Hello, everyone. Welcome back. I now have with me Greg Gorgas, the President and CEO of Artelo Biosciences. So Artelo is a lipid signaling company with a focus on cancer supportive care. This is an area that we don't think gets enough attention in favor of cancer therapeutics, but it can often be just as important to ensure that a patient can remain on and tolerate treatment as it is to ensure that the treatments they're getting are actually effective. With that, Greg, why don't you give us a brief two to three-minute overview of what Artelo does? Thanks very much for the opportunity, Michael, and to be with the Maxim team. It's our privilege. Artelo was founded in 2017. It was founded on the promise that if we modulated the lipid signaling, or more specifically, the endocannabinoid system, we could affect human health and bring medicines to the market for which there's no FDA-approved treatments. And one of the lead assets, which I hope we'll get a chance to talk about, is for cancer-related anorexia or cachexia. No FDA-approved treatment for that. Our second program going into the clinic is for chemotherapy-induced peripheral neuropathy. That affects cancer treatment for a number of people. And then, more broadly, our platform has expanded beyond just cancer supportive care to direct treatment for cancer or dermatologic conditions or some CNS conditions, so we've really been pleased with the expansion of our franchise. All right. Thank you for that overview. Now, there may be some perception out there incorrectly that Artelo is in the cannabinoid space, and while you do have some targets that are targeting the endocannabinoid system, it really is an incomplete picture. Now, this may be a bit more complicated than something we can cover in a 25-minute conversation, but I think if we could start out high level, could you give a brief description of what exactly the role that lipid signaling plays in disease and the treatment of disease? Yeah, I appreciate that, and there is misperception because when you say the word cannabinoid, people think of cannabis, and we are not a company that has ever touched the plant, nor do we intend to. But our bodies are built with an endocannabinoid system. That system is part of a large, complex system of really where lipids play a very important role in the body. Lipids are the biochemical compounds that we know that include fats and oils. A lot of people think of omega-3 fatty acids, or they get a lipid profile done when they get their blood work, or they've heard the term lipidomics. Lipids are very important in the body in that they form the phospholipid bilayer of cells. So they're responsible for cell structure. They're how cells consume energy, but they're also how cells communicate. Mm-hmm ... within themselves and with each other. It's known for a long period of time that this is a very, very interesting druggable target, and because lipids are so important in almost every aspect of our body, it's a really interesting area for development and it wasn't until the folks at Stony Brook University were able to identify specific and potent chemistries that modulated lipid signaling that we were able to really unlock the opportunity to build drugs in this space. Mm-hmm. Now, we've done. You know, because we're a leader in this area, we've really enriched our science page of our website, and so for. You're right. In 25 minutes, we could spend all of that time just on this one question. We would just invite people to go to artelobio.com, flip to the Science page, and read about the promise of lipid signaling. Mm-hmm. And with that, I'd like to transition and start talking about your lead asset, ART-2713. To start off, could you just talk a little bit about what exactly is cancer-related anorexia and cachexia? This is actually an area where we've seen Pfizer move in. They have a monoclonal antibody, suggesting that the unmet need there is significant enough to justify the cost of bringing forward a biologic. So why is this such an important aspect of the disease to treat? I've been almost, it's 30-plus, and it's approaching 40 years in the space. There has never been a drug to treat cancer anorexia. Anybody that's been around this, the space or been around cancer patients know of which I speak, and if you haven't, you at least can recall pictures of Steve Jobs or Toby Keith or others that are more famous and in the news that have experienced cancer, and you've seen them basically shrivel up and pass away. Unfortunately, that's a very common experience, and it's not an uncommon experience for those that are experiencing cancer. In fact, it's estimated that up to 80% of late-stage cancer sufferers suffer from what is known as cancer anorexia-cachexia syndrome, or CACS. Mm-hmm. I'll just describe what that is. It's a loss of appetite. It's a loss of weight. It's a loss of fatty tissue. It's a loss of muscle. It's a loss of quality of life and an actual loss of life itself. Not only are there no FDA-approved treatments for cancer anorexia, there is no recommended off-label treatments by the American Society of Clinical Oncology. Mm-hmm. Physicians are resorting to milkshakes. They're resorting to nutritional counseling, maybe short course of steroids, which can be immunosuppressive, but there's really nothing good to treat this. So no wonder Pfizer is in the space, and we're pleased with the results. If anybody that cares about cancer patients, as we do, you would be thrilled with... They were able to show in their phase II study that you can, at their very highest dose, affect the appetite and the weight gain of cancer patients. Mm-hmm. We have a small molecule, in contrast to a biologic, and naturally people think of, you know, pricing comparisons to that. Listen, we're rooting for the cancer patient. We believe if our drug also shows similar results to Pfizer's, they could be used in synergy. There are different mechanisms of action. They could be used sequentially, and it might be that you prefer the less expensive one to start off for those patients at risk. So we believe there's room for both of us, and we're just happy to see, not only in our results, but in their results, some eventual movement in this space, and after 40 years, and having a mom and a mother-in-law that passed away of cancer, I can tell you that this also means a lot to me personally. What kind of link is there between CACS and cancer outcomes? We do know that those that are able to maintain their weight do actually live longer. Our trial, and same with Pfizer's, is only three months. Mm-hmm. We're not really measuring survival in that three-month period. These are all patients that are expected, both in their trial and ours, to have a life expectancy in excess of the duration of the study. We're not directly measuring survival. Whether the journey is towards survival or it's a journey towards hospice and eventual death, quality of life is important in all of these patients, and if you're well enough to fight, you know, and take chemotherapy and not have the dose reduced every time you visit your physician, there may be a promise in there. I don't want to overpromise on this. Mm-hmm. What we're aiming to do is address quality of life and the weight gain in those patients today. It'll be long-term studies to see whether Pfizer's drug or ours or anybody else's can affect survival. But what exactly is the mechanism for ART-2713 in this indication? It's interesting to ask that because everybody thinks about the weight loss drugs right now. Yeah. With the weight loss drugs just make you feel not hungry, and you're satisfied, or you're not hungry. So it's an off switch. Basically, those drugs are an off switch. I'm summarizing, and then it's very pedestrian the way I'm saying it, but it's an off switch for the hunger sensation that the patients are experiencing. Ours is the opposite of that. It's an on switch. So it targets receptors in the gut region. It's full of these cannabinoid receptors. People know when they take, for example, and I'm not linking us to cannabis, and our drug doesn't even mimic something that's in cannabis, but cannabis users have gotten the munchies, again, a pedestrian term. And so we know that targeting these receptors does cause an appetite stimulation. The problem with cannabis is it also has some side effects that cancer patients really aren't desiring, and so what's interesting about our drug is not only is it an on switch as opposed to an off switch for that appetite stimulation, but our drug, excuse me, is also peripherally selective, meaning it gives you the medicinal benefit below the neck, but none of that psychoactivity that plagues cannabis above the neck, so it's the hunger without the high, and we- Mm ... think that that is really interesting, for the cancer patient. Do you talk about any prior data that is out there that supports the mechanism and supports this for weight gain? This is not originally our drug. It was originally AstraZeneca's drug, and AstraZeneca developed it, was developing it as an anti-pain drug, and one of the side effects they saw in their five Phase I studies was profound weight gain. In fact, the weight gain, we have the slide up on our website, shows a contrast between those getting placebo and those getting active drug with a p-value of 0.0001, and that's anybody that understands statistics knows that's pretty significant, and this was just in 12 days. It was on the basis of that we said, as cancer drug developers or cancer supportive care drug developers, this is something very, very interesting. Cancer patients are quite beat up. Mm-hmm. And so, not only having something that stimulates appetite but also works in the periphery and doesn't cause profound side effects is also something important as we consider development of this drug. Mm-hmm. So that actually transitions into the next question that I wanted to ask you because it seems like the drug is somewhat de-risked based on that previous data from an efficacy perspective. But as you mentioned, these are fragile patients, so safety is especially important. Have you shown any safety issues or tolerability issues, or is there a relatively clean profile for ART-2713? I'm glad you asked that, because it's been the one of the bigger surprises to us. Our safety profile in the cancer patients, you know, AstraZeneca was treating people with low back pain or molar extraction pain. Mm-hmm ... pain patients, otherwise healthy volunteers. We're going into fragile, cancer patients. And we started at extremely low doses, 150 micrograms, and escalated up to 650 micrograms. I'm happy to report that in our phase II study, there were no dose delays, no dose reductions, no dose continuances due to side effects. There were no grade three or four toxicities reported. There was one patient that had some mild diarrhea that took some Imodium, but continued on with their therapy for their full course, and so we're very, very pleased. And now in the phase II, we start at 650 micrograms in the same patient population, and escalate up to 1,300 micrograms, and to date, we have not seen any of that. Mm ... toxicity that we were, you know, thought might have been a concern at the beginning of the trial. So we're very, very pleased with the safety profile that we've seen to date with it within the Cancer Appetite Recovery Study, which is our phase I/II study that's ongoing at the moment. Now, as you mentioned, you have a phase I/ II that's ongoing right now. Could you just give us an update on where that is? What are the timelines for data, and then what sort of endpoint? 'Cause you're in the phase II portion now, correct? Yeah, so we added in the phase II portion a little bit more than we had in the phase I. So we're measuring lean body mass- Mm-hmm ... appetite, weight gain, obviously, quality of life, that's a validated questionnaire, and then also, the patients are wearing, it's called a MotionW atch. It's kind of like a Fitbit watch, although it doesn't signal to you, "Get up out of bed," or, you know, "Off the couch," but it just records your activity. 'Cause our expectation is if you're healthier, you're gonna be out of bed more, and we all know that from our personal lives. So those are the measurements in the phase II. We're on track to finish enrollment towards the end of this year. When I say towards, you can look at that, you know, December 31st from the January perspective or the December, but it's real close to that we expect- Mm ... to finish enrollment. Now, finishing enrollment doesn't finish the trial and announce the data, because I said earlier, these patients are on for 12 weeks, and then we have a one-month safety follow-up. So I would expect that we would be able to release data sometime next summer on the phase II portion. On the phase I, though, we will be presenting that data at the Sarcopenia and Cachexia Wasting Disorders meeting in Washington, DC, the first week of December. Mm-hmm. So exciting stuff to look forward to on this program. Now, to transition to your novel preclinical compound, ART-2612, this targets fatty acid- binding proteins. So could you describe what these compounds are and what they do in the body? So let's talk about fatty acid- binding proteins. They're exactly what the term says. They're proteins that bind fatty acids. And I said earlier, people take in from the fruits, nuts, vegetables, animal protein, fatty acids, it's what cells, you know, use for energy. But they don't migrate or signal without a chaperone or a helper. And the analogy that I like to use is maybe an envelope or a package, where you put the contents, in this case, the fatty acids, in the envelope, and then shuttle that envelope to, you know, through the postal system of our bodies to where it belongs. Other people have used an Uber driver analogy. They've used a taxi driver analogy, a bus driver analogy, but all of those analogies are just meant to show that you're carrying the payload or shuttling it to its, its location, and that's exactly what fatty acid- binding proteins do. We're the leading company in the world in inhibiting fatty acid- binding proteins. You might say, "Well, why would you wanna inhibit something that normally functions well in the body and, and does what it's supposed to do?" It is, but let's say in cancer, breast cancer, for example, you can have 20 times that of normal buses, taxis, envelopes, packages, whatever you wanna call it, but carriers of fatty acids- Mm ... that's feeding cancer. And so when it's overexpressed or upregulated, you wanna bring that back down to a normal level. And so the mechanism is when that's out of alignment, to bring that back into alignment, and that can have potential therapeutic benefit. Now, the reason I say we're the leading company is we're the first in with an FDA approval, an IND, an investigational new drug approval, to go into the clinic with a selective fatty acid- binding protein 5 inhibitor. And so that's pretty exciting for the industry. It's pretty exciting for the target that others have searched for. It's exciting for the folks at Stony Brook University, but I think it's most exciting for those of us here at Artelo. Now, there are a number of fatty acid- binding proteins out there. Mm. So why go after FABP5, and in particular, how does this play a role in your lead target, chemotherapy-induced peripheral neuropathy? Okay, so there are 10, let's call them 10 buses, and, you know, sometimes you take bus number three, the bus number five. It's a overly simplistic way of... Because I'm not being fair to the biology here. But different fatty acid-binding proteins, isoforms, FABPs, let's say five, manage a certain lipid profile, and others might be with different lipid profiles. And we also know that they're found in different locations in the body. So FABP7 may be expressed more in the CNS, FABP5 in the periphery and work better for pain. So it depends on the disease you're going after, and the isoforms and the inhibitors. And not all FABP inhibitors, FABP5 inhibitors are created equal, too, and they also filter lipids in different ways based upon our different chemistry. I would say, with a little bit of pun intended, this is the artistry at Artelo, and there's a little pun in there, but, it's what our scientists are exploring. It's what's got potential partners very excited about the science that we're developing, and it's given rise to new intellectual property that we've filed around this as well. So I hope that answers, Michael, your question to some degree. Now, how common is it for cancer patients undergoing chemotherapy to experience peripheral neuropathy? It's very common. In fact, 40%, and just think about that, four out of every 10 cancer patients experience peripheral neuropathy, but it's more pronounced with certain types of chemotherapy, so for example, the platinums or taxanes, which are very common in, let's say, colorectal cancer treatment or breast cancer treatment, it can be 80%-90% of those patients experience peripheral neuropathy. Just think nerve pain, nerve pain that is fast onset, usually within the first 30 days of treatment. It can last many, many years, even after treatment. It's so painful that most cancer patients will say to their physician, "Switch me off of this chemotherapy, or stop this chemotherapy for a while," 'cause the pain is so unbearable. You can't even open a refrigerator door, go in and grab a carton of milk or a glass of milk without putting a glove on. It's that intense a pain. In fact, physicians have said, "I know if a patient's experiencing it, because they show up for their appointments in slippers rather than tying their own shoes," so it is very common, and it is for which there's no FDA-approved treatment, and so this is something that I think has to be addressed for cancer patients, and we're thankful we have this opportunity. Yeah. No, it seems like another case where you need that support in order to get these patients to complete their treatment regimens. Now, what have you demonstrated preclinically? Are there any preclinical models out there for CIPN that you've completed? Yeah, so remember I said it's nerve pain, and we have five preclinical studies that we've completed in peripheral neuropathy. Some of them have been prevention studies, where we actually treat concurrent with the onset of the chemotherapy, and we've been able to prevent it. Some are treatment after it's already started, and one of those studies was with diabetic neuropathy, which is caused by a disease, not an assault of chemotherapy. I'm most excited about the prevention opportunity, because if we can give cancer patients the ability to prevent this from happening in the first place. Those that have experienced pain know if you can get in front of pain, it's much better than trying to react to it and treat it. We also put out data this last summer on cancer bone pain. I believe this was in breast cancer patients. Could be in a colorectal. I'm confusing a couple things in my head, but it doesn't matter. It's up on our website. The press release is there. You can verify on the data, but it... the data looked really good in cancer bone pain as well. So, and we have an ongoing study in osteoarthritis right now. So it seems across a number of potential pain indications, this drug looks very promising. What other areas do you expect that this could be potentially effective, looking beyond cancer? Well, I mentioned cancer. Yeah, I mentioned cancer earlier, Michael, and that was because this envelope or bus driver carrier it seems to be relevant in a number of cancers. A number of cancers, not just breast cancer that I mentioned, but colorectal, ovarian cancer, just to name a few. We have data in anxiety where this approach inhibiting fatty acid-binding protein 5 looks very promising. We have data in psoriasis that's already been publicly announced. We're doing an atopic dermatitis study as we speak. And so dermatology is another field. And so I've mentioned anxiety, cancer, dermatology, and of course, pain and inflammation, which we've just covered. That could be with the same compound, ART-2612, or it could be from our extensive library. We have over 100 of these compounds that we've licensed in and are covered under our rich patent estate. Now, what sort of IP do you have out there for FABPs? And then could you touch just a little bit on the competitive landscape? You mentioned that you're at the forefront, but is there anyone else that's looking down this path? Yeah, no one, no one directly with an FABP inhibitor. We licensed an entire library from Stony Brook University. And so we got a lock on this early in 2000- late 2017. We have 15 issued patents, both in the U.S. and outside the U.S. And 26 patents that are either filed by Stony Brook, licensed to us exclusively, or our own patents from our own inventions as partners with them in this process. So if you add those two together, you're over 40 patents if they were all issued. We don't perceive there to be a risk on that. So it's worldwide, it's to the target, it's to the compositions that we own, as well as the uses in the different disease areas that I've mentioned. All right. And you do have a third program out there. We can't talk about it too much, as we are coming up on our time, but I would like to see if you'd just touch briefly on ART-1211, and why co-crystallization is so important when you're talking about a CBD-based asset. Co-crystals are not new, but let me just give you a couple of brief bullet points. One is that CBD, and this is the backbone of this co-crystal, CBD is an important drug. Jazz thought so. It paid $7.2 billion for it when it was acquired. It's FDA-approved for two rare forms of childhood epilepsy. Anybody who, like I did, watched the FDA review this and saw the impact that it's had, not only on children, but families, would see how important of a drug. But it's not a very good pharmaceutical drug. It's got very low bioavailability, poor absorption, and it's not delivered in a convenient tablet form. Mm-hmm. It's in a liquid. We wanted to set out and fix that and fix the pharmaceutical inelegance that was there, so to speak, and that has to do with polymorphism, which would extend our time, so I won't explain that. The FDA guidance in simplicity is to create a co-crystal. Mm. A co-crystal is a unique form combined with another, a chemical that holds it in a particular shape. What we found from creating a co-crystal... By the way, there are 20 other co-crystals that are in the marketplace today. Blockbuster drugs like Lexapro, for example, was a co-crystal. There are four main advantages that we have. One is we have an issued patent both in the United States and in jurisdictions around the world through the end of 2038, which means if somebody wants to build a co-crystal just like ours, they violate our patent estate. That gives us a good chance of market exclusivity. Second is that we have better physical properties. Right now, we have multiple formulations, solid tablet forms, that we can go into the clinic next year, one of the big milestones that we have coming. Third is that we've shown in both rats and dogs, pharmacokinetic improvements to our drug. And last but not least, multiple studies in anxiety and depression, these are mouse or rodent models of anxiety and depression, where one-third of the amount of CBD in the co-crystal is able to provide efficacy, and three times that amount of CBD is either deleterious or has no effect in these models, and we've done that consistently. So the pharmacology is fantastic. This is an A student in our portfolio, that every time it gets tested, it comes in with an A on its scorecard, and I think it's a real sleeper value driver within the Artelo franchise. All right. Greg, we're coming up on our time here, so thank you so much for being with us. Before we close, just give me 10 seconds. What is the next event that investors should watch for Artelo for? We said that we're close to finishing enrollment of phase II of the cancer anorexia study, and we are in startup mode for the single ascending dose study with the fatty acid-binding protein 5 inhibitor, and both of those are competing for data towards in the second quarter of next year as data releases, as one of five potential clinical readouts next year. All right. Thank you very much, Greg. Thanks, Michael.