Ladies and gentlemen, thank you for standing by, and welcome to the Cara Therapeutics and Tvardi Therapeutics merger announcement conference call. Please be advised that today's conference is being recorded. I will now hand the conference over to today's moderator, PJ Kelleher, Tvardi Investor Relations. Please go ahead. Thank you, Operator, and good morning, everyone. Earlier today, Cara Therapeutics and Tvardi Therapeutics issued a joint press release announcing the signing of a definitive merger agreement. A copy of this press release is available on each company's respective website at caratherapeutics.com and tvarditherapeutics.com. Joining me on today's call are Chris Posner, Chief Executive Officer of Cara Therapeutics, and Imran Alibhai, Chief Executive Officer of Tvardi Therapeutics. Before I turn the call over to Chris, I would like to remind everyone that this discussion and the accompanying presentation will contain forward-looking statements based upon the current expectations of Cara and Tvardi, which include but are not limited to statements regarding the expected timing, completion, effects, and potential benefits of the transaction, and the future expectations and plans and prospects for the combined company. Such statements represent management's judgment and intention as of today and involve assumptions, risks, and uncertainties. Cara and Tvardi undertake no obligation to update or revise any forward-looking statements except as required by law. Slide 2 provides an overview of these forward-looking statements and the risks and uncertainties that could cause actual outcomes and results to differ materially from those contemplated in these forward-looking statements. Please refer to this slide for more details on these forward-looking statements and other important information. Furthermore, Cara intends to file a registration statement and accompanying proxy statement and prospectus with the SEC relating to the proposed merger. Please be advised to read, when available, the proxy statement and the prospectus and other relevant documents filed with the SEC, as these will contain important information about Cara Therapeutics, Tvardi Therapeutics, and the transaction. Once available, these documents can be obtained free of charge from the SEC at sec.gov or on Cara Therapeutics' website. I'll now turn the call over to Chris Posner, Chief Executive Officer of Cara Therapeutics. Chris? Thank you, PJ, and thanks to everyone for joining us on today's call. This morning, we announced the proposed merger of Cara Therapeutics and Tvardi Therapeutics, a private company developing novel oral small-molecule therapies targeting STAT3 to treat fibrosis-driven diseases. STAT3 is a highly validated but historically undruggable transcription factor and is a central catalyst in fibrosis-driven diseases. Imran will do a deeper dive into the science and the status of Tvardi's ongoing clinical trials in a moment. Following a comprehensive review of strategic alternatives for Cara Therapeutics that we initiated on July 1, along with my fellow Cara board members, we concluded that this merger is in the best interest of our shareholders while also allowing us to continue on our mission to improve patients' lives. As we will discuss in more detail shortly, this is an exciting time for Tvardi, with line of sight to two phase II data readouts next year and a cash runway for the combined company into the second half of 2026. The merger has been approved by the boards of directors of both companies and is expected to close in the first half of 2025, subject to customary closing conditions, including the approval of both companies' respective stockholders. Upon close, the combined company will be renamed Tvardi Therapeutics, will be based in Houston, Texas, and trade on the NASDAQ Exchange under the symbol TVRD. As mentioned, the combined company will focus on advancing Tvardi's pipeline of novel oral small-molecule therapies targeting STAT3, a central mediator in the pathogenesis of fibrosis in diseases with significant unmet need, such as idiopathic pulmonary fibrosis, or IPF, and hepatocellular carcinoma, or HCC. In addition, concurrent with entering into the merger agreement with Tvardi, Cara also entered into an asset purchase agreement with Vifor Fresenius Medical Care Renal Pharma, pursuant to which, at the consummation of the transaction, Cara will sell to VFMCRP, and VFMCRP will acquire from Cara certain assets and rights for the development, manufacture, and commercialization of Korsuva, Kapruvia, as well as certain associated liabilities. The asset purchase agreement is subject to certain conditions to closing, including the consummation of the merger with Tvardi. Now, let's review the key details of the proposed all-stock transaction. The combined company will be well-capitalized, including $28 million from a concurrent Tvardi financing, which, combined with Cara's anticipated cash at the closing of the merger, is expected to provide cash runway for the combined company into the second half of 2026. Ownership of the combined company is expected to be 83% for Tvardi investors and 17% for Cara stockholders, subject to adjustment based on Cara's net cash at closing and before giving effect to the Tvardi financing. As mentioned, based on Tvardi's current operating plan, this cash balance is expected to fund the combined company's operations into the second half of 2026, well past two critical phase II data readouts and the commencement of phase III trial preparation activities, if positive. The existing Tvardi management team, headed by CEO Imran Alibhai, will lead the combined company, and we are confident in their ability to drive significant long-term value for shareholders. The board of directors will include a total of seven members, six members selected by Tvardi and one member selected by Cara. We would like to extend our thanks to the Cara and Tvardi boards for their support in having unanimously approved this transaction. Subject to shareholder approval and customary closing conditions, we expect the transaction to close in the first half of 2025. With that, I'll now turn the call over to Imran, Chief Executive Officer of Tvardi Therapeutics, to tell us more about the company. Over to you, Imran. Thank you, Chris, and thank you to everyone joining the call this morning. We believe this merger and concurrent financing represent a truly transformative step forward in our quest to introduce a new class of breakthrough medicines for fibrosis-driven diseases. With a strengthened balance sheet and the many benefits conferred by NASDAQ exchange listing, I believe we are very well-positioned to advance our clinical programs through potentially value-creating milestones in 2025 and beyond, beginning with two important phase 2 data readouts next year, as I will discuss in more detail momentarily. I would like to thank Chris and the entire Cara Therapeutics board of directors for seeing the significant value that I believe will be realized through this transaction. At this point, I'd like to provide a brief overview of Tvardi, our science, and our clinical programs. Tvardi is focused on targeting STAT3, an incredibly well-known transcription factor that is a central mediator for fibrosis-driven diseases. Historically, it has been highly validated, yet undruggable target within the fibrosis-driven disease cascade. Based on the insights of our founders, who have deep expertise in STAT3 biology, we have designed orally-delivered small molecules that target STAT3. Our lead molecule, TTI-101, has the potential to serve as a disease-modifying therapy in IPF. In IPF models, we've observed not only reversal of fibrosis but also restoration of lung function. Our ongoing phase II blinded data suggests encouraging trends in lung function in patients with IPF. In addition, we are well-positioned to have a differentiated therapeutic impact in hepatocellular carcinoma, another fibrosis-driven disease. We have seen signs of responses both in monotherapy and in combination therapy from completed trials as well as ongoing clinical trials. From a timing perspective, we will have multiple near-term catalysts expected in the next year. For our lead program in IPF, we expect phase 2 unblinded data in the second half of 2025. Shortly thereafter, we will have phase 1B/2 top-line data from our HCC study, and then finally, we are ready to move forward with our second STAT3 inhibitor, TTI-109, which we expect an IND submission in the first half of 2025. Why STAT3? When you consider the major cascades we associate with fibrosis-driven diseases, there are a multitude of canonical cascades, including growth factors like TGF-β, cytokines like IL-6, and non-receptor tyrosine kinases, all of which coalesce onto STAT3 and induce its activation. STAT3 then homodimerizes and heads to the nucleus, where it is involved in a variety of diseases like IPF, hepatocellular carcinoma, and systemic sclerosis. Intrinsically, STAT3 activation leads to proliferation and survival, but also extrinsically, it leads to immune suppression. So what we've designed is a small molecule that is orally delivered that binds to STAT3 and inhibits its activation, thereby preventing homodimerization in the transcriptional cascades we associate with disease. What we do not do is have any effect on STAT3, the protein. Why do I mention this? Because STAT3 exists as a monomer in the electron transport chain. So previous attempts, and even current attempts to drug STAT3, have been to hit the protein and move it out of the system. And the problem with that has been that others have witnessed toxicities, toxicities like peripheral neuropathies that don't go away and lactic acidosis, i.e., mitochondrial toxicities. We have actually demonstrated in papers that we have no effect on mitochondrial cellular respiration. Two, across the 150 patients we've treated to date, we have not seen one example of mitochondrial toxicities related to our drug. So we think we found a better way to drug STAT3. So when we think of the pathway of fibrosis, what is interesting, there are multiple pathways leading to disease. If you focus your attention to the middle of the page, there is an intrinsic component and an extrinsic component, both of which STAT3 is involved with. When we see STAT3 activation, what happens to pro-proliferative cells is that they become proliferative, and they lead to deposition and scarring. But below the line in the immune system, we also see immune suppression. In that, we see the upregulation of MDSCs and Tregs, which then leads to the concomitant downregulation of CD8 cell activity. In the presence of our molecule, we've now demonstrated in vitro, in vivo, and now clinically that, one, we can downregulate the pro-proliferative activities at the cellular compartment, i.e., above the line, and then below the line, we can actually lead to immune activation because we see a downregulation of MDSC activity with a concomitant upregulation in CD8 cell activity. And we've published this numerous times. These insights are actually driven by the people on this page. Our scientific advisory board is led by our two founders, David Tweardy and Ron DePinho. David actually was one of the first groups to identify STAT3 30 years ago, not only its function, but its also its structure. He also happens to be the head of internal medicine at MD Anderson. So if there ever was a KOL in the field of STAT3, it's him. The other co-founder is Ron DePinho. He's the past president of MD Anderson, a prolific entrepreneur, and was elected to the National Academy for his work in aging. We're also buttressed by our scientific advisory board and our clinical programs by the who's who of oncology and folks like Keith Flaherty, Lisa Lancaster, and Jeff Swigris across oncology, as well as IPF. Our board is composed of folks who have been there and done that. Our chairman is Sujal Shah. Sujal was the past CEO of CymaBay, which earlier this year, excuse me, was acquired by Gilead Sciences for $4.3 billion. Mike Wyzga was the CFO of Genzyme, which was acquired for $20 billion. Our management team currently is composed of myself. My background is a PhD. My career started on the buy side, working at MPM Capital as well as Alexandria Venture Investments, both in private and public equities. I then transitioned to healthcare investment banking, and this is my second operating role. My first was at DNAtrix, and then I was picked off to be the first employee here at Tvardi Therapeutics. We're also supported by our CFO, Dan Kahn, who was classically trained as an M&A and securities lawyer. He then transitioned to banking at Morgan Stanley, where he was an M&A and securities banker. He then had multiple investment roles as well as operating roles and came to us at the beginning of 2023 as our CFO. And then finally, we have our Chief Medical Officer. John is a medical oncologist. He spent over 10 years at Emory University and has quite a breadth of experience on the development side. He was at Lilly, where he was involved in mid-stage trials for an approved therapy in HCC, as well as working at HUTCHMED before joining us, where he was critically important in leading the NDAs for their molecules in Europe, the U.S., and worldwide. On this page is our pipeline. Today, we'll primarily focus on idiopathic pulmonary fibrosis, our lead indication with TTI-101. We'll touch briefly on HCC, our second trial, again with TTI-101, and then we'll wrap up with TTI-109. TTI-109 is an oral small molecule which is structurally related to, yet chemically distinct from TTI-101, and is designed to enhance our ability to target STAT3. An IND application for TTI-109's first human study is expected in the first half of 2025. We look forward to providing more details about our second molecule, 109, in fibrosis-driven diseases as they become available, so first, let's move to IPF. IPF is an incredibly well-known disease. It is a rare chronic interstitial lung disease characterized by inflammation, progressive fibrosis, and then eventually death. Patients with IPF have a poor prognosis with a median mortality of two to three years. It is an orphan disease, which TTI-101 has orphan designation, yet the prevalence is quite high. We see almost 150,000 patients in the United States. There are two currently approved molecules. One is Ofev, and the other is Esbriet. Between the two of them, they've had peak sales of almost $5 billion. Unfortunately, neither reverse nor halt clinical decline, and only 25% of patients in the U.S. even initiate the standard of care. We therefore believe there is a significant commercial opportunity for a differentiated IPF treatment. Let's hone in on the role of STAT3 in fibrotic-driven diseases. In any fibrotic-driven disease, you see an initial event or injury that triggers a host of fibrotic signaling cascades, which include major drivers such as IL-6 and TGF-β, as well as a host of other signaling cascades like Hedgehog and Notch. Interestingly, all of them coalesce and activate into STAT3. Consequently, STAT3 induces a transcription program of a multi-step disease pathway, beginning with clotting and coagulation, inflammatory cell migration, fibroblast proliferation, and then eventually ECM deposition or fibrosis. This is so well genetically validated that haploinsufficiency of STAT3, meaning knocking out one of the two alleles of STAT3, completely protects animals from the development of fibrosis. However, if you knock out IL-6 completely or knock out TGF-β receptor completely, you still see the formation of fibrosis. That demonstrates to us there is redundancy in the signaling cascades. However, there is no redundancy at the STAT3 transcription factor level, again suggesting that STAT3 is a central catalyst in the fibrotic cascade. We've studied the role of STAT3 and inhibition of STAT3 across a myriad of fibrosis-driven diseases. Here is one such example in sclerosis, in which these genetically engineered mice have thickening of their hypodermis or thickening of their skin, which is very similar to what we see in patients with sclerosis or scleroderma. When we then treat with our molecule TTI-101, we show reversal of this hypodermal thickness shown on the right-hand side. When we look at the biomarkers, we see these animals hugely upregulate our target, phospho- STAT3. And then again, when we treat with TTI-101, we see a statistically significant decrease in the amount of phospho- STAT3, almost extinguishing back to zero levels. What's very interesting is when you look at all of the other pro-fibrotic mediators, we show statistically significant decreases in Col1, TGF-β, IL-6, and CTGF. Every one of these mechanisms has been individually targeted in clinical trials. We can downregulate all of them with a single molecule and it doesn't matter the model. In this paper that we published, not only did we show it in a genetically engineered mouse shown here, but even in a chemically induced mouse of systemic scleroderma, can we show the reversal of the fibrosis and the downregulation of pro-fibrotic markers? We initially selected IPF as our initial foray into human clinical trials. Why is that? When you look at the pathogenesis of IPF, there are three major compartments in the lung that lead to the pathogenesis of the disease: epithelial cells, fibroblasts, and macrophages. When you stay in an IPF patient's lungs, what you can see is activation or hyperactivation of our target, phospho-STAT3, in every compartment. However, when you look at a normal patient, we see no phospho-STAT3 in their lungs. Similarly, when we induce pulmonary fibrosis in an animal model, we see hyperactivation of phospho-STAT3. You ask, why does any of this matter? Because it's already been demonstrated that patients with high STAT3 die much, much faster. Shown in the middle of this page is a Kaplan-Meier plot. In red are IPF patients who have high STAT3. And you can see their survival probability is around 30%. Patients with low STAT3 have a much higher probability of survival, around 80%. So we took all this data and went into what is the gold standard model of pulmonary fibrosis, which is known as the bleomycin model. In this model, you take a mouse who's untreated, and you stain with Masson's trichrome to look at its lung architecture, and then on the right-hand side, we do something that most people don't. We actually measure the effect of the fibrosis and look at lung function, and they, like us, when they are placebo-treated, respire around 97% or have oxygen saturation around 97%. When you then give them bleomycin, which is an old cancer drug, this induces this pulmonary fibrosis shown in the middle panel here, and what we see is a honeycombing cascade of fibrosis. This is very similar to what we see in IPF patients, and then on the right-hand side, we see these animals then develop hypoxia, and their ability to bring in oxygen or have oxygen saturation drops below 85%. Again, very similar to what we see in IPF patients. We then wait 14 days after the bleomycin and deliver TTI-101, and what we can show is a reversal of the fibrosis. This, in and of itself, is compelling because most folks, when they do this experiment, they give their drugs simultaneously or even prophylactically and say, "Look, we can prevent fibrosis," but we know that's not the human condition. That's interesting, but what we've not seen anyone publish is this on the right-hand side. Once we start treating the animals with TTI-101, we can restore lung function back to near wild-type levels. We've repeated this experiment numerous times, and we've seen the same exact effect, and so we went back to the drawing board to really understand how are we mechanistically different from other therapies. What we've published very recently at the CHEST conference is that what we know is that in a normal patient, or normal in human, excuse me, a normal individual, they have deposition and degradation, and they work in concert to keep a balance. When we have IPF patients, unfortunately, the balance is tipped towards scarring and deposition. We also know that in IPF patients, they have decreased T cell responses. In the presence of our molecule, based on our mechanistic studies, we can tip the balance the other direction in the fact that we hit both compartments. One, we actually decrease deposition, but two, we can also increase degradation by inducing T cell activity. So we've taken all of this data and compiled it. And we've demonstrated, one, we have a very well-established target where STAT3 correlates with high mortality in IPF patients and is clearly a central catalyst in the fibrotic pathway. Two, we believe we have compelling biological activity where we've observed TTI-101 to reduce fibrosis and improve lung function in models of IPF. And then three, we actually had clinical proof of mechanism. We actually started our work in the clinic in oncology. And we could do something in oncology we couldn't do in IPF, and that is take biopsies. And so what we were able to do in our phase one oncology trial, we were able to take patients' pre-treatment and on-treatment biopsies and measure levels of our target, phospho- STAT3. And what we were able to demonstrate is that across all patients, we saw a decrease of 55% of our target. In patients who had stable disease, i.e., their tumor stopped growing, we saw an almost 80% decrease in phospho-STAT3. We compiled this data set in an IND application and went to the pulmonary division at the FDA, and we requested to move directly into a phase II trial. They agreed with us, and they said there was no need to do a SAD/MAD study in healthy volunteers. We have now initiated the trial on this page. This is known as the REVERT IPF trial. This is an all-U.S. trial where we are enrolling 75 patients. As a reminder, our drug is orally dosed twice a day. The treatment period is a 12-week study where it is a double-blind study, randomized and placebo-controlled of two doses of our molecule, 800 and 400 versus placebo. We can be used alone or in combination with nintedanib and enrolling mild to even more moderate IPF subjects relative to our competitors. Now, this is the first time we're in this patient population, so we'll obviously be looking at safety and PK. But the exploratory objectives to look for efficacy will also be the phase three endpoints, endpoints like change in forced vital capacity, which is the only approved FDA endpoint, but we'll be looking at a host of other phase III endpoints like quantitative lung fibrosis through high-resolution CTs as well as six-minute walk tests. And then we've also incorporated a validated set of biomarkers that are prognostic of disease in the IPF patient population. We expect to report this data out in the second half of next year. To sum up our key takeaways in TTI-101 and IPF, STAT3 has incredibly well-established biology as a central mediator in fibrosis. We believe our approach is differentiated because we believe that not only are we able to target intrinsically what's occurring at the cellular level, but also we're able to target extrinsically the ability to overcome immune suppression. Our clinical proof of concept is underway with clinically relevant endpoints and a collection of STAT3 mediated biomarkers. Finally, the answer will be forthcoming, near-term clinical milestone, because we expect to report out this data in the second half of 2025. Switching gears briefly to hepatocellular carcinoma, HCC, or liver cancer, is our second indication of interest. This is a disease of fibrosis in which the liver becomes inflamed and fibrotic and eventually forms hepatocellular carcinoma. When you think about the pathogenesis of this disease, that's STAT3. These are the canonical functions of STAT3: inflammation, fibrosis, and then cancer, so the way we study this in an animal model was to look at a genetically engineered mouse who, over an 11-month period, develops inflammation, develops fibrosis, and then forms cancer, and so what we did is we then treated the animals after the formation of the tumors after 11 months, and then what we saw was a statistically significant reduction in the hallmarks associated with inflammation, including decreases in ALT, decreases in AST, and shown here, decreases in microsteatosis. We saw significant decreases in fibrosis, and we completely abolished tumor growth in this model, so this then drove us into a clinical trial, and in the clinical trial, we enrolled patients across a variety of advanced solid tumors. We particularly enriched the trial for HCC or liver cancer patients. In our trial, we observed durable partial responses in which patients' tumors shrunk more than 30%. We observed this in a variety of patients, including gastric, ovarian, and shown here, multiple HCC patients. Here are two examples. Now, I'll just focus on the partial responder B at the bottom of this page. This is a patient who had failed standard lines of therapy, including lenvatinib, a tyrosine kinase inhibitor, nivolumab, and anti-PD-1, and had very large tumors shown in the bottom left. With TTI-101 monotherapy, we observed significant reductions in some of his tumors, and he maintained this response for almost 14 months, and so we took a step back and looked at the phase one oncology data holistically. In this monotherapy study of patients suffering from advanced cancers, we observed, in pharmacokinetics, the exposures aligned and were, in fact, above the level required for efficacy in preclinical oncology and fibrosis models. We also observed at trough levels at the recommended phase two dose, we were above, not the IC50, but the IC90 for STAT3-induced growth. And as previously discussed from our pharmacokinetic perspective, with paired biopsies after six weeks of treatment with TTI-101, we showed a decrease in our target of activated STAT3. TTI-101 was very well tolerated with oral dosing twice a day. And finally, we observed biological activity, and that supported the mechanistic data that our STAT3 inhibitor should be working at the tumor level in the cellular compartment, but if you think about the mechanism, it should also be working in the tumor microenvironment in the immune compartment. We've actually demonstrated in preclinical models that the combination of our molecule with checkpoint inhibition is additive and synergistic. For example, when you take a humanized mouse and implant it with human HCC tumors and you treat it with the standard of care, which is a checkpoint inhibitor plus bevacizumab, you see a nice effect, the gray versus the green. When you add TTI-101 to the mix, the effect is definitely additive and probably synergistic. And not only do we have proof of concept preclinically, we have proof of concept that was already established in danvatirsen, a molecule generated by Ionis. Ionis outlicensed this molecule to AstraZeneca, and they tested their STAT3 antisense oligonucleotide plus immune checkpoint inhibition in a phase 11 trial. They observed more than a doubling of the response rates when they combined their molecule with ICI therapy. However, the program was eventually discontinued because of a high rate of adverse events, including thrombocytopenia and transaminitis, very onerous dosing with IV therapy three times a week in the first week and then once weekly, and they themselves said they don't actually inhibit STAT3 in the tumor, only in the tumor microenvironment, and thus they probably saw this activity in combination. From our perspective, we don't see these adverse events. We have oral dosing twice a day, and as I demonstrated in the previous slide, we actually can hit the target directly in the tumor, and this was further compounded by the fact we saw similar activity with our monotherapy trial. The patient that I highlighted earlier was a patient who came onto our trial who had failed nivolumab very quickly after one cycle for immune checkpoint inhibition. And in orange are the sum of his targets, in which you can see with TTI-101 monotherapy, he had a massive reduction in the sum of his targets, which he maintained for 14 cycles or 14 months. Unfortunately, he had progression due to a non-target lesion, so he had to come off therapy. Now, the physician on trial understood our therapy, and he said, "You should have changed his tumor microenvironment. So even though we've discontinued TTI-101, I'm going to rechallenge him with immune checkpoint inhibition." And when he did, we saw a response. Now, we would never run a clinical trial like this, but all this data together suggests to us not only are we seeing activity in the tumor itself, but we may be seeing activity in the tumor microenvironment, which would suggest this molecule could be used in monotherapy as well as in combination. Thus, we designed a trial when we looked at the landscape that fit these criteria. When you think about the treatment landscape shown on the bottom of this page, frontline therapy currently, one of the standards of care is an anti-PD-L1 combination with anti-VEGF therapy. The response rate in this patient population is anywhere between 10%-27%. Eventually, all patients move on and progress because we see very few complete responses in frontline therapy. They then move to second-line therapy, which is a host of tyrosine kinases and anti-VEGF therapies with response rates less than 5%. And then finally, we move to third line where there are no approved therapies. So as we contemplated how we could fit in the landscape, we could definitely be in last line as monotherapy, and then we could potentially be in second line to overcome resistance by adding back to a PD-1 inhibitor or be in frontline where we could show synergy between the existing molecules like we had shown in our preclinical models. Thus, we built a trial that allowed us to do all of these things simultaneously. The trial, again, is an all-U.S. trial. It is currently open and enrolling across 21 U.S. sites. We have three separate lines shown on this page. Cohort A are the monotherapy patients, patients who are in last line where there are no available therapies that can confer clinical benefit. Cohort B are patients in second line who have demonstrated progression with an anti-PD-1 or PD-L1 in frontline, and then we're simply adding TTI-101 to pembrolizumab, a PD-1 inhibitor, to see if we can overcome that resistance, and then finally, we're looking at treatment naive patients where we're trying to see if we can show that TTI-101 is synergistic to the existing therapies like we've done in preclinical models. We expect this data to read out at the end of next year, so the key takeaways for HCC are we have very well-established biology of STAT3. We think we have a differentiated approach because STAT3 inhibition could have a dual therapeutic effect, not only at the cellular compartment, but overcoming immune suppression. Three, we have clinical proof of concept, which is underway with a phase two trial, which I just described to you across three different cohorts. And finally, we expect to have data at the end of the year. That concludes my prepared remarks. We hope you take away from this morning's call that we are extremely excited about this transaction, which will allow Tvardi to build on our deep expertise in STAT3 biology and potentially introduce new hope to patients suffering from fibrosis-driven diseases leading with IPF and then followed by HCC, which both represent multi-billion-dollar commercial opportunities. To recap our upcoming milestones, we announced the transaction today. We expect the transaction to close in the first half of next year. Thereafter, with our lead program, we anticipate phase 2 unblinded data in IPF in the second half of the year. Thereafter, we anticipate the phase 1b topline data from our ongoing HCC trial. Finally, in the first half of next year, we plan to submit an IND to the FDA for our second candidate, 109, with the goal of initiating first-in-human trials shortly thereafter. I would again like to thank Chris and the Therapeutics Board for recognizing the value of this merger, as well as the investors who expressed confidence in our company and our vision through the participation in our concurrent financing. We look forward to providing future updates on our continued progress. Thank you again for your interest in this transaction and the new Tvardi Therapeutics. Please have a good day. This concludes today's conference call. Thank you for participating. You may now disconnect.