We can get started. Thank you, everyone, for joining us. I'm Spencer Kent from the TD Cowen Healthcare Investment Banking team in San Francisco. Pleased to welcome Skye Bioscience today for a presentation, and I'd like to introduce Puneet Arora, Chief Medical Officer of the company, and I'll turn it over to you for the presentation. Thank you very much. Thank you, and thank you for having us here today. I'm here, as you heard, representing Skye Bioscience. I am the Chief Medical Officer. I am an endocrinologist by training, so I'm really delighted to be talking today about obesity and other metabolic disorders and telling you more about our lead molecule, nimacimab, and the program that we are running to treat obesity and overweight disorders with this medication. Just a disclaimer, as always, that we have a lot of forward-looking information and conversation today, so you should be looking at our SEC filings and doing adequate research on that. We, as Skye Bioscience, our mission is to develop medicines to treat obesity and metabolic disease, and these are the areas that we are firmly focused on. We believe that we are developing clinically and commercially differentiated medications. We want to redefine the landscape for the treatment of metabolic disorders, and of course, obesity is what we are focusing on first. Our lead molecule is nimacimab. Nimacimab is a new and a distinct class of CB1 inhibitors, which is a pathway that has been known for a while now and is validated. Nimacimab, we believe, has the potential to become a leader in treating patients with obesity and also its related metabolic disorders. A bit more about Skye Bioscience. Since August of 2023, we have raised $107 million in equity capital. We are very well supported by specialist life sciences investors, and these are top-tier investors, and we feel fortunate to have such good backing. Last year was a big year for us. We were uplisted to the Nasdaq in April and added to the Russell 2000 Index in 2024, and we are currently funded to run through Q3 of 2027. We have a very strong leadership team, and we are fortunate also to be backed by a very strong board. Overall, a lot of experience with drug development and with building companies and very good advice that takes us forward on our clinical program. N imacimab, our lead molecule, has IP and composition of matter protection through 2035. We do have a novel biologic pipeline, and our R&D team is focused on GPCR antibody targets, biomarkers, and other metabolic pathways. We have coming up this year, and we'll talk a little bit more about it, near-term data inflection points. Our phase IIa trial is running right now, and we expect data this year. We also have full CMC capabilities, which of course is extremely important, including GMP manufacturing, to support future clinical trials and the trial that is underway now. We believe at this point that there are significant opportunities that remain in the anti-obesity medication market. It is true that the incretins are wonderful drugs. We've had a revolution in the treatment for obesity. The GLP-1s and the associated incretins with it have opened up the opportunity to treat obesity as a disease and very much as a chronic disease and have proven the point that we can target biologic pathways effectively to treat obesity. However, this first generation of drugs that we are seeing continues to have some issues, and we believe that there's more that can be done to treat obesity effectively and to treat it in a manner that is sustainable and to get healthy weight loss for people. Some of these things include the GI issues that we see with incretin drugs. Both Wegovy and Zepbound cause significant rates of nausea and diarrhea and also vomiting, which tends to restrict how long people can take these drugs. In fact, now that so many people are taking these drugs, there is a lot of real-world data that is available, and Blue Health Intelligence recently reported that 30% of patients drop out after treatment after the first four weeks, and most don't stay for the minimum of 12 weeks that is required to get meaningful weight loss. Wegovy's STEP trials showed that there was about a 15% non-responder rate, so there is certainly a fraction of patients who don't respond to GLP-1 drugs and would benefit from alternate pathways. Along with that, there is the question of how much lean mass loss you get in the total weight loss. We all understand that losing some lean mass is a part of weight loss physiologically. When you lose weight by any mechanism, including by intensive lifestyle modification, a certain fraction of that weight is going to be lost as lean mass. We, as physicians, will always counsel our patients to avoid losing a larger fraction of lean mass so that you end the process more healthy with a better muscle fat ratio. Ideally, we would like to lose no more than 25% of the weight lost as lean mass. However, the trials with Wegovy actually show that the fraction of mass lost as lean mass can be as much as 40%. The opportunity remains to improve tolerability in terms of treatment of weight loss. Tolerability allows these drugs to be taken for the longer term and to get more effective weight loss and to find the right combinations that can go with the GLP-1 backbone to improve the parameters of weight loss and to make it more sustainable and healthier. In a broad sort of manner, we can divide our approaches to weight loss as targeting central mechanisms and targeting peripheral mechanisms. When we look at the incretin drugs that are largely used at the moment, this includes the GLP-1s, of course, but also combinations as in Zepbound with GIP and now upcoming with glucagon, although drugs with glucagon tend to target liver disease more than they do obesity at this point. These drugs overwhelmingly act by acting on central receptors and causing a decrease in appetite and caloric restriction. This is like akin to going on a crash diet and eating less. These drugs are obviously very effective and have created a revolution in terms of people being able to achieve weight loss. This brings along with it, as we've already alluded to, adverse events, including nausea, vomiting, and diarrhea. The non-incretin approaches tend to target peripheral organs, on the other hand. We know now that when we look at metabolic disease in general, and obesity, of course, is a part of that spectrum, and many important metabolic diseases like diabetes are in some ways associated with obesity, there are a number of organs outside of the brain and the CNS which are critical in terms of the root cause of these diseases. This includes the liver, the kidney, the muscle, and adipose tissue. Targeting these organs can address the fundamental drivers of these diseases. There are two paths to weight loss or to energy modulation in general. One is how you take energy in, which is addressed very well by the current incretins and the GLP-1 medications. The other is how you spend energy. When you lose weight, you very quickly decrease the amount of energy you spend, which mitigates all the benefits that you're getting from the reduction in calorie intake. This also leads to a very quick regain of weight as soon as either these drugs are stopped or you let up in any way on the efforts to decrease your calorie intake. The effort in terms of targeting peripheral organs includes a number of other targets like increasing energy expenditure, targeting adipose tissue to reduce inflammation, which the CB1 pathway does very well when you block it, to reduce fat mass, to also control the increased production of leptin, and to reestablish key pathways with insulin and leptin by reestablishing sensitivity because obesity brings along with it resistance to both leptin and to insulin. Leptin is important because leptin signals from adipose tissue in the periphery to the brain and brings about satiety, and so it modulates energy intake. A productive shift in these appetite-regulating hormones can curb both calorie intake and also, by various actions in these peripheral organs, the actual use of energy. We are looking now at both sides of the scale. Now, the CB1 pathway, which we are targeting with nimacimab, is a pathway that's been validated for weight loss. This is a conserved pathway, important in our evolution. Rimonabant was a drug that was approved approximately two decades ago. It was a very exciting time then because no other drug had shown 10% weight loss, and rimonabant could do that. Rimonabant was withdrawn because it preferentially went into the brain in its distribution and caused neuropsychiatric side effects, and therefore this first generation of CB1s was abandoned. Many others were being developed as well. The second generation of CB1 antagonists that we're seeing now are more peripherally restricted. We recently saw data from monlunabant. This was last year. This is a drug that's being produced by Novo Nordisk. This is also a small molecule like rimonabant and, relatively speaking, is very much peripherally restricted. What we saw with monlunabant was in the phase II, at 16 weeks, the placebo-adjusted weight loss was about 6%, which was double what we had seen with rimonabant and certainly comparable with what we see with oral semaglutide at the same time point. We also see that with both rimonabant and with monlunabant, the GI tolerability is significantly improved compared to the GLP-1 drugs. In terms of efficacy and also in terms of tolerability, the CB1 antagonist pathway is well validated by both the results that we've seen from rimonabant and from monlunabant. The press release from Novo did suggest that being a small molecule, monlunabant continued to leak a little bit into the CNS, thus causing some neuropsychiatric effects and some continuing concern over that. We believe that nimacimab, being an antibody, has a distinct advantage here because antibodies, being large molecules, do not leak across the blood-brain barrier, and therefore that will mitigate these neuropsychiatric effects while still bringing the benefit of this weight loss and this validated clinical effect that we are seeing. Nimacimab is a CB1-inhibiting antibody. It inhibits the receptor. It's an engineered IgG4. As an antibody, it's peripherally restricted, and it doesn't accumulate in the CNS or in the brain despite multiple weekly doses. It's very specific, as antibodies tend to be, for the CB1 receptor. It actually binds to the receptor at an allosteric site and is both a potent inhibitor as an antagonist to this receptor, so it will antagonize the binding of endogenous ligands, but it also functions as an inverse agonist and is actually twice as potent as rimonabant here. Now, looking a bit more at the CB1 pathway, when you have overstimulation of this pathway, which tends to occur in people who are obese and who have metabolic disorders, a number of deleterious effects occur, including in adipose tissue, where the tissue tends to get more inflamed and has de novo fatty acid synthesis. The fat is being produced in a form where storage is preferred, and you get storage of fat in adipose that's causing obesity. The adipose tissue stops breaking down fat and making it available for energy consumption, so lipolysis is decreased. Besides that, we can look at other organs. For example, in the kidney, we know that there is associated kidney disease with obesity and metabolic disorders. Stimulation of the CB1 pathway causes increased inflammation and fibrosis in the kidney and in the liver and the pancreas, where, again, there is an increased production of new fat and storage of this fat in organs where storage of fat is clearly deleterious and causes significant long-term consequences. It also reduces insulin signaling and increases fibrosis. Nimacimab, which is targeting a clinically validated pathway and is peripherally restricted, can block all of these actions and therefore have beneficial effects on both weight loss and all the associated metabolic comorbidities. Being an antibody, it also has a long half-life. We believe the half-life is about 21 days, and this could support monthly dosing. Also, based on data that we've seen from rimonabant, blocking this particular receptor, which is a CB1 receptor, can cause a relative preservation of lean mass as compared to what we see with the GLP-1 drugs today. Given the fact that the mechanism of action is predominantly peripheral, although clearly it will also moderate the intake of food and therefore energy consumption, we believe that there is a strong case to be made for combinations with incretin because the mechanisms are complementary. Here I'm showing you something that I was talking about earlier, which is the fact that this antibody to the CB1 receptor doesn't get distributed to the brain. It doesn't cross the blood-brain barrier. These experiments were done in non-human primates, specifically in cynomolgus monkeys, and you can see both data from CSF levels, which are an indicator of what is in the CNS. Also, on those pictures that you can see on the right, those are actually the distribution of nimacimab in these monkeys. The drug has been tagged with iodine-124, and then PET scans have been taken, and you can see that there is no distribution in the brain. In order to establish that this mechanism of antagonizing CB1, which is otherwise validated, works with an antibody that is completely restricted to peripheral action, of course, we are getting central action. It's indirect. The drug just doesn't cross the blood-brain barrier. That always raises the questions of, well, do you still see the weight loss simply because the antibody is novel? We wanted, in order to show this, we established a DIO model where we knocked in the human receptor for CB1, given that the antibody binds to the human receptor and not to the murine receptor. This allows us to use nimacimab in this model. Here you can see some early results from this model that we've established. What we're doing here is giving approximately a month of dosing with nimacimab in a dose-dependent manner. You can see that at the high dose, we had a 16% weight loss in these DIO mice. As a positive control, you can also see with the green lines over here, semaglutide, and you can see weight loss with semaglutide as well. The model works and is validated. This gives us proof of mechanism in these DIO mice that a peripherally restricted antibody will cause weight loss in the same way as the original CB1 antagonists that we've seen. Nimacimab is capable of restoring metabolic homeostasis in adipose tissue. It will directly decrease inflammation. It decreases the excessive production of leptin. In that process and by other direct action, it's able to restore the signaling of leptin in the hypothalamus, which restores satiety signals and reduces energy consumption. It also has beneficial actions on resistance. In the liver, it decreases fibrosis and steatosis. It is capable of reducing MASH and MAFLD, which are comorbidities associated with obesity, has similar effects on the GI tract and certainly on the muscle, where it allows the muscle to continue to have a higher metabolic rate and consume energy, which is important in maintenance of weight loss. I mentioned earlier that the mechanism of blocking CB1 receptors is complementary to the action of incretins. This table just shows you the various mechanisms that we're using right now to target weight loss. You can see that a lot of what the CB1 antagonists do is complementary because of its peripheral action to what the GLP-1s are doing. The GLP-1s largely decrease appetite, increase satiety, delay gastric emptying, and stimulate insulin secretion. Adding to this CB1 antagonism gives you insulin and leptin sensitivity, preserves lean mass, has much better GI tolerability. These two mechanisms of action together, we hope, can have additive and optimistically some synergistic effects. Now, the population of obese people today, for a variety of reasons, which we will not go into, worldwide and certainly in the U.S., is very large. This ranges from people who are overweight and at risk to people who are morbidly obese. If we look at people who may need help in terms of losing weight, a large number of these actually exist in the overweight and the Class I obesity class s o...