Ladies and gentlemen, greetings and welcome to MBX Biosciences conference call. Today's call is being recorded, and all lines have been placed on mute, and all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. As a reminder, this conference is being recorded. It is now my pleasure to turn the call over to MBX Biosciences Senior Director of Investor Relations and Communications, Jim DeNike. Thanks, Shannon. Good morning, everyone, and thank you for joining us. Today, we issued a press release reporting results from our phase 1 single-ascending and multiple-ascending dose trial of MBX 1416 in healthy volunteers. The press release and presentation are available on our website. Joining me on the call today are Kent Hawryluk, Co-Founder, President, and CEO, and Dr. Sam Azoulay, Chief Medical Officer. Rick Bartram, our Chief Financial Officer, is also joining for Q&A. Today's call and presentation include forward-looking statements. These statements are based on our current expectations and projections and are subject to risks, uncertainties, and assumptions. I encourage you to review the risk factors and other disclosures outlined in our most recent SEC filings, all of which are available on our website. I'll now turn the call over to Kent. Thank you, Jim. Good morning and happy New Year. Before we walk through the MBX 1416 data, let's provide a quick overview of MBX for those that are new to the story. MBX Biosciences is a clinical-stage biopharmaceutical company founded by global leaders in peptide drug design and development. We are pioneering a platform technology called Precision Endocrine Peptide, or PEP, which was created by our scientific co-founder, Dr. Richard DiMarchi. PEPs are engineered to have optimized pharmaceutical properties, including extended time action and consistent drug exposures, as well as convenient, infrequent dosing regimens. Our lead program, MBX 2109, is an investigational parathyroid hormone, or PTH, peptide pro-drug therapy for hypoparathyroidism. We have orphan drug designation in the United States and are conducting a phase II clinical trial with enrollment completion expected this quarter and top-line results expected in the third quarter of this year. Our second program, and subject of our call today, MBX 1416, is a long-acting GLP-1 antagonist and a potential therapy for post-bariatric hypoglycemia, or PBH. MBX also has an obesity portfolio, including MBX 4291, a GLP-1/GIP coagonist pro-drug, which we believe has the potential for once-monthly dosing, improved GI tolerability, and greater weight loss than current market leaders. This candidate is currently in IND-enabling studies with an IND submission planned for the second quarter of this year. Turning to our MBX 1416 program and slide two, PBH is a rare, chronic, and serious complication of bariatric surgery with a substantial patient burden. We estimate a U.S. prevalence of over 90,000 patients, and there are currently no approved pharmacotherapies for PBH, representing a significant unmet medical need. PBH typically presents six months to three years after Roux-en-Y gastric bypass and vertical sleeve gastrectomy procedures. Anatomical changes from these surgeries cause nutrients to rapidly leave the stomach and enter the small intestine. When PBH patients eat, excessive GLP-1 release occurs, which stimulates insulin secretion and reduces glucose in circulation. Severe hypoglycemia can result, leading to serious neuroglycopenic symptoms, including confusion, seizures, and loss of consciousness. PBH is a debilitating disease that can be extremely disruptive to patients' lives because timing of hypoglycemia is unpredictable, can occur multiple times per day, and may require an injection of glucagon as a rescue. This uncertainty creates a fear factor, limits ability to drive and work, and commonly causes people to socially isolate, further diminishing quality of life. Even with recent advancements in obesity medicines, bariatric surgery remains the gold standard for significant and sustained weight loss in severely obese patients. Given the chronic nature of PBH and absence of any approved pharmacotherapies to treat it, we believe there is, and will continue to be, a meaningful need for an effective treatment. The standard of care for PBH, as described on slide three, mainly focuses on dietary intervention such as frequent small meals or avoidance of high glycemic index foods. Compliance with this regimen may be challenging for patients. There are also off-label medications with limited clinical data, and they are often poorly tolerated. Surgery is a last resort but highly invasive, and outcomes may be unpredictable. Use of a GLP-1 inhibition-based mechanism has been clinically validated as a potential therapy to reduce the frequency and severity of hypoglycemic episodes in patients with PBH. A GLP-1 antagonist, avexitide, which has a half-life of approximately two hours, is in phase III development as a daily injection to treat PBH. Our goal with our MBX 1416 program is to be the first once-weekly drug approved to treat PBH. It is designed to be a highly potent, long-acting GLP-1 receptor antagonist. Leveraging our PEP platform, a human GLP-1 peptide sequence was structurally modified to inhibit GLP-1 at the GLP-1 receptor with enhanced potency, stability, and solubility. To achieve sustained drug exposures throughout the day and night and convenient once-weekly dosing, fatty acylation has been incorporated to enhance binding to albumin. We believe by inhibiting GLP-1, we'll be able to prevent severe hypoglycemia from occurring, thereby eliminating patients' need for glucagon injections or surgery, which will vastly improve their quality of life. The MBX 1416 phase I clinical trial, described on slide four, was a randomized, double-blind, placebo-controlled study designed to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of MBX 1416 in healthy adult volunteers. The trial was conducted in the United States and enrolled a total of 69 subjects. The single-ascending dose portion of this phase I trial evaluated 32 healthy adults equally randomized to receive placebo or subcutaneous MBX 1416 doses of 10 milligram, 30 milligram, 100 milligram, and 200 milligram. The multiple-ascending dose portion of the trial evaluated 23 healthy adults equally randomized to receive placebo or subcutaneous MBX 1416 doses of 10 milligram, 30 milligram as two injections, and 30 milligram as one injection once weekly for a total of four weeks. An additional drug-drug interaction, or DDI, cohort evaluated rosuvastatin and acetaminophen pharmacokinetics in the presence and absence of MBX 1416 in 14 subjects. We will cover the top-line results in more detail shortly, but overall, we are very pleased with the positive phase I results that showed that MBX 1416, when evaluated in healthy volunteers, was generally well tolerated with a favorable safety profile and a pharmacokinetic profile supportive of once-weekly dosing. We observed no meaningful impact of MBX 1416 on rosuvastatin exposure, and MBX 1416 appeared to slightly accelerate first-hour gastric emptying, as expected with GLP-1 antagonism. Also, MBX 1416 appeared to increase GLP-1 peak within 60 minutes of a mixed meal tolerance test, suggesting a PD signal in healthy adult volunteers that may translate into a therapeutic benefit in PBH patients. Based on these results, we intend to initiate a phase II trial in patients with PBH in the second half of 2025 to further optimize dosing, pending alignment with the FDA on our proposed study design. We now have two programs in clinical development that validate our PEP platform technology. I would now like to invite Sam to discuss the top-line results of the SAD, MAD, and DDI cohorts in more detail. Thank you, Kent, and good morning, everyone. Let's start with subject demographics in the MBX 1416 phase I studies, as shown on slide six. Demographics were diverse and balanced across all cohorts. The mean ages were 41.9 in the SAD, 39.9 in the MAD, and 35.9 years in the DDI cohort. The sex of the participants was balanced across both the SAD and DDI cohorts, with more males than females in the MAD cohort. Participants' race, ethnicity, weight, and BMI were also balanced across each group. Turning to slide seven, overall, no serious adverse event and no grade 4 adverse event were observed in the study. In the SAD and DDI cohort, no grade 3 or 4 adverse events were observed. In the MAD cohort, no grade 4 adverse events were observed, while five subjects experienced a total of six grade 3 adverse events, all injection site reaction, or ISR, with four subjects in the 30 mg cohort and one subject in the 10 mg cohort. Grade 3 treatment-emergent adverse events observed in this study were related to erythema, defined as redness, at the injection site greater than 10 cm in size. Except for adverse events related to ISR, no pattern or imbalance between MBX 1416 and placebo were observed for any adverse event. As outlined on slide eight and previously mentioned, ISR was the most common adverse event incurred receiving MBX 1416 and were mostly mild or moderate. Given injectable peptides are known to cause ISR, we proactively collected all ISR, including mild reaction, using a dedicated form and using the FDA toxicity grading scale. ISRs were observed in 73% of participants who received MBX 1416 compared to none in the placebo group. In 88% of the subjects with ISR, they were mild or moderate and were predominantly characterized by erythema, as I said, redness, in 95% of subjects with an ISR, minimal or no pain, and resolution generally within approximately seven days. No systemic clinical manifestation was observed in association with the ISR. No subjects withdrew voluntarily from study treatment. Histological characterization of a grade 3 ISR, which developed in a participant from the MAD 30 mg cohort, suggests a commonly observed reaction with peptide therapeutics, a delayed-type hypersensitivity ISR. ISR has been reported with several GLP-1 agonists that are marketed for the treatment of type 2 diabetes and obesity, including liraglutide, lixisenatide, exenatide, and tirzepatide. For example, weekly exenatide had a peak of incidence of ISR between two and four weeks, with no more ISR occurring after 14 weeks. Considering the unmet medical need in the severe disease and the characteristics of the ISR, we believe at this stage the risk-benefit profile of MBX 1416 remains favorable. In addition, we will continue to monitor ISR and deploy mitigation strategies that have been effective with other peptide drugs as part of our phase II dose selection program. Next, let's look at the laboratory values as summarized on slide nine. We are very pleased to see no clinically meaningful changes. No changes in body weight were observed across the study, and mean changes in vital signs from baseline were generally small and not dose-related. Mean changes from baseline in clinical chemistry, including glucose and hematology value, were generally small, with no apparent pattern of dose dependence. Mostly isolated and transient reduction in hemoglobin were noted in a few participants from both the SAD and MAD cohorts in both the active and placebo group. None of these reductions were deemed clinically significant by the investigator or were reported as adverse events. Finally, mean changes from baseline in ECG parameters were generally small and not dose-related, with no clinically meaningful changes in the corrected QT interval observed. Now, let me turn to our PK and PD observation from the phase I trial. Slide 11 confirms that MBX 1416 exposure and PK profile were in line with our expectation based on the molecule design. Concentration increased in a dose-proportional manner in both the SAD and MAD cohorts. In the MAD cohort, steady state was achieved after the third dose, approximately 14 days after the third dose. Importantly, the half-life of MBX 1416 was approximately 90 hours, which supports our once-weekly dosing regimen. The peak-to-trough ratio is approximately 2.5, which shows MBX 1416 exposure is maintained throughout the week. In addition, there was low inter-subject variability. Slide 12 illustrates the pharmacodynamic effect on GLP-1 observed during two mixed meal tolerance tests performed in the MAD cohort. The 10 mg dose is shown in blue, and the 30 mg dose is shown in green. We are very encouraged to see that despite the small sample size, there is an increase in GLP-1 that reached statistical significance at a few early time points, including at 45 minutes on day nine at both 10 mg and 30 mg doses, and at 30 minutes on day 23 at 10 mg, while borderline significant at 30 mg. As a comparison, increase in GLP-1 peak following mixed meal tolerance tests has been observed with Avexitide in healthy volunteers. As expected in healthy subjects, no meaningful changes from baseline or between MBX 1416 and placebo were observed in the other parameters measured during the mixed meal tolerance test, for example, glucose, insulin, or C-peptide. We are anticipating changes in these parameters in PBH patients based on the apparent increase in GLP-1 and MBX 1416 hypoglycemia. To efficiently evaluate MBX 1416 effect on gastric emptying and potential drug-drug interaction with statin, we added a cohort in our phase I study, and the results are summarized on slide 13. Consistent with the expected effect of GLP-1 antagonism, MBX 1416 at 45 mg appeared to slightly accelerate first-hour gastric emptying, as demonstrated by a small increase in acetaminophen exposure in the presence of MBX 1416 compared to acetaminophen alone administered at 1,000 mg. Exposure of rosuvastatin, a commonly prescribed statin, increased only slightly in the absorption phase in the presence of 45 mg of MBX 1416 compared to 10 mg of rosuvastatin administration alone. MBX 1416 had no effect on total rosuvastatin exposure, as measured by AUC 0 to infinity. This corroborates our belief that the small early change in rosuvastatin exposure was caused by accelerated gastric emptying rather than the direct inhibitory effect of MBX 1416 on the transporters that mediate rosuvastatin cellular uptake, such as OATP1B1 and OATP1B3. Overall, we are very pleased with the outcome of this evaluation, and we believe that MBX 1416 will not impact usage and dosing. This concludes my summary of the top-line results from the phase I MBX 1416 trial, and at this time, I will turn the call back to Kent for a look ahead for our program in 2025. Thank you, Sam. Slide 14 summarizes the key results observed from the trial. As I mentioned in my opening remarks, we are pleased with the positive phase I results that showed in healthy volunteers that MBX 1416 was generally well tolerated with a favorable safety profile, as well as a pharmacokinetic profile supportive of once-weekly dosing. We observed no meaningful impact of MBX 1416 on rosuvastatin exposure and a slight acceleration in first-hour gastric emptying, as expected with GLP-1 antagonism. We also observed an increase in GLP-1 peak during the first hour after a mixed meal tolerance test, which is an encouraging signal in healthy volunteers that we believe may translate into a therapeutic benefit in patients with PBH. Based on these results, we intend to initiate a phase II study in patients with PBH in the second half of this year to further optimize dosing, pending alignment with the FDA on our proposed study design in an end-of-phase I meeting with the FDA expected in mid-year. As you can see on slide 15, we have multiple important value inflection points anticipated in 2025, including the next steps outlined for the MBX 1416 program and an IND submission for our MBX 4291 program in obesity, and a key phase II top-line data readout in Q3 for our MBX 2109 program in hypoparathyroidism. We believe the next 12 months will be a transformative time for MBX, and we look forward to providing you with further updates on each of our programs. With that, we will open it up for questions. Operator, please poll for questions. Thank you. To ask a question, please press star 11 on your telephone and wait for your name to be announced. To withdraw your question, please press star 11 again. Our first question comes from the line of Jessica Fye with JPMorgan. Your line is now open. Great. Good morning, guys. Thanks for taking our questions. I guess first, how should we think about a phase II design here? Should we think of this as looking similar to what Eiger ran? And then separately, can you elaborate on the ISR AEs that you saw in the MAD portion of the trial? And maybe just explain to us, what does a grade 3 ISR look like, and how does that look like broken down across the different dose levels? Thank you. Okay. Thank you, Jess. So two-part question. And just the first part, we do plan to proceed with a phase II trial in the second half of this year following successful end-of-phase I meeting with the FDA mid-year. At this time, we're not providing more details on the study design, and we'll do so after aligning with the agency and kicking off the study. I'll turn it over to Sam to address your second part of the question. Yeah. I think mainly the ISRs were manifested by erythema, and the grade 3 was defined by the size of the erythema, which was in size more than 10 cm. That's what triggered a grade 3. In fact, what was very interesting is that the healthy volunteers didn't request to be withdrawn or didn't request any additional treatment. They just noticed it and said, "Well, I have this erythema." And the investigator thought it was important decided to withdraw three of the subjects, one at 10 mg and two at 30 mg. So again, back to your question, the grade was defined by the size or only by the size, and that's what defines the grade 3. And the spread across the dose, I think we see an increase with the dose. The 10 mg see a little bit less adverse event, less ISR than the 30 mg. Thank you. Thank you. Our next question comes from the line of Michael Yee with Jefferies. Your line is now open. Hey, guys. Thanks for taking our questions. This is Kyle from Michael Yee. So on the PD curves on slide 12, could you please elaborate further on the shape of the curves? I guess specifically on day nine, why is there a seesawing effect? And on day 23, why does the curve look different than day nine? And how would you expect this to translate to PD signals in patients? And how would you compare and contrast this to what's observed with amylase PD signals? Thank you. Yeah. So what you can see on day nine, there is a consistent effect on day three, there is a consistent effect around between 30 minutes and 60 minutes and the different effect later. So that's why we really took as a value the early observation that was observed at both 10 mg and 30 mg. So that's why that was very important to have this consistency in effect. The second comment is related to, we're still in healthy volunteers, right? And we have a small population. The number of subjects were 6 and 12, respectively, for the different dose. So we were very happy with the results to see these results, but we are conscious that the sample size is still limited. Yeah. So there is publication showing that with avexitide, there is also an increase in GLP-1 peak, increase of peak in GLP-1. So we have found an interesting publication where we see a similar effect. And back to your question about what we expect later is really to see an effect on insulin, on C-peptide, but also on the glucose nadir that will be, how can I say, predictive of the clinical benefit on symptoms. So that's what we, and for this, we will wait for data on patients in our phase II program to see this effect. Okay. Thank you. Thank you. Thank you. Our next question comes from the line of Annabel Samimy with Stifel. Your line is now open. Hi, all. Thanks for taking my questions. Just had a quick one. I guess, what are some of the determinants that you're going to be looking at to identify the appropriate dose selection going forward into phase II? What should we be looking out for? Is it strictly based on the SAEs, or are you looking at certain levels, PK levels specifically? Thanks. Thank you, Annabelle. I'll have Sam address that. Yeah. First, we don't have any SAEs in this phase I study. And I think we are ready to go to patients, in fact. We have enough data today from our phase I to move to patients. And in the patient population, we'll be looking at the pharmacodynamic effect to continue to look at the pharmacodynamic effect, such as glucose nadir, such as insulin, C-peptide, and also looking at symptoms improvement. Yeah. Just reinforcing the point that we saw statistically significant PD effect at both the 10 mg and 30 mg dose in this phase I study. Okay. Thank you. Thank you. As a reminder, to ask a question at this time, please press star 11 on your touch-tone telephone. Our next question comes from the line of Seamus Fernandez with Guggenheim Securities. Your line is now open. Oh, great. Thanks for the question, so just a couple of questions here, guys. The dynamics around the comparison to exenatide. Exenatide also happened to have a fairly high rate of autoantibody production that was related to this. Have you looked at related to some of the ISRs, I believe, so have you looked at autoantibody development, not necessarily neutralizing antibodies, but it does appear interesting looking at the sort of time course, seeing that this is occurring on the third or fourth dose for the Grade 3 erythema. Just interested to get a better understanding if you've looked at autoantibodies developing in this patient population, and then any speculation, because it doesn't look like Avexitide has the same ISR rate, at least in what's presented in the public domain. Just trying to get a sense of how different your GLP-1 antagonist is in terms of its design and if there's any speculation as to what might be causing the ISRs. Thanks. Thank you, Seamus. The ADA standard kind of analysis will be forthcoming. Probably present that at a medical meeting. Just taking a step back, this design was taking a human GLP-1 sequence with some structural modifications to create a GLP-1 antagonist and fatty acylation for the longer half-life that we've seen, the 90 hours. We believe that this was designed for greater homology, for greater stability, solubility, and potency. We have about, from in vitro assays, about 10-fold greater potency in inhibition at the GLP-1 receptor than Avexitide. We believe that we are well-positioned to have a best-in-class once-weekly treatment for this chronic serious disease with a tremendous unmet medical need. Thank you. That concludes our Q&A session. At this time, I would like to turn the call back over to Kent Hawryluk for closing remarks. Thanks, Shannon. I'd like to thank everyone for joining us today and for your continued interest in MBX. 2025 promises to be a pivotal year for our company with a number of key value inflection points anticipated throughout the year, including phase II evaluation of MBX 1416 in PBH patients, top-line results from our ongoing phase II trial in hypoparathyroidism, and our IND submission for our obesity candidate, MBX 4291. We look forward to providing further updates on these and other programs in development throughout the year and hope to see you at a future investor conference or medical meeting. This concludes today's conference call. Thank you for your participation. You may now disconnect.