IGC Pharma FY 2025 Earnings Call - IGC81 Shows Early Agitation Relief and Potential Disease Modification in Alzheimer's

Conference Operator: Ladies and gentlemen, greetings and welcome to the IGC Pharma Fiscal Year End 2025 Shareholder Update Call. At this time, all participants have been placed on a listen-only mode. If you have any questions or comments during the presentation, you may press Star 1 on your phone to enter the question queue at any time, and we will open the floor for your questions and comments following management’s remarks. It is now my pleasure to turn the floor over to your host, Roslyn Christian, with IMS Investor Relations.

Roslyn Christian, IMS Investor Relations, IGC Pharma: Thank you, and I want to welcome everyone to the IGC Pharma Fiscal Year End 2025 Shareholder Update Call. For those calling in by phone, a slide presentation to accompany today’s remarks is available on our website at igcpharma.com. Before we begin, I’d like to remind everyone that this conference call may contain forward-looking statements based on our current expectations and projections regarding future events and are subject to change based on various important factors. In light of these risks, uncertainties, and assumptions, you should not place undue reliance on these forward-looking statements, which speak only as of the date of this call. For more details on factors that could affect these expectations, please see our filings with the Securities and Exchange Commission. On the call today with Ram Mukunda, CEO of IGC Pharma, and Claudia Grimaldi, CFO.

The team will provide an update on the business, followed by a question-and-answer session. With that, I would like to turn the call over to management. Please go ahead, Ram.

Ram Mukunda, CEO, IGC Pharma: Thank you, Roslyn, and thank you all for participating in this conference call. We have about 20 slides that I would like to present as part of our year-end shareholder update. To give you a brief overview, as many of you know, IGC Pharma develops therapies for Alzheimer’s disease and other chronic conditions. Our lead asset, IGC81, is currently in a phase two trial for agitation in Alzheimer’s dementia, and I will present some data that shows that we are also advancing this towards trials as a potential disease-modifying therapy. We have worked this year on an AI platform and integrated AI into our R&D program, and we’ve also worked on an early detection system for Alzheimer’s that I will go over. During part of our AI exercises, what we discovered was that one of our Alzheimer’s candidates is potentially also a GLP-1-based candidate.

It’s an agonist at GLP-1, which opens up the market for metabolic disorders. The operational highlights for the financial year 2025 include significant progress on the Kalma trial. That’s our phase two trial on agitation. We’ve added several new sites, as I will show you. We’ve also advanced IGC81 as a disease-modifying therapy. We worked on our new diagnostic model, which we’re calling MINT-AD, and we’ve also grown our pipeline into the GLP-1 portfolio. To give you an update on the progress on our phase two trial, just to remind everyone, agitation in Alzheimer’s dementia impacts about 76% of Alzheimer’s patients. There are about 50 million Alzheimer’s patients worldwide and about 7 million in the US. Agitation in Alzheimer’s is a group of very hard-to-manage behaviors, and these include physical aggression, verbal aggression, wandering, pacing, excessive motor movements, among several other behaviors. Now, these are not just hard to manage.

Agitation leads to long-term hospitalization, leads to separation of families, higher mortality, higher use of medications, and it has been shown that it accelerates cognitive decline. Currently, there is one FDA-approved medication. It’s called Brexpiprazole. It costs around $17,000 a year, and it takes about 6-10 weeks to work. It comes with a black box warning. It is also an atypical antipsychotic. Our phase two trial currently is about 146 participants. It’s a multi-center, double-blind, randomized placebo-controlled trial, and the primary endpoint is to look at agitation or the reduction in agitation compared to placebo at week six. Separately, we are also looking at agitation at week two. The inclusion criteria is essentially the patient has to have Alzheimer’s, and the patient also has to have clinically significant agitation.

We use a scale called the NPI to essentially grade the patient’s agitation level, and they have to score a four or more in order to participate in the trial. As I said, we currently have about 22 sites. In financial year 2024, we added several of the sites in the U.S. as well as in Canada. In 2025, during the financial year, we added several more sites, and subsequent to the financial year, we added more sites. Currently, we have about 22 sites, and part of the reason why the trial initially was a little bit slow is because this particular patient is very difficult to recruit. They’re highly agitated, and our patients live at home with a caregiver, so essentially we’re targeting and we have to recruit the dyad, the patient and the caregiver. It’s been a difficult process.

However, we have increased our reach considerably by using geotargeting around each of these sites where we now have Facebook ads targeting patients that live within a 15-minute radius, and then we are going to expand that to about a 30-minute radius and then to a 45-minute radius. This is now starting to work, and we are starting to bring in a lot more patients to each of these sites. I am very confident that we can accelerate the completion of this trial. We did release interim data on the first 30 patients, and what we found is very encouraging. We found that our medication acts within two weeks. If you look at this particular slide, the magenta-colored graph or the line is our active medication compared to our active placebo, which is the blue line.

As you can see, in week two, there’s a considerable difference between the placebo group and the active group, and that difference continues through to week six, which is our end of trial. When you compare this or when you overlay this, and this is not a direct comparison with the existing drug, but if you overlay this with the published results from the approved drug, what you see is the approved current medication takes about six weeks to start to act. At week two, there’s practically no difference between their placebo and their active, which is marked in the black that you see on this particular graph. We have statistically and clinically significant reduction of agitation at the end of trial, which is week six, and we see a very strong indication that our medication works as early as week two.

This is a striking differentiator between our medication and the existing approved medication. Now, to remind our shareholders and the participants, in preclinical research, what we had found is that our medication modifies amyloid as well as tau. These are the two hallmarks of Alzheimer’s. These are plaques and tangles. What we discovered is that our medication is a potential disease-modifying drug. When we went to phase one, we also discovered that it reduces neuropsychiatric symptoms, and that’s why we launched a phase two on agitation, which is one of the neuropsychiatric symptoms, and we slowed down launching a trial on IGC81 as a disease-modifying therapy.

What we see is from the preclinical and some of the data that we’ve gotten from phase one, as well as from the interim results on phase two, that this drug is potentially a disease-modifying therapy because it reduces plaques, it reduces tangles, it also enhances mitochondrial function in an Alzheimer’s. We found that in an Alzheimer’s mouse model. It improved spatial memory in an Alzheimer’s mouse model. It crosses the blood-brain barrier, and it also supports long-term, it has long-term neuroprotection properties. We are looking at this drug. We are now preparing this as a disease-modifying. We will be launching a trial on IGC81 as a disease-modifying therapy.

Looking at our current, just to remind everyone, again, agitation in Alzheimer’s, the way we got here was even though the preclinical data pointed to disease modification, our phase one clinical data showed that we had clinical and statistically significant decreases in neuropsychiatric symptoms, including in agitation. We launched our phase two on agitation. This year, we did a lot of work on our AI diagnostic platform, and essentially what we’re doing is we are downloading and curating and harmonizing a total of about 108 databases from around the world. We’re using these databases to train an Alzheimer’s model with three aims. One is to identify groups with high risk factors for Alzheimer’s. We’re looking at groups of risk factors for Alzheimer’s. The second thing that this model will do is to predict cognitive decline two to five years in advance.

The idea behind this model, behind this AI model, is to deploy it as a doctor’s tool to help general practitioners diagnose their patients. What we found is that in Alzheimer’s, false negatives are very high. To give you an example, a patient walks into a general practitioner’s office, and the caregiver might complain that, "Oh, this person’s forgetting things," and it might get attributed to aging or a normal part of aging. In fact, that person may actually have cognitive decline, and that person may actually be coming down with Alzheimer’s.

This model will allow the doctor to be able to input various factors, various elements, including clinical data, demographic data, and the model will then group those into risk factors and say, "This particular patient is at a high risk or at a moderate risk or at a mild risk for getting Alzheimer’s." It will predict cognitive decline in a timeframe of two to five years in advance. We think this model is very exciting. We’ve already tested the model, and based on the initial results that we’re getting, we’re very excited that this model will actually work and be very useful for doctors. We’ve called this model MINT-AD, and MINT stands for Multimodal Interpretable Transformer for Alzheimer’s. We’ll be releasing a lot more news about this model throughout this financial year.

Just to give you some highlights on our team’s achievements, we were recognized by the NIH for innovation. We were selected as one of the top 15 finalists in the NIA, which is the National Institute on Aging Prepare Challenge for Early Alzheimer’s Detection. We’re very proud of that. The beta version of MINT-AD is up and running, and it’s able to differentiate, and it’s able to look at risk factors and identify risk factors. We also used AI tools to discover that one of our Alzheimer’s candidates is also an agonist at GLP-1. Now, that potentially opens this drug up for other metabolic disorders. We have about five platform drugs: IGC81, which is in a phase two. We have LMP, which targets neuropsychiatric symptoms and AD pathology. We have the TGR platform, which targets amyloid plaque, and that essentially is for early to moderate Alzheimer’s.

We also have IGCM platform, which targets both plaques and is a GLP-1 agonist. The IGCC platform targets tau, and it also targets GLP-1. These are our other platform drugs that we are currently developing. As I mentioned, one of our drugs is a GLP-1, and this could potentially help us target a multi-billion dollar global market for things like weight management or type 2 diabetes. There are considerable synergies between neuroprotection and metabolic regulation via the GLP-1, so it is not unusual that these molecules would actually target GLP-1 as well. We have a very diversified pipeline with GLP-1 candidates as well as Alzheimer’s candidates that could capitalize on emerging markets and create substantial long-term value for our shareholders. On the financial front, we are very focused on minimizing dilution and maintaining a clean cap table. We have renewed the $12 million line of credit that we have.

We are funding our business through selective capital raises, and we’re very focused on deploying capital efficiently to advance our drugs through clinical trials at a low cost per patient. To give you an example, in a phase two trial, typically costs between $100,000-$150,000 per patient. We’re able to do this for about half the cost. We have an in-house CRO or a clinical research team that manages these trials, and we’re able to keep the cost very low. We have multiple pending clinical and AI milestones that we hope will lead to a reduction of the cost of capital for the company. In addition, the board has aligned management’s incentives that include stocks, options, and bonuses with those of the investors. We now have performance-based stock options and bonuses. There are several upcoming milestones that you should be focused on.

One of them is to initiate high-end enabling studies for expanding our pipeline. Second would be to complete the phase two trial and to expand IGC81 as a disease-modifying treatment with phase two trial targeted for late calendar year 2025. With that, I’d like to thank everyone for participating in this conference call. Operator, please open this up for questions. Certainly. Everyone at this time, we’re conducting a question-and-answer session. If you have any questions or comments, please press star one on your phone at this time. We do ask that while posing your question, please pick up your handset if you’re listening on speakerphone to provide optimum sound quality. Once again, if you have any questions or comments, please press star one on your phone. Please hold while we pull for questions. Thank you. Your first question is coming from Gene Carter from Old Mill Capital Partners.

Your line is live. Hey, guys. Thanks for taking my questions and congrats on all the progress. Just a couple for me. Could you provide us with a bit more insight into the competitive landscape, specifically what other drugs that are available to Alzheimer’s patients right now? Gene, thank you for that question. Yes, the current Alzheimer’s treatment landscape primarily includes cognitive enhancers like Aricept, Memantine. These help with cognitive symptoms, but they don’t alter the course of the disease. Recently approved disease-modifying therapies like lecanemab, donanemab for early Alzheimer’s, now both of these target amyloid plaque. These drugs have generated a significant amount of attention, but there are challenges, including cost, delivery via infusion, and strict eligibility requirements tied to biomarkers and imaging. Now, on the agitation side, which is where IGC81 is, agitation impacts, as I mentioned, about 76% of Alzheimer’s patients.

There’s one drug, Brexpiprazole, and this was approved last year. Now, this is effective in some cases, but it does carry a black box warning. It has a late onset, meaning it takes about six weeks to start acting. It’s an atypical antipsychotic, and it’s often used very cautiously because of concerns around side effects in older populations. IGC81, our drug, is differentiated in several ways. For one, it’s an oral investigational therapy. It’s a liquid formulation that individuals would take one dropper full in the evening and one dropper in the morning. That’s the dosing that we’re currently testing in the phase two. So far, all of the data shows that it’s well tolerated, and it’s potentially multifunctional. That means impacting agitation, but also helping with sleep. And based on our preclinical data, it could also impact core neuropathological features like neuroinflammation, mitochondrial dysfunction.

I think IGC81 can be positioned as a complementary or alternative solution to current options, particularly in symptomatic management where there are very large gaps currently. Got it. That’s very helpful. Thank you. You guys have added some trial sites over the past six months, as you mentioned. Do you feel that you have enough sites to complete the current trial, or do you anticipate having to add additional sites? Gene, currently, we have about 22 sites under contract, and these are mostly in the US, and we have several in Canada. We are now currently using a geotargeting strategy around each of the clinical sites. What we do is go on to Facebook, and we use Facebook targeting around, right now, it’s about a 15-minute or a 20-minute radius around each of the sites.

This has increased our registrations and enrollment by about 200%. Our aim is to keep expanding this and increasing the radius, say, from 15 minutes to maybe 30 minutes to 45 minutes. We are hoping that we can expand our enrollment to about 500%. Based on the current recruitment, current velocity, which we are adding, the existing sites are projected to meet our enrollment targets. We anticipate maintaining the current site network. We do not plan to add new sites. However, if enrollment slows or there are unforeseen delays, we have contingencies. We have talked to other sites as well in the northeast and in the Midwest. We would be able to very quickly add more if they are needed. Got it. Makes sense. All right. That is very helpful. Congrats on the progress again, and thanks for taking my questions. Thank you.

Your next question is coming from Ed Wu from Ascendient Capital. Your line is live. Yeah. Congratulations on all the progress. My question is, you mentioned that you’re going to use Facebook to do the geotargeting. Is that going to increase the cost of the clinical trials to have to utilize this social media for recruitment? Ed, that’s an excellent question. We have done the calculations, and we are budgeting about $1,000 per new recruited patient. So we’re almost halfway through. We need another, call it 80 patients to complete the trial. So 80 times $1,000. That’s sort of our budget. It is not going to increase the cost of the trial considerably. It will add, it’ll increase it marginally. That sounds good. Have you given an updated timeline of when we may expect either the next interim data or for the completion of the trial?

Ed, we do not plan to look at interim data, where we are very encouraged by the interim data on the first 30 patients. As you know, we had very good P-values at the end of trial. We had P-value of less than 0.05, which essentially means that the trial is going well. There is a differentiation between the active group and the placebo group. We also saw excellent results, very low P-values for sleep, both at two-week mark as well as at the six-week mark. We are very encouraged by the interim data that we already saw. We do not plan to do another interim look. If we were to do that, there would be a penalty, and we would have to increase the number of patients. To avoid the penalty, what we are going to do is focus on completing the trial.

We are very confident at the current rate at which we’re going that we’re trying to get this trial done this fiscal year and get the results out. Great. Thank you, and I wish you guys good luck. Thank you. Thanks, Ed. Thank you. Your next question is coming from James Malloy from Alliant Global Partners. Your line is live. Hey, Ram. Thanks for taking my question. What’s the current expectation for the Kalma trial top line? I think with last guidance, maybe I missed it, was last guidance in February was suggesting maybe second half of this year. Any updates on that? And then for the plaque tangle trial, could you walk us through what that will look like and sort of size, cost, and time to run that, please? Thank you. Thanks, Jim.

As far as the current Kalma trial is concerned, I think we are almost halfway to—we expect to finish the trial this fiscal year, meaning March of next year. That is sort of our timeline. Internally, we are more aggressive, but I think that is a pretty good indication as to when we think we can finish that trial. The other areas, what we found is IGC81 has a lot of potential as far as amyloid or tangles or mitochondria are concerned in Alzheimer’s. That is something that would position IGC81 as a disease-modifying therapy. Our aim is to run a phase two trial. We are looking at several different trial designs. There is one thing that we do need to finish before we can launch that particular trial.

We’re talking to a couple of different universities of teaming up and even applying for grants to do that particular trial because there is a lot of interest around amyloid therapy. There’s a lot of interest around tau. And our particular medication, IGC81, has shown that it can work on tau. It can decrease tau. It can decrease tangles and enhance mitochondrial functioning. This is something that’s very unique to IGC81. We’re very excited about that. The phase two trial would be a trial that’s probably around—it would be a pilot study. It wouldn’t be a very large trial. It would be a trial with maybe 50 patients or so. In terms of cost, as you know, we have an internal CRO, and our cost structure is considerably lower than if we were to use one of the larger CROs.

I think I did say that typical trials cost between $100,000-$150,000 per patient, and we’re at half of that. In terms of cost, I think that’s something that’s not going to cost us millions and millions of dollars. It’s something that we can contain the cost and get that trial done. It’s a very exciting area for us because it positions the drug as a disease-modifying, as a potentially disease-modifying therapy. All right. Excellent. One of the key things that hits a lot of Alzheimer’s drugs is ARIA. Any thoughts on—I presume you haven’t seen any indications of that yet. Still waiting on the data, of course. Any thoughts on what you want to see there? Yes. We’ve talked long and hard about ARIA. They are connected to the monoclonal antibodies that are the current two therapies, lecanemab and donanemab.

Our medication is not a monoclonal antibody. We do not expect ARIAs, and currently, we have not seen any. This is something that we think can be very safe and a considerable alternative to the two existing therapies because, as I said, ours would actually target several of the hallmarks of Alzheimer’s. It would target the amyloid plaque, and preclinically, we have been able to show that it targets tangles and increases mitochondrial functioning, which is another pathway to try and get to this disease. That is a very exciting area for us. The safety, obviously, key. How do you think I am positioning versus traditional cannabis that gets used a lot in the space? Personal experience of friends, friends’ parents who are going through Alzheimer’s and taking cannabis, and it is very effective. How does IGC sort of position against something along those lines? Should the drug pan out?

It’s a great question, Jim. There’s a couple of different things to think about. One is that cannabis on its own is not the solution. Our drug is a combination. It includes THC as well as another molecule in a liquid formulation. It is very different from just smoking weed. That is one. Second, the replicability and the actual potency is, as you know, it’s a medication. The tolerance levels are very, very low. The tolerance, it’s in a very—when we say the drug has 2.5 milligrams, it has 2.5 milligrams. It does not have 5 milligrams, or it does not have 1.5 milligrams. That is very important. Replicability is very important. Tolerance levels are very important. It is a medication. The combination is very important.

Lots of differentiators between a drug that we are producing and, as you said, someone that can just go out and get cannabis and use cannabis. The dosing levels are also very important. Smoking cannabis is not something that you would, for example, give—you would not give your 80-year-old or 85-year-old mom or dad cannabis to smoke because they could fall. In that aging population, falls is a very big problem. They could have cardiac issues, lots of issues with just using cannabis. There is a very big difference between a medicine that is produced after a phase one trial, a phase two trial, a phase three trial versus just going out and buying cannabis. Absolutely. Absolutely. Final question then, mechanistically, looking at G&A kind of down in the fourth quarter pretty dramatically.

Is that sort of the levels we should expect going forward or more around the $1 million a quarter level that had been sort of throughout fiscal 2025? No, I think what we’ve essentially done is what I’ve done is to refocus the company or to focus the company entirely on three things. Number one, getting the trial done as quickly as we can. Number two, launching the phase two trial as a disease-modifying therapy. Number three, deploying a beta version of MINT-AD, which is another thing that we’re very excited about because there are 400 million people around the world that have preclinical Alzheimer’s, meaning that they have amyloid plaque buildup in their brain, but they are not showing any symptoms. They are at risk. Currently, you need a PET scan or a recently approved blood biomarker to even detect those.

What we’re developing is an AI model, a foundation model for Alzheimer’s that can, based on clinical data, based on demographic data, based on socioeconomic data, do three things or do two things. One is to cluster the risk factors and say that this individual that walks into a general practitioner’s office is at risk for Alzheimer’s and to grade that risk in terms of mild, moderate, or high. The second thing it would do is to predict and say that in the next two years, cognitive decline based on a couple of different scales is possible. This is sort of the projection going out two years. That helps a doctor to intervene. We’re very excited with that as well. That’s something that we’re very focused on developing.

It can be a tool for general practitioners in America in rural areas where neurologists might not be available or specialized help might not be available, and PET scans might not be available. That is something that we could deploy on the web, and doctors can actually use it to diagnose and as an aid, as a doctor’s aid. We have essentially refocused; we are focusing on these three things. I think that is why the G&A is down, and the G&A has been cut to refocus the company into completing the phase two trial, launching the second phase two trial, and getting MINT-AD to beta testing. Great. Thank you for taking the questions. Thank you. That concludes our Q&A session. I will now hand the conference back to Ram Mukunda for closing remarks. Please go ahead. Thank you. I want to thank everyone for joining our call.

In closing, I want to say that we are committed to addressing one of the most devastating diseases that we all face. For investors, we believe that IGC is at a very exciting juncture with key milestones for the current financial year, where, as I said, we’re hyper-focused on getting the phase two trial done, and positive results from that can potentially move our valuations considerably. We want to launch IGC81 as a disease-modifying therapy, and acceptance by the FDA of that trial would also be something that would move our valuations out of the symptoms area to actual disease modification, which commands considerably higher valuations. We think that MINT-AD on its own is something that’s worth an incredible amount and can also move our valuations. This is a very exciting time for our investors. We want to thank all of you for being with us.

As we have said before, we are building a future. We are not just building therapies. We are not just developing therapies, but we are building a future where Alzheimer’s is no longer an insurmountable challenge. Thank you, everyone. Thank you. Everyone, this concludes today’s event. You may disconnect at this time and have a wonderful day. Thank you for your participation.