Hi, good morning. It's our pleasure to have MBX Biosciences with us today, who is best known for its Precision Endocrine Peptide Canvuparatide for hypoparathyroidism, but they've also leveraged their program to various conditions in the cardiometabolic space. Specifically, they have MBX 1416, a GLP-1 antagonist for post-bariatric hypoglycemia, and also MBX 4291, which is a dual agonist that has the potential for monthly administration. First, though, I do want to give the floor to CEO Kent Hawryluk and Chief Medical Officer Salomon Azoulay and Rick Bartram, CFO, just for a few minutes to talk about the recent Kaniparutide news, which for all intent and purpose was very positive. Maybe we can get into the other programs. Ken, go right ahead. Thank you Annabelle. We're really delighted to be participating in Stifel's CardioMetabolic Virtual Conference and I would like to thank you and the team for your ongoing support. It's really a transformational year for the company and I'm excited to share an update on our progress. Just a reminder, this presentation includes forward looking statements. I encourage you to look at our risk factors and other disclosures outlined in our most recent SEC filings, which are available on our website. If you could proceed on the slide. MBX Biosciences is a clinical-stage biopharmaceutical company founded by global leaders in peptide drug design, development, and commercialization. We are pioneering a novel platform technology called Precision Endocrine Peptide, or PEP, and each of our drug candidates we believe has the potential to be best in class with blockbuster revenue potential. One example, to demonstrate what our technology can do, we took a peptide hormone, PTH, that has a half-life of about an hour and engineered it into a therapy that can be given once weekly and deliver continuous infusion-like drug exposure. That molecule that you referenced, Annabelle, once-weekly Canvuparatide, is a potential PTH replacement therapy prodrug with best-in-class profile. We were just so thrilled to present our positive phase II results last week. I know we'll be discussing those a little bit further, but I wanted to really share some key takeaways. You know, 79% responder rate at six months, that was an increase from 63% at 12 weeks. These results are really quite competitive. To put that into some perspective, the once-daily injectable has on its U.S. label a 69% responder rate at six months and we look at some really other measures of success. Every patient completed the trial and 94% elected to enroll in the two-year open-label extension study and we view that as a strong testament to interest from patients in remaining on our weekly therapy. Other secondary endpoints reinforced the clinical proof of concept and demonstrated stable precision control of calcium in HP patients. Looking at the safety and tolerability, really strong, no treatment-related SAEs, no discontinuations. We believe these results really underscore the potential of once-weekly Canvuparatide to establish a new standard of care in adults with HP and really increase our conviction as we advance to a Phase III registration study. Our second program, MBX 1416, is a potential first-in-class treatment for post-bariatric hypoglycemia or PBH, and we are underway with a Phase II-A study in PBH patients. In addition, MBX Biosciences has an obesity portfolio of differentiated PEP candidates, including MBX 4291, which is an ultra-long-acting GLP-1/GIP co-agonist prodrug, which we believe has the potential for once-monthly dosing as well as improved GI tolerability and greater weight lowering than current products and candidates. Additionally, we have other obesity candidates in lead optimization and look forward to sharing more about those as they approach IND. It's important to note that we are in a very strong cash position on a pro forma basis. Our June 30, 2025, cash was approximately $412 million, taking into account net proceeds from our follow-on offering last week, and this cash on hand is expected to extend our operating runway into 2029 and allow us to achieve really important value-creating milestones across all of our pipeline assets, including the phase III registration study in Canvuparatide. Given the topic today, I'd like to provide a brief overview of our lead obesity asset, MBX 4291, and it was invented by Dr. Richard DiMarchi, our scientific founder, who was the inventor of the first GLP-1/GIP co-agonist at our previous company, Marcadia, which was acquired by Roche and then later by Novo Nordisk as MB2. What we did is take an active drug that is designed to perform like tirzepatide, albeit with novel composition of matter. Importantly, we apply two of our PEP technologies, prodrug and fatty acylation, to provide gradual controlled release, continuous infusion-like drug exposure, and long time action. As you see illustrated there on the right, this transformation to active drug occurs in the system under physiologic conditions, pH and temperature, requiring no enzymes. This is very analogous to our technology that's clinically validated in our Canvuparatide program. These advances are really important because we believe that in chronic use, a once-monthly that has tolerability across the entire month and is efficacious will be the market leader. If we turn to some data in non-human primates, this really shows that our pharmacokinetic profiles are superior to tirzepatide. If we look at the black triangles representing tirzepatide concentrations, you see this rapid rise to Cmax and then the concentration falling off. Thus, the molecule is dosed weekly. We do know from talking to KOLs that this fast rise to Cmax is what is associated with the GI intolerability of the incretin class. Instead, in contrast, let's look at the empty black squares showing a slow steady rise to Cmax and then a prolonged exposure measured out to three weeks. Turning to repeat dosing, we see this effect continue. In fact, on the left we see nice dose proportionality, and on the right with four once-weekly dosing, we have flat as a board PK profile. I mean you can't get more infusion-like than this exposure with a peak to trough of about one. This is important again to support our hypothesis that in chronic use our molecules should be better tolerated, which could allow patients to get to a higher dose level and achieve greater weight lowering aims. In fact, in these normal non-human primates that we tested MBX 4291 in once-weekly dosing, we see a really remarkable weight lowering. Particularly remarkable as this is not an obesity model. These are normal NHPs. This is extremely competitive weight lowering, and importantly, it was tolerated by the monkeys. We believe that this will set us up for a successful phase I study, which is underway in the high BMI adults, 30 BMI or above. It is a SAD four-week MAD followed by a 12-week Part C study in the target population where we aim to demonstrate once-monthly dosing as well as other points of differentiation such as better tolerability and weight loss. With this study, we can really position MBX Biosciences as a leader in obesity. I will turn it over to Annabel for questions. That's great. My question around your obesity portfolio was precisely what you just answered. What was in the preclinical studies that gives you confidence of this differentiation? I guess one of the things that I saw in that chart, in the non-obesity model you saw some very good weight loss. It seems that when the drug was taken away it seemed to have a much slower, I guess, return of the weight. How should we think about the durability of the prodrug, your prodrug post dosing? Obviously one of the issues with obesity drugs that we know and that's been cited by physicians as well as payers for that matter, which is what's causing some of the problems with reimbursement, is that persistence. Maybe you can talk about how you can improve persistence and how you can improve the tail of the weight loss after treatment. It's a really excellent point there, Annabel. In addition, we have demonstrated in vitro that we have the same degree of activity at both of the GLP-1 and GIP receptors, as tirzepatide. This was by design, though we have a novel molecule and of course then have a prodrug of it. I think that speaks to how we are leveraging the gold standard today in weight lowering with these two mechanisms that obviously Dr. Richard DiMarchi has been involved with for many years. In terms of the durability of effect, I think that our prodrug has advantages in terms of adherence and reducing discontinuations. Our goal really would be to keep patients on drug. I think once monthly will become the standard of care, and we'll really look to demonstrate that in the phase I Okay, great. How do you measure, I guess, tolerability in some of these preclinical models? Do you have a chance? I mean, I think you noted before that it's the time, I guess the fast rise creates the tolerability issue. Do you see that playing out in any way in these preclinical non-primate models? We have observed that the monkeys were able to tolerate these high doses, and as you see, lose considerable amount of weight, approaching 20% in four weeks. We think that's really important. There's no better model than humans. We are very thrilled to be underway with our phase I study in the high BMI adults and will be very much looking forward to reporting that, looking at the side effects, right? Nausea, vomiting, discontinuations, all of these measures that I think we just haven't seen the ultra-long actings yet prove they've cracked that code of tolerability. Okay, can you talk to us about how you're going to be reporting out these different stages of your trial? You've obviously got part A, part B, part C. How is that all? Going to be reporting out what we've communicated. Annabel, is that our full phase I data set will be complete in 2027, and we'll provide more specific guidance as the study advances. Okay, got it. You did mention that you have a portfolio. Here I'd love to hear a little bit how you, I guess, construct this portfolio as the landscape is evolving around you. Obviously, GLP-1/GIP is a validated target. Amylin is emerging. Glucagon is emerging. How do you think about all those potential additions to the PEP platform to create that obesity portfolio? There are a number of important validated targets in obesity. We're very familiar with all of them. Again, Richard not only invented the first GLP-1/GIP co-agonist, but also the first triple agonist before retatrutide. Very familiar with glucagon and amylin as well. We've been quite reticent to share what our preclinical programs are, given the competitive nature of the obesity field. I think it's safe to say we're looking at best-in-class profiles that leverage our ability to deliver this continuous infusion-like drug exposure, which we know is so important for tolerability, and more to come as these assets approach IND. We do believe generally that this is a heterogeneous population and a very large market opportunity, so there'll be room for multiple product choices that kind of deliver precision medicine to the patients based on their need. Okay, and then one last question on this. Would you be looking to do these as proprietary programs, or do you plan on partnering out obesity? In obesity it is. These are large registration studies and large sales forces required. Generally, it's strategic to have a corporate partner, and we fully expect to partner these programs at a strategic time for the company. Got it. All right. I'm working backwards in your pipeline, going with all the cardiometabolic drugs first. I'll hit on Canvuparatide, I promise, because I know you want to talk about that. Maybe we can touch on MBX 1416, because obviously that's the next one that's going to be emerging. That is the GLP-1 antagonist for post-bariatric hypoglycemia. Maybe we can just set the stage and talk about this indication a little bit, and I guess the market, for that matter, how you think about this evolving as GLP-1s are clearly changing the landscape quite a bit. We see tremendous unmet need in post-bariatric hypoglycemia, PBH. This has clearly been more recently understood as a disease with the rise of bariatric surgery. This is a chronic condition. No approved pharmacotherapies at present time. We see an opportunity to be first in class. The mechanism is clinically validated GLP-1 antagonism. That, I think, is really good for us. We can kind of follow a well-trodden path from a development and regulatory standpoint, and I think deliver a best-in-class profile. With the once-weekly, you know, half-life we've shown in our phase I of 90 hours, that's substantially longer than the half-life of the once-daily injectable that's in phase III. That's, you know, 2-3 hours as a comparison. We know from talking to physicians that having the full day and night coverage is important for prevention, which fits our profile. This disease causes a rise in GLP-1 that's unnatural, right? Given the changed anatomy, the rapid rise or transit of nutrients to the gut. A GLP-1 antagonist is the right approach that will bring down insulin in PBH patients and prevent the glucose in the deer or the hypoglycemia. GLP-1s would be not a safe approach for these patients given the disease state. With this increased GLP-1 and, you know, aspect of your question, we see bariatric surgery remaining the gold standard. There's really no substitute for the speed and durability of that effect, particularly in the severe obese population. It really lines up nicely for this program. Okay, got it. Maybe Sam, you can review some of the phase I data for the PBH program. I guess it's similar to what we saw in the phase I Canvuparatide. It was also in healthy volunteers. Maybe you can tease out some of the characteristics that you saw that gets you excited about the program and its potential for success. Thanks, Annabel. Yeah, definitely what we saw is a long half-life as Kent was alluding to with 90 hours, which is excellent and should cover the week, but most importantly the night, as in this hypoglycemic event, as you know, are completely unpredictable. The fact that the patient will be covered during the day and the week will be a great, great advantage. What really was exciting was this PD activity, which was we looked at those following mixed meal tolerance test. We looked at really pharmacodynamic effects such as insulin, glucose, et cetera, but we, as expected, it's healthy volunteers and we didn't see that much. However, we saw a GLP-1 increase and it was a good signal during this mixed meal tolerance test. In terms of reproducibility, we observed it following two mixed meal tolerance tests, we observed it after 10 mg and 30 mgs. So it's really a good signal and opens the path now to the phase II-A, where we should expect in patient not only to confirm this effect, but also to see the effect on insulin, C-peptide, et cetera, and certainly the glucose nadir, which is what we want to increase in order to make sure that the chance of hypoglycemia decreases substantially. Okay, this is again one of those counterintuitive things when you're looking at healthy volunteers. When you have a mixed meal test and you see a GLP-1 increase, but you have a GLP-1 antagonist, can you square that for people in case it gets confusing? Yeah, it's just the action on the receptor. You're blocking the receptor. The negative GLP-1 increase, that's as simple. That's a very quick image. We can go for longer on this, but just a quick summary. Okay, great. Obviously, when you think about GLP-1 antagonism, you think of the opposite effect on weight loss versus weight gain. Just get people comfortable with the fact that GLP-1 antagonists are not going to result in weight gain for these patients. We did not observe anything in animal models, we did not observe anything in human in healthy volunteers. Also, the competition has not observed increase in weight or any increase in glucose, significant increase in glucose. We are confident that in this population, with our GLP-1 antagonist, we will be targeting hypoglycemia with very, very few adverse events, such as glycemia and others. We are confident here. Okay, great. As you mentioned earlier, there's no treatment right now for hypoglycemic events. There is, obviously. Amylyx is doing once daily. Is there anything from their trials, from some of the activity that they've seen, that gets you more comfortable or excited about your potential program to do similar? What kind of paradigm could potentially do to Yorvipath? Is that a direct parallel that you can draw, and I guess, what can you take from some of the Amylyx trials that you can bring into your program that gets you excited? Annabelle, if approved, it would be good for PBH patients. We're very comfortable with the playbook of going from once daily to once weekly. We've just seen in most every indication, you have a rapid adoption of the once weekly option, typically first for convenience, but then you see real world clinical benefits from better adherence or just greater consistent exposure. We think that we're really well positioned. Again, I think looking at prevention, you want to make sure you have the full day and night coverage, not just temporary, because these episodes of hypo can occur anytime and they're devastating, often requiring a medical intervention such as a glucagon injection or EM or ER visit. Great. When can we see that data? When are you expecting to see the data? Currently we're indicating we'll have the phase II-A data next year. We'll provide more specificity as the trial advances. Glad that the trial's underway. Okay. We have just a few minutes. I do want to touch on Canvuparatide because that is very exciting. I know that everyone probably has heard about it already, but just to go through some of the specifics of the trial. It was great. I think you have all your information you need to go into the phase III. How do you dose select based on what you've observed in the phase II? 400, 600 did not quite get there, but the total pool did. How do you decide what to start with as far as dosing? Go ahead, Sam. Yeah, so it's a dose finding study, just by definition, phase II dose study. What we have to do is to select the initial dose, a starting dose, right, because it's a customized medication. We'll be titrating up from that dose. As usual, you're looking at efficacy and you're looking at tolerability, and you want the right balance between the two, and that's exactly how we'd be selecting the starting dose. Okay. As you think about the tolerability, I'm thinking a little bit about the adverse events, like the hyperglycemia. There was an incidence of hyperglycemia initially. How do you minimize that? Since it's temporary and it was just during that fixed dosing period, it's probably not as much of a concern because it's not a chronic situation of hyperglycemia. Are you trying to manage hyperglycemia specifically, or is it just, you know, we should just come to expect it? It's something that you have to manage as patients are coming off of supplementation. Hyperglycemia is something you would expect in this population. As a reminder, you titrate up at a time where patients are still taking active vitamin and calcium supplement. It is an interaction between the drug and the supplements that might lead to hypercalcemia. For our dose finding study, for our dose findings. For the starting dose, we'll be looking at the ones that really create the less risk of hypercalcemia when you initiate the treatment and how we are going to minimize this hypercalcemia event. If you look at the occurrence of hypercalcemia, it's mainly during the titration phase. That is what we expect to adjust in our phase III trial, knowing that the level of hypocalcemia you have seen is not worrisome at all. Okay, what are the other points that you're trying to differentiate from your path? I think you're talking about possibly urinary calcium and the urinary calcium excretions. What can you do there as far as differentiation in your label? Certainly urine calcium is one of the indications we can get into the label. Your VPAs didn't get it. What we saw from phase II study is very encouraging. What we saw, the decrease we saw in the target population of patients with elevated urine calcium at baseline, and you see this reduction. I think if we can confirm this in phase III in alignment with the FDA, that's something really we can target as an indication. Okay, great. I'm getting the signal that our time's up. I guess we're going to have to carry on at another point. I guess the end of phase II meeting is in 4Q, and I guess we'll hear the next steps from there. We look forward to requesting the end of phase II meeting and aligning with the agency on a global phase III registration study design and providing an update on our timelines and plans when that's all squared away. What a transformative year, and these data that we talked through really reinforce our PEP platform technology that I think is going to position us extremely well, not only in hypoparathyroidism, but in other areas like obesity. This is just the start with MBX 4291, and we have a lot of promise there and look forward to sharing more. Excellent. Thank you so much. Thanks for your time. Take care.