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 slide 2. I'm very excited to discuss the positive data from cohort 1 of our phase Ib clinical trial of LTI-03 in idiopathic pulmonary fibrosis. On today's call, we'll be joined by Cory Hogeboom, Aileron's Chief Scientist, and we are pleased to have an expert in the field, Dr. Andreas Günther, Head of the Center for Interstitial and Rare Lung Diseases of the Justus Liebig University in Gießen, Germany. I'd now like to turn the call over to Cory Hogeboom for a brief overview of LTI-03 and the cohort 1 data. Cory? Thanks, Brian. It's my pleasure today to discuss the data from cohort one of the phase Ib clinical trial, evaluating low dose 2.5 mg BID of LTI-03 for 14 days in patients diagnosed with idiopathic pulmonary fibrosis or IPF. The phase Ib study is a two-cohort safety trial, and we expect to report results of cohort two, which will evaluate high dose 5 mg BID of LTI-03 in this patient population in the third quarter of 2024. LTI-03 is a novel Caveolin-1 related peptide that has a unique dual mechanism of action. It has shown the ability to both reduce pro-fibrotic signaling, as well as protect critical cells in the lung epithelium, which could potentially protect healthy lung tissue and restore lung function. 12 patients were enrolled in cohort 1 of the ongoing phase Ib clinical trial, 3 in the placebo arm and 9 in the active arm. Patients had a bronchoscopy at baseline, received a low dose of LTI-03, 2.5 mg BID, twice a day for 14 days or placebo, followed by a bronchoscopy on day 14 and 7 days of follow-up. The primary endpoint of this study is safety and tolerability, with key exploratory biomarker endpoints in blood, BAL, and deep bronchial brushings. Key findings from cohort 1 show that LTI-03 reduced expression of multiple pro-fibrotic proteins in both pathologic basal-like cells and fibroblasts, stimulated production of a factor indicative of type 1 epithelial cell health, and did not induce inflammation in peripheral blood mononuclear cells. I'll now turn the call over to, Dr. Andreas Günther, who will walk through detailed findings from cohort 1 portion of the phase Ib study. Andreas? So hello, everybody. Cory, thank you for these explanations. I may probably shortly introduce myself. My name is Andreas Günther. I'm a pulmonary and critical care physician in the University of Gießen in Germany. I'm now running an ILD center for many years, 20 years now, and I'm active both in basic and translational research, as well as in clinical studies in the field of interstitial lung diseases. So I think I'm quite familiar with the disease as such, which really deserves novel treatment modalities. And as Cory figured out, the interest in LTI-03 largely stems from the observation that for the first time, to my understanding, in the history of IPF-related research and drug identification, we are talking about a drug with a dual function, both the fibroblast and the mesenchyme, as well as the epithelium. Which is of fundamental importance from our understanding, as the disease seems to be triggered by the epithelium and the mesenchyme, the activated fibroblasts taking over the function of an executor of fibrosis by producing large amounts of collagen, making the lungs stiff and impairing gas exchange. So as a result of the preceding preclinical and the first clinical studies in normal, healthy volunteers, it was decided to move on with the phase Ib. The clinical trial design you will find on the slide, phase Ib clinical trial design. This study actually is still in progress, but has been looking at two dosing cohorts, one, the low dosing cohort, 2.5 milligram BID, and a high-dose cohort, including 5 milligram BID. The first cohort, the 2.5 milligram BID, has been already conducted, and we are able now to look at some data that have been generated in the context of this trial. The overall study design was to include patients with an IPF diagnosis not longer than three years ago. Patients should have had no anti-fibrotic therapy in the two months prior to baseline investigations. A total of 24 patients as planned, ultimately to be included into this trial. Of course, the primary endpoint-... was safety and tolerability. As you are aware from the preceding discussions, LTI-03 was provided as a dry powder for inhalation. It was the firm belief of the company, as well as the advisors, that an inhalative approach could have genuine advantages versus a systemic administration. You are probably aware of the ongoing discussions that some drugs that are supposed to work in IPF may probably not appropriately be dosed with regard to the treatment of fibrosis, because the side effects limit their use once they are systemically provided. So an inhalative approach, from our understanding, includes the clear advantage of being able to appropriately dose the drug to reach the lung, the distal lung compartment, without causing significant spread over in systemic side effects. As a result, LTI-03 has been designed to be given as a dry powder to patients with IPF, and we strongly believe that by doing so, it is able to reach the distal lung of these patient population and to impact the fibrotic pathways in the distal lung of these patients. As you can see, patients underwent after screening an initial bronchoscopy to assess the baseline conditions in each individual patient followed by a 14 days treatment of the drug. And then after 14 days, the patients were bronchoscoped again, and during the bronchoscopy, we did two major investigations or procedures. First, the patients received a bronchoalveolar lavage, and the lavage fluid was aliquoted and sent in for analysis. The patients also underwent deep bronchial brushings, which to us reflects a kind of a complementary invasive approach to sample the distal lung. The lavages will certainly reach primarily the alveolar compartment, as it has been shown in numerous clinical investigations in the past. And the deep bronchial brushings will probably primarily assess distal bronchioles, as well as alveolar space, because of the flux of fluids through the alveoli to the distal bronchial compartment. So we think we did our best to sample the distal lung in this particular patient cohort, undergoing this placebo versus verum inhalation over a time period of 14 days. In both samples, in the lavages obtained at baseline or at day zero, and the bronchoscopy undertaken at day 14, several parameters were assessed. These parameters can be found on the following slide, phase Ib clinical trial called One Low Dose, which also is a kind of a summary. Now, it is important to state that all these markers that had been chosen are known to be playing a significant role in idiopathic pulmonary fibrosis, so at least there are prognostic data available showing the importance of these markers. They also have been shown to be of relevance in our previous ex vivo studies employing human IPF precision-cut lung slices with a placebo or a standard of care, or LTI-03 treatment, and were found to be therapeutically addressed and impacted by the treatment with LTI-03. One can clearly say that these markers are not only of importance in the natural course of the disease, but are also targets of the LTI-03 treatment, and therefore are potentially able to reflect the activity of the drug in the distal lung compartment. For easier reading, the markers are here grouped according to their pathway they are addressing and the cells they are addressing. For example, collagen one, IL-11, CXCL7, typical fibroblast, myofibroblast markers. TSLP, Gal-7, are markers that are associated with basal-like epithelial cell activity, cells that seem to play a significant role in the evolution of the disease and the aggravation of the disease. And then soluble RAGE, as you may have heard from Cory before, a marker that, that is indicative of, let's say, alveolar epithelial health, and that we have been observing to be a very good marker to reflect LTI-03 activity on the epithelium. As I said, and a very new aspect in IPF treatment to not only address fibroblast biology, but also to try to overcome the chronic injury in the type two cells and other alveolar epithelial cells, as mentioned before. So if we now have a look at these markers, you will see on the consecutive page, which is called LTI-03 phase I Biomarker Support Data, Gal-7 and TSLP. You can see that in case of these two compounds, LTI-03 treatment in patients with IPF, and we're talking about three patients receiving placebo versus eight patients receiving active low-dose treatment. Both of these markers were found to be suppressed by the LTI treatment in a statistically significant way. This is already quite impressive, as I think, because having in mind the relatively low number of placebo patients, reaching significance at all is already quite a challenge, I would say. And you can see from the distribution of the data that this is quite stunning. So these basal cell markers are clearly suppressed, indicating or implicating a beneficial drug effect on this particular IPF-relevant epithelium population. The data are shown as a delta between post-dose and pre-dose. So one may argue that there seems to be some change over time, for example, in the placebo cohort. I think this is absolutely okay, as it may reflect the natural evolution of the disease with an overall increase of these markers over time, which would reflect, to some extent, disease severity. We also have to keep in mind that these patients underwent an invasive procedure 14 days before, and that may also probably cause some reaction in the distal lung. And then, of course, also we have some aspect of sampling, where just particularly sampling a small part of the lung, and we may probably not be able every time to again, reach the very same locus of sampling after 14 days when we re-bronchoscope the patients. So here, a very clear signature with regard to basal cell markers, as we have been seeing in the ex vivo human IPF precision-cut lung slices. In the following slide, which is called LTI-03 Phase I, the biomarker support data IL-11 and collagen one, alpha one, you can see that, especially with regard to collagen one, there's also a significant reduction in the amount of collagen in the active group versus the placebo group. Collagen one is probably the best investigated biomarker indicating progression and onset of fibrosis, and has been also found to be of prognostic implication. So I think it is clearly visible that LTI-03 in these patients affects fibrosis by reducing this biomarker. As you can see on the left hand, the data are not as clear, and especially they don't reach significance for IL-11. But still, if you look at the data distribution and having in mind, again, the overall very limited N number in the placebo group, I think it is. There's a clear signature or a trend in the correct and right direction. If we turn to the next slide, we can see LTI-03 phase Ib biomarker support data, phospho-SMAD2/3 and total SMAD2/3. You will see that there's not that much of a change between active and placebo arms, which at a first glance may be somewhat confusing. But I can say that TGF-beta signaling pathways, especially through this SMAD, is notoriously difficult to capture in experimental settings. And I think it is not unpredictable that it is much more difficult to see significant changes in response to LTI-03 treatment with regard to this particular marker. I think that PAI-1, a readout parameter of TGF-beta signaling, is still on the list of things to be addressed and studied, and I'm looking forward to these data. On the forthcoming figure, which is focusing on soluble RAGE and CXCL7, you can see that, as anticipated from the more basic experiments being done in the past and also on the basis of the ex vivo human IPF precision-cut lung slice data, we can see a trend to an increase in soluble RAGE, which is promising, as I would say. I mean, it does not, again, reach significance because of the reasons mentioned before: low numbers, scattering of the data, especially in the placebo arm. But I think that if you look at the distribution of the primary data, there is a clear trend to an increase of soluble RAGE, which may be much more prominent and easily to depict in the patient cohort receiving the higher dose of LTI-03, and I'm looking forward to these data. With regard to CXCL7, you can see a drop in the plasma concentration, which is what we would expect based on previous data. And again, there is a trend visible from the raw data, which does not seem to reach significance in this case. And finally, one slide further, we can see one graph depicting changes in pAKT. So here there is not that much of a big difference with regard to the placebo versus active treatment, which I think is okay. We cannot see a clear trend here, so it seems to be rather unchanged. And that brings me to my, to my overall interpretation of the dataset. I mean, it's pretty clear that the primary purpose of this study was to assess safety and tolerability, which was observed, so it appears to be a safe application process to deliver LTI-03 as a dry powder. And that's the first and very important information. And with regard to the readout parameters of LTI-03 efficacy, I think overall it is fair to say that we do see changes in the biomarkers that are consistent with LTI-03 anti-fibrotic and pro-epithelium protective actions. These changes do not necessarily reach significance in all of the investigated parameters, which again, to me is explainable by the overall limited number of placebo patients. The number of calculations are, for sure, have been done on the basis of safety tolerability assessments, and not with regard to the secondary endpoints, as we have been looking at them right now. But for me, this drug still, after looking at this data, has all the attitudes that I would like to see to go further with a phase II study. Especially having in mind that, again, this drug seems to target both the epithelium of the alveoli of the diseased lungs as well as the mesenchyme. For this reason, it would be my expectation that, in contrast to existing drugs, the efficacy of this drug could be better as compared to the standard of care. And with this, I would like to thank you. Thank you, Dr. Günther, for your perspective, and thanks to Cory as well. We are excited about these results and look forward to continuing to progress LTI-03, as well as LTI-01, through the clinic, beginning with the LTI-03 high-dose cohort 2 readout, expected in the third quarter of 2024. We look forward to keeping you updated on the clinical development of LTI-03, and we'll now open up the call to questions. All right. No further questions. Thank you all for your time today. Appreciate the-