As a reminder, this conference call is being recorded. I would now like to turn the call over to your host for today's conference, Krista Fogarty, Lipocine's Principal Accounting Officer. You may now begin your presentation. Good morning. This is Krista Fogarty, Principal Accounting Officer of Lipocine, and I would like to thank everyone for joining today's call discussing LPCN 2401 for chronic obesity management, including clinical trial results. We issued a press release with these results earlier today. The release is currently available on our website at lipocine.com and has been filed with the SEC on Form 8-K with the SEC and is available on the SEC's website at sec.gov. An archive of this webcast will be available on our website later today. Leading the call today is Lipocine's President and CEO, Dr. Mahesh Patel. Dr. Patel is joined by Lipocine's Senior Director of Clinical Development, Dr. Benjamin Bruno, Lipocine's Chief Medical Director, Dr. Anthony DelConte, and Lipocine's Corporate Development Advisor, Dr. Mark Rampe. In addition, Dr. Chidu Chidambaram, Lipocine's Senior Vice President of Research and Product Development, is also on the line and will be available during the Q&A session. Before we begin our prepared remarks, I need to remind you that certain statements that we will make in this presentation are forward-looking statements within the meaning of the Private Securities Litigation Reform Act. These forward-looking statements reflect Lipocine's judgment and analysis only as of today, and actual results may differ materially from current expectations based on a number of factors affecting the company's business. Accordingly, you should not place undue reliance on these forward-looking statements. For a more thorough discussion of the risks and uncertainties associated with forward-looking statements to be made in this conference call and webcast, we refer you to the disclaimer regarding forward-looking statements included in our press release. We do not undertake any obligation to update or alter any forward-looking statements, whether because of new information, future events, or otherwise. I will now turn the call over to Dr. Mahesh Patel. Mahesh? Thanks, Krista, and good morning, everyone. I'm Mahesh Patel, President, CEO, and co-founder of Lipocine. I'm pleased to report that today Lipocine announced positive LPCN 2401 clinical results from our previously completed Phase II trial in participants with metabolic dysfunction-associated steatohepatitis. Before we discuss the results and get to the slides, let me provide a little background. Currently, we are in the midst of an obesity epidemic in the U.S. 74% of adults older than 20 are either obese or overweight. Obesity is defined by excess body fat. Excess body fat increases the risk of death and major comorbidities. Therefore, the main goal of a product intended to be used for medical weight loss is long-term reduction in fat mass, leading to reduced morbidity and mortality. Recently approved GLP-1 receptor agonists, namely semaglutide and tirzepatide, have become the bedrock of weight management therapies for patients who are obese or overweight with at least one weight-related comorbid condition and are indicated as an adjunct to a reduced-calorie diet and increased physical activity. Current clinical use of this agent is primarily focused on achieving weight loss without regard to overall body composition. Weight loss achieved is not solely attributed to loss of fat mass. However, as up to 40% of weight loss is driven by lean mass loss, which includes muscle and bone. In the long term, loss of lean mass has an adverse impact on mortality and morbidity. Moreover, patients are unable to maintain the lost weight upon discontinuation of GLP-1 receptor agonists. That is, the lost weight is regained rapidly, potentially mostly as fat mass, and as the body has adjusted to the reduced basal metabolic rate with a loss of calorie-burning muscle mass. So first, let's get some housekeeping out of the way with a note regarding forward-looking statements. Okay, let's dive into the presentation. LPCN 2401 is an oral proprietary product candidate comprising an anabolic androgenic receptor agonist, an alpha tocopherol, an antioxidant, and metabolic modifier, two actives in a single dosage form. Let me review plausible mechanism of action that informed the design of our product candidate. In individuals with obesity, the excess adipose tissues stimulate release of inflammatory mediators, predisposing them to a pro-inflammatory state and oxidative stress. Through their anti-inflammatory effects, androgen and alpha tocopherol decrease the activation of cytokines and adhesion molecules. Alpha tocopherol also serves as a free radical scavenger and protects against oxidative stress, including stress from osteoclasts, and also helps in maintaining membrane fluidity. In addition to its anti-inflammatory effects, the androgen receptor agonist component of LPCN 2401 is expected to stimulate muscle satellite activator, FGF2, and modulate muscle growth suppressors, including myostatin in skeletal muscle. Androgen agonism is known to play a beneficial role in glucose and lipid homeostasis, including increased insulin sensitivity, induction of fat breakdown, and reduced lipid production. Hence, 2401 has the potential to improve body composition through its multimodal mechanism. Now I'll pass the call over to Lipocine's Chief Medical Director, Dr. Anthony DelConte, to discuss the importance of body composition and unmet needs in obesity management. Tony? Thanks, Mahesh. The importance of lean mass or fat-free mass, which includes both muscle and bone content, is illustrated in this slide. The ideal body composition is around 70% lean mass for women and 90% for men. The role of muscle in health and disease prevention and the dangers of rapid lean mass loss have been well established. Research from the University of Minnesota demonstrates the importance of body composition on weight regain post-cessation of calorie restriction. During the semi-starvation period, both lean and fat tissue are lost, with more fat than lean mass loss, similar to what is observed with GLP-1 use. When caloric intake is increased, there's a rapid regain of weight and fat mass, whereas the increase in lean mass is much slower. Eventually, the amount of fat and weight gain is greater than what was lost, a phenomenon known as weight overshoot or fat overshoot. This is an analogous situation that we will see later on with incretin mimetics, where the weight is gained rapidly upon discontinuation of therapy. The observed hyperphagia, or excessive calorie intake, persisted until the muscle mass returned to baseline levels. The consequence of excessive body fat can greatly diminish overall health. These include the risk of death and major comorbidities such as Type 2 diabetes, hypertension, dyslipidemia, cardiovascular disease, osteoarthritis of the knee, sleep apnea, and some cancers. Furthermore, having excess fat in the android region is strongly associated with negative health outcomes. Increased visceral fat can also increase the risk of certain health conditions such as diabetes, prediabetes, and heart disease. So with incretin mimetics, while they've become a bedrock of weight management, they do have some limitations. Results published in the New England Journal show that GLP-1 agonist treatment led to a 15%-21% rapid weight loss, but up to 40% of the total weight loss was from lean mass, which is cause for concern. In addition, the greatest amount of weight is lost in the first four to five months. Further weight loss can be achieved, although due to the slower rate of loss, it takes longer to reach the ultimate goal. An additional limitation is seen from another publication on the right panel. Once GLP-1 therapy is discontinued, weight begins to rebound. If the patterns of weight gain follow those seen post-discontinuation, post-diet discontinuation, the risk is that much of the gain will be fat, not lean mass. Despite the popularity of GLP therapy, there's still a huge unmet medical need. Although injectables are acceptable, an oral agent is preferred by patients. The loss of lean muscle mass remains a problem, and an improved body composition where muscle is preserved and not lost would be preferred. A new therapy would need to minimize the rebound weight gain, particularly that of gaining fat over muscle. Overall, there would need to be an improvement in the risk-benefit profile with a focus on achieving an ideal body composition. Now I'll turn it over to Ben to share the LPCN 2401 preclinical and clinical study results. Ben? Thanks, Tony. I'm going to cover the rationale, design, and top-line results of this Phase II clinical study before turning it back over to Dr. DelConte to discuss safety findings. But before we get to the clinical study, I wanted to share one slide regarding animal study data generated with LPCN 2401, specifically in a rabbit model of metabolic syndrome. Control male rabbits were fed a regular diet, RD, and all others were given a high-fat diet to induce sequelae similar to what is seen in humans with metabolic syndrome. Those given a high-fat diet were co-administered either vehicle, a placebo, or one of two treatments. Treatment A is a testosterone ester monotherapy, and treatment B, LPCN 2401, is a combination of the same testosterone ester plus alpha tocopherol. LPCN 2401 resulted in a significant improvement in glucose tolerance and reduction in visceral fat, not only compared to placebo but also compared to treatment A. The black line on the graph represents the results for the control rabbits, which were fed a regular diet. As you can see, the high-fat diet plus vehicle resulted in a significant worsening of glucose tolerance. Treatment A administration improved OGTT, but the results were still significantly worse than what is seen with the control rabbits. On the other hand, LPCN 2401 administration resulted in a significant improvement in glucose tolerance, both compared to vehicle and treatment A, and brought glucose tolerance in line with the control rabbits. Regarding visceral adipose tissue, administration of treatment A reduced VAT, and the VAT reduction with LPCN 2401 was superior to that seen with treatment A. Now onto the clinical study design. This was a three-arm, blinded, randomized, placebo-controlled trial that enrolled men with metabolic dysfunction-associated steatohepatitis, a liver condition common in men with obesity, dyslipidemia, Type 2 diabetes, and hypertension. Participants were randomized one-to-one-to-one to one of three oral treatments: treatment A, testosterone undecanoate monotherapy; treatment B, LPCN 2401, a combination of testosterone undecanoate with alpha tocopherol; or treatment C, matching placebo capsule. Participants received one of three treatments for 36 weeks, during which there were DEXAs performed at baseline, week 20, and week 36. DEXA is a validated tool for accurately measuring body composition, including fat and lean mass and bone mineral content. Pre-specified endpoints in the study included changes in lean and fat mass. It is important to note that this study enrolled both hypogonadal and eugonadal men. Low testosterone was not a requirement for study eligibility. The baseline characteristics for the body composition analysis set are presented in this slide. This set is comprised of all individuals who had sufficient DEXA data for evaluation. Specifically, it included all participants who had a baseline and at least one post-baseline DEXA scan. Baseline characteristics were well balanced between treatment groups. Average age was in the early 50s and BMI in the mid-30s. Importantly, all 40 participants met criteria for the use of approved weight loss drugs, namely BMI 30 or above or BMI over 27 with at least one weight-related comorbidity. Next, we will move on to the trial results. All LPCN 2401 results presented are for week 36, last observation carried forward. LPCN 2401 significantly improved body composition compared to placebo. The graph on the left shows the placebo-adjusted% change from baseline, and all presented results are significantly superior to placebo, with p less than 0.05. 2401 improved the fat-to-lean mass ratio by more than 10%, which was driven by both a reduction of fat mass and an increase in lean mass. LPCN 2401 also reduced the android fat by more than 4%. The amount of fat in the android region is highly correlated with the amount of whole-body visceral fat, particularly in men. LPCN 2401 also significantly increased bone mineral content. The intervention was observed to be weight-neutral, with fat mass loss mostly offset by lean mass gains. If we compare the body composition changes seen with LPCN 2401 to those results published for injectable incretin mimetics, we can see the similarities and differences, in particular with regards to the changes in lean mass. First, comparing the changes seen with injectable semaglutide to LPCN 2401, we can see that both treatments resulted in reductions in fat mass as a percentage of total mass and increases in lean mass as a percentage of total mass. However, semaglutide actually resulted in a significant reduction in total lean mass, whereas LPCN 2401 resulted in a significant increase in total lean mass. The percentage of the total mass that consists of lean mass, the center bars, increased with semaglutide, but that is due to the loss in fat mass being greater than the loss in lean mass. Overall, semaglutide treatment resulted in a loss of lean mass. Comparing tirzepatide and LPCN 2401, it can be seen that the percent of fat loss is greater with tirzepatide, at about 26% at week 72 versus 7% at week 36 with 2401. But tirzepatide-treated participants also experienced loss in lean mass, over 8% loss from baseline. To our knowledge, data for change in lean mass as a percentage of total mass are not available for tirzepatide. The participant populations for both of these incretin mimetics studies were over two-thirds female. Many weight loss studies have found that men lose more lean mass than women, so it is likely that the loss of muscle in men is greater than the study-wide averages shown here. It is important to note that the incretin mimetic data are derived from published reports of different clinical trials at different points in time, with differences in trial design, size, and patient populations. No head-to-head clinical trials have been conducted. Now I'd like to show data on other biomarkers, both of weight-related comorbidities as well as other DEXA findings, including comparisons to treatment A monotherapy. At week 36, there was a nonsignificant trend towards improvement in blood pressure and hemoglobin A1c with LPCN 2401 compared to placebo. Systolic and diastolic blood pressure were reduced by about five and four millimeters of mercury, respectively. An absolute decrease in hemoglobin A1c was almost 0.5%. When we compare these results to those of treatment A, we can see that the beneficial effects were only observed with LPCN 2401. The DEXA data regarding whole-body fat mass and lean mass changes were similar with the two therapies. However, LPCN 2401 did significantly reduce android fat compared both to monotherapy and placebo. The differential effects seen here on A1c and android fat with LPCN 2401 and treatment A are in line with the findings in the rabbit study. Finally, LPCN 2401 significantly increased bone mineral content, both compared to treatment A and placebo, altogether suggesting that LPCN 2401 may provide multiple benefits over testosterone ester monotherapy. Now I'll turn it back over to Dr. DelConte to discuss safety findings. Tony? Yeah. Thank you, Ben. So LPCN 2401 was well tolerated with the rates and severities of treatment-emergent adverse events and serious AEs similar to placebo. While no LPCN 2401-treated participants discontinued treatment due to a treatment-emergent AE, there were four placebo-treated participants who discontinued study drug due to treatment-emergent AEs. There were no adverse events of diarrhea, nausea, or vomiting with 2401. Also, there were no AEs related to androgenic effects, including benign prostatic hyperplasia, prostate-specific antigen increase, or hypertension. One participant had an AE of peripheral edema with 2401 compared to two participants on placebo. Muscle spasms, a common adverse effect of other agents under development for the preservation of muscle mass, were not reported by any 2401-related or treated subjects. There were no cardiovascular events or drug-induced liver injuries reported with 2401 use. In fact, LPCN 2401-treated participants had significant improvements in numerous liver health markers, including reduced liver fat, reductions in liver injury markers such as ALT and AST, and NASH resolution upon biopsy. I'll now turn the call over to Lipocine's Corporate Development Advisor, Dr. Mark Rampe, to discuss the prospects of LPCN 2401 for obesity management. Great. Thank you, Tony. Let's take a moment to talk about a growing epidemic in the U.S.: patients with obesity and those who are overweight. In the U.S., 74% of adults over the age of 20 are either obese or overweight. The medical costs resulting from obesity were estimated to be $173 billion in 2019, and the population, known as those with diabesity, patients with obesity and diabetes, has grown to approximately 110 million, more than one in three adults in the United States. There are an estimated 24 million obese elderly patients, a group that is most vulnerable to losing muscle mass. The number of GLP-1 agonist users in the U.S. is projected to reach 30 million by the year 2030. There is tremendous interest in these therapies. Recent polls show that 38% of men and 51% of women would be interested in taking a prescription drug for weight loss. I would also like to discuss some of the recent trends and complications in weight management. In just over three years, obesity in the U.S. increased from 31% to approximately 42% of the population. Over that same time frame, the prevalence of severe obesity has nearly doubled. Although incretin mimetics have become very popular, there remain a number of issues, including substantial lean mass loss, weight regain following cessation of therapy, including the potential for both fat overshoot as well as unclear challenges with the long-term use of these products. In summary, we are very excited to share the news today regarding the potential of LPCN 2401, a novel oral treatment for obesity and weight management. The data we discussed today showed significant body composition improvement in men with at least one obesity-related comorbidity. This included decreased fat mass combined with an increase in lean body mass, reduced android fat, and increased bone mineral content. We believe that LPCN 2401 has potential to improve body composition in combination with incretin mimetics to help maintain weight loss, ameliorate muscle loss, and amplify fat loss. This includes the potential to help patients maintain weight loss once their GLP-1 therapy is discontinued, as well as to prevent fat overshoot and accelerate muscle rebound. LPCN 2401 is a novel oral formulation that was well tolerated with adverse event rates similar to placebo. We believe that 2401 has potential to be used in combination with the currently approved incretin mimetic therapies. The clinical and preclinical data we have generated to date are encouraging and support further evaluation of LPCN 2401 as an aid to quality weight loss while preserving lean muscle mass. Now back to Mahesh to discuss the next steps and concluding remarks. Thanks, Mark. In conclusion, these positive results that are differentiating LPCN 2401 from androgen receptor agonist monotherapy have immense potential implications. In the evolving obesity management landscape, these results are particularly relevant as there is a growing understanding by physicians and patients alike that, in totality, weight loss in obesity management improves health, but not all weight loss can be deemed healthy. The maintenance of lean mass is critical. These results are a prelude to further assessment of LPCN 2401 as a cotherapy with incretin mimetics such as semaglutide, active and marketed Ozempic, and Wegovy, and other GLP-1 agonists or dual agonists. To address the critical unmet needs as current users of these therapies are losing lean mass at an alarming rate and extent, we believe LPCN 2401 could represent a safe option with meaningful effectiveness to address some of the serious unmet needs in obesity and weight management. We look forward to meeting with the FDA to discuss next steps in further development of 2401. This concludes our prepared remarks for the day. At this point, we'll turn over a call to our operator for Q&A. Thank you. We'll now be conducting a question-and-answer session. If you'd like to ask a question at this time, please press star one from your telephone keypad, and a confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to withdraw your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment, please, while we pull for questions. Once again, that is star one. Thank you. Thank you. And our first question will be coming from the line of Oren Livnat with H.C. Wainwright. Please proceed with your questions. Thanks. Really interesting data. I have a few questions. First, can you just remind us what the rationale is for the coformulation with the vitamin E, and what do we know about the, I guess, monotherapy efficacy of vitamin E as we try to tease out the differences between these treatment arms A and B? And I have a couple of follow-ups. Thanks. All right. Well, hi. Good morning. Yeah, our design rationale was that, combined androgen receptor agonist like testosterone ester would contribute toward the androgenic effects, basically as a myostatin inhibitor. And vitamin E is a powerful antioxidant that, in concert, could help modulate lipids as a fat burner. At the same time, it'd be a free radical scavenger counteracting reactive oxygen species. So we believe that, in concert, I guess it would bring benefits in terms of lipolysis to lipogenesis as well as inhibiting the myostatin to help improve the mass of skeletal muscles, functionality, and quality. Okay. And can you just remind us so this came out of the LiFT study, right? So I guess can we talk, I think, first of all, is that correct? And can you help us understand how that population differs or doesn't differ from the overall obesity market and the indicated GLP and GIP populations? Yes, that's correct. It came out of the LiFT study, and I'll pass it on to Ben to address the question. Ben? Yeah. The LiFT study was looking at the NASH population now considered MASH, metabolic dysfunction-associated steatohepatitis. And this is really one of the most common comorbidities seen in an obese population. It's really the liver manifestation of obesity. So it is very common that in someone with obesity, you would have a fatty liver or steatohepatitis. So in terms of the differences in the populations, there isn't a very big difference. This is also the study was done in a pre-cirrhotic population. So this isn't some group of people that are having impaired liver function to the level where it's affecting the actual ability of the liver to do its job. So this is kind of the earlier stages where obesity has led to liver dysfunction. So if you looked at people in the obese population, a very large percentage of. Okay. And since the obvious value here is to combine with GLPs and GIPs, I guess, do we know or from the literature, what you understand with the mechanism, if there would be any interaction between these drugs? Is there any reason to think the lean muscle mass-building properties of 2401 would behave differently in somebody taking these weight loss therapies? Good question. We believe there's an opportunity as a cotherapy with GLP-1 agonist or dual agonist. I'll have Chidu, our head of R&D, answer. Potential to. Yeah. Thanks, Mahesh. Yeah, there are some literature data out that, in a molecular basis, mechanistically, they've shown that GLP-1 receptor as well as the androgen receptor work in concert, meaning we require one to work with the other to do the job better. So we are anticipating to have at least a additive or synergistic effect when you combine this androgen receptor agonist with GLP-1. Okay. Just lastly, you said your next step is to go to the FDA, obviously. But you have a few irons in the fire now, Mahesh, across different therapeutic areas. Where do you anticipate this fitting into your development or partnering scheme in relation to the neurology franchise and other products that are sitting in your two-partner bucket? Thanks. Well, given the tremendous unmet need and we remain opportunistic, at this juncture, we're not ruling out or ruling in developing ourselves or partnering. Obviously, our input and feedback we get from FDA will help us decide if we do it internally or partner it, but we're keeping all optionality, I think, given the huge unmet need and positive results. All right. Thanks. I look forward to following up separately. Congrats. All right. Thanks, Brian. Thank you. As a reminder to ask a question, you may press star one at this time. Our next questions are from the line of Matt Kaplan with Ladenburg Thalmann. Please proceed with your questions. Hey. Good morning, Mahesh. Thanks for taking the questions. Just wanted to follow up on Oren's question in terms of the use of 2401 potentially in the future. Do you foresee it being used as a monotherapy in this population, potentially, in terms of looking at obesity and weight management? Yeah. I'll start out, and then, Mark, you can chime in. I think it could be used as a combination therapy to preserve muscle mass, but there is a desire to discontinue, not be on the GLPs for a variety of reasons, and I guess to prevent the rebound and overshoot that Tony talked about, it could be used as a monotherapy as you wean off or discontinue from GLP. Mark or Tony, do you have anything else to add? No. No, I don't. Okay. Thanks. And then in terms of next steps, going to meet with the FDA, what are you thinking of in terms of proposing for next steps in the clinical development? Yeah. Have Ben address that. I think, as quickly as possible, we're going to meet with the FDA to get feedback on a study design that we have in mind to run further assessment as a cotherapy with GLP-1, Ben. Yeah. As Mahesh said, really, what we're planning to discuss with the FDA is the potential to test this in combination with GLP-1 therapies, look at some of these similar endpoints we looked at today in terms of lean mass preservation, fat mass loss, and overall weight loss as well. So the data that we have, as well as the literature data, it really does support testing in combination with GLP-1s, and we expect that to be the next step, the next trial that we perform. However, we do have to discuss this with FDA. Will you also look at its impact upon GLP-1 discontinuation and that segment? Yeah. That's definitely something we are very interested in, looking at what happens if you stop GLP-1, maybe as you were taking 2401 or starting 2401 after discontinuing GLP-1s, to see if you can prevent that fat rebound as well as improve that lean mass. We're also going to be discussing the potential of including women in this clinical development program, given there is also a large unmet need in women. They make up a big percentage of the GLP-1 users, and they also experience lean mass loss with these agents, as we saw in the data today. So there will have to be some dose determination. It would likely be about one-tenth of the dose that we have used in this study, given the female population. But there is a really large unmet need in both the male and female populations, so we will be discussing both with FDA. Great. Thanks. Thank you. We have reached the end of our question-and-answer session, and I'll turn the call over to Mahesh Patel for closing remarks. All right. Thanks, Rob, and thanks all of you for your participation today. Appreciate it. This will conclude today's conference. Let me disconnect your lines at this time, and we thank you for your participation. Have a wonderful day.