Kyntra Bio (KYNB) Q2 2026 earnings call transcript

Thank you, Latonia, and good afternoon, everyone. Thank you for joining today to discuss KYNTRA BIOS' second quarter, 2026 financial and business results. I'm Gaia Shemes from Lifestyle Advisors. Joining me on today's call are Thane Wedig, Chief Executive Officer, David DiLuccia, Chief Financial Officer, and Carl Gatton, 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'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 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. kyntrabio. com.

With that, I would like to turn the call over to the CEO, Stane Wedding.

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, 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 roxidustat, our potential treatment for anemia due to lower-risk mild dysplastic syndromes. Then David De La Chia, our CFO, will review the financials, after which we will open the call for your questions.

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 ROX-DUSTAT 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 U. S. diagnosed every year with drug-treatable, castration-resistant metastatic disease is substantial.

Targeting CD46, a novel tumor-selected multifunctional epitope that helps tumors evade complement-dependent cytotoxicity, could help address this need. Moving to slide five, 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 tumorigenesis, as well as during the progression from localized castration-sensitive prostate cancer to metastatic castration-resistant.

Third, an estimate of 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 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 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, FG3180, 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 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 II 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 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, 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%. 20% of the 25 resistivival 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 mg per kg adjusted body weight dose utilizing the expansion phase of the trial, providing early evidence of a dose-response relationship. 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 seven months of median radiographic progression-free survival in biomarker unselected patients across the entire cohort of 44 patients. Importantly, in patients who have 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%. In addition to the efficacy measures, the ISP 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 I monotherapy trial with the aim to build upon the 8 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 FG3180 was associated with greater PSA 50 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, This is a trend of greater PSA 50 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 II monotherapy trial. Slide 9 lays out the design for this Phase II 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 III dose based on efficacy, safety, and PK measures. All patients in this 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-nabel trial is on track for the fourth quarter 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 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 I trial.

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 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 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 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 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 FG3246 in this patient population.

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 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 mildisplastic syndromes program on slide 13. There are approximately 50,000 patients with anemia associated with lower-risk MDS in the U. S. , 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 roxidustate 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 Rosadustat 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-talk 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 roxidustat 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 Luzbatercept, 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 RoxyDucet favorably in the treatment paradigm of lower-risk MDS.

Slide 16 provides an overview of the Phase 3 trial. Following our interactions with the FDA, we have now finalized the protocol for the Phase III study, 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 Roxageustat internally or with a strategic partner, which aligns with our goal of initiating the study in the fourth quarter of 2026.

To summarize the RoxyDustat 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 RoxyDustat 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?

Thank you, Thane. For the second quarter of 2026, total revenue was negative $1.5 million compared to $1.3 million for the same period in 2025. Total operating calls and expenses for the second quarter of 2026 were $16.1 million, compared to $13.4 million for the second quarter of 2025. R&D expenses for the second quarter of 2026 were $6.8 million, compared to $5.9 million in the second quarter of 2025. SG expenses for the second quarter of 2026 were million compared to million in the second quarter of 2025 During the second quarter of 2026 we recorded a net income from continuing operations of million or net income per basic and diluted share compared to a net loss of million or net loss per basic and diluted share one year ago Now shifting towards cash.

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. Thank you, and I will now turn the call back over to Faye.

Thank you, Dave. We entered the second half of 2026 with promising momentum. We will continue our disciplined execution of the FG3246 and FG3180 program with results from the interim analysis of the Phase II monotherapy trial expected in the fourth quarter of 2026, and continue the Phase III enabling activities for RoxyDustat with the goal of initiating the Phase III trial in lower-risk MDS in the fourth quarter of 2026.

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

Thanks, Alex, for the call. I'm going to hand that question over to Carol Datum, our VP of product development. Carol?

Thank you for the question. So, 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.

There are some intervals in between. There are some intervals in between, yes.

And Alex, there will be very specific guidance to the sites on the 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.

Hey, thanks, Matt, for the question. So, the start of the phase three, as we've 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's a consideration, while we also evaluate strategic partners as well. And so we're running a parallel path with both of these. And at the end of the day, we're going to make the decision that we believe is in the best interest of shareholders. There are some dynamics in 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 that was previously held by AstraZeneca during the development of the CKD program.

When we negotiated those rights back from AZ, if we were to develop Roxadustat on our own and commercialize on our own, we would owe AZ a mid-single-digit loyalty on net sales. If we were to partner the program with a strategic and somebody else were to develop and commercialize, AZ would then be entitled to 35% of any economics that would accrue to KYNTRA BIO. 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.

No, it's a great question. And so, the RS kind of dynamic with respect to RS positive and RS negative, there's clearly a larger need in the marketplace for RS negative patients, given the fact that loose battercept has not been able to really show any sort of a benefit relative to ESAs in that particular patient population, and the fact they're not indicated in the second-line setting for RS negative patients. And so, you know, the understanding of that dynamic, you know, 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. We're 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 ROX-DUCE-DEP works across both of those patient populations.

But the RS-negative opportunity or the Matterhorn data, you know, we'd be pursuing this regardless of the opportunity for RoxyDustat 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 myodospastic syndrome.

Did that get us your question, Matt?

The only thing I would add is you asked around how Matterhorn informed the Phase 3 design, and it's obviously been a significant driver of the Phase 3 design, 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. And to Thane's point, the analysis also shows that ROXA-DUSTAT improves transfusion dependence and hemoglobin across RS positive and negative. And so that is also reflected in the phase 3 design.

Yeah it a great question Mike and I appreciate the question I go ahead and kick it off and then Carol I hand it over to you for additional commentary So to your point we clearly are allowing prior pluvicto 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, 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 3246 based upon prior Pluvicto exposure. 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 BASE-2 trial.

Carol, go ahead.

No additions from my side.

Yeah, it very well could. I think what we've found is that, you know, you don't see, you know, an immediate or instantaneous adoption, especially in therapy where ARPIs have been, you know, 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 treated, flu-victor treated patients? And so it's clearly an important consideration for us.

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. As we think about the design of a global phase three, 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 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.

No, thanks, Mike. Carol, you want to take that one?

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

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 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.

Correct. Yes, we are. Absolutely. We definitely are. And in fact, in the phase one monotherapy trial, there was a really nice CT DNA effect with FG3246.

I appreciate it, Mike.

Sure. Thanks, Jay. Good to hear from you. Carol, you want to take that one, and then I'll add on?

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 leeticians to understand how responses are similar or different in different patient subpopulations. And 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 3180. 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, is from the post-chemo setting into the pre-chemo setting into then the hormone-sensitive setting.

And so those are certainly part of our life cycle considerations moving forward. Dane, back to you.

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 three design, But this is speaking with some KOLs. They believe that a PSMA approach will continue to be kind of 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 four to six months of additional RPFS when you switch from one ARPI to another. And so they think that a PSMA approach like Pluvicto or other PSMA-directed therapies would be standard of care once a patient has progressed on an ARPI. 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. And so, again, it's more anecdotal than anything. We'll continue to, as Carol said, explore it. It will 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.

You bet.

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.