FibroGen, Inc

Hello, and thank you for standing by. Welcome to FiberGen Third Quarter 2025 Earnings Conference Call. At this time, all participants are on a listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press Start 11 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press Start 11 again. I would now like to hand the conference over to Gaia Seamus. You may begin.

Thank you, Amanda. Good afternoon, everyone, and thank you for joining us today to discuss FibroGen's third quarter 2025 financial and business results. I'm Gaia Chamis from Lysa Advisors. Joining me on today's call are Thayne Wettig, Chief Executive Officer, and David DeLucia, Chief Financial Officer. Following the prepared remarks, we will open the call to your questions. I would like to remind you that remarks made on today's call include forward-looking statements about FibroGen. Such statements may include, but are not limited to, collaboration with AstraZeneca and Astellas, financial guidance, the initiation, enrollment, design, conduct, and results of clinical trials, regulatory strategies, and potential regulatory results, research and development activities, commercial results and results of operations, risks related to our business, and certain other business matters. Each forward-looking statement is subject to risks and uncertainties that could cause actual results and events to differ materially from those projected in that statement. A more complete description of these and other materials risks can be found in FibroGEN's filing with the SEC, including our most recent Form 10-K and Form 10-Q. FibroGen does not undertake any obligation to update publicly any forward-looking statements, whether as a result of new information, future events, or otherwise. The press release reporting the company's financial results and business updates and a webcast of today's conference call can be found on the investor section of FibroGen's website at www.fibrogen.com. With that, I would like to turn the call over to C.L. Fein.

Thank you, Gaia. Good afternoon, everyone, and welcome to our third quarter 2025 earnings call. On today's call, I will provide an update on our ongoing efforts with a focus on our three main priorities, the completion of the sale of fibrin in China, the continued progress with our lead asset, FG3246, a potential first-in-class antibody drug conjugate targeting CD46, and its companion PET imaging agent in metastatic castration-resistant prostate cancer, and the path forward for roxidustat as a potential treatment for anemia due to lower-risk mild dysplastic syndromes. Then David De La Chia, our CFO, will review the financials, after which we will open the call for your questions. On slide three, I would like to start with the sale of VibraGen China to AstraZeneca that we recently completed for approximately $220 million. This was a truly transformative transaction that provided us with the most efficient means to access the company's cash held in China, extending our cash runway into 2028. Following the transaction, we successfully paid off the term loan facility with Morgan Stanley tactical value. Second, we continued to progress FG-3246 and FG-3180 in metastatic castration-resistant prostate cancer, or MCRPC, and initiated the Phase II monotherapy trial of FG3246 and FG3180 earlier this quarter. Additionally, we expect the top-line results from the investigator-sponsored trial of FG3246 in combination with enzalutamide in MCRPC to be presented at a medical conference in the first quarter of 2026. Third, as we have previously stated, We had a successful type C meeting with the FDA in July, providing us with a clear regulatory path forward for Roxidustat. We remain on track to submit the phase three trial protocol for Roxidustat for the treatment of lower risk mild dysplastic syndromes in patients with high transfusion burden later this quarter. We are confident that with our mid and late stage assets, simplified capital structure, and upcoming near term catalysts across both clinical programs, We are well positioned to advance meaningful therapeutic options for patients and significant value for shareholders. I will now provide a brief overview of our FG3246 and FG3180 programs in MCRPC. Slide five summarizes the high unmet need in late stage prostate cancer. Approximately 290,000 men are diagnosed with prostate cancer each year in the U.S. with about 65,000 drug-treatable patients where the cancer has metastasized and become castrate-resistant. This group of patients has a grim five-year survival rate of approximately 30%, underscoring the significant opportunity for new life-extending treatments. We believe that FG3246 could be this new treatment option and estimate the total addressable market to be well over $5 billion annually. On slide six, we highlight the novelty of CD46, a tumor-selective target that has several distinguishing features. First, CD46 is upregulated during tumorigenesis and helps tumors evade complement-dependent cytotoxicity. Second, its expression is also upregulated in the progression from localized castration-sensitive prostate cancer to metastatic castration-resistant prostate cancer. and further overexpressed following treatment with androgen signaling inhibitors. Notably, CD46 is highly expressed in MCRPC tissues with lower interpatient variability and higher median expression compared with PSMA, making it an attractive therapeutic target. Turning to slide seven, FG3246 is our potential first-in-class ADC in development for MCRPC. The ADC combines the YS5 antibody with an MMAE payload to specifically target the tumor-selective epitope of CD46. YS5 is a fully human IgG1 monoclonal antibody that was engineered to specifically target the tumor-selective epitope of CD46, whose expression is limited in normal tissue. FG3246 represents an androgen receptor agnostic approach clinically differentiating it from other prostate cancer treatments currently in development, many of which target PSMA. The companion PET imaging agent, FG3180, utilizes the same YS5 targeting antibody as FG3246 and is also under clinical development. We believe that having a patient selection biomarker would not only allow us to better enrich the patient population in a future Phase III trial, It could also enable differentiation of FG3246 in the prostate cancer treatment paradigm. In addition, FG3180 could represent an important commercial opportunity as a companion diagnostic to FG3246, similar to the existing PSMA PET agents. Slide 8 recaps the top line results from the two FG3246 clinical trials to date. On the left side, we highlight the Phase I monotherapy study, where a median radiographic progression-free survival of 8.7 months was observed in patients with MCRPC that were heavily pretreated and were not biomarker-selected. PSA reductions of greater than 50% were achieved in 36% of these patients. On the right, we highlight the previously reported preliminary efficacy data from the Phase Ib portion of the investigator-sponsored combination study with enzalutamide which demonstrated a preliminary estimate of 10.2 months of radiographic progression-free survival, with PSA declines observed in 71% of available patients. The top-line results from the IST are expected to be presented at a medical conference in the first quarter of 2026. Together, these results highlight what we believe is compelling clinical activity with FG3246, with competitive RPFS results compared to other approved and investigational treatments in both the monotherapy and combination settings. Moving to slide nine, based on the phase one monotherapy results, we initiated the FG3246 phase two monotherapy dose optimization trial in September. We plan to enroll 75 patients in the post-ARPI pre-chemo setting across three dose levels to determine the optimal dose for phase three based on efficacy, safety, and PK parameters. It is important to note that FG3180 will be an integral part of the study as we seek to demonstrate the correlation between CD46 expression and response to the ADC in this all-comers population. One other important design element is the use of GCSF as primary prophylaxis to mitigate grade three or greater neutropenia commonly seen with MMAE payloads and also experienced in the phase one monotherapy trial. The addition of GCSF is designed to reduce dose interruptions and downward adjustments and may enable a better tolerated and more consistent treatment with the ADC. An interim analysis of the Phase II trial is planned for the second half of 2026 and will include efficacy, safety, PK, and exposure response data that will be reported as they become available given the open-label design of the trial. On slide 10, I'd like to highlight three important steps we have taken with the design of the Phase II monotherapy trial with the aim of building on the 8.7 months of RPFS demonstrated in the Phase I monotherapy trial. Leveraging the preliminary evidence of an exposure-response relationship, the Phase II study will use three of the highest doses from the Phase I dose escalation and expansion study. Second, primary prophylaxis with GCSF will be utilized to potentially mitigate neutropenia, which could enable more consistent exposure to the ADC with fewer dose interruptions or adjustments early in the course of treatment. This could consequently extend the duration of therapy and potentially enhance the efficacy of the ADC. Third, enrolling healthier patients in earlier lines of therapy versus the five median lines of therapy in the Phase I trial. Together, we believe that these design elements have the potential to improve upon the Phase I results and achieve an RPFS of 10 months or greater, which we believe is the benchmark for commercial competitiveness. Slide 11 shows our long-term development strategy for FG3246 and FG3180, which provides us with important optionality in prostate cancer. We have a well-designed Phase II monotherapy trial in the post-ARPI pre-chemo setting in MCRPC to attempt to further build upon the 8.7 months of RPFS demonstrated in the Phase I monotherapy study. In addition, the Phase II study will explore the correlation between CD46 expression and response to the ADC, potentially validating FG3180 as a predictive patient selection biomarker in future studies. We are confident that our development pathway for FG3246 unlocks sequential or parallel registrational pathways, as FG3246 will be evaluated in multiple lines of therapy, in monotherapy and or in combination with an ARPI, and in an all-comers population or patients with high expression of CD46. Slide 12 highlights the recent and upcoming catalysts for the FG3246 and the FG3180 program. Looking ahead, we expect the top line results from the IST of FG3246 in combination with enzalutamide to be presented at a medical conference in the first quarter of 2026. With the recent initiation of the Phase II monotherapy trial, we expect to report the interim results in the second half of 2026. To summarize on slide 13, FG3246 targets a novel epitope on prostate cancer cells with first-in-class potential. given there are no other CD46 targeted projects in clinical development. Targeting CD46 with FG3246 has already demonstrated promising early efficacy signals with an acceptable safety profile, both in monotherapy and combination settings. We are excited for the upcoming milestones and look forward to updating you as the program progresses. Turning out to Oxidustat, Slide 15 highlights the unmet need and the potential for Oxidustat in the approximately 49,000 patients with anemia associated with lower-risk MDS in the U.S. alone. Current treatments are effective in less than 50% of patients. With no oral options currently on the market or in late-stage development, a significant opportunity exists to offer a potential new treatment that is durable with convenient oral administration to patients in the second-line and beyond settings. Moving to slide 16, I would like to briefly highlight the data from a post-hoc analysis in a subgroup of patients with anemia of lower risk MDS who entered the Phase III Matterhorn study of roxidustat with a high transfusion burden. In this analysis, using the international working group definition for high transfusion burden of four or more RBC units in two consecutive eight-week periods, roxidustat showed a meaningful treatment effect with 36% of patients achieving transfusion independence for greater than or equal to eight weeks versus only 7% in the placebo group with a nominal p-value of 0.041. These results are highly similar to the pivotal trial results for the two most recently approved therapies for anemia associated with lower-risk MDS. Based on these results, as we turn to slide 17, Our target indication for roxidustat is in patients with lower MDS and high transfusion burden who are refractory to or ineligible for prior ESA treatment, where we believe roxidustat has the potential to elevate the standard of care in the second line and beyond treatment settings. In July, we had a positive type C meeting with the FDA, where we aligned on key design elements and a regulatory path forward for roxidustat. The potential pivotal phase three trial, summarized on slide 18, will include patients requiring four or more RBC units in two consecutive eight-week periods prior to randomization, who, as I alluded to on the previous slide, are refractory to, intolerant to, or ineligible for prior ESAs. We also agreed with the FDA on important dosing elements, including the starting dose of 2.5 milligrams per kilogram, and on the management of potential thrombotic risk, which could include trial eligibility, dose modification, and discontinuation criteria. We are currently evaluating eight-week and 16-week RBC transfusion independence as the primary endpoint for the trial. The team continues to work diligently on finalizing the Phase III protocol, and we remain on course for submission in the fourth quarter of this year. We are currently exploring our clinical development options, which include maintaining Roxidustat as a wholly owned asset and running the phase three trial on our own or partnering the program. We are actively engaged in this process and will ultimately choose the path that we believe is in the best interest of shareholders. To summarize on slide 19, there is significant opportunity for Roxidustat in anemia associated with lower risk MDS with no other oral treatments currently available or in late stage development. Furthermore, we believe our target indication would support an orphan drug designation, which, if granted, would provide us with seven years of data exclusivity in the U.S. This potential exclusivity, combined with an attractive market opportunity and an efficient commercial model, represents a substantial economic opportunity for Roxadustat in anemia associated with lower-risk MDS. With that, I will now turn the call over to Dave to discuss the company's financials. Dave?