Good morning, welcome to Travere Therapeutics' business update call. Today's call is being recorded. At this time, I would like to turn the conference over to Nivi Nehra, Vice President of Corporate Communications and Investor Relations. Please go ahead, Nivi. Thank you, operator. Good morning, and thank you all for joining us to discuss Travere Therapeutics' exclusive licensing and collaboration agreement with Everest Medicines. Today's call will be led by Dr. Eric Dube, our President and Chief Executive Officer. Eric will be joined in the prepared remarks by Dr. Jula Inrig, our Chief Medical Officer. Chris Cline, our Chief Financial Officer, will join us for the Q&A. Before we begin, I'd like to remind everyone that statements made during this call regarding matters that are not historical facts are forward-looking statements within the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements are not guarantees of performance. They involve known and unknown risks, uncertainties, and assumptions that may cause actual results, performance, and achievements to differ materially from those expressed or implied. Disclaimer on the company's press release issued earlier today, and 10-K present our views only as of the date such statements are made, and Travere specifically disclaims any obligation to update such statements to reflect future information, events, or circumstances. With that, let me now turn the call over to Eric. Eric? Thank you, Nivi. Good morning, and thank you all for joining us. Earlier this morning, we were very pleased to announce that Travere has entered into an exclusive licensing and collaboration agreement with Everest Medicines for civorebrutinib, also known as EVER001, a potential best-in-class reversible BTK inhibitor. Under the agreement, Travere will receive development and commercialization rights to civorebrutinib in global markets outside of China and certain countries in East and Southeast Asia. This is an exciting and strategic transaction for Travere. We've been engaged on this program for some time, and now we are entering into this agreement from a position of strength with the ability to execute on these development programs quickly once the deal closes. Notably, the transaction brings a potential best-in-class product candidate into our rare kidney portfolio, with proof of concept clinical evidence in primary membranous nephropathy, or PMN, and a compelling mechanistic rationale across several immune-mediated rare kidney diseases, including immune-mediated FSGS, minimal change disease or MCD, and potentially others. While civorebrutinib is initially anchored in PMN, a disease with no approved medicines today, its multi-indication potential is an important part of what makes this transaction strategically compelling and why we view it as a potential pipeline and a product. Importantly, civorebrutinib will bring a distinct immune-mediated mechanism to our portfolio alongside FILSPARI nephroprotective role. In immune-mediated FSGS, FILSPARI and civorebrutinib would give Travere two distinct medicines with complementary profiles, and we see that as an important opportunity to further address unmet need in FSGS over time. Cevobrutinib will also provide further long-term growth potential and diversification alongside and beyond FILSPARI and pegtibatinase while remaining closely aligned with the areas where Travere has the greatest expertise and ability to execute. With this transaction, we are building on the momentum of our current portfolio, including recent strong performance in FSGS and IgA nephropathy. Travere has built its leadership by advancing medicines for rare diseases with significant unmet need and limited treatment options. With FILSPARI, the first medicine ever approved in FSGS and the first non-immunosuppressive medicine approved in IgA nephropathy, we have demonstrated our team's ability to successfully advance a rare kidney medicine from clinical development through commercialization. With pegtibatinase, we are also advancing and developing the first potential disease-modifying therapy for classical homocystinuria. Cevobrutinib fits naturally with Travere's expertise, infrastructure, and longstanding commitment to the rare disease community. It is a rare kidney disease product candidate and a development opportunity where we believe our clinical, regulatory, and commercial capabilities can add significant value. Everest is a biopharmaceutical company with a strong track record in the development and commercialization of innovative medicines. We look forward to collaborating with their team to advance this program globally. With that, I'll turn the call over to Jula to walk through the scientific rationale and clinical data in more detail. Jula? Thank you, Eric. We are very excited about civorebrutinib because it brings together several attributes we look for in a development candidate. A compelling mechanistic rationale, proof of concept evidence in a rare kidney disease with high unmet need, and biologic rationale to support the potential for the treatment of several immune-mediated kidney diseases. Patients impacted by primary membranous nephropathy carry a high disease burden, which often includes fatigue, massive swelling with weight gain, and brain fog, which not only impacts their quality of life but also their ability to attend school or work. Patients with primary membranous nephropathy need therapies that can rapidly reduce both disease activity and proteinuria to minimize ongoing kidney damage and the symptoms and complications of persistent nephrotic syndrome. While current off-label immunosuppressive approaches can be effective in some patients, they are often associated with delayed onset of action, prolonged B-cell depletion, and increased risk of hypogammaglobulinemia and infections. There remains a significant unmet need for treatments that provide earlier disease control with less impairment of immune function to reduce the burden of chronic immunosuppression. We believe civorebrutinib has a differentiated potential best-in-class profile. Let me start with the mechanism. It is an oral covalent reversible inhibitor of Bruton's tyrosine kinase, or BTK. Its covalent reversible mechanistic profile is relatively unique within the BTK inhibitor class and is an important part of its differentiated profile. In simple terms, this means civorebrutinib is designed to bind strongly to BTK while also allowing that binding interaction to detach and be reversible. Reversibility is important because it may allow for targeted immune modulation as needed. BTK is a key mediator of B-cell receptor signaling and plays an important role in B-cell activation, maturation, proliferation, and differentiation into antibody-producing cells. That biology is highly relevant in immune-mediated kidney diseases, where B-cell activation and autoantibody production can contribute directly to kidney injury. In primary membranous nephropathy, for example, the disease is often driven by autoantibodies, most commonly anti-phospholipase A2 receptor, or anti-PLA2R, antibodies that target the podocyte. This leads to immune complex formation and deposition in the basement membrane and podocyte injury. This disruption in the kidney's filtration barrier results in significant proteinuria and over time leads to progressive kidney damage. Anti-PLA2R antibody levels are clinically meaningful because they reflect active autoantibody-driven disease and can help guide treatment decisions. Importantly, reductions in anti-PLA2R antibodies are often an early sign that the underlying immune process is being controlled, with reductions in proteinuria that follow as the filtration barrier begins to recover. By targeting BTK, civorebrutinib is designed to modulate B-cell signaling upstream of autoantibody production. Importantly, this is distinct from B-cell-targeted approaches such as anti-CD20 antibodies, which deplete B cells, and APRIL/BAFF inhibitors, which target pathways involved in B-cell and plasma cell survival. BTK inhibition is intended to regulate the immune signaling pathways that drive pathogenic B-cell activity without depletion of B cells. civorebrutinib may also have beneficial targeted immunomodulatory effects compared to B-cell-targeted approaches, including effects on myeloid lineage immune cells. That is important because multiple immune-mediated kidney diseases involve both autoantibody biology and inflammatory immune signaling that can contribute to glomerular injury, proteinuria, and progressive kidney damage. The covalent reversible nature of civorebrutinib is also central to why we are excited about this asset and its differentiated profile. It was designed to combine high potency and selectivity with reversible BTK inhibition, supporting a targeted and potentially flexible approach to immune modulation in chronic autoimmune kidney diseases with the goal of limiting side effects traditionally associated with immunosuppression. The fact that civorebrutinib is a pill is also important. Many immune-modulating therapies used today or in development are IV or subcutaneous biologics. An oral medicine could offer meaningful convenience for patients and physicians, particularly in chronic diseases where treatment burden, adherence, flexibility, and the ability to adjust therapy are important considerations. Taken together, the profile of civorebrutinib is compelling. It is orally administered, targeted, designed to provide reversible immune modulation, and has the potential to address B-cell and autoantibody-driven disease processes that are relevant across multiple immune-mediated kidney diseases. Let me turn briefly to the clinical evidence. civorebrutinib is being evaluated in an ongoing phase I-B/II-A study in patients with anti-PLA2R antibody positive PMN. This is an open-label, single-arm study with highly encouraging results to date that provide important clinical support for the mechanism. Across the study, civorebrutinib demonstrated rapid and sustained reductions in anti-PLA2R antibodies and proteinuria with stable eGFR. Cohort one evaluated 100 milligrams once daily for four weeks, followed by 100 milligrams twice daily, while Cohort two evaluated 200 milligrams twice daily. At week 12, anti-PLA2R antibody levels declined by approximately 62% in Cohort 1 and 87% in Cohort two, supporting the rapid immunologic activity observed in this study. There were also meaningful reductions in proteinuria, with declines of approximately 77% and 80% in Cohorts one and two at weeks 36, respectively. These responses, together with improvements in serum albumin and stable kidney function, provide important clinical support for the mechanism. We view the rapid reduction in anti-PLA2R antibodies as particularly meaningful because it is a direct marker of immunologic disease activity in primary membranous nephropathy and believe it also differentiates civorebrutinib from other assets in development for PMN. From a safety perspective, civorebrutinib was generally well-tolerated in the data reported to date. Beyond PMN, we are particularly interested in immune-mediated FSGS and minimal change disease. Everest recently initiated an exploratory phase II basket study that includes FSGS, MCD, and IgA nephropathy, which we believe is consistent with the broader mechanistic rationale for civorebrutinib across immune-mediated kidney diseases. This is another area where civorebrutinib may fit well with Travere's rare kidney disease portfolio. In FSGS, FILSPARI has an established role as a nephroprotective therapy, and civorebrutinib adds a distinct immune-mediated mechanism that may broaden Travere's ability to help patients, including those outside FILSPARI's current indications. There is clear portfolio fit with continued innovation in FSGS, potentially addressing different aspects of the disease biology. Our priority following the close of this transaction will be to work closely with Everest Medicines, FDA, and global regulators to align the next stages of global clinical development, including the path forward in PMN and our plans to evaluate civorebrutinib in FSGS minimal change disease and potentially other indications. We are excited by the science, encouraged by the clinical proof of concept in PMN, and confident that Travere is the right company to advance this product candidate given our experience in rare kidney disease development and commercialization. With that, I'll turn the call back to Eric. Eric? Thank you, Jula. We're excited to collaborate with Everest Medicines, whose work has established an important clinical foundation for civorebrutinib. Together, we look forward to advancing the program towards its next stage of development, with the shared goal of advancing innovation in areas of significant unmet need for patients living with rare kidney disease. To summarize, we believe this transaction is an excellent strategic fit for Travere for three key reasons. First, civorebrutinib is a differentiated oral BTK inhibitor with potential best-in-class attributes, including rapid onset of action, convenient oral administration, and a potentially favorable safety profile with proof of concept in PMN. Second, civorebrutinib will bring pipeline and a product potential across multiple immune-mediated kidney diseases to Travere's rare kidney disease portfolio. Importantly, we believe continued innovation in immune-mediated kidney disease, including FSGS, will involve approaches that address multiple aspects of disease biology. With civorebrutinib, we will have the potential to add a distinct but complementary profile alongside FILSPARI and its nephroprotective role. Third, we are entering into this transaction from a position of strength, supported by strong performance of FILSPARI in both FSGS and IgA nephropathy. With our established clinical development, regulatory and commercial expertise, and infrastructure, we believe civorebrutinib has the potential to become a meaningful, long-term growth driver alongside and beyond FILSPARI and pegtibatinase. With that, I'll turn the call back over to Nivi for Q&A. Nivi? Thank you, Eric. Operator, we can now open up the line for Q&A. Thank you. We will now begin the question and answer session. As a reminder, we ask that you limit yourself to one question. If you have another question, please rejoin the queue. To ask a question, please press star one to raise your hand. To withdraw your question, press star one again. We ask that you pick up your handset when asking a question to allow for optimum sound quality. If you are muted locally, please remember to unmute your device. Please stand by now while we compile the Q&A roster. We will now take the first question from the line of Joseph Schwartz with Leerink Partners. Your line is open. Great. Thanks. Congrats on this deal. I was wondering if you could share civorebrutinib's actual kinome selectivity panel in terms of the fold selectivity over TEC, ITK, EGFR, and ERBB2, four. Also, what is the residence time and occupancy half-life at BTK versus the off targets, and does platelet function recover between doses? Thanks. Good morning, Joe. Thanks so much for the question. Starting off with the specific questions for Jula, why don't you take that, and you can share what's available to date? Yeah. Thanks, Joe, for the question. Part of the rationale for civorebrutinib is because it has such a high selectivity for BTK. There is some data that Everest has put out with regards to selectivity over EGFR, ITK, and TEC, and it has a better profile when you compare it to many of the other BTK inhibitors with regards to selectivity. That's why we believe that we're going to have a better potential safety profile versus others. What we've seen to date, while I don't think you asked about the platelet activity in between doses. What I can tell you is the safety data that we've seen to date, and there's been a little over 150 patients and healthy volunteers exposed, and we haven't seen the off-target decreases in platelet count and other adverse effects that have been seen with some of the earlier generation BTK inhibitors. That's helpful. Thank you. Thanks, Joe. Your next question comes from the line of Vamil Divan with Guggenheim Securities. Your line is open. Good morning. This is Arseniy on for Vamil. Maybe just to follow up on that question and ask more generally. When we compare it to CD20, obviously it's oral, but what is the main potential advantage? Would it be safety, speed of onset? Then in terms of safety, practically, can you interrupt the treatment if the patient has an infection or is going for surgery? Do you preserve vaccine response when you're taking this inhibitor versus CD20? Just any color on the differentiation would be helpful. Thanks, Arseniy. Jula? Yeah. Part of the reason we're excited about civorebrutinib is because it's highly selective and it modulates B-cell signaling, unlike CD20-targeted therapies that broadly deplete B cells. We do believe that with functional B-cell modulation rather than B-cell suppression, that can help you potentially reserve some immunoglobulin so you don't see widespread immunoglobulin, IgG, IgM, IgA depletion, rather than targeting intracellular signaling to reduce the formation of those pathogenic autoantibodies. That's what gives us the confidence that this could potentially be safer over the long term versus B-cell depletion. Then the other aspect that gets us excited is oftentimes when you're targeting early B-cell line lineage, such as CD20, it takes longer to reduce that antibody formation because you're waiting for the B-cell survival and you're not targeting the plasma cells that are producing the antibodies. The onset of action with this mechanism that we've seen in the phase I/II data with the reduction in PLA2R occurring very early and then followed by proteinuria reduction also gives us the confidence that this is a solid approach to continue to development. Thank you. Your next question comes from the line of Anupam Rama with J.P. Morgan. Your line is open. Hey, guys. Thanks so much for taking the question and congrats on the deal here. Maybe building off the last question, can you speak to the off-treatment data that you're seeing here and what that could mean from a formulation and/or dosing frequency considerations in the future? Thanks so much. Thanks, Anupam. Jula? Yeah. We do see continued durability of off-treatment. It is still very early to be able to discuss that. We haven't made final decisions around dosing or duration. Once the deal closes, we'll be able to give more details around our strategy and planning for that. I think what you're getting at, is this a long-term treatment? Is this induction treatment? The fact that there is some durability off-target is promising. Those decisions around duration of treatment haven't been determined yet. Thanks so much for taking the question. Your next question is from the line of Prakhar Agarwal with Cantor Fitzgerald. Your line is open. Hi, thank you for taking my questions and congrats on the deal. Maybe on the PMN indication first, I think other BTKs like zanubrutinib has some data in PMN as well. Just as a follow-up, what could a development pathway look like in PMN? Thank you so much. Thanks, Prakhar. Jula? Yeah. The only other BTK inhibitor that has early data provides proof of concept that the mechanism likely works. I think you mentioned, it's zanubrutinib. That is a slightly different mechanism. That is an irreversible covalent BTK inhibitor. We do believe that the fact that we are covalent reversible has the potential for a better safety profile overall with regards to why we believe in civorebrutinib as a potential best-in-class for patients with primary membranous nephropathy. Your next question is from the line of Gavin Clark-Gartner with Evercore ISI. Your line is open. Hey, guys. I guess just to follow up on Prakhar Agarwal's question a little bit more specifically. Last we saw, Everest Medicines was planning to start the registrational PMN study this year. Is that still your plan? On this topic, it seems like 72-week complete renal response is a pretty established registrational endpoint, even based on recent conversations. Is that what you're planning to pursue, or are you discussing a different path with regulators? Thank you. Gavin, thanks so much for the questions. With regard to timing, we'll be able to talk a bit more of that after the deal closed. Certainly part of our intent is to make sure that we can move very quickly, moving forward. Jula, do you want to comment on regulatory interactions and endpoints? Yeah. Again, when the deal closes, we'll have greater ability to share more with regards to the endpoints, but you're not far off with regards to it's known that you can utilize complete remission and select time frames for it, but we'll provide more after the deal closes as far as our strategy and plans for our phase III design. Okay. Thanks. Your next question comes from the line of Laura Chico with Wedbush Securities. Your line is open. Good morning. Thanks very much for taking the question. I guess I had one more bigger picture strategic question. Obviously there's a lot of reasons to stay in rare nephrology, but I'm curious what other disease areas or therapeutic verticals were considered, when you were seeking out other assets, and would you consider still seeking additional assets in rare nephrology? Thank you. Good morning, Laura. Thanks for the question. We certainly have been looking broadly within the rare nephrology space, but not limited there. If we think about the work that we're doing in pegtibatinase, there are a number of other areas that we've been interested in. For us, this one was the right asset, not only for the reasons clinically and strategically that we've talked about, but also the timing of development, being able to take that over and move through the next phase of development. We'll continue to evaluate other potential assets, and we'll look within and beyond rare nephrology. With what we have now, particularly the pipeline and uphill potential, we're very excited about bringing this into our portfolio. Your next question comes from the line of Mohit Bansal with Wells Fargo. Hi, this is Sadia Rahman on for Mohit. Thanks for the question. Yeah, it looks like very robust data in China. I'm just curious how you expect that data to translate to a Western population. Specifically, can you comment on any differences in background treatment usage in China versus the U.S.? Thanks. Thanks, Sadia. Jula, I'll turn that one over to you. Thanks for the question. We do believe that the efficacy data, based on what we understand of the underlying disease biology within primary membranous, will translate into comparable efficacy as well as safety. Obviously, we still have to do the development plan to demonstrate that, but no reason for us to believe that we won't see similar treatment effects and safety within a different population, including U.S. Again, we will plan to do this globally. More to come on that. All right. Thank you. Your next question comes from the line of Alex Thompson with Stifel. Your line is open. Hey, great. Thanks for taking our question. I was wondering if you could comment on whether we should expect to see more follow-up data from the phase I-B/II study. It looks like the cutoff here was about a year ago. Curious if we should expect more data in the near term. Thank you. Thanks, Alex. Jula? Actually, Everest is planning on presenting data later this week at ERA. More to come soon. Your next question comes from the line of Maury Raycroft with Jefferies. Your line is open. Hi, this is Farzan on from Maury. A quick question on the safety profile. How are you thinking about potential for liver toxic notes that have hindered other BTK inhibitors in the systemic autoimmune trial and potential class read-throughs? Farzan, thanks for the question. Jula, would you like to comment on that? BTK inhibitors are not interchangeable. They can differ quite a bit in binding profile, reversibility, selectivity, potency, dosing, as well as the underlying patients that you study the medicine in. I would say that cevobrutinib is differentiated from other BTK inhibitors because it's covalent reversible with high potency and selectivity, as well as reversible target engagement. The data that we've seen today, as I mentioned earlier, in healthy volunteers and PMN patients, has shown that cevobrutinib has been generally well-tolerated. With regards to AEs, we haven't seen the AEs that have been associated with some of the earlier irreversible BTK inhibitors, such as things like neutropenia or cardiac effects, as well as the liver safety concerns. We do know that there's a potential class risk around liver, and that, as I mentioned earlier, depends on how you dose and other aspects. We have not seen safety signals to date to raise concern. Obviously, we will do careful evaluations of safety throughout our development plan as well. Perfect. Thank you so much. Your next question comes from the line of Jason Zemansky with Bank of America. Your line is open. Thank you. Good morning. Appreciate you taking our questions, congrats on the deal. Appreciate that can't talk necessarily about timelines yet, maybe can you outline what are the steps needed to get civorebrutinib into a pivotal study? What needs to happen in order to get that underway? Just give an idea of what needs to happen next. Thanks. Jason, thanks so much for the question. This is something that we'll comment more on once the deal closes, once it is in our hands. Certainly our intent is to move quickly once we have the asset. Your next question is from the line of Yigal Nochomovitz with Citi. Your line is open. Hi, this is Caroline on for Yigal. Congrats on the deal, and thanks for taking our question. Can you tell us more about your strategy positioning this asset alongside FILSPARI in overlapping indications? Would you pursue it as a monotherapy or combination, or only in patient subsets that fall outside of FILSPARI's current label? Thanks. Thanks so much, Caroline, for the question. We are certainly excited about the potential to have another potential medicine for particularly FSGS, and there's a very clear role for both FILSPARI and civorebrutinib. As you might know, FSGS is a heterogeneous disease, and some patients really would benefit from medicines that address more than one aspect of their disease. For example, FILSPARI being nephroprotective, whereas something like civorebrutinib would be addressing the immune-mediated disease biology. What we're particularly excited about is that this would give Travere two distinct medicines with complementary profiles that we see the potential to be able to address that over time. With regard to the development and the strategy there, that's something that we are not going to be commenting on today, but certainly look to the future to be able to provide more detail. Ladies and gentlemen. Thank you. This concludes the question and answer session of today's conference call. I will now hand the call back over to Nivi. Thank you everyone for joining today's call. Have a great rest of your day. This concludes today's call. Thank you all for attending. You may now disconnect.