Q2 2026 Kyntra Bio Inc Earnings Call

August 13, 2026

Speaker #1: Later, we will conduct a question-and-answer session. If you would like to ask a question at that time, please press star 11 on your telephone and wait for your name to be announced.

Operator: If you would like to ask a question at that time, please press star one one on your telephone and wait for your name to be announced. 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 LifeSci Advisors. Please go ahead.

Speaker #1: Please be advised that today’s conference is being recorded. I would now like to hand the conference over to your speaker today, Gaia Shamus of LifeSci Advisors.

Speaker #1: Please go ahead.

Gaia Vasiliver-Shamis: Thank you, Latonia, and good afternoon, everyone. Thank you for joining today to discuss Kyntra Bio's Q2 2026 financial and business results. I am Gaia Shamis from LifeSci Advisors. Joining me on today's call are Thane Wettig, Chief Executive Officer, David DeLucia, Chief Financial Officer, and Karel Gottem, 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 Kyntra 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.

Speaker #2: I'm Kila Tonya, and good afternoon, everyone. Thank you for joining today to discuss Kintra Bio's second quarter 2026 financial and business results. I'm Gaia Shamus from LifeSci Advisors.

Speaker #2: Joining me on today's call are Thane Wettig, Chief Executive Officer; David DeLucia, Chief Financial Officer; and Carol Gaddam. Vice President of Product Development. Following the prepared remarks, we will open the call to your questions.

Speaker #2: I would like to remind you that remarks made on today's call include forward-looking statements about Kyntra 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.

Gaia Vasiliver-Shamis: I would like to remind you that remarks made on today's call include forward-looking statements about Kyntra 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.

Speaker #2: Each forward-looking statement is subject to risks and uncertainties that could cause actual results and events to defer materially from those projected in that statement.

Gaia Vasiliver-Shamis: Each forward-looking statement is subject to risks and uncertainties that could cause actual results and events to differ materially from those projected in the statement. A more complete description of these and other material risks can be found in Kyntra Bio's filing with the SEC, including our most recent Form 10-K and Form 10-Q. Kyntra 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 Kyntra Bio website at www.fibrogen.com. With that, I would like to turn the call over to the CEO, Thane Wettig. Thane?

Speaker #2: A more complete description of these and other material risks can be found in Kintra Bio's filings with the SEC, including our most recent Form 10-K and Form 10-Q.

Speaker #2: 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 update and a webcast of today's conference call can be found on the Investors section of Kintra Bio website at www.kintrabio.com.

Gaia Vasiliver-Shamis: 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 Kyntra Bio website at www.fibrogen.com. With that, I would like to turn the call over to the CEO, Thane Wettig. Thane?

Speaker #2: With that, I would like to turn the call over to the CEO, Thane Wettig. Thane?

Speaker #3: 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.

Thane Wettig: Thank you, Gaia. Good afternoon, everyone, and welcome to our Q2 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 FG-3246, our potential first-in-class antibody drug conjugate targeting CD46 and its companion PET imaging agent in metastatic castration-resistant prostate cancer. And second, with roxadustat, our potential treatment for anemia due to lower risk myelodysplastic syndromes. Then David DeLucia, our CFO, will review the financials, after which we will open the call for your questions. Starting with slide 3, I would like to highlight our mid and late-stage programs and upcoming catalysts.

Speaker #3: First, with FG-3246, our potential first-in-class antibody-drug conjugate targeting CD46, and its companion PET imaging agent in metastatic castration-resistant prostate cancer. And second, with roxadustat, our potential treatment for anemia due to lower-risk myelodysplastic syndromes.

Thane Wettig: And second, with roxadustat, our potential treatment for anemia due to lower risk myelodysplastic syndromes. Then David DeLucia, our CFO, will review the financials, after which we will open the call for your questions. Starting with slide 3, I would like to highlight our mid and late-stage programs and upcoming catalysts.

Speaker #3: Then David DeLucia, our CFO, will review the financials after which we will open the call for your questions. Starting with slide 3, I'd like to highlight our mid and late-stage programs and upcoming catalysts.

Speaker #3: The phase 2 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.

Thane Wettig: The phase II monotherapy trial for FG-3246 and its companion diagnostic FG-3180 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 Q4 of this year. With our roxadustat program, the protocol for the phase III trial has been finalized, and we are advancing towards our goal of initiating the registrational trial in Q4 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 FG-3246 and FG-3180 program in mCRPC. The unmet need for new treatments for the 65,000 men in the US diagnosed every year with drug-treatable castration-resistant metastatic disease is substantial.

Speaker #3: With our Roxadustat program, the protocol for the phase 3 trial has been finalized, and we are advancing towards our goal of initiating the registrational trial in the fourth quarter of 2026.

Speaker #3: With the 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.

Speaker #3: Let's start with the FG3246 and FG3180 program in mCRPC. The unmet need for new treatments for the 65,000 men in the U.S. diagnosed every year with drug-treatable, castration-resistant metastatic disease is substantial.

Speaker #3: Targeting CD46, a novel tumor-selective multifunctional epitope that helps tumors evade complement-dependent cytotoxicity could help address this need. Moving to slide 5, what sets CD46 apart from non-PSMA tumor antigen targets for metastatic prostate cancer centers on four key points.

Thane Wettig: Targeting CD46, a novel tumor-selected multifunctional epitope that helps tumors evade complement-dependent cytotoxicity could help address this need. Moving to slide 5. What sets CD46 apart from non-PSMA tumor antigen targets for metastatic prostate cancer centers on four key points. First, it is highly expressed in prostate cancer and other tumors, yet with limited expression in normal tissue. Second, CD46 is upregulated during tumor genesis 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. 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 6 highlights FG-3246, our CD46-targeting potential first-in-class ADC, which combines the YS5 antibody with an MMAE payload.

Speaker #3: First, it is highly expressed in prostate cancer and other tumors, 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.

Speaker #3: Third, an estimated 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 higher median expression in mCRPC tissues, which makes it a compelling non-PSMA therapeutic target.

Speaker #3: Slide 6 highlights FG3246, our CD46 targeting potential first-in-class ADC, which combines the YS5 antibody with an MMAE payload. MMAE is the payload for five currently marketed ADCs, the generated approximately 5 billion dollars in worldwide revenue in 2025, making it a well-characterized therapeutic approach for treating solid tumors.

Thane Wettig: 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, FG-3180, 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 III trial while also differentiating FG-3246 in the prostate cancer treatment paradigm. It also represents an important commercial opportunity as a companion diagnostic to FG-3246, similar to the existing PSMA PET agents, which generated revenue of almost $2 billion in 2025.

Speaker #3: 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 FG3180 utilizes the same YS5-targeting antibody and is being developed under its own IND.

Speaker #3: We believe that having a patient-selection biomarker could enable us to potentially enrich the patient population in a Phase 3 trial while also differentiating FG3246 in the prostate cancer treatment paradigm.

Speaker #3: 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 dollars in 2025.

Speaker #3: FG3180 is an important part of our ongoing Phase 2 trial, where we will assess the correlation between CD46 expression as measured by the PET agent and response to FG3246.

Thane Wettig: FG-3180 is an important part of our ongoing phase II trial, where we will assess the correlation between CD46 expression as measured by the PET agent, and response to FG-3246. 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 FG-3246 across two distinct trials. We believe these results, summarized on slide 7, are competitive when compared to other approved and investigational treatments. In the phase I monotherapy trial highlighted on the left part of the slide, FG-3246 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%.

Speaker #3: 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.

Speaker #3: 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 7 are competitive when compared to other approved and investigational treatments.

Speaker #3: In the Phase 1 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 a PSA50 response of 36%.

Speaker #3: 20 percent of the 25 resistive available 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 trial, providing early evidence of a dose response relationship.

Thane Wettig: 20% of the 25 RECIST 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 trial, providing early evidence of a dose-response relationship. In the top line results from the phase I-B/II investigator-initiated study at UCSF summarized on the right side, combination of FG-3246 with enzalutamide demonstrated encouraging antitumor activity with 7 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 FG-3246 and enzalutamide achieved a meaningful median RPFS of 10.1 months with a PSA50 response of 40%.

Speaker #3: In the top line results from the phase 1B2 investigator-initiated study at UCSF summarized on the right side, combination of FG3246 with Enzalutamide demonstrated encouraging anti-tumor activity with 7 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 FG3246 and Enzalutamide achieved a meaningful median RPFS of 10.1 months with a PSA 50 response of 40 percent.

Speaker #3: 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 3 or greater neutropenia compared to the phase 1 monotherapy trial. This approach is now designed into our ongoing phase 2 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 1 monotherapy trial, with the aim to build upon the 8.7 months of RPFS demonstrated in the phase 1 trial.

Thane Wettig: In addition to the efficacy measures, the IST provided us with important insights into the adverse event profile of the ADC. The use of G-CSF prophylaxis led to a significant decrease in grade 3 or greater neutropenia compared to the phase I monotherapy trial. This approach is now designed into our ongoing phase II 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 I monotherapy trial, with the aim to build upon the 8.7 months of RPFS demonstrated in the phase I trial. Moving to slide 8, an additional insight we gained from the IST is that higher tumor uptake of FG-3180 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 FG-3180.

Speaker #3: Moving to slide 8, in additional insight we gained from the IST is that higher tumor uptake of FG3180 was associated with greater PSA 50 response.

Speaker #3: 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 this small number of patients.

Thane Wettig: 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 of greater PSA50 response to FG-3246 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 FG-3246. We aim to further characterize this association as part of the ongoing phase II monotherapy trial. Slide 9 lays out the design for this phase II monotherapy trial, where we will enroll 75 patients in the post one ARPI pre-chemo setting across three dose levels, with the primary objective to select the optimal phase III dose based on efficacy, safety, and PK measures.

Speaker #3: 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 2 monotherapy trial.

Speaker #3: Slide 9 lays out the design for this Phase 2 monotherapy trial, where we will enroll 75 patients in the post-1 ARPI, pre-chemo setting across three dose levels.

Speaker #3: With the primary objective to select the optimal phase 3 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.

Thane Wettig: All patients in the study will be treated with FG-3180 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 Q4 of this year and will include PSA50 response, ORR, safety, PK, and exposure response data. Futility will be assessed by a composite response rate of PSA50 and ORR. Importantly, we expect mature RPFS data to become available throughout 2027 as patients continue their treatment with FG-3246 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 I trial.

Speaker #3: The interim analysis of this open-label trial is on track for the fourth quarter of this year, and will include PSA50 response, ORR, safety, PK, and exposure-response data.

Speaker #3: Futility 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.

Speaker #3: 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.

Speaker #3: 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. Second, primary prophylaxis with GCSF is being utilized to mitigate neutropenia—an approach which was successfully implemented in the Phase 2 portion of the IST.

Thane Wettig: First, we are testing three of the highest doses from the phase I monotherapy study, 1.8, 2.4, and 2.7 milligrams per kilogram. Second, primary prophylaxis with G-CSF 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 3 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 FG-3246. Third, we are enrolling patients who are earlier in the progression of mCRPC versus the median five prior lines of therapy in the phase I 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 FG-3246 in this patient population.

Speaker #3: We believe reducing the incidence of grade 3 or greater neutropenia should lead to fewer dose interruptions or adjustments, extending the duration of therapy, and enabling more consistent exposure to the ADC.

Speaker #3: Of FG3246. And third, we are enrolling patients who are earlier in the progression of MCRPC versus the median 5 prior lines of therapy in the phase 1 trial.

Speaker #3: 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.

Speaker #3: Together, we believe these design elements have the potential to improve upon the phase 1 results and achieve a median RPFS of 10 months or greater which can be viewed as a threshold for commercial competitiveness.

Thane Wettig: Together, we believe these design elements have the potential to improve upon the phase I 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 II 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 Q4 of this year. To conclude this update on FG-3246, we are actively enrolling patients in our phase II monotherapy trial in the post one ARPI pre-chemo mCRPC setting, with important design elements in place that we believe could enable FG-3246 to surpass the 8.7 months of median RPFS demonstrated in the phase I trial.

Speaker #3: Slide 10 shows the sites that are participating in the ongoing Phase 2 trial. We now have 23 sites live at top-tier U.S. institutions, and we continue to be encouraged by our progress to date.

Speaker #3: 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 2 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 1 trial.

Speaker #3: We look forward to the interim analysis in the fourth quarter of this year. Moving on to the roxadustat lower-risk myelodysplastic syndromes program on slide 13.

Thane Wettig: We look forward to the interim analysis in Q4 of this year. Moving on to the roxadustat lower risk myelodysplastic 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 is a significant opportunity for an effective, durable, convenient oral treatment that works across multiple lines of therapy. Slide 14 highlights why we believe roxadustat can be that treatment.

Speaker #3: There are approximately 50,000 patients with anemia associated with lower-risk MDS in the US, with current therapies effective in less than 50 percent of these patients.

Speaker #3: With no oral options currently on the market or in late-stage development, there is a significant opportunity for an effective, durable, convenient oral treatment that works across multiple lines of therapy.

Speaker #3: Slide 14 highlights why we believe roxadustat can be that treatment. In a post-hoc analysis of high transfusion burden patients from our previous phase 3 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 roxadustat achieved transfusion independence for at least eight straight weeks versus only 7% in the placebo group, with a nominal p-value of 0.041.

Thane Wettig: In a post-hoc analysis of high transfusion burden patients from our previous Phase 3 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 roxadustat 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 roxadustat can raise the standard of care across multiple lines of treatment.

Speaker #3: 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 Roxidustat can raise the standard of care across multiple lines of treatment.

Speaker #3: 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 3 Matterhorn study, roxadustat demonstrated similar rates of transfusion independence across both RS-positive and RS-negative patients.

Thane Wettig: 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, roxadustat 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 roxadustat 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 that luspatercept, 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.

Speaker #3: Primary research that we have conducted with practicing clinicians indicates that Roxidustat has the potential to be a useful treatment in both of these patient segments.

Speaker #3: The RS negative opportunity which represents a majority of lower-risk MDS patients is especially relevant given Lispazosept, 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.

Speaker #3: We believe that demonstrating similar efficacy across the entire patient population could position roxadustat favorably in the treatment paradigm of lower-risk MDS. Slide 16 provides an overview of the Phase 3 trial.

Thane Wettig: We believe that demonstrating similar efficacy across the entire patient population could position roxadustat 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 the protocol for the phase III study, which includes a primary endpoint of 8-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 roxadustat internally or with a strategic partner, which aligns with our goal of initiating the study in Q4 2026.

Speaker #3: Following our interactions with the FDA, we have now finalized a protocol for the Phase 3 study, which includes a primary endpoint of 8-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.

Speaker #3: We continue to explore the opportunity to develop Roxidustat internally or with strategic partner which aligns with our goal of initiating the study in the fourth quarter of 2026.

Speaker #3: To summarize the roxadustat 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 roxadustat as a compelling commercial opportunity.

Thane Wettig: To summarize the roxadustat 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 roxadustat as a compelling commercial opportunity. We've continued 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?

Speaker #3: We continue to make important progress with the phase 3 enabling activities. With that, I will now turn the call over to Dave to discuss the company's financials.

Speaker #3: Dave?

Speaker #2: Thank you, Thane. For the second quarter of 2026, total revenue was negative 1.5 million dollars compared to 1.3 million dollars for the same period in 2025.

David DeLucia: Thank you, Thane. For Q2 2026, total revenue was -USD 1.5 million compared to USD 1.3 million for the same period in 2025. Total operating costs and expenses for Q2 2026 were USD 16.1 million, compared to USD 13.4 million for Q2 2025. R&D expenses for Q2 2026 were USD 6.8 million compared to USD 5.9 million in Q2 2025. SG&A expenses for Q2 2026 were USD 9.3 million compared to USD 7.1 million in Q2 2025. During Q2 2026, we recorded a net income from continuing operations of USD 12 million, or USD 2.96 net income per basic and diluted share, compared to a net loss of USD 13.7 million, or USD 3.38 net loss per basic and diluted share 1 year ago. Now shifting towards cash.

Speaker #2: Total operating costs and expenses for the second quarter of 2026 were $16.1 million, compared to $13.4 million for the second quarter of 2025.

Speaker #2: R&D expenses for the second quarter of 2026 were 6.8 million dollars compared to 5.9 million dollars in the second quarter of 2025. SG&A expenses for the second quarter of 2026 were 9.3 million dollars compared to 7.1 million dollars in the second quarter of 2025.

Speaker #2: During the second quarter of 2026, we recorded a net income from continuing operations of $12 million, or $2.96 net income per basic and diluted share.

Speaker #2: Compared to a net loss of $13.7 million, or a net loss of $3.38 per basic and diluted share one year ago. Now, shifting towards cash.

Speaker #2: As of June 30th, we reported $95.7 million in cash, cash equivalents, investments, and accounts receivable. We expect the company to have a cash runway into 2028, enabling us to continue to invest in our U.S. pipeline opportunities.

David DeLucia: As of 30 June, we reported $95.7 million in cash equivalents, investments, and accounts receivable. We expect the company to have a cash runway into 2028, enabling us to continue to invest in our US pipeline opportunities. Thank you, and I will now turn the call back over to Thane.

Speaker #2: Thank you. I will now turn the call back over to Thane.

Speaker #3: Thank you, Dave. We entered the second half of 2026 with promising momentum. We will continue our disciplined execution of the FG-3246 and FG-3180 programs, with results from the interim analysis of the Phase 2 monotherapy trial expected in the fourth quarter of 2026.

Thane Wettig: Thank you, Dave. We enter the H2 of 2026 with promising momentum. We will continue our disciplined execution of the FG-3246 and FG-3180 program with results from the interim analysis of the phase II monotherapy trial expected in the Q4 of 2026, and continue the phase III enabling activities for roxadustat, with the goal of initiating the phase III trial in lower risk MDS in the Q4 of 2026. With that, I would now like to turn the call over to the operator for Q&A.

Speaker #3: And continue the Phase 3 enabling activities for roxadustat, with the goal of initiating the Phase 3 trial in lower-risk MDS in the fourth quarter of 2026.

Speaker #3: With that, I would now like to turn the call over to the operator for Q&A.

Operator: Certainly. As a reminder, to ask a question, please press *11 on your telephone and wait for your name to be announced. To withdraw your question, please press *11 again. Please stand by while we compile our Q&A roster. Our first question will come from the line of Alex Ramsey of William Blair. Your line is open.

Speaker #4: Certainly. As a reminder, to ask a question, please press *11 on your telephone and wait for your name to be announced. To withdraw your question, please press *11 again.

Speaker #4: Please stand by while we compile our Q&A roster. Our first question will come from the line of Alex Ramsey of William Blair. Your line is open.

Speaker #5: Hi, this is Alex on for Andy. So for the upcoming phase 3 trial of roxadustat, the dosing regimen begins with 2.5 mg per kilogram, with potential for titrating up to 3.5.

Alex Ramsey: Hi, this is Alex on for Andy. For the upcoming phase III trial of roxadustat, the dosing regimen begins with 2.5 mg per kg, with potential for titrating up to 3.5. We were just wondering how that determination is made, and if it is based on tolerability or efficacy, and how long after starting the treatment the assessment is made. Also what the titration interval is from both a timing and a dosing perspective.

Speaker #5: So we were just wondering how that determination is made, and if it's based on tolerability or efficacy, and how long after starting the treatment the assessment is made.

Speaker #5: And then also, what the titration interval is from both a timing and dosing perspective.

Speaker #3: Yeah, thanks, Alex, for the call. I'm going to hand that question over to Carol Adam, our VP of Product Development. Carol?

Thane Wettig: Yeah. Thanks, Alex, for the call. I am going to hand that question over to Carol Adam, our VP of Product Development. Carol?

Thane Wettig: Yeah. Thanks, Alex, for the call. I am going to hand that question over to Carol Gaddum, our VP of Product Development. Carol?

Speaker #5: Thank you for the question. So, uptitration or downtitration is based on an assessment of benefit and risk, as you have highlighted. An assessment for a change in dose is possible every six weeks, based on what we see from a benefit and risk perspective.

Carol Adam: Thank you for the question. Up titration or down titration is based on an assessment of benefit and risk, as you have highlighted, and the assessment is, or a change in dose is possible every six weeks based on what we see from a benefit and risk perspective.

Carol Gaddum: Thank you for the question. Up titration or down titration is based on an assessment of benefit and risk, as you have highlighted, and the assessment is, or a change in dose is possible every six weeks based on what we see from a benefit and risk perspective.

Speaker #5: Perfect. Thank you so much. And so, in that, is it straight from 2.5 to 3.5 if they go up in dose, or is there some interval in between?

Alex Ramsey: Perfect. Thank you so much. Is it straight from 2.5 to 3.5 if they go up in dose, or is there some interval in between?

Carol Adam: There are some intervals in between. There are some intervals in between.

Carol Gaddum: There are some intervals in between. There are some intervals in between.

Speaker #5: There are some intervals in between. There are some intervals in between, yes. Okay, perfect. Thank you so much.

Alex Ramsey: Okay.

Carol Adam: Yes. Mm-hmm.

Carol Gaddum: Yes. Mm-hmm.

Alex Ramsey: Okay, perfect. Thank you so much.

Thane Wettig: Yeah, Alex, there will be very specific guidance to the sites on the titration either up or down based upon a number of factors, including hemoglobin level and the rate of rise of that hemoglobin level as well.

Speaker #3: And Alex, there will be very specific guidance to the sites on the titration, either up or down, based upon a number of factors, including hemoglobin level.

Speaker #3: And the rate of rise of that hemoglobin level as well.

Speaker #5: Perfect. Thank you so much.

Alex Ramsey: Perfect. Thank you so much. Mm-hmm.

Speaker #4: And our next question will be coming from the line of Matthew Keller of HC Wainwright. Your line is open.

Operator: And our next question will be coming from the line of Matthew Keller of H.C. Wainwright. Your line is open.

Matthew Keller: Hey, good afternoon, everyone. Thanks for taking our questions. I guess on the roxadustat program as well, first, I was wondering if you would remind us, how contingent are you starting the phase III on a partner? Then a follow-up to that, I was wondering how has the MATTERHORN data changed your calculus at all on potentially partnering that program?

Speaker #6: Hey, good afternoon, everyone. Thanks for taking our questions. So I guess on the Roxa program as well, first, I was wondering if you could remind us, how contingent are you starting the phase 3 on a partner?

Speaker #6: And then a follow-up to that, I was wondering, how has the Matterhorn data changed your calculus at all on potentially partnering that program?

Thane Wettig: Hey, thanks, Matt, for the question. The start of the phase III, as we have stated previously, we are undergoing both the opportunity to develop internally as well as partner the program. To develop internally, we would have to bring in capital in order to do that, and so that is a consideration while we also evaluate strategic partners as well. We are running a parallel path with both of these. At the end of the day, we are going to make the decision that we believe is in the best interest of shareholders. There are some dynamics in play related to economics. If you think about the license that we wholly own in North America and South America, that was a license that was previously held by AstraZeneca during the development of the CKD program.

Speaker #3: Hey, thanks, Matt, for the question. So, the start of the Phase 3, as we've stated previously, we are undergoing both the opportunity to develop internally, as well as to partner the program.

Speaker #3: To develop internally, we would have to bring in capital in order to do that, and so that's a consideration while we also evaluate strategic partners as well.

Speaker #3: And so, we're running a parallel path with both of these. At the end of the day, we're going to make the decision that we believe is in the best interest of shareholders.

Speaker #3: There are some dynamics at play related to economics. So, if you think about the license that we wholly own in North America and South America, that was a license previously held by AstraZeneca during the development of the CKD program.

Speaker #3: When we negotiated those rights back from AZ, if we were to develop Roxidustat on our own and commercialize on our own, we would owe AZ a mid-single-digit royalty on net sales.

Thane Wettig: When we negotiated those rights back from AstraZeneca, if we were to develop roxadustat on our own and commercialize on our own, we would owe AstraZeneca a mid-single-digit royalty on net sales. If we were to partner the program with a strategic and somebody else were to develop and commercialize, AstraZeneca would then be entitled to 35% of any economics that would accrue to Kyntra Bio. So that is one consideration from an economic perspective. Clearly, there are strategic and operational considerations that we continue to evaluate. As I said, we are going to ultimately make the call that we believe is in the best interest of shareholders.

Speaker #3: If we were to partner the product or the program with a strategic, and somebody else were to develop and commercialize it, AZ would then be entitled to 35% of any economics that would accrue to Kyntra Bio.

Speaker #3: So that's one consideration from an economic perspective. Clearly, there are strategic and operational considerations that we continue to evaluate. And as I said, we're going to ultimately make the call that we believe is in the best interest of shareholders.

Speaker #6: Yeah, it totally makes sense. And then, can you comment at all about how the RS data is maybe playing into that, if at all?

Matthew Keller: Yeah, it totally makes sense. Can you comment at all about how the RS data is maybe playing into that, if at all? If I may, kind of an adjacent question, did the RS data also influence the potential phase III design at all? Sorry, I am going to pepper you with a couple there.

Speaker #6: And if I may kind of an adjacent question, did the RS data also influence the potential phase 3 design at all? Sorry, I'm going to pepper you with a couple there.

Thane Wettig: No, it is a great question. The RS kind of dynamic with respect to RS positive and RS negative, there is clearly a larger unmet need in the marketplace for RS negative patients, given the fact that luspatercept has not been able to really show any sort of a benefit relative to ESAs in that particular patient population. In fact, they are not indicated in the second-line setting for RS negative patients. The understanding of that dynamic obviously plays into how we think about the opportunity, how we think about the clinical design, how we think about the ultimate forecast should we be successful in the phase III trial.

Speaker #3: No, that's a great question. And so yeah, the RS kind of dynamic with respect to RS positive and RS negative, there's clearly a larger unmet need in the marketplace for RS negative patients, given the fact that Bruce Batterstep has not been able to really show any sort of a benefit relative to ESAs in that particular patient population.

Speaker #3: And the fact they're not indicated in the second-line setting for RS negative patients. And so the understanding of that dynamic obviously plays into how we think about the opportunity, how we think about the clinical design, how we think about the ultimate forecast should we be successful in the phase 3 trial.

Speaker #3: We're going to make sure that we enroll the requisite number of both RS positive and RS negative patients in the phase 3 trial so that we can have the power to be able to demonstrate that Roxidustat works across both of those patient populations.

Thane Wettig: We are going to make sure that we enroll a requisite number of both RS positive and RS negative patients in the phase III trial so that we can have the power to be able to demonstrate that roxadustat works across both of those patient populations. But the RS negative opportunity or the MATTERHORN data, we would be pursuing this regardless of the opportunity for roxadustat to perhaps show a differential benefit in RS negative patients relative to RS positive patients. But it clearly does give us, we think, a really nice commercial opportunity across both segments, but especially in the RS negative population, which makes up more than 50% of the total patients who have lower risk myelodysplastic syndrome. Did that answer your question, Matt?

Speaker #3: But the RS negative opportunity or the Matterhorn data we'd be pursuing this regardless of the opportunity for Roxidustat to perhaps show a differential benefit in RS negative patients relative to RS positive patients.

Speaker #3: But it clearly does give us, we think, a really nice commercial opportunity across both segments, but especially in the RS-negative population, which makes up more than 50% of the total patients who have lower-risk myelodysplastic syndrome.

Speaker #3: Did that get at your question, Matt?

Matthew Keller: It absolutely did. Thank you so much for the color. I really appreciate it.

Speaker #6: It absolutely did. Thank you so much for the color. I really appreciate it.

Speaker #3: Yeah, you bet. And Dave or Carol, anything to add to that?

Thane Wettig: Yeah. Dave or Carol, anything to add to that?

Speaker #5: Thank you. The only thing I would add is you asked about how Matterhorn informed the Phase 3 design, and it has obviously been a significant driver of the Phase 3 design. We went through a comprehensive analysis of what variables were driving outcomes—Roxa versus placebo—and isolated transfusion burden as the key variable, and have designed the Phase 3 trial accordingly.

Carol Adam: Thank you. The only thing I would add is you asked around how MATTERHORN informed the phase III design and has obviously been a significant driver of the phase III design, went through a comprehensive analysis of what variables were driving outcomes, roxadustat versus placebo and isolated transfusion burden as the key variable and have designed the phase III trial accordingly. To Thane's point, the analysis also shows that roxadustat improves transfusion independence and hemoglobin across RS positive and negative. So that is also reflected in the phase III design.

Carol Gaddum: Thank you. The only thing I would add is you asked around how MATTERHORN informed the phase III design and has obviously been a significant driver of the phase III design, went through a comprehensive analysis of what variables were driving outcomes, roxadustat versus placebo and isolated transfusion burden as the key variable and have designed the phase III trial accordingly. To Thane's point, the analysis also shows that roxadustat improves transfusion independence and hemoglobin across RS positive and negative. So that is also reflected in the phase III design.

Speaker #5: Accordingly, and to Thane's point, the analysis also shows that Roxidustat improves transfusion dependence and hemoglobin across RS positive and negative. And so that is also reflected in the phase 3 design.

Speaker #6: That makes sense. Thank you.

Matthew Keller: Makes sense. Thank you.

Speaker #4: And our next question will be coming from the line of Michael King of Rodman & Renshaw LLC. Your line is open.

Operator: Our next question will be coming from the line of Michael King of Rodman & Renshaw LLC. Your line is open.

Speaker #6: Thanks for taking the question, guys. If I could, I'd like to pivot to 3246 and 3180. A couple of questions on the program. I'm just curious, how do you guys look at it as far as I know it's one to two prior lines and one prior ARPI?

Michael G. King Jr.: Thanks for taking the question, guys. If I could, I'd like to pivot to FG-3246 and FG-3180. Couple of questions on the program. I'm just curious how you guys look at it as far as, I know it's one to two prior lines and one prior ARPI, but I'm just curious what you anticipate the enrollment might be for individuals who have been treated with lutetium-177, and whether you can enrich enrollment for that population. The reason I'm asking is I'm trying to think about whether there's any element in the design of the phase II that could propel you towards some kind of an accelerated approval strategy.

Michael King: Thanks for taking the question, guys. If I could, I'd like to pivot to FG-3246 and FG-3180. Couple of questions on the program. I'm just curious how you guys look at it as far as, I know it's one to two prior lines and one prior ARPI, but I'm just curious what you anticipate the enrollment might be for individuals who have been treated with lutetium-177, and whether you can enrich enrollment for that population. The reason I'm asking is I'm trying to think about whether there's any element in the design of the phase II that could propel you towards some kind of an accelerated approval strategy.

Speaker #6: But I'm just curious, what you anticipate the enrollment might be for individuals that have been treated with lutetium 177? And whether you can enrich enrollment for that population and the reason I'm asking is I'm trying to think about whether there's any element of the design of the phase 2 that could propel you towards some kind of an accelerated approval strategy.

Speaker #3: Yeah, that's a great question, Mike. And I appreciate the question. I'll go ahead and kick it off. And then Carol, I'll hand it over to you for additional commentary.

Thane Wettig: Yeah, it's a great question, Mike, and I appreciate the question. I'll go ahead and kick it off and then Carole, I'll hand it over to you for additional commentary. To your point, we clearly are allowing prior Pluvicto treated patients into the trial. At the outset of the trial, we kind of had an estimate as it relates to what percent of patients were going to be previous Pluvicto treated patients. This far into the trial, while we're not disclosing our enrollment stats yet, what we can say is about 30% of patients who have been enrolled into the trial and randomized, were previously treated with Pluvicto, and we've got a pre-specified analysis based upon prior Pluvicto exposure or not.

Speaker #3: So to your point, we clearly are allowing prior Plovitdo treated patients into the trial. We at the outset of the trial, we kind of had an estimate as it relates to what percent of patients were going to be previous Plovitdo treated patients.

Speaker #3: This far into the trial, while we're not disclosing our enrollment stats yet, what we can say is about 30% of patients who have been enrolled into the trial and randomized were previously treated with Plovitdo.

Speaker #3: And we've got a pre-specified analysis based upon prior Plovitdo exposure or not. So we've got that built into the SAP, so that we will be able to clearly determine if there is any sort of differential impact or effect from 3246 based upon prior Plovitdo exposure.

Thane Wettig: So that we've got that built into the SAP so that we will be able to clearly determine is there any sort of a differential impact or effect from FG-3246 based upon prior Pluvicto exposure. Haven't really thought about the ability to go for accelerated approval in that particular patient population if we showed a really nice benefit, but it's an interesting thought. Ultimately, we're going to be data-driven based upon the outcome of the phase II trial. So Carole, go ahead.

Speaker #3: I haven't really thought about the ability to go for accelerated approval in that particular patient population if we showed a really nice benefit, but it's an interesting thought. Ultimately, we're going to be data-driven based upon the outcome of the Phase 2 trial.

Speaker #3: Carol, go ahead.

Speaker #5: No additions from my side.

Carol Adam: No additions from my side.

Carol Gaddum: No additions from my side.

Speaker #6: I just wonder if there has been any inflection, because I mean, I know it's early days, but Novartis just recently received first-line indication, so I wonder if that 30% proportion might increase going forward from here.

Michael G. King Jr.: I just wonder, has there been any inflection? Because, I know it's early days, but Novartis just recently received first-line indication. I wonder if that 30% proportion might increase going forward from here.

Michael King: I just wonder, has there been any inflection? Because, I know it's early days, but Novartis just recently received first-line indication. I wonder if that 30% proportion might increase going forward from here.

Speaker #3: Yeah, it very well could. I think what we've found is that you don't see an immediate or instantaneous adoption, especially in the early therapy where ARPIs have been really cemented as standard of care, both in the castration-sensitive phase as well as if they haven't been previously treated with an ARPI in the castration-resistant phase as well.

Thane Wettig: Yeah, it very well could. I think what we've found is that, you don't see an immediate or instantaneous adoption, especially in the area of therapy where ARPIs have been really cemented as standard of care, both in the castration sensitive phase as well as if they haven't been previously treated with an ARPI in the castration resistant phase as well. So it's something we'll continue to keep an eye on. We're closely evaluating the patients who are enrolled to understand, are we seeing an inflection in previously Pluvicto-treated patients, and so it's clearly an important consideration for us.

Speaker #3: So it's something we'll continue to keep an eye on. We're closely evaluating the patients who are enrolled to understand if we are seeing an inflection in previously treated Plovitdo-treated patients.

Speaker #3: And so it's clearly an important consideration for us.

Speaker #5: Yeah, and I would just add to that that there is obviously the dynamic around enrollment, and that is obviously also highly driven by the sites in particular and the treatment practice at the individual sites.

Carol Adam: Yeah, I would just add to that there is obviously the dynamic around enrollment, and that is obviously also highly driven by the sites, in particular, and the treatment practice at the individual sites. As we think about the design of a global phase III, we're obviously very closely monitoring market shares in the pre and CRPC setting and then the metastatic setting, to understand eligibility criteria, but also how we even set up the control arm and what is the appropriate prior line of therapy. So point well taken around there being a lot of movement in that space.

Carol Gaddum: Yeah, I would just add to that there is obviously the dynamic around enrollment, and that is obviously also highly driven by the sites, in particular, and the treatment practice at the individual sites. As we think about the design of a global phase III, we're obviously very closely monitoring market shares in the pre and CRPC setting and then the metastatic setting, to understand eligibility criteria, but also how we even set up the control arm and what is the appropriate prior line of therapy. So point well taken around there being a lot of movement in that space.

Speaker #5: As we think about the design of a global Phase 3, we're obviously very closely monitoring market shares in the pre-mCRPC setting and then the metastatic setting to understand eligibility criteria, but also how we even set up the control arm and what is the appropriate prior line of therapy.

Speaker #5: So, point well taken around there being a lot of movement in that space.

Speaker #6: Yeah, yeah, yeah. Sorry to keep belaboring this point, but one other question I wanted to ask and that is I know PET imaging is your key guide towards response, but I'm wondering, is it possible to get both pre and post-treatment biopsy from these individuals because I'm just curious about the expression the levels of expression of PSMA prior to therapy and post-therapy to see if there's any correlation or with the level of expression with PSMA sort of are you going to be more active serving the post-PSMA setting less active or indifferent to PSMA?

Michael G. King Jr.: Yeah. Sorry to keep belaboring this point, but one other question I wanted to ask, and that is, I know PET imaging is your key guide towards response, but I'm wondering, is it possible to get both pre- and post-treatment biopsy from these individuals? Because I'm just curious about the levels of expression of PSMA prior to therapy and post-therapy to see if there's any correlation or with the level of expression with PSMA. Are you going to be more active sort of in the post-PSMA setting, less active or indifferent to PSMA?

Michael King: Yeah. Sorry to keep belaboring this point, but one other question I wanted to ask, and that is, I know PET imaging is your key guide towards response, but I'm wondering, is it possible to get both pre- and post-treatment biopsy from these individuals? Because I'm just curious about the levels of expression of PSMA prior to therapy and post-therapy to see if there's any correlation or with the level of expression with PSMA. Are you going to be more active sort of in the post-PSMA setting, less active or indifferent to PSMA?

Speaker #3: No, no, thanks, Mike. Carol, you want to take that one?

Thane Wettig: No. Thanks, Mike. Carol, you want to take that one?

Speaker #5: Sure. Yeah, it's certainly a very interesting scientific question. And we're doing a lot in terms of tissue collection, PSMA scans, PET scans, and our 3180 scans as much as possible to understand how it evolves over time.

Carol Adam: Sure. Yeah. It's certainly a very interesting scientific question, and we're doing a lot in terms of tissue collection, PSMA scans, PET scans, and our FG-3180 scans, as much as possible to understand how it evolves over time. As you can appreciate, there are limitations as to the burden that you can put on patients.

Carol Gaddum: Sure. Yeah. It's certainly a very interesting scientific question, and we're doing a lot in terms of tissue collection, PSMA scans, PET scans, and our FG-3180 scans, as much as possible to understand how it evolves over time. As you can appreciate, there are limitations as to the burden that you can put on patients.

Speaker #5: As you can appreciate, there are limitations as to the burden that you can put on patients. So this is a bit more on the best effort basis, but it's certainly a key question to address.

Thane Wettig: Sure

Carol Adam: It is a bit more on a best effort basis, but it's certainly a key question to address. What I would also just say is, in this disease area, the tissue availability is limited given the disease, often just being bone disease and also tissue availability if it's soft tissue disease. So, we're coming up against some challenges here in terms of disease, but we're doing all we can to address that scientific question.

Carol Gaddum: It is a bit more on a best effort basis, but it's certainly a key question to address. What I would also just say is, in this disease area, the tissue availability is limited given the disease, often just being bone disease and also tissue availability if it's soft tissue disease. So, we're coming up against some challenges here in terms of disease, but we're doing all we can to address that scientific question.

Speaker #5: And what I would also just say is, in this disease area, the tissue availability is limited given the disease, often just being bone disease, and also limited tissue availability if it's soft tissue disease.

Speaker #5: So we're coming up against some challenges here in terms of disease, but we're doing all we can to address that scientific question.

Speaker #6: Well, I know the Prostate Cancer Working Group just updated their guidelines to encourage the use of ctDNA. I don't know, are you going to be looking at ctDNA in these patients?

Michael G. King Jr.: Well, I know the Prostate Cancer Working Group just updated their guidelines to encourage the use of ctDNA. I don't know, are you going to be looking at ctDNA in these patients?

Michael King: Well, I know the Prostate Cancer Working Group just updated their guidelines to encourage the use of ctDNA. I don't know, are you going to be looking at ctDNA in these patients?

Carol Adam: Correct. Yes, we are.

Carol Gaddum: Correct. Yes, we are.

Speaker #5: Correct. Yes, we are.

Thane Wettig: Absolutely. We definitely are. In fact, in the phase I monotherapy trial, there was a really nice ctDNA effect with FG-3246.

Speaker #3: Absolutely. We definitely are. In fact, in the phase 1 monotherapy trial, there was a really nice ctDNA effect with FG3246.

Speaker #6: Okay. All right. I think I've exhausted my questions for now. Thank you.

Michael G. King Jr.: Okay. All right. I think I have exhausted my questions for now. Thank you.

Michael King: Okay. All right. I think I have exhausted my questions for now. Thank you.

Speaker #3: I appreciate it, Mike.

Thane Wettig: I appreciate it, Mike.

Speaker #4: And our next question will come from the line of Jay Olson of Oppenheimer. Your line is open, Jay.

Operator: Our next question will come from the line of Jay Olson of Oppenheimer. Your line is open, Jay.

Speaker #7: I failed. I have to see.

Jay Olson: Oh, hey. Congrats on all the progress, and thanks for taking our questions. We had a couple questions, starting with FG-3246. Can you just talk about how you're thinking of positioning FG-3246 as a differentiated non-PSMA approach to metastatic CRPC? Is the greatest opportunity in PSMA-low or PSMA-negative patients, or do you see CD46-targeted therapy as potentially complementary to PSMA-directed approaches? Then just on roxadustat, from a longer-term perspective, how are you thinking about eventually moving into the first-line setting? Thank you.

Speaker #6: Oh, hey. Congrats on all the progress. And thanks for taking our questions. We had a couple of questions. Starting with 3246, can you just talk about how you're thinking of positioning 3246 as a differentiated non-PSMA approach to metastatic CRPC?

Speaker #6: Is the greatest opportunity in PSMA-low or PSMA-negative patients, or do you see CD46-targeted therapy as potentially complementary to PSMA-directed approaches? And then just on ROCs, from a longer-term perspective, how are you thinking about eventually moving into the first-line setting?

Speaker #6: Thank you.

Thane Wettig: Sure thing. No, thanks, Jay. Good to hear from you. Carol, you want to take that one and then I'll add on?

Speaker #3: Sure. No, thanks, Jay. Good to hear from you. Carol, do you want to take that one, and then I'll add on?

Speaker #5: Sure. Yeah, I think these are exactly the type of questions we're looking to address with the Phase 2. And that's why we're allowing prior litigation to understand how responses are similar or different in different patient subpopulations.

Carol Adam: Sure. Yeah. I think these are exactly the type of questions we're looking to address with the phase II, and that's why we're allowing prior lutetium to understand how responses are similar or different in different patient subpopulations. To the prior question, we're also doing the scans to really understand where the patients fall and where there's the greatest unmet need and where we have the most compelling value proposition for FG-3180. So I think all strategic options are here on the table, and it ultimately will be data-driven. Then to your point around moving up lines, I think that's what we've traditionally seen, right? Is from the post-chemo setting into the pre-chemo setting into the hormone-sensitive setting. So those are certainly part of our life cycle considerations moving forward. Thane, back to you.

Carol Gaddum: Sure. Yeah. I think these are exactly the type of questions we're looking to address with the phase II, and that's why we're allowing prior lutetium to understand how responses are similar or different in different patient subpopulations. To the prior question, we're also doing the scans to really understand where the patients fall and where there's the greatest unmet need and where we have the most compelling value proposition for FG-3180. So I think all strategic options are here on the table, and it ultimately will be data-driven. Then to your point around moving up lines, I think that's what we've traditionally seen, right? Is from the post-chemo setting into the pre-chemo setting into the hormone-sensitive setting. So those are certainly part of our life cycle considerations moving forward. Thane, back to you.

Speaker #5: And to the prior question, we're also doing the scans to really understand where the patients fall, where there's the greatest unmet need, and where we have the most compelling value proposition for 3180.

Speaker #5: So, I think all strategic options are here on the table, and it ultimately will be data-driven. And then, to your point around moving up lines, I think that's what we've traditionally seen, right? It's from the post-chemo setting into the pre-chemo setting, and then into the hormone-sensitive setting.

Speaker #5: And so those are certainly part of our life cycle considerations moving forward. Thane, back to you.

Speaker #3: Yeah, thanks. Carol and Jay, maybe one other comment. And this just comes from discussions with clinicians in this space. And this isn't based upon dozens of interviews like we would do as we would contemplate a phase 3 design, but this is in speaking with some KOLs they believe that a PSMA approach will continue to be kind of standard of care in this pre-chemo setting.

Thane Wettig: Yeah. Thanks, Carol, and Jay, maybe one other comment, and this just comes from discussions with clinicians in this space. This isn't based upon dozens of interviews like we would do as we would contemplate a phase III design, but this is in speaking with some KOLs. They believe that a PSMA approach will continue to be standard of care in this pre-chemo setting. What they also talk about is with the ARPIs, they're being used more in the castration-sensitive phase, and that clinicians are shying away from this ARPI switch approach just because you only get an incremental 4 to 6 months of additional RPFS when you switch from one ARPI to another. They think that the PSMA approach, like Pluvicto or other PSMA-directed therapies, would be standard of care once a patient has progressed on an ARPI.

Speaker #3: What they also talk about is that with the ARPIs, they're being used more in the castration-sensitive phase, and that clinicians are shying away from this ARPI switch approach just because you only get an incremental four to six months of additional RPFS when you switch from one ARPI to another.

Speaker #3: And so they think that the PSMA approach, like Pluvicto or other PSMA-directed therapies, would be standard of care once a patient has progressed on an ARPI.

Speaker #3: Once a patient then progresses on a PSMA-directed therapy, they tend to think about a different target, but they also tend to think about a different modality.

Thane Wettig: Once a patient then progresses on a PSMA-directed therapy, then they tend to think about a different target, but they also tend to think about a different modality. So if they were on an RLT that targeted PSMA, they then might think about an ADC that targets a different epitope, like CD46. So they wouldn't go from an RLT that targets PSMA to an ADC that targets PSMA. They also may not go from an RLT that targets PSMA to an RLT that targets another epitope. Again, it's more anecdotal than anything. We'll continue to, as Carol said, explore it. It'll be heavily driven by what we see in our phase II trial. But yeah, it's something that we think about a lot as we contemplate what a phase III design could look like.

Speaker #3: So, if they were on an RLT that targeted PSMA, they then might think about an ADC that targets a different epitope like CD46. So, they wouldn't go from an RLT that targets PSMA to an ADC that targets PSMA.

Speaker #3: They also may not go from an RLT that targets PSMA to an RLT that targets another epitope. And so, again, that's more anecdotal than anything.

Speaker #3: We'll continue to, as Carol said, explore it. It'll be heavily driven by what we see in our Phase 2 trial. But yeah, it's something that we think about a lot as we contemplate what a Phase 3 design could look like.

Jay Olson: Great. Thanks for taking the questions.

Speaker #6: Great. Thanks for taking the questions.

Speaker #3: You bet.

Thane Wettig: You bet.

Operator: I would now like to turn the call back to Thane for closing remarks.

Speaker #4: And I'd now like to turn the call back to Thane for closing remarks.

Speaker #3: Yeah, we appreciate everybody joining us for today's second quarter earnings call and your continued interest in Kyntra Bio. Enjoy the rest of your day, guys.

Thane Wettig: Yeah. We appreciate everybody joining us for today's Q2 earnings call and your continued interest in Kyntra Bio. Enjoy the rest of your day, guys.

Operator: This concludes today's conference call. Thank you for participating. You may now disconnect.