During the presentation, please feel welcome to submit questions using the Zoom Q&A interface at the bottom of your screen. After the presentation, we'll open to your questions. With that, Eric, I'll turn it over to you.
Great. Thank you very much, and I appreciate everyone listening in today to learn a little bit about our company, InMed Pharmaceuticals. Before we get started, I'd like to point out that we are a publicly listed company on the Nasdaq under the symbol INM, and as such, it's important that I point out that we will be using forward-looking statements in the presentation today. A copy of this slide is available in the slide deck that has been posted. InMed is a drug development company looking at drugs that are targeting the CB1 and CB2 receptors in the human body. Our lead drug candidate, INM-901, targets neural inflammation in neurodegenerative diseases such as Alzheimer's.
It's a proprietary, orally bioavailable, disease-modifying therapeutic that targets the CB1, CB2 pathways, and can cross the blood-brain barrier, which is important in this disease. Additionally, we have other drug development candidates in our R&D pipeline, including INM-089 for ocular disease, where we're focusing on dry age-related macular degeneration, and INM-755 in dermatology, where we've completed a phase II study in a rare genetic skin disorder called epidermolysis bullosa. I'll talk a little bit about our leadership team and our capital market structure at the end of the presentation. I won't go into too much detail about Alzheimer's disease. I think we're all familiar with it at this point, and we've all been touched in our lives somehow by this.
The most recognized hallmarks of Alzheimer's disease are the buildup of these proteins, amyloid beta, and tau, which can cause basically a gunking up of the system in the brain. You know, emerging research is talking more and more about the role of neuroinflammation in this disease pathway. I'd like to focus on that and explain why we are pursuing this with our candidate INM-901. If you think of the traditional view of how this disease develops, it became evident that amyloid beta and tau were built up to a large extent in Alzheimer's patients, much more so than you'd see in a normal patient without the disease.
The theory was that these proteins and this buildup was leading to neuronal damage, which then resulted in inflammation as a cleanup response. You know, if you stick to this line of thinking, then of course, if you take out amyloid beta and tau, reduce those through pharmaceutical intervention, then none of these other things would happen. The thinking has shifted over the last couple of years to look at this more as a cycle, so that any of these things can happen in any order, which then trigger the others to happen as well. As an example, neuroinflammation can be measured in patients with Alzheimer's disease, you know, years or even decades before the disease manifests itself and starts to show signs and symptoms.
Neuroinflammation might actually be one of the, you know, precursors or leading causes that start this whole vicious cycle. You know, with that in mind, we're looking at it as a driver of disease, not as a result of some disease process. What plays a role in this neuroinflammation? There are two cell types in the brain that are responsible for this, the microglial cells and the astrocytes. Under normal circumstances, these cell types basically resolve neuroinflammation and have anti-inflammatory actions in different modes of action, but they both contribute to that reduction in neuroinflammation. However, in a chronic setting, these can switch from a protective state to a destructive state. In these instances, they start to express pro-inflammatory cytokines that can lead to neurodegeneration.
Really what you wanna do is to either prevent the transition to the destructive state or actually reverse it to go back to the protective state. But we, you know, are very clear that these two cell types are responsible for the neuroinflammatory response in diseases such as Alzheimer's. We also know that the microglial cells and the astrocytes have these CB1 and CB2 receptors, and these are responsible for regulating inflammation in these cell types. Just as an example here, the activation of CB2 receptors promotes the transition towards a reparative anti-inflammatory state from the reactive state. You know, these receptors are playing a role in modulating the inflammation. What we're doing is using a drug to target these receptors to trigger this transition back to a reparative anti-inflammatory state versus the reactive one.
That's both with the CB2 receptors as well as the CB1 receptors. The CB1 receptors are probably more responsible for a neuroprotective effect than an anti-inflammatory, effect, but they both play an important role in diseases such as Alzheimer's. Now that we know which cell types and what receptors on those cells are, playing a role, we have now a drug, INM- 901, that can specifically, attach to these cells at those binding receptors for CB1 and CB2 and have important, effects in reducing inflammation, in the brain. You can see here that there's two particular, approaches that we are blocking here. One is the expression of inflammasomes, and the other is the expression of pro-inflammatory cytokines. There's a list of them that, we think we can have an important impact on.
By blocking that pathway, we think we can reduce inflammation in the brain and have a positive outcome in diseases such as Alzheimer's disease. We've seen a number of things in preclinical testing that support this theory. We have seen a neuroprotective effect such that the neurons that have undergone an amyloid beta insult, the presence of INM-901 regulates their cell death and protects these cells from cell death. We've seen a neuroprotective effect. We've seen a neurogenesis effect. As these neurons become mature neurons, what you like to see is the healthy branching of the neurites, but also an elongation such that these can reach out and have communication with other neurons.
In diseases such as Alzheimer's, these both shrink in their length, and the branches are not as robust as you'd see here in a mature neuron. In the presence of 901, we see both an elongation and additional branching in vitro studies. We've also seen a reduction of amyloid beta itself. We don't think this is the most important aspect of what our drug is doing, but nevertheless, it's better to see the reduction than not see the reduction. We think the real effect here is in neuroinflammation, and this is gonna be the most important attribute of INM-901. In Alzheimer's disease, you see a whole suite of proteins, these biomarkers that are elevated and causing inflammation.
However, in the presence of INM-901 in Alzheimer's model, we see a stark reduction of all of these pro-inflammatory markers in the test subjects. We're having exactly the effect that we think is necessary to treat the neuroinflammatory component of Alzheimer's disease. You know, we have this theory. We want to test this theory out in a proof of concept study in the mouse model. There's a particular mouse model called the 5xFAD mouse model. This is a genetic knockout model where these mice have been bred to develop very early on a amyloidosis type disease that is reflective of Alzheimer's disease. We had a very robust and very long-term study design to test the effects of INM-901 in this animal model.
You can see here the 5 different test groups that we had. A wild type just means a normal mouse that does not have the genetic mutation. There's the normal mice who had no drug. We also treated some of the normal mice with our drug to see if there's any ill effect. The 5xFAD mice, some of them, did not receive any drug. We had two arms where they received either low dose or a high dose of INM-901. When they were two months old, they were injected twice weekly for seven months. This is a very long-term study with a very robust design with five different treatment groups.
We tested a number of different behavioral criteria in these animals to try and measure, first of all, whether a diseased mouse reacts differently than a normal mouse, and then whether a diseased mouse that's been treated with INM-901 behaves differently than the diseased mice who did not receive any treatment. We looked at a whole host of different tests. There were five tests in this study. We also had an earlier short-term study where we did additional types of testing. Just to give you an example of how these tests are designed, let's start with the Barnes maze test. This involves having a very large disk that has holes drilled in it, and you put the mouse in the middle, and you know, you have to think, how would a normal mouse behave?
They would investigate ways to hide. They're very anxious animals. They don't like to be in open spaces. All of these holes are just basically, you know, cut through, and if they go into them, they'll fall to the ground. One of these has a little chamber that they can hide in. You can move this chamber around for each different mouse. Basically, you train the mouse to know where that chamber is. You then take him away and bring him back, and you measure how long it takes each mouse to find the chamber. The chamber's gonna be in the same place.
How long does it take for them to recognize their environment and then go back to the place where they can hide? You'd think that a normal mouse after being trained would know to go find that chamber very quickly. Indeed, that was the case. You then take the diseased mice who have you know poor cognition poor memory all of the signs and symptoms that you would see with an Alzheimer's patient. How long does it take them to then go and find where the chamber is? Indeed, these animals took a little bit longer. You know, they're confused. They're not as anxious. They don't understand that they're in danger by being in an open space. They you know just don't remember where the chamber is. You have those two extremes.
Looking at diseased mice who received INM-901, how did they behave? In all instances, they behaved more like the normal mouse than they did with the untreated diseased mouse. These are the kinds of tests that we run to look at a number of different outcomes, including behavior, cognition, memory, these kinds of things. I'll show you some data from that in a second. Additionally, we collected brain tissue and blood and did a number of microbiological tests to look at things like the expression of the pro-inflammatory cytokines that I mentioned earlier, and other disease markers to see how, you know, the different mice measured against one another. This is the outcome from the behavioral studies.
Just by way of how to read this data, you can see here on the Barnes test that I just explained to you know, it takes here about 20 seconds for the trained mouse to find the chamber where he can hide. By comparison, the diseased mice who have not been treated with drug took about 100 seconds. Sorry, I don't know why that changed here. Then you look at the diseased mice who received drug, both a low dose and a high dose. We see a number of things. First of all, we see that the treated mice, diseased mice, behave, you know, closer to a normal mouse than a diseased mouse would. You also see a dose effect. The more drug they receive, the better they responded.
It's very important to see in these kinds of studies. Across all of these different tests, you see the same thing. You see a reduction towards normal in the diseased mice who are treated with our drug. That's a very interesting, very important finding, and it certainly is very exciting for us as we continue to develop this drug. Likewise, when you look at the blood analyses and the number of different plasma inflammatory markers that we looked at, so IL-1β , NfL, IL-2, et cetera, you see the normal mouse and how much of this protein would be expressed in their blood. You see the diseased mice where you have an increase in these inflammatory markers. Inflammation is definitely taking place in these animals.
They're otherwise healthy, so it's not coming from some other disease. It's definitely coming from the increase in amyloid beta in these animals. You see again the low dose and the high dose. In just about every case, we see the dose effect, the high dose responding better than the low dose, but we definitely see a return to normal of these pro-inflammatory markers. Again, you know, we see not only in the blood that there's a strong reduction in the pro-inflammatory markers, but we also see a cognitive outcome in the other behavioral tests that you can probably correlate to say there's definitely something going on here. We know that in the blood and in the tissue, we're seeing some important reductions.
Apparently that's leading to an improvement in memory, cognition, locomotion, and a number of other outcomes. Taken together, it's a very exciting data from this robust study that we've conducted. Taking a look in summary at INM-901, we saw significant reduction in all of these biomarkers in a very robust long-term animal model. We conducted a second inflammation study with something called LPS-induced inflammation. Independent of Alzheimer's, we see a different study resulting in the same thing, and that is reduction in the inflammasome markers and IL-1β , which we think contribute to neurodegeneration. There's two different tests here that are showing similar results. We know that we have a direct impact on neural inflammation, and it's independent of whether it's amyloid beta or tau pathology.
You know, this type of treatment may be useful in other kinds of neurodegenerative diseases beyond Alzheimer's. We saw in vitro studies this neuroprotective effect. We saw the validation using mRNA data to support the other observations that we saw in behavioral tests. We saw some neuronal regeneration that promotes the outgrowth of the neurites. You know, it's a very robustly bioavailable drug. We can orally formulate this. We think that's gonna be important for the treatment of patients in the clinical setting. We're very excited about this. We think the data it points directionally in the right way. We are continuing to conduct other studies. We'll be reporting on those in the next couple of weeks as the data becomes available.
We're very excited about this, the opportunity for INM-901. Gonna shift now and talk about dry age-related macular degeneration. A lot of people have heard of macular degeneration, usually in the wet form. It's very well known here in Vancouver where we're based. The first treatment for that, for wet AMD came from a company called QLT, which is one of the foundational biotech companies here in Vancouver. Dry AMD is a little bit different. It's a much larger patient population. It progresses more slowly, but nevertheless can lead to complete vision loss and blindness. We think the unmet medical need in this space remains high, and there's a good opportunity for something that is disease-modifying to play an important role in this disease.
What is dry AMD? At the back of the eye, the retina, you start to have this damage caused by a breaking down of the different elements of the eye. This will continue unabated and spread until it covers everything including the optic nerve, where you then lose sight. If you look at a normal retina, the top being the inside of the eye and the bottom being the outside of the eye, you can see the different layers here of the retina, the photoreceptor cells, the retinal pigment epithelium, and the choroid. What happens in dry AMD is that you have a deterioration of these middle layers that cause a thinning of the retina.
You know, the idea here is to find a way to stop this progression in its tracks, and if possible, reverse this so that you can have improved vision. We have done a number of studies looking at the potential for INM-089 to impact these different components of the disease. This is just an example of one study where the red-stained tissue here, and then it's further identified by this dotted line, shows you the control, which is an intact retinal pigment epithelium. In the diseased model, you can see that there's huge gaps in the retinal pigment epithelium. There's very poor integrity or lack of the RPE itself.
In the subjects treated with INM-089 in these preclinical studies, you can see a much better restoration and protection of the RPE using INM-089. There's just a very small gap here. Definitely a huge improvement in the RPE, and you know, again, something that looks more normal than it does diseased here. There's a number of different studies we've conducted. This is just one of them, and we're very excited about this opportunity as well. In summary, INM-089 is also a signaling ligand for CB1 and CB2. We've demonstrated the preservation of retinal function in an animal model of AMD.
This is something that's delivered by retinal injection, which is very standard for drugs that work at the back of the eye and is in line with current clinical practices across the world. Something that we think will be very effective. Proactively protecting the retinal ganglion cells, which are the nerve cells that give you vision. This is actually where the investigation actually started when we were looking with a previous generation drug at glaucoma. We saw this protection of the retinal ganglion cells. We are also seeing this with the dry AMD model. You know, again, it's a very interesting opportunity, and we're very excited about its continued development. I'll touch briefly on INM-755.
This is a drug that we took through phase IIA studies, looking at chronic severe itch in a very devastating skin condition called epidermolysis bullosa. This is a genetic condition where the integrity of the skin is very, very poor, very low, such that a simple brush or scratch can cause a very severe wound and, you know, is very difficult to treat because it doesn't heal. The patients who enrolled in this study, we were taking all comers. We were looking to validate what we saw in preclinical testing that this drug has an impact on pain, on itch, on inflammation, and helping to heal these wounds.
However, the patients that enrolled were primarily non-wound itch, so they would have just a very, you know, severe chronic itch area that, you know, because of the lack of integrity of the skin, they couldn't really do anything about. You can't scratch it 'cause you'll just open the skin and cause a wound there. So it may sound like, you know, nothing important for us, but for patients with this disease, it's very severe. Chronic severe itch, you know, presents itself in a number of other diseases as well, not just epidermolysis bullosa. We had 18 patients were clinically assessed, and 12 of those had a meaningful improvement in their itch score. We used a very high, what's the right word?
Very good skin cream, that, you know, would in and of itself actually help just because the moisturizing content of the cream itself would probably help reduce itch in some instances. Nevertheless, despite this very, very good cream that we used, which had its own effect, on top of that, the addition of INM-755 had a clearly more meaningful effect in these patients, you know, above and beyond what the cream alone would have done. This is an interesting opportunity. You know, it falls into the category of we can't do everything at the same time. We're looking for a partner to move this into phase III clinical testing.
You know, we you know, don't have the resources to be able to do that ourselves. You know, that search continues, and you know, hopefully we'll be able to find a happy home for this product because we think it holds a lot of promise in severe chronic itch. Corporate standpoint, we have a very experienced pharmaceutical drug development team, starting with discovery all the way through to commercialization. You know, we're small, but we're very robust and have very experienced individuals in their respective fields of expertise. Board of directors, everything from small biotech to large pharma, including a Wall Street representative.
We have a very active board who, you know, likes to roll their sleeves up and get involved with the company, and we're very excited to have them all on board with us. Just a financial snapshot, the reporting as of December 31. About $7 million in the bank. That's enough to get us into the fourth quarter of this year. Shares outstanding, this is a, you know, fully diluted at about 7 million, so very low float. Of course, you know, the way the markets have been over the last year, you know, we've been on that roller coaster as well, with the market cap, you know, somewhere around $4 million at this point.
You know, incredibly low for a company that has the technology that we have, you know, the team that we've assembled, the cash that we have, and, you know, just the opportunity in the right disease categories with very strong product candidates. Key value drivers. Both INM-901 in Alzheimer's and INM-089 in dry macular degeneration are on essentially the same timeline at this point. For INM-901, which we are prioritizing, we're targeting a pre-IND meeting with the FDA in the third quarter of this year. We need to complete some additional IND-enabling pharmacology and toxicology studies. You know, we look to be in clinical trials in 2027. You know, from a preclinical standpoint, we've shown just about everything I think we can show.
We can, you know, do additional studies, but we don't think it's gonna convince us any more that we have a very important candidate here. We wanna get to human trials as quickly as possible. Similarly, INM-089 on the same timeline, you know, maybe a quarter behind. You know, it's gonna come down to our ability to attract the funding that we need to develop two products at once. Otherwise, we will be focusing on INM-901. We have the ability to discover other novel candidates for other diseases, and we have a very nice patent portfolio protecting some of that. You know, as things develop, we'll be looking at possibly developing other candidates.
You know, equally important is, you know, trying to execute on strategic initiatives that include things like strategic partnerships, co-development opportunities, and of course, investment to be able to accelerate these programs as much as possible. We think we have the right candidates, we have the right people, we have the right company in place, and now we just need to execute. With that, I will stop and throw it over to the moderator.
Great. Well, thank you very much, Eric, for the presentation. We have time for a couple of questions. Let's start with that slide you just shared around the milestones.
Sure.
Sounds like one of the most exciting milestones is that pre-IND meeting for INM-901.
Right.
Could you talk a little bit about, you know, kind of between now and that meeting, what you're looking to put together and, you know, sort of any risks that there are to staying on the timeline?
Yeah, there's not a lot of risks at this point. We have to assemble all the data that we have thus far on the product into the proper documentation to conduct the pre-IND meeting. What we wanna do is get in front of the FDA, you know, kind of introduce the product and the program, talk about the pathway that we foresee, talk about the data that we've assembled, and, you know, basically say, "Listen, this is what we're thinking. Does this align with what the expectations are of the FDA?" Are there any ways that we may be able to accelerate things?
I mean, most importantly, you know, can we find a pathway that we both agree to, you know, as we approach human clinical testing that may be able to, you know, move us quicker down the timeline? We continued to conduct some of these IND-enabling pharmacology and toxicology studies. We have an ongoing one with, you know, kind of a dose-ranging study in two species. We're doing the work. It's all gonna dovetail together, you know, as we advance over the next couple of quarters.
Great. Thanks. Then one more from the audience. You mentioned the strong IP portfolio. Could you talk a little bit, yeah, about, you know, sort of what you own and how that sets you up for go-to-market strategy of either in-house or sort of out-licensing?
Yeah. You know, the key patent is around these particular class of compounds and the ability to modify them in a way that may enhance their clinical efficacy, or maybe even enhance how they're formulated or delivered. We have a very broad patent there. We have a number of other patents that are related to the use of these compounds, that are related to the manufacturing of these compounds. You know, we're very well positioned to advance these knowing that we have very significant freedom to operate in the space that we're active in. In terms of out-licensing, you know, if.
Just to give you an example, if someone were to say, "We think the CB1, CB2 pathway may be an interesting target in X disease," you know, we could work with someone to develop a suite of compounds that they can then test, you know, leading to finding a drug target, compound that can then be further developed. We're very well situated for that, where we're very good. We have a great deal of expertise in how to make these compounds, which is not as straightforward as you might think. You know, we're very glad to have that. Most companies our size, you know, they don't have the, what's called CMC, the chemistry manufacturing control component. We're very well suited in that arena.
Great context. With that, we are at time. I'd like to thank you, Eric, for sharing the InMed Pharmaceuticals story with us, and also thank everybody listening for spending time with us today.
Thank you.