lot of people roll their eyes. But every time I go to another company’s website and look for their publications, they are proud on having seven or twelve. INmune Bio has 70!
There are two very important points about this number. We didn’t ask for any of this. Scientists came to us and asked to use the drug to help them unravel the mysteries of the CNS in whatever disease they were interested in. The second thing is these studies were all done at different institutions by people with different levels of training; a graduate student, a postdoctoral student, or an attending. No matter whose hands we put this drug in, it worked.
Then have that translate into man suggests that we are really working with a drug that targets, what I would say, quite fundamental biology. This gives us comfort to make the investments. We are not holding our breath hoping for success. We are confident of success. We are curious what new and interesting stuff we are going to learn.
The other thing is I just want to nuance a little bit what C.J. says. He uses the word biomarkers to mean both inclusion criteria and efficacy criteria. I tend to split it. When I think about biomarkers, I like to segregate the inclusion criteria, the enrichment criteria, from the biomarkers we’re using to look at drug response; the efficacy biomarkers. We chose these based on, shall we say, informed insight. It all goes back to understanding the drug, the disease and a drive to eliminate the guess work often found in clinical development programs.
We had no idea that the biomarkers would be as powerful as they are, and the influence that had on the design of our phase 2 trials. We think that efficient use of biomarkers in CNS drug development is a very important secret sauce that is an important part of the recipe to our success. Because of these biomarkers with are not doing all comer trials. We have figured out a way to select the patients that match the pathophysiology of their disease, which has glial dysfunction, with the way our drug works, which is neutralizing soluble TNF.
So, CJ, you were talking about how your pre-clinical translated so well into the clinic. You guys just came out with some pre-clinical white matter data in MS and maybe you can talk a little bit about the work you’re doing with Imeka and the importance of remyelination along with the importance of this recent data you came out with.
The process of neuronal death starts with the loss of synapses. The second thing to go is the loss of white matter – myelinated axons. Finally, the gray matter, the cell bodies, degenerate.
Every neurodegenerative disease is going to have loss of synapses, white matter, and gray matter. The reason we talk about neurodegeneration of gray matter is because that’s the point of no return. I think the reasons there’s been an over-emphasis on gray matter is because that’s the point at which we have to keep patients from advancing to. In contrast to gray matter, white matter changes happen early and white matter can be repaired. We think there are clear advantages to shifting the focus to white matter degeneration because we have biomarkers to identify white matter pathology and the opportunity to reverse the disease process.
The data that was just presented by Lesley Probert’s group showed that white matter was improved within the cortex in an animal model of Multiple Sclerosis. We never looked to see if there were changes in white matter within the brain outside of those big white matter tracks, this is a unique finding. They were also able to get a much clearer picture of how the immune cells of the brain, the microglia and astroglia, were behaving during this process. What Leslie was able to show was that the microglia and astroglia were behaving in a way that facilitated repair, although they do different things. Leslie is now looking more closely at exactly what they are doing.
I don’t think this will be unique to Multiple Sclerosis and I would expect if we looked at an Alzheimer’s model or any other model of neurodegenerative disease, we would see very similar things. And this is exactly why I think white matter will be important for all our CNS programs and why we will continue to use white matter biomarkers in our clinical development programs.
Three additional points on this. CJ brought up the astrocyte. Astrocyte and microglial cells are 50% of the cells in your brain. He just said is that 50% of the cells in the brain participate in this repair function. What’s even more interesting is until recently, nobody knew what the hell an astrocyte does.
Historically, it was said that the 40% of the astroglial cells in the brain were performing a nurse-maid function. They make sure everything’s healthy. Actually, that is correct. But how they do it wasn’t clear. Now we’re beginning to understand that astroglial cells are major players in many aspects of the brain. Our understanding is incomplete, but we know that X-Pro helps them get them into the repair mode.
Another important point that drug development, like medicine, is driven forward by technology. And part of the reason that demyelination has only been discussed in MS is because you have a billboard out there saying, “This disease has demyelination.” This “billboard” uses technology to measure demyelination that is 20 years old. Think about the cell phone you had 20 years ago. Yep…that is what MS drug development has been depending on. Little wonder there is limited innovation in the space.
We never had the technology available to that allowed us to look at the dynamics of myelination in live humans. We had a low technology snapshot trying to see into the complicated biology of demyelination. Now, with better imaging, progress will be made. Beyond MS where the signposts for demyelination are much more subtle compared to a billboard sized demyelination in MS, precision is required.
As our technology improves, specifically the technology that Imeka is bringing our development programs, we’re beginning to see pathology that we didn’t know exist and we’re beginning to understand that it plays a part in the clinical disease that the patient has. Today we can see re and demyelination in diseases where it has not been considered important. In the future, I believe for every CNS disease, the pathology and treatment discussions will include a discussion of myelin biology. Personally, I think one of the most interesting differentiating elements of XPro is it’s ability to promote remyelination. The obvious application is MS, but I think by no means is it the only application of this unique attribute.
R.J., this has been great. How about we finish with you discussing your strategic priorities and what investors should be looking for from INmune over the next 12-24 months.
Today we haven’t spoken about our NK (Natural Killer Cell) platform INKmune, but we expect to continue to enroll patients in our P1 trial which we will readout as they occur. Now with Alzheimer’s, and I want C.J. to really comment a little bit more on the TRD depression story, we have not emphasized TRD enough lately because we’ve been so head down on Alzheimer’s. Our Alzheimer’s programs are rolling. Unfortunately, because these are blinded randomized trials, the news flow is going to be relatively low until they read out.
Fortunately, we’re not waiting two or three years to read them out, we should have top line data in 2023. We are focused on execution of these trials, enrolling the patients. To be clear, when I say top line data, I mean the EMACC, the cognitive endpoint. The effects on cognition are what people want to understand. But let me remind you of a couple of important elements in those phase 2 trials.
First is that all patients get drug for at least nine months, probably 12 months, after they reach the primary end-point of the trial. That is, we roll them into an extension trial. This is critically important, because the FDA, the company and investors want to know how durable the response is and how safe long-term use of the drug is in this elderly group of patients.
Let me use the Mild Cognitive Impairment (MCI) trial as an example. If you’re a 65-year-old with MCI in the three month trial that gets a great clinical response the first thing everyone will ask is, “Well, that’s great for three months. What happens when you treat the patient longer?” Because of the extension trial, we’ll be able to answer this question. Next, we beleive separating mild AD from MCI is key. Admittedly they are a continuum of the same disease, the predictability of cognitive decline is different. Cognitive decline in patients with mild AD patients is reliable. It’s a little more complicated, more unreliable in the MCI patients.
A lot of what C.J. is doing, in the MCI trial, is we are exploring an additional suite of biomarkers to try to help us understand which MCI patients that are going to be converting to AD – identify those that are whose cognitive dysfunction is progressing. The data suggests that the conversion rate is generously 20% per year. Patient enrichment strategies are critical in this group of patients.
We hope combining our simple enrichment required criteria, patients must be APOE4 positive, with what we will learn from all the efficacy biomarkers included in the trial, will help us design enrichment criteria for a pivotal MCI trial that has high percentage patients that will convert to Alzheimer’s disease. These are the patients you want to treat in the clinical trial. C.J., before you get into TRD, anything you want to add there?
No, I just want to clarify the MCI and mild AD. There are two studies right now, and the reason for that is because our biomarkers manifests differently in MCI and mild AD. Therefore, we have to study them separately. Now, the primary endpoint for both studies is EMACC. I suspect that the EMACC will be a good cognitive endpoint for both MCI and AD patients and we will be able to lump them together for a registration trial. But we will let the data tell us that. But the expectation I have for those two AD programs is that they will become one.
Now, on to TRD. We will be starting the TRD study this summer. This is a program that’s based on a proof-of-concept study Andy Miller’s group at Emory University ran with a non-selective TNF inhibitor nearly a decade ago. Andy is PI of this study. Not only does he have experience and a deep understanding of inflammatory-related biomarkers in TRD patients, selecting them, measuring them; he also has experience with TNF inhibitors, showing proof of concept that the targeting TNF actually works. We designed a study that’s supported by the National Institute of Health to look at the biomarkers that reflect inflammation induced biological changes in major depression.
What Andy’s group has shown, led by Jen Felger, is that inflammation causes a loss of connectivity between brain regions, and this can be measured via functional MRI. The hypothesis is that XProTM can restore connectivity. Right now, it’s planned as a two-year study. We’re going to do our best to try and speed that along so we can advance more quickly to a proof of concept, phase 2 study.
The TRD market is big. The need is big and real. And I think the likelihood of success in TRD is as good, if not better, than even in AD.
Awesome. Thank you both for your time and thoughts. This is very exciting and we’re really looking forward to seeing what you can deliver to both patients and investors over the next couple years and beyond.
Disclosures and Disclaimers
XPro1595™ (XPro™) is a next-generation inhibitor of tumor necrosis factor (TNF) that acts differently than currently available TNF inhibitors in that it neutralizes soluble TNF (sTNF) without affecting trans-membrane TNF (tmTNF) or TNF receptors. XPro™ could have potential substantial beneficial effects in patients with Alzheimer’s disease by decreasing neuroinflammation. For more information about the importance of targeting neuroinflammation in the brain to improve cognitive function and restore neuronal communication visit this section of the INmune Bio’s website.
About INmune Bio, Inc.
INmune Bio, Inc. is a publicly traded (NASDAQ: INMB), clinical-stage biotechnology company focused on developing treatments that target the innate immune system to fight disease. INmune Bio has two product platforms that are both in clinical trials: The Dominant-Negative Tumor Necrosis Factor (DN-TNF) product platform utilizes dominant-negative technology to selectively neutralize soluble TNF, a key driver of innate immune dysfunction and a mechanistic driver of many diseases. DN-TNF product candidates are in clinical trials to determine if they can treat cancer (INB03™), Mild Alzheimer’s disease, Mild Cognitive Impairment and treatment-resistant depression (XPro™). The Natural Killer Cell Priming Platform includes INKmune™ developed to prime a patient’s NK cells to eliminate minimal residual disease in patients with cancer. INmune Bio’s product platforms utilize a precision medicine approach for the treatment of a wide variety of hematologic and solid tumor malignancies, and chronic inflammation. To learn more, please visit www.inmunebio.com.
Forward Looking Statements
Clinical trials are in early stages and there is no assurance that any specific outcome will be achieved. Any statements contained in this press release that do not describe historical facts may constitute forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any statements contained in this press release that do not describe historical facts may constitute forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any forward-looking statements contained herein are based on current expectations but are subject to a number of risks and uncertainties. Actual results and the timing of certain events and circumstances may differ materially from those described by the forward-looking statements as a result of these risks and uncertainties. INB03™, XPro1595, and INKmune™ are still in clinical trials or preparing to start clinical trials and have not been approved by the US Food and Drug Administration (FDA) or any regulatory body and there cannot be any assurance that they will be approved by the FDA or any regulatory body or that any specific results will be achieved. The factors that could cause actual future results to differ materially from current expectations include, but are not limited to, risks and uncertainties relating to the Company’s ability to produce more drug for clinical trials; the availability of substantial additional funding for the Company to continue its operations and to conduct research and development, clinical studies and future product commercialization; and, the Company’s business, research, product development, regulatory approval, marketing and distribution plans and strategies. These and other factors are identified and described in more detail in the Company’s filings with the Securities and Exchange Commission, including the Company’s Annual Report on Form 10-K, the Company’s Quarterly Reports on Form 10-Q and the Company’s Current Reports on Form 8-K. The Company assumes no obligation to update any forward-looking statements in order to reflect any event or circumstance that may arise after the date of this release.TW Research's Disclaimers & Disclosures: TW Research may have been compensated for writing this article. For a full list of disclaimers and disclosures, please visit http://