Kyntra Bio, Inc.

Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Gaia Shamis of Lifespy Advisors. Please go ahead.

Thank you, Latonya, and good afternoon, everyone. Thank you for joining today to discuss Kintra Bio's second quarter 2026 financial and business results. I'm Gaia Shamis from Lifespy Advisors. Joining me on today's call are Thane Wettig, Chief Executive Officer, David DeLucia, Chief Financial Officer, and Carol Gadom, 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's 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 Bio's 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, Thane Wettig. Thane?

Thank you, Gaia. Good afternoon, everyone, and welcome to our second quarter 2026 earnings call. On today's call, I will provide an update on the important progress we have made across our clinical portfolio. First, with FG3246, are potential first-in-class antibody drug conjugate targeting CD46 and its companion PET imaging agent in metastatic castration-resistant prostate cancer. And second, with roxidustat, our potential treatment for anemia due to lower-risk mild dysplastic syndromes. Then David DeLucia, our CFO, will review the financials, after which we will open the call for your questions. Starting with slide three, I'd like to highlight our mid- and late-stage programs and upcoming catalysts. The Phase II monotherapy trial for FG3246 and its companion diagnostic FG3180 in the post-ARPI pre-chemo setting in metastatic castration-resistant prostate cancer continues to actively enroll patients and we are on track for the results from the interim analysis in the fourth quarter of this year. With our Roxidustat program, the protocol for the Phase III trial has been finalized and we are advancing towards our goal of initiating the registrational trial in the fourth quarter of 2026. With a simplified capital structure and cash runway into 2028, we remain committed to executing on our strategic vision and look forward to the upcoming catalysts for both clinical programs. Let's start with the FG3246 and FG3180 program in MCRPC. The unmet need for new treatments for the 65,000 men in the US diagnosed every year with drug-treatable and David DeLucia. We also have a number of patients who are suffering from metastatic cancer. We also have a number of patients who are suffering from metastatic cancer. yet with limited expression in normal tissue. Second, CD46 is upregulated during tumorigenesis as well as during the progression from localized castration-sensitive prostate cancer to metastatic castration-resistant prostate cancer. Third, an estimate 50 to 70% of patients have high CD46-expressing tumors. And finally, relative to PSMA, CD46 expression is more uniform with lower interpatient variability and with higher median expression in MCRPC tissues, which make it a compelling non-PSMA therapeutic target. Slide six highlights FG3246, RCD46 targeting potential first-in-class ADC, which combines the YS5 antibody with an MMAE payload. MMAE is the payload for five currently marketed ADCs, that generated approximately $5 billion in worldwide revenue in 2025, making it a well-characterized therapeutic approach for treating solid tumors. The YS5 antibody offers an androgen receptor agnostic and non-PSMA approach, differentiating it from many of the prostate cancer treatments currently in development. As with the ADC, our companion imaging agent, FGE3180, utilizes the same YS5 targeting antibody and is being developed under its own IND. We believe that having a patient selection biomarker could enable us to potentially enrich the patient population in a phase three trial while also differentiating FG3246 in the prostate cancer treatment paradigm. It also represents 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. FG3180 is an important part of our ongoing phase two trial where we will assess the correlation between CD46 expression as measured by the PET agent and response to FG3246. Our aim is a clinically differentiated therapeutic in a competitive yet highly unsatisfied MCRPC market. Importantly, we are the only non-PSMA program in mid to late stage development that combines a therapeutic with a companion PET imaging agent. The excitement we have in this program comes from the clinical results for FG3246 across two distinct trials. We believe these results, summarized on slide seven, are competitive when compared to other approved and investigational treatments. In the phase one monotherapy trial highlighted on the left part of the slide, FG3246 demonstrated a median RPFS of 8.7 months in patients with MCRPC who were heavily pretreated and were not biomarker selected, with PSA50 response of 36%. Twenty percent of the 25 resist-evaluable patients achieved an ORR with a meaningful duration of response of 7.5 months. It is important to note that all of these ORRs were demonstrated at the 2.7 milligram per kilogram adjusted body weight dose utilized in the expansion phase of the providing early evidence of a dose-response relationship. In the top line results from the Phase 1B2 investigator-initiated study that UCSF summarized on the right side, combination of FG3246 with enzalutamide 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 only one prior ARPI, the combination of FT-3246 and enzalutamide achieved a meaningful median RPFS of 10.1 months with a PSA 50 response of 40%. In addition to the efficacy measures, the IST provided us with important insights into the adverse event profile of the ADC, the use of GCSF prophylaxis, led to a significant decrease in grade three or greater neutropenia compared to the phase one monotherapy trial. This approach is now designed into our ongoing phase two monotherapy study where our objective is to keep more patients on their initial dose without the same degree of dose interruption or reduction experienced in the phase one monotherapy trial with the aim to build upon the 8.7 months of RPFS demonstrated in the phase one trial. Moving to slide eight. An additional insight we gained from the IST is that higher tumor uptake of FG3180 was associated with greater PSA50 response. The PET imaging on the right is from a patient with clear and meaningful expression of CD46 after exposure to FG3180. The bottom row of the table on the left shows that 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 PSA50 response to FG3246 versus those with a lower SUV with a nominal p-value that just missed being statistically significant despite the small number of patients. This is the first observed association between CD46 expression and response to FG3246. We aim to further characterize this association as part of the ongoing phase two monotherapy trial. Slide nine lays out the design for this phase two monotherapy trial where we will enroll 75 patients in the post-1 ARPI pre-chemo setting across three dose levels with the primary objective to select the optimal phase three dose based on efficacy, safety, and PK measures. All patients in the study will be treated with FG3180 in order to further explore the correlation between CD46 expression and response to the ADC in this biomarker unselected trial. The interim analysis of this open label trial is on track for the fourth quarter of this year and will include PSA 50 response, ORR, safety, PK and exposure response data. Putility will be assessed by a composite response rate of PSA 50 and ORR. Importantly, we expect mature RPFS data to become available throughout 2027 as patients continue their treatment with FG3246 and the trial progresses toward completion. On slide 10, we'd like to emphasize the three design elements we have incorporated with the aim of improving upon the 8.7 months of median RPFS demonstrated in the Phase 1 trial. First, we are testing three of the highest doses from the Phase 1 monotherapy study, 1.8, 2.4, and 2.7 milligrams per kilogram. primary prophylaxis with GCSF is being utilized to mitigate neutropenia, an approach which was successfully implemented in the Phase II portion of the IST. We believe reducing the incidence of Grade III or greater neutropenia should lead to fewer dose interruptions or adjustments, extending the duration of therapy, and enabling more consistent exposure to the ADC of FG3246. and third, we are enrolling patients who are earlier in the progression of MCRPC 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, we believe these design elements have the potential to improve upon the phase one results and achieve a median RPFS of 10 months or greater, which can be viewed as a threshold for commercial competitiveness. Slide 10 shows the sites who are participating in the ongoing phase two trial. We now have 23 sites live at top tier U institutions and we continue to be encouraged by our progress to date. We remain on track for the interim analysis of 36 patients in the fourth quarter of this year. To conclude this update on FG3246, We are actively enrolling patients in our Phase II monotherapy trial in the post-1 ARPI pre-chemo MCRPC setting with important design elements in place that we believe could enable FG3246 to surpass the 8.7 months of median RPFS demonstrated in the Phase I trial. We look forward to the interim analysis in the fourth quarter of this year. Moving on to the Roxodustat lower risk mild dysplastic syndromes program on slide 13. There are approximately 50,000 patients with anemia associated with lower risk MDS in the US, with current therapies effective in less than 50% of these patients. With no oral options currently on the market or in late stage development, there's a significant opportunity for an effective, durable, convenient oral treatment that works across multiple lines of therapy. Slide 14 highlights why we believe roxidustat can be that treatment. In a post-hoc analysis of high transfusion burden patients from our previous Phase III Matterhorn study using the international working group definition for high transfusion burden of four or more RBC units in two consecutive eight-week periods, we saw that 36% of patients treated with roxidustat achieved transfusion independence for at least eight straight 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. Turning to slide 15, based on these results, our target indication is intended to be for the treatment of anemia in patients with lower-risk MDS who are refractory to or ineligible for prior ESA treatment, where we believe Roxiduset can raise the standard of care across multiple lines of treatment. We believe we also have a unique opportunity to demonstrate transfusion independence across both RS-positive and RS-negative patients. As presented in our most recent disclosure at EHA, the European Hematology Association, in a post-hoc analysis of the Phase III Matterhorn study, Roxidustat demonstrated similar rates of transfusion independence across both RS-positive and RS-negative patients. primary research that we have conducted with practicing clinicians indicates that Roxiduset has the potential to be a useful treatment in both of these patient segments. The RS negative opportunity, which represents a majority of lower risk MDS patients, is especially relevant given Lusbatracept, the market leading brand in the treatment of lower risk MDS, has not demonstrated clinically differentiated efficacy in this segment of the lower risk MDS population and is not indicated for use in the second-line setting in RS-negative patients. We believe that demonstrating similar efficacy across the entire patient population could position roxiducet favorably in the treatment paradigm of lower-risk MDS. Slide 16 provides an overview of the Phase III trial. Following our interactions with the FDA, we have now finalized a protocol for the Phase III which includes a primary endpoint of eight-week transfusion independence over the first 24 weeks of the trial with key secondary endpoints of 12, 16, and 24-week transfusion independence over 48 weeks. We continue to explore the opportunity to develop Roxidustat internally or with a strategic partner which aligns with our goal of initiating the study in the fourth quarter of 2026. To summarize the Roxidustat opportunity in lower-risk MDS on slide 17, with a substantial unmet need, no oral therapeutic options on the market or in late development, significant potential in RS-negative patients, and an orphan drug designation in hand, we see Roxidustat as a compelling commercial opportunity. We continue to make important progress with the Phase III enabling activities. With that, I will now turn the call over to Dave to discuss the company's financials. Dave?