Kyntra Bio, Inc. (KYNB) 2026 Q2 法說會逐字稿

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

Thank you, Latonia, and good afternoon, everyone. Thank you for joining today to discuss Kyntra Bio’s second quarter 2026 financial and business results. I’m Gaia Shamis from LifeSci Advisors. Joining me on today’s call are Thane Wettig, Chief Executive Officer; David DeLucia, Chief Financial Officer; and Carol Gaddum, 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.

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.kyntrabio.com.

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

Thank you, Gaia. Good afternoon, everyone, and welcome to our second quarter 2026 earnings call. On today’s call, I will provide an update on the important progress we have made across our clinical portfolio.

First, with FG-3246, our potential first-in-class antibody drug conjugate targeting CD46 and its companion PET imaging agent in metastatic castration-resistant prostate cancer. 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’d like to highlight our mid and late-stage programs and upcoming catalysts. The Phase 2 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 the fourth quarter of this year. 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. 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. 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 tumorigenesis as well as during the progression from localized castration-sensitive prostate cancer to metastatic castration-resistant prostate cancer. Third, an estimate 50% to 70% of patients have high CD46-expressing tumors. 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. 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 3 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.

FG-3180 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 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 1 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 pre-treated and were not biomarker selected, with PSA50 response of 36%.

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 1/b2 investigator-initiated study at UCSF summarized on the right side, combination of FG-3246 with enzalutamide demonstrated encouraging anti-tumor activity with seven months of median radiographic progression-free survival in biomarker unselected patients across the entire cohort of 44 patients. Importantly, in patients who had progressed on only one prior ARPI, the combination of FG-3246 and enzalutamide achieved a meaningful median rPFS of 10.1 months with a PSA50 response of 40%.

In addition to the efficacy measures, the IST provided us with important insights into the adverse event profile of the ADC. The use of G-CSF 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.

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.

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 2 monotherapy trial.

Slide 9 lays out the design for this Phase 2 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 3 dose based on efficacy, safety, and PK measures. 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 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 FG-3246 and the trial progresses toward completion.

On slide 10, we would like to emphasize the three design elements we have incorporated with the aim of improving upon the 8.7 months of median rPFS demonstrated in the Phase 1 trial.

First, we are testing three of the highest doses from the Phase 1 monotherapy study, 1.8, 2.4, and 2.7 milligrams per kilogram. Second, primary prophylaxis with G-CSF is being utilized to mitigate neutropenia, an approach which was successfully implemented in the Phase 2 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 1 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.

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.

Slide 10 shows the sites who are participating in the ongoing Phase 2 trial. We now have 23 sites live at top-tier US 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 FG-3246, we are actively enrolling patients in our Phase 2 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 1 trial.

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. 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. 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. 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. 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 majority of lower risk MDS patients, is especially relevant given 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. 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. Following our interactions with the FDA, we have now finalized the 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. 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 the fourth quarter of 2026.

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 have continued 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. 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 costs 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&A expenses for the second quarter of 2026 were $9.3 million compared to $7.1 million in the second quarter of 2025.

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, compared to a net loss of $13.7 million, or $3.38 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 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. I will now turn the call back over to Thane.

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 program with results from the interim analysis of the Phase 2 monotherapy trial expected in the fourth quarter of 2026, 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.

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

(Operator Instrucitons) Alex Ramsey, William Blair.

Hi, this is Alex on for Andy. For the upcoming Phase 3 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’s based on tolerability or efficacy, and how long after starting the treatment the assessment is made. What the titration interval is from both a timing and a dosing perspective?

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

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.

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? Or some --

There are some intervals in between. There are some intervals in between.

Okay.

Yes.

Okay, perfect. Thank you so much.

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.

Perfect. Thank you so much.

Matthew Keller, H.C. Wainwright.

Hey, good afternoon, everyone. Thanks for taking our questions. I guess, on the roxadustat program as well. First, I was wondering if you could remind us how contingent are you starting the Phase 3 on a partner? And then a follow-up to that, I was wondering is how has the MATTERHORN data changed your calculus at all on potentially partnering that program?

Hey. Thanks, Matt, for the question. The start of the Phase 3, 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. That’s a consideration while we also evaluate strategic partners as well.

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. 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 royalty 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. That’s one consideration from an economic perspective. Clearly, there are strategic and operational considerations that we continue to evaluate. As I said, we’re going to ultimately make the call that we believe is in the best interest of shareholders.

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? 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.

No, it’s a great question. So the RS 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 luspatercept 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 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. We’re going to make sure that we enroll a 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 roxadustat works across both of those patient populations.

But the RS-negative opportunity, or the MATTERHORN data, we’d 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?

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

Yeah. David or Carol, anything to add to that?

Thank you. The only thing I would add is, you asked around how MATTERHORN informed the Phase 3 design. It has obviously been a significant driver of the Phase 3 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 3 trial accordingly.

To Thane’s point, the analysis also shows that roxadustat improves transfusion independence and hemoglobin across RS positive and negative. That is also reflected in the Phase 3 design.

That makes sense. Thank you.

Michael King, Rodman & Renshaw, LLC.

Thanks for taking the question, guys. If I could, I would like to pivot to FG-3246 and FG-3180. Couple of questions on the program.

I am just curious how you guys look at it as far as -- I know it is one to two prior lines and one prior ARPI, but I am just curious what you anticipate the enrollment might be for individuals who have been treated with Lutetium-177? Whether you can enrich enrollment for that population. The reason I am asking is, I am trying to think about whether there is any element of the design of the Phase 2 that could propel you towards some kind of an accelerated approval strategy.

Yeah, it’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.

So 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, 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 2 trial.

Carol, go ahead.

No additions from my side.

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.

Yeah, it very well could. I think what we’ve found is that you do not see an immediate or instantaneous adoption, especially in the area of therapy where ARPIs have been really cemented as standard care, both in the castration-sensitive phase, as well as if they have not been previously treated with an ARPI in the castration-resistant phase as well.

So it is something we will continue to keep an eye on. We are closely evaluating the patients who are enrolled to understand, are we seeing an inflection in previously Pluvicto-treated patients? It is clearly an important consideration for us.

Yeah. 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 3, we are obviously very closely monitoring market shares in the pre and mCRPC setting, and then the metastatic setting to understand eligibility criteria, but also how you 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.

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. I am wondering, is it possible to get both pre- and post-treatment biopsy from these individuals? Because I am just curious about the levels of expression of PSMA prior to therapy and post-therapy to see if there is any correlation 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?

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

Sure. Yeah. It is certainly a very interesting scientific question. And we are 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.

Sure.

This is a bit more on a best effort basis, but it is 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 is soft tissue disease.

So we are coming up against some challenges here in terms of disease, but we are doing all we can to address that scientific question.

Well, I know the Prostate Cancer Working Group just updated their guidelines to encourage the use of ctDNA. I do not know, are you going to be looking at ctDNA in these patients?

Correct. Yes, we are.

Absolutely. We definitely are. In fact, in the Phase 1 monotherapy trial, there was a really nice ctDNA effect with FG-3246.

Okay. All right. I think I’ve exhausted my questions for now. Thank you.

I appreciate it, Mike.

Jay Olson, Oppenheimer.

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 mCRPCs? 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 roxadustat, from a longer-term perspective, how are you thinking about eventually moving into the first-line setting? Thank you.

Sure thing. 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 Lutetium-177 to understand how responses are similar or different in different patient sub-populations.

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. 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.

Yeah. Thanks, Carol. 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 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. 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.

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. 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.

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 2 trial. But yeah, it’s something that we think about a lot, as we contemplate what a Phase 3 design could look like.

Great. Thanks for taking the questions.

You bet.

And I’d now like to turn the call back to Thane for closing remarks.

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.

This concludes today’s conference call. Thank you for participating. You may now disconnect.