Hello, and thank you all for joining today's call. I'm Brian Windsor, President and Chief Executive Officer of Aileron Therapeutics. Before we begin, I'd like to remind you that various remarks we will make today constitute forward-looking statements for purposes of the safe harbor provisions under the Private Securities Litigation Reform Act of 1995, as outlined on this slide. Joining on today's call are Dr. Cory Hogaboam, Aileron's Chief Scientific Officer, and we are pleased to have a leading expert in the field, Dr. Andreas Günther, who is the Head of the Center for Interstitial and Rare Lung Diseases of the Justus Liebig University in Gießen, Germany. I'm very excited to discuss the safety and positive biomarker data from Cohort 2 of our Phase I-B clinical trial, which evaluated treatment of 5 mg BID of LTI-03 for 14 consecutive days in subjects with idiopathic pulmonary fibrosis. We believe that the results are remarkable and support advancement to a phase II study. We observed dose-dependent effects of LTI-03 in Cohort 2, which support the findings observed in the Cohort 1 data at a lower dose, 2.5 mg BID of LTI-03 for 14 consecutive days. Some highlights that we observed in the high-dose Cohort 2 arm of LTI-03 included dose-dependent trends were observed in five biomarkers, including collagen 1A1, CXCL7, TSLP, GAL7, and surfactant protein D, or SPD, which provide evidence of active LTI-03 pharmacodynamics. Also, statistical significance of three biomarkers observed in Cohort 2 mirrored the findings in Cohort 1, and the combined dataset showed even stronger results, with four results showing statistical significance. In Cohort 2, we also measured surfactant protein D, or SPD, which is an indicator of epithelial cell health. LTI-03 demonstrated a 5% decrease in SPD after a 14-day treatment course. We are highly encouraged by this result since the current standard of care for IPF, which is the drug marketed under the brand name Ofev, reduced SPD by 4% at 12 weeks in the INMARK clinical trial. 2023 sales for OFEV were EUR 3.5 billion, which equated to about $3.8 billion. We are highly encouraged that LTI-03 was able to have a meaningful reduction in SPD only 14 days after treatment. On the safety front, phosphorylated AKT, or pAKT, which is the safety biomarker, was not activated in PBMCs in either cohort, which we were pleased to see. We believe that the data in the phase I-B study strongly reinforces the potential of LTI-03 to improve lung function and reverse the course of IPF. With a dual mechanism of action and the possibility of disease-modifying effects, we believe that LTI-03 could meaningfully impact the current treatment paradigm. We believe that LTI-03 has potential to meet the current high unmet need for IPF patients. The global IPF market is estimated to reach $11.7 billion by 2031. Currently, there are two drugs that are approved: nintedanib, better known under the brand name OFEV, which I referenced earlier, and pirfenidone, which is marketed under the brand name Esbriet. Both drugs offer very modest clinical benefit, only slowing disease progression for about a year, and are expensive. Median survival is still two to five years from diagnosis, so there's a real need for something that impacts both pro-fibrotic pathways as well as epithelial cell health. We believe LTI-03 could have a measurable impact for IPF patients. Now, I'd like to go in and discuss data slides in detail. I want to start just with a recap of what our target is: caveolin-1, which is a key regulator in fibrosis. The caveolin-1 protein is dramatically related to fibrosis, with a high propensity to hypertrophic scarring and, conversely, high content of caveolae, resulting in a low propensity for hypertrophic scarring. Caveolin is found in many cell types in the fibrosed lung. Caveolin has a regulatory effect in fibrosis, and it affects this regulatory function through a 20-amino acid sequence called the caveolin scaffolding domain, or CSD. You can see this in the purple region in the illustration on the right-hand side. This region binds and connects with proteins with a caveolin binding domain, affecting their phosphorylation status and their trafficking, and thus affects the trafficking of a large number of proteins, many involved in multiple fibrosis pathways. Next slide. Unfortunately, caveolin is basically lost in a fibrotic state. This paper by Naftali Kaminski and Augustine Choi showed that it's dramatically downregulated in IPF, both at the transcript level and the protein level. So this really kind of begs the question: if your target is missing, then what do you have to target? Next slide. The answer is a little non-intuitive, but very effective. LTI-03 is a portion of that caveolin scaffolding domain region of caveolin-1. It is a seven-amino acid peptide. It is this FTTFTVT sequence, which is really at the center of that CSD region. And when we put this peptide into a cell system, a tissue culture system, a living system, it sort of acts like it's mimicking Cav1 activity, binds proteins, affects their phosphorylation, and thus apparently affects trafficking of a large number of proteins, many involved in fibrosis. We've seen tremendously positive things in the preclinical studies with LTI-03. This peptide is given by dry powder inhalation for direct-to-lung delivery. Next slide. Here is the design of the current phase I-B study that we have just completed in IPF patients. This was for patients with a diagnosis of less than three years, and they could not have been on previous antifibrotic therapy for at least two months of baseline. So treatment naive or washout for two months. This study involved 24 patients total, nine active and three placebo in each dosing group. The low-dose data, which we have released previously, is 2.5 mg LTI-03 BID. The high dose that we're talking about today is 5 mg BID. These are dosed sequentially for 14 days. We do require for these patients a bronchoscopy at screening and also a bronchoscopy at a 14-day follow-up because, although our primary endpoint is, of course, safety and tolerability for these patients, we are looking at key exploratory endpoints, which are multiple biomarkers. These are ones that we're able to get through plasma as well as direct lung contact. We determined statistical significance for biomarker movement as a p-value of less than 0.05. Next slide. I've been through this summary, but just to highlight again, we did have dose-dependent movement of five of the biomarkers, a statistical significance of three biomarkers in the Cohort 2 with four statistical significance sets in the combined dataset. We were able to measure surfactant protein D, and our safety biomarker was not activated in either cohort. Next slide. Here is a table of the results that we have. And so, kind of from left to right, we see a positive trend in the Cohort 2, whether we had one or not, whether that was statistically significant in Cohort 2. And then next to that, whether we saw a positive trend when we combined datasets from Cohort 1 and Cohort 2, and then whether that dataset was statistically significant. And then finally, on the right-hand side, whether the dataset was dose-dependent from Cohort 1 to Cohort 2. And so you can see, kind of just focusing on the Cohort 2 data, that we did have positive results for the collagen 1A1, IL-11, CXCL7, TSLP, GAL7, surfactant protein D, and phosphorylated AKT. I would note that one of the biomarkers we looked at in Cohort 1, sRAGE, which was evaluated for that cohort, we were not able to evaluate in this cohort due to multiple protocol violations. We did see statistically significant results with CXCL7, TSLP, and GAL7, and then even better statistical significance results with IL-11, CXCL7, TSLP, and GAL7, and then finally, dose-dependency of collagen 1 A1, CXCL7, TSLP, GAL7, and SPD. So maybe I can go into specifics on the graphs. Next slide. So this is the graph for galectin- 7, or GAL7. We did see both significant effects and dose-dependent decreases. So on the left, you have a graph just of cohort two relative to placebo. We did have a statistically significant decrease in GAL7 relative to placebo. On the right-hand side, you see the combined dataset. The light blue circles are the cohort one values. The dark blue are the cohort two, obviously a statistically significant result for the combined dataset versus placebo. So very good result with GAL7. Next slide. TSLP, another marker that we saw good results in the Cohort 1. We also had really good results in Cohort 2. So on the left, Cohort 2 value versus placebo, p-value of 0.01, obviously statistically significant and obviously lower, and then the combined dataset also greater significance when we combine the dataset versus placebo. I would note that GAL7 and TSLP are both found in the basal-like cell in the fibrosed lung. This is a cell type, an aberrant cell type. This is specific to IPF, is not found in a normal lung, and really only found in the deeply fibrosed portion of the lung, so one question that I get a lot is, with an inhaled peptide, how do you know that you're getting to the right spot of the lung? How do you know that your drug is going to do what you have seen it do in preclinical studies? Having markers, GAL7 in particular, that is specific to these basal-like cells, having these move significantly to us is real evidence that the drug is getting where it needs to go and doing what we believe it's supposed to do. Next slide. IL-11, another marker with which you're probably familiar. We had a significant decrease in the combined dataset, not one that was dose-dependent. We saw a pretty good drop in IL-11 versus placebo in both groups. You can see the cohort 2 on the left just missed significance, and the combined dataset was statistically significant on the right-hand side relative to placebo. Next slide. Collagen 1A1, we did have a dose-dependent decrease. Neither group was statistically significant, but we did have a good decrease in Cohort 2 relative to placebo, and then a nice dose-responsive effect. You can see the combined Cohort 1 and Cohort 2 values there on the right-hand side, so dose-dependent decrease of collagen. Next slide. SMAD was one that didn't show a beneficial effect in Cohort 2, and neither did it show a beneficial effect in, I'm sorry, in Cohort 1, and neither did it show an effect in Cohort 2. It was pretty flat in both groupings. We measured the delta for phosphorylated SMAD or pSMAD on the bottom, and then also delta for the total SMAD relative to beta-tubulin on the top, and you can see with the cohort two, looks about like the cohort one values, and the combined dataset on the right-hand side, again, pretty flat versus placebo. Next slide. CXCL7, we've had both significant and dose-dependent decreases. You can see the Cohort 2 data on the left-hand side, a significant decrease versus placebo, and then the combined dataset, even greater significance when we combine Cohort 1 and Cohort 2, again, dose-dependent, which is CXCL7. Next slide. Phosphorylated AKT, this is measured in peripheral blood mononuclear cells, or PBMCs. This is a safety marker for us. We did not want to see movement of phosphorylated AKT relative to placebo because this would have possibly indicated inflammation being caused by LTI-03. In Cohort 1, we did not see movement relative to placebo, and neither in Cohort 2 did we see any sort of elevation relative to placebo. You can see the Cohort 2 completely flat there relative to placebo and the combined dataset. So no inflammation per this biomarker and a good safety measurement for us. Next slide. Surfactant protein D, or SPD. This is one that we measured in plasma, which is important to us moving ahead in the clinic because it'll be much easier to get plasma samples going forward than, obviously, samples that require a bronchoscopy. SPD is a new compound that we were able to measure for the Cohort 2, again, taken out of plasma. Although not statistically significant, we did have a decrease in surfactant protein D of about 5% relative to placebo. On average, we're able to go back and run plasma samples from Cohort 1 and saw a dose-dependent effect, so a stronger effect with Cohort 2. SPD is an important one for us going forward, and we're glad that we had this movement. SPD is really a function of epithelial cell health. And for us to see this sort of movement down in SPD lets us know that LTI-03 is potentially protecting the barrier of epithelial cells. This is really kind of a measure of barrier epithelial cell health. When the barrier is dysfunctional, you get leakage of SPD into the plasma, and that's why we wanted to see a decrease in SPD relative to placebo, which we did, so good biomarker for us going forward. Next slide. SPD was also decreased by OFEV in a clinical trial, so this is a table looking at the effects of nintedanib on circulating biomarkers of IPF. This is the INMARK clinical trial. You can see some good names up there involved in this clinical trial, but we did see movement of SPD. Sorry, this red box is moved up, but the SPD values are what we really want to highlight. In nintedanib versus placebo, they looked at a fold change in SPD at week 12, and it corresponded to a 4% decrease in surfactant protein D in this trial. Now, of course, we measured this at a different time point, a much earlier time point, did see a 5% decrease. These trials are obviously different in design, but for us, this was really good evidence that we're able to affect a biomarker also affected by one of the two approved standard of care drugs. So this will be an important biomarker for us going forward. So really, really pleased with the biomarker results that we've seen, the Cohort 2 results similar to Cohort 1, and then importantly, the dose dependency that we saw in Cohort 2 versus Cohort 1. So that's really my summary of the data slides. I would like to now turn the call over to Dr. Andreas Günther for his thoughts on the study. Hello everybody. From Gießen in Germany, my name is Andreas Günther. I'm Professor of Internal Medicine, and I'm the Head of the Center for Interstitial and Rare Lung Diseases at the Justus Liebig University in Gießen, Germany. I have been working on preclinical projects in the context of LTI-03, and I'm participating in the phase I-B trial that is the focus of our today's discussion. So I'm familiar with both the preclinical dataset as well as the data that just recently came out of this particular trial. As you know, the phase I-B trial was involving 24 patients with idiopathic pulmonary fibrosis in order to prospectively randomized explore the ability of LTI-03 delivered as a dry powder via inhalation to impact significant pathways for fibrosis in the human lung. In total, 18 patients received LTI-03 versus six patients who received placebo. The duration of the trial was 14 days, and the patients underwent bronchoscopy at baseline for routine purposes as well as bronchoscopy after 14 days. During these bronchoscopies and extensive sampling of biomaterials, including deep bronchial biopsies as well as bronchoalveolar lavage, and also sampling of blood-based biomarkers was performed to answer the question if LTI-03, as observed in preclinical settings and in ex vivo experiments, would be able to impact very important signaling pathways forwarding fibrosis. First, I would like to state that we were pleased to see that obviously there were no major safety aspects. The dose and the drug seemed to be well tolerated. There were only minor adverse events, which are in line with dry powder inhalation, such as slightly increased coughing in some pulmonary patients participating, but there were overall no significant safety signals, which makes us believe that it is absolutely feasible to continue with this program in terms of safety. With regard to the biomarkers, I would like to mention that several of these biomarkers had been on the list of the company, and the focus or the reason why the company chose this was because these markers were, A, found to be either prognostic in patients with IPF, or at least found to be clearly differentially regulated, and B, these markers were found to be impacted by the drug in preceding preclinical in vitro as well as ex vivo studies employing human IPF tissues in the sense of high precision-cut lung slice experiments. The markers that were on the agenda are collagen 1A1, IL-11, CXCL7, thymic stromal lymphopoietin, TSLP, and galectin-7, GAL7. Now, some of you will certainly know some of these markers, especially collagen, which is an imprint of the ongoing fibrotic reaction. Others, such as IL-11, for example, indicate some inflammatory changes that are observed in patients with IPF and altered macrophage biology, such as CXCL7. There are also markers that not only have been shown to be of relevance for the fibroblasts, the key effector cell in lung fibrosis, but also in basal cells, which recently have been shown to contribute to the pathobiology of IPF. In this regard, TSLP and GAL7 have been shown to be impacting basal cell biology to be increased in patients with IPF and were therefore on the target list. Now, all of these markers have been found to be upregulated in IPF. All of these markers in preceding preclinical trials have been shown to be downregulated by LTI-07, oh, I'm sorry, LTI-03. The expectation was that, similar to the preclinical and ex vivo studies, patients who received LTI-03 would similarly show a decline and a reduction in collagen 1A1, CXCL7, IL-11, TSLP, and GAL7. As you will see and hear from the colleagues from Aileron, this is indeed what happened. As you can see, the study showed that not only was there a positive trend when pulling together all data from the two cohorts versus the placebo group, there was a positive trend for a regulation via LTI-03, there was also statistical significance, at least with regard to IL-11, CXCL7, TSLP, and GAL7. And I think this is of importance because we have to keep in mind that IPF perceives a rather heterogeneous disease with a spatial heterogeneity. So even when doing a bronchoscopy with a bronchoalveolar lavage or a deep bronchial brushing, you cannot be entirely sure that you would reach similarly concerned parts of the lung from one patient to the next one. So there is usually a kind of a scattering of data, but having in mind that it is quite stunning to see that in this trial, treatment with LTI-03 significantly reduced the expression of collagen 1A1, CXCL7, TSLP, and GAL7. Now, since LTI-03 also seemed to affect pathways that are of impact for basal-like cells, there was also a question coming up if that would also hold true for alveolar type 2 cell, which is the most important cell type in IPF, probably because that's where the injury and the fibrosis starts. So type 2 cells in IPF lungs usually show signs of their chronic injury, and one very prognostic marker of that is the basolateral secretion of a surfactant protein called SPD. SPD in serum has been found to be clearly prognostic. The higher the value, the more likely the probability of death and exacerbation. So it was an obvious question to also ask if treatment with LTI-03 would be capable of impacting plasma SPD levels. As you can see from the data that are presented to you, although not reaching significance, there was a clear tendency to a reduction of SPD by about 5% in this rather short time period of two weeks. As a kind of a comparison, it is probably important to state that the authorized drug nintedanib is also able of reaching a decrease in SPD by 4%, but that's obviously reached after a much longer treatment period. One could, of course, speculate if patients that receive LTI-03 for a longer time period may show an even better response in terms of SPD. One could interpret this dataset in that probably there is also a kind of a beneficial effect of LTI-03 on the alveolar type 2 cells, a phenomenon that has been studied in preclinical experiments before and has been found to be a valid observation. Taken together, my interpretation of this dataset is that on a quite substantial list of biomarkers, LTI-03, which is primarily supposed to be anti-fibrotic but also probably acting epithelial protective, seems to do its job, seems to beneficially affect pro-fibrotic signaling pathways in the distal lung of IPF subjects, resulting in a reversal of the pro-remodeling pro-fibrotic activity of these pathways. And also, of significant importance, it seems to be safe. We are looking forward to continue with LTI-03 in a phase II trial, and we hope that we will see comparably beneficial effects. Thank you. Thank you, Dr. Günther, for your perspective. Really appreciate that. I want to remind everyone of the Ask a Question button in the upper right-hand corner of your screen if you have a question. With the phase I-B safety and biomarker results, along with a robust preclinical safety package reported in our phase I-A study, we believe that we are well positioned to advance the clinical program for LTI-03. We look forward to a phase II study for LTI-03, and we also look forward to keeping you updated on developments and appreciate your support of Aileron. Dr. Cory Hogaboam with me, and I will now open the call up to answer any questions. All right. There are no questions. So with that, we conclude our data call on the cohort two data for the phase I-B study of LTI-03. Thank you again for your time. Have a good day.