Kyntra Bio, Inc.

Thank you for standing by, and welcome to Kentra Bio's fourth quarter and full year 2025 earnings conference call. At this time, all participants are in a listen-only mode. After the speaker presentation, there will be a question and answer session. To ask a question during the session, you will need to press star 1-1 on your telephone. To remove yourself from the queue, you may press star 1-1 again. I would now like to hand the call over to Gaia Shamus, with LifeSci Advisors. Please go ahead.

Thank you, operator. Good afternoon, everyone. Thank you for joining today to discuss KintraBio's fourth quarter and full year 2025 financial and business results. I'm Gaia Chamis from LifeSci Advisors. Joining me on today's call are Zane Wettig, Chief Executive Officer, David Ilchia, Chief Financial Officer, and Carol Gedum, Vice President of Product Development. 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 Kintra Bio. Such statements may include, but are not limited to, collaborations 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 material risks can be found in Kintra BIOS filing with the SEC, including our most recent Form 10-K and Form 10-Q. Kintra Bio 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 Kintra Bio website at www.kintrabio.com. With that, I would like to turn the call over to the CEO, Zane Wedding. Zane?

Thank you, Gaia. Good afternoon, everyone, and welcome to our fourth quarter and full year 2025 earnings call. On today's call, I will provide an update on the continued progress with FG3246, a potential first-in-class antibody drug conjugate targeting CD46 and its companion PET imaging agent in metastatic castration-resistant prostate cancer, as well as the path forward for roxidustat as a potential treatment for anemia due to lower-risk modest plastic 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'd like to start by highlighting the transformational year we had in 2025. We completed the sale of Hybrids in China to AstraZeneca, paid off our senior secure term loan, and extended our cash runway into 2028. This enabled us to start the phase two trial for FG3246 and FG3180 in the post-ARPI pre-chemo setting in metastatic castration-resistant prostate cancer, where we are actively enrolling patients at multiple sites in the U.S. We recently reported the top-line results presented at ASCO-GU from the investigator-sponsored trial of FG3246 in combination with enzalutamide in MCRPC, and we remain on track to report the interim results from our ongoing Phase II monotherapy trial of FG3246 and FG3180 in the second half of 2026. We also made important progress with Roxidustat with the submission of the Phase III protocol for lower risk modest plastic syndromes and the receipt of orphan drug designation for MDS. We expect feedback on the Phase III trial design from the FDA in the coming weeks with the aim of initiating the Phase III trial in the second half of this year. We began 2026 rejuvenated, rebranding FibroGent to Kentra Bio to better reflect the momentum and energy of a company focused on oncology and rare disease. We remain confident that with our mid and late stage assets, simplified capital structure, and upcoming catalysts across both clinical programs, we are well positioned to create meaningful therapeutic options for patients and significant value for shareholders. Moving to our FG3246 and FG3180 program 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 with metastatic disease that has become castration 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 FG3246 could be this new treatment option and estimate the total addressable market to be well over $5 billion annually in the US alone. Slide six depicts 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 non-PSMA 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, 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 with its own IND. We believe that having a patient selection biomarker would not only allow us to better enrich the patient population in a future phase three 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, which generated revenue of almost $2 billion in 2025. Slide 8 highlights the design of the investigator-initiated Phase 1B-2 trial of FG3246 in combination with enzalutamide and MCRPC, for which top line results were presented at the recent ASCO-GU meeting. These results, shown on slide nine, demonstrated encouraging anti-tumor activity with seven months of median radiographic progression-free survival in biomarker unselected patients across the entire cohort of 44 patients. Importantly, in patients who had progressed on one prior ARPI, the combination of FG3246 and enzalutamide achieved a median RPFS of 10.1 months. and demonstrated a PSA50 response of 40%. Notably, on slide 10, higher tumor uptake of FG3180 was associated with PSA50 response, underscoring the potential for FG3180 as a PET imaging biomarker for patient selection. On the right-hand part of the slide is an example of a PET image from the IST captured after treatment with FG3180 highlighting significant CD46-expressing tumors. The table on the left shows the correlation between tumor uptake of FG3180 and PSA50 response. Patients with a higher average maximum standardized uptake value, or SUV, of a target lesion when normalized to the SUV of the blood pool demonstrated a trend to greater response to FG3246 as measured by PSA50 versus those with a lower SUV, with a nominal p-value that just missed being statistically significant. This data demonstrates for the first time an association between CD46 expression and response to FG3246. Further evaluation of FG3180 is an important part of the ongoing Phase II monotherapy trial. Finally, on slide 11, the combination of FG3246 and enzalutamide had a similar safety profile to what was observed in the FG3246 phase 1 monotherapy trial. Importantly, the incidence of grade 3 or greater neutropenia was substantially reduced with the utilization of GCSF prophylaxis when compared to the phase 1 monotherapy trial. This approach is an important design element of our ongoing phase 2 monotherapy trial. In summary, the results of the IST provide us with the key insights that further validate design elements in our ongoing phase 2 monotherapy trial. which we believe has the potential to improve upon the median RPFS observed in the Phase I monotherapy trial, which I will cover in greater detail next. Briefly on slide 12, we recap the top-line results from the Phase I monotherapy study of FG3246, which we believe are competitive when compared to other approved and investigational treatments. These results demonstrated a median RPFS of 8.7 months in patients with MCRPC that were heavily pretreated and were not biomarker selected. PSA reductions of greater than 50% in this population were achieved in 36% of these patients. Moving to slide 13, 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 3 based on efficacy, safety, and PK parameters. It is important to note that FG31AD will be an integral part of the study as we seek to further explore what was demonstrated in the Phase 1B-2 combination trial and determine whether there is further correlation between CD46 expression and response to the ADC in this all-comers Phase 2 trial. An interim analysis of the open-label Phase 2 trial is planned for the second half of and will include PSA50, ORR, safety, PK, and exposure response data. Importantly, we expect mature RPFS data to become available in 2027 as patients continue on their treatment with FG3246 and the trial progresses toward completion. On slide 14, I'd like to highlight three important steps we have taken with the design of the ongoing phase two monotherapy trial which were further validated with the IST results as we aim to improve upon the 8.7 months of median RPFS demonstrated in the Phase I monotherapy trial. First, leveraging earlier evidence of an exposure-response relationship, the Phase II study is using three of the highest doses from the Phase I dose escalation and expansion study. Second, primary prophylaxis with GCSF is utilized to mitigate neutropenia, which was successfully demonstrated in the phase two portion of the recently disclosed IST. The mitigation of neutropenia could enable more consistent exposure to the ADC with fewer dose interruptions or adjustments early in the course of treatment, which could extend the duration of therapy and potentially enhance the efficacy of the ADC. Third, we are enrolling healthier patients in earlier lines of therapy versus the median five prior lines of therapy in the phase one trial, The 10.1 months of median RPFS demonstrated in the IST in patients who progressed on only one prior ARPI underscores the potential of FG3246 in this patient population. Together with the insights from the IST results, we believe that these design elements have the potential to improve upon the Phase I results and achieve a median RPFS of 10 months or greater, which we believe is the benchmark for commercial competitiveness. Slide 15 highlights the recent and upcoming catalysts for the FG3246 and FG3180 program. We are actively enrolling patients and are on track to report the interim results from the Phase II monotherapy trial in the second half of this year. To summarize, on slide 16, 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 and no non-PSMA approaches in mid- to late-stage development with a companion PET imaging approach. Targeting CD46 with FGD3246 has already demonstrated promising early efficacy signals with an acceptable safety profile, both in monotherapy and combination settings. We have a well-designed Phase II monotherapy trial in the post-ARPI pre-chemo setting in MCRPC to further to attempt to further build upon the 8.7 months of median RPFS demonstrated in the Phase 1 trial. We are looking forward to the interim readout later this year, and we'll update you as the program progresses. Turning now to Roxidustat. Slide 18 highlights the unmet need and the potential for Roxidustat in the approximately 49,000 patients with anemia associated with lower-risk MDS in the U.S. alone. Current treatments, as measured by transfusion independence, 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 across multiple lines of therapy. Moving to slide 19, I would like to quickly 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 at least 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 20, our target indication for Roxidustat is in patients with lower risk MDS who are refractory to or ineligible for prior ESA treatment, where we believe Roxidustat has the potential to elevate the standard of care across multiple treatment lines. In addition, We believe we have an opportunity to demonstrate efficacy across both RS-positive and RS-negative patients. When looking at the prevalence of the disease, RS-negative patients make up more than 50% of patients in lower-risk MDS. There is a great opportunity to potentially move up-line and help these patients, given that luspatercept is not approved in the second-line setting in RS-negative patients. Moving to slide 21, after aligning with the FDA last summer on key design elements, of a Phase III trial, we submitted the final protocol to the FDA and expect to receive their feedback in the coming weeks. We are currently exploring the opportunity to develop Roxidustat internally or with a strategic partner and aim to initiate this study in the second half of 2026. To summarize on slide 22, there is significant opportunity for Roxidustat in anemia associated with lower-risk MDS with no other oral treatments currently available or in late-stage With Roxadustat being granted orphan drug designation, we believe that a minimum of seven years of regulatory exclusivity, combined with an attractive market opportunity and 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? Thank you, Thayne.