NKTR - NASDAQ

Nektar Therapeutics

NKTR·NASDAQ

$59.23

+1.1%

HealthcareBiotechnology

Nektar Therapeutics, a biopharmaceutical company, focuses on discovering and developing medicines in areas of unmet medical need in the United States and internationally. The company's products include Bempegaldesleukin, a CD122-preferential interleukin-2 (IL-2) pathway agonist, which is in phase 3 clinical trial to treat metastatic melanoma, renal cell carcinoma, muscle-invasive bladder cancer, squamous cell carcinoma of the head and neck, and adjuvant melanoma; phase 2 clinical trial for the treatment of renal cell carcinoma, non-small cell lung cancer, and urothelial cancer; phase 1/2A clinical trial to treat squamous cell carcinoma of the head and neck; phase 1/2 clinical trial for the treatment of solid tumors; and phase 1B clinical trial to treat COVID-19. It is also developing NKTR-358, a cytokine Treg stimulant that is in phase 2 clinical trial for the treatment of systemic lupus erythematosus and ulcerative colitis, as well as phase 1B clinical trial to treat atopic dermatitis and psoriasis; NKTR-255, an IL-15 receptor agonist, which is in phase 1/2 clinical trial for the treatment of non-Hodgkin's lymphoma and multiple myeloma, and head and neck cancer and colorectal cancer; and NKTR-262, a toll-like receptor agonist that is in phase 1/2 clinical trial to treat solid tumors, as well as various other drug candidates. The company has collaboration agreements with Takeda Pharmaceutical Company Ltd.; AstraZeneca AB; UCB Pharma S.A.; F. Hoffmann-La Roche Ltd; Bausch Health Companies Inc.; Pfizer Inc.; Amgen Inc.; UCB Pharma (Biogen); Bristol-Myers Squibb Company; Baxalta Incorporated; Eli Lilly and Company; Merck KGaA; and SFJ Pharmaceuticals, Inc. Nektar Therapeutics was incorporated in 1990 and is headquartered in San Francisco, California.

Statements Value Model

At a Glance

Live Snapshot

Market Cap$1.16B

EPS-9.7300

P/E Ratio-6.09

Earnings Date08/06/2026

Earnings Call Transcript

NKTR • 2024 • Q4

Operator

Good day, and thank you for standing by. Welcome to the Nektar Therapeutics Fourth Quarter 2024 financial results conference call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question-and-answer session. [Operator Instructions] Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Vivian Wu. Please go ahead.

Vivian Wu

Thank you, Crystal, and good afternoon, everyone. Thank you for joining us today. With us on the call are Howard Robin, our President and Chief Executive Officer; Dr. Jonathan

Howard Robin

Thank you, Vivian. Thank you all for joining us today. 2024 was a productive year for Nektar, and I'm very proud of our team for executing on important clinical development milestones for our lead autoimmune pipeline program, rezpegaldesleukin, also known as RE

Brian Kotzin

Thank you, Howard. It's great to be back at Nektar. As Howard mentioned, I've had the great pleasure to work on RE

Jonathan Zalevsky

Thank you, Brian. It's exciting to be working with you on a daily basis again. As Howard mentioned, we announced in January that we completed enrollment in the RE

Sandra Gardiner

Thank you, J

Operator

Thank you. [Operator Instructions] And our first question will come from Yasmeen Rahimi from Piper Sandler. Your line is now open.

Yasmeen Rahimi

Good afternoon, team. Thank you so much for all the great updates, and we're very much looking forward to the data across both of the studies for this year. I guess, the first question is, you guys have shown in the earlier stage really phenomenal dose responses in the EASI scores. Would love to understand how you're thinking about dose response across the three-dose arms. And then, secondly, if you could just maybe remind us, what is the criteria or responder analysis defined for patients to be eligible to go from the induction phase to the maintenance phase? And I'll jump back in the queue.

Howard Robin

Jonathan Zalevsky

Sure. Yeah. Thanks, Yas. So, the first question about the dose response, so we addressed that with three different cohorts that addressed both dose level and regimen. So, two of our dose cohorts evaluated the 24 microgram per kilogram dose. One of those evaluated that dose twice a month, the other cohort at once a month. And we changed the frequency there because that was sort of designed to model the pharmacodynamic profile of the Tregs that we measure in the blood. And so, that's why we wanted to have the same [Cmax] (ph) one time with different exposures in the once-a-month versus twice-a-month set. So that was the goal there, to assess that based on the PK-PD knowledge. And then, we also selected 18 micrograms per mil dose twice-a-month. That dose is higher than the 12 microgram per kilogram that we used in the Phase 1b study. We felt that that dose 12, while it did separate a little bit from placebo, was a little bit on the lower efficacy side. So, we wanted to evaluate a higher dose level than 12 micrograms per kilogram in the Phase 2b. And that's why we chose 18 micrograms per kilogram, halfway between 12 and 24 from the Phase 1b study. So, that's our expectations around the design of the Phase 2b. And then, in terms of the criteria for patients moving from the induction to the maintenance arms of the study, at the end of the 16-week induction, patients that have an EASI-50 or better response are eligible to be re-randomized to enter into the maintenance. And then, in the maintenance, they're re-randomized to stay on the same dose level that they were on in the induction portion of the study. But now the regimen is either once a month or once every three months. So, we use that EASI-50 criteria for advancement from induction to maintenance.

Yasmeen Rahimi

Thank you, J

Operator

Thank you. Our next question will come from Julian Harrison from BTIG. Your line is open.

Julian Harrison

Hi. Thank you for taking my questions. First on the Phase 2b atopic dermatitis data expected next quarter, I'm wondering if you could talk about what kind of efficacy bar either on EASI or IgA you think would be commercially viable and worthwhile to advance RE

Howard Robin

Yeah, that's a good question. I think, we've done a lot of homework in that area, especially recognizing that Amgen just released its data on OX40. So, I'll let J

Jonathan Zalevsky

Yeah. Thanks, Julian. So, we definitely see at least two different versions of activity. Obviously, like, there's ranges of EASI, that are active and that are desirable to achieve. And also, the separation from placebo, both features are very important. We like what we saw in our Phase 1b study, right, which showed both the dramatic separation from placebo in terms of placebo-adjusted and also an 83% change from baseline. So, we're looking to replicate that kind of data in our Phase 2b, but we also acknowledge that as a drug with a novel mechanism and an agent that's already shown a remittive effect as we've shown in the Phase 1b that even efficacy in the range of Dupixent, the standard of care currently, would also be a very successful outcome for us. We're definitely aware of the recent results in the field, including Amgen's ROCA data. And I think that data is probably considered a little bit underwhelming by some of the folks that have addressed and looked at that data. And we think that we're in a great position to replicate the Phase 1b results that we had with RE

Howard Robin

And always remember that this isn't a zero-sum game and it really is a quite underserved market with a very serious disease and having a novel mechanism is certainly going to be appreciated by patients and physicians, I'm sure of that.

Julian Harrison

Got it. Thank you. That makes a lot of sense. And then, one more, if I may. I'm curious how you're thinking about your rights to dapirolizumab in light of the recent litifilimab royalty monetization. Are there any differences compared to litifilimab that are worth noting?

Howard Robin

Jonathan Zalevsky

Yeah. They're different mechanisms of action, of course, right? One is a BDCA2 inhibitor that's targeting more of the plasmacytoid arm. And, of course, that drug has shown activity in both systemic lupus and cutaneous lupus. And it seems like it has maybe even more potential in the cutaneous form of the disease, whereas dapi, right, is a CD40 ligand targeting agent, right, so it addresses different mechanisms of action. And then -- so that's mechanistically, both of the drugs have demonstrated, I think, impressive results in Phase 2. And obviously, dapi has positive Phase 3 data as well.

Julian Harrison

All right. Excellent. Thank you.

Operator

Thank you. Our next question will come from Jay Olson from Oppenheimer. Your line is open.

Jay Olson

Oh, hey, congrats on all the progress, and thank you for providing this update. Maybe another question on the topline Phase 2 atopic dermatitis results in the second quarter. Can you just talk about the scope of data that you're planning to share in that topline release and maybe some of the secondary endpoints we should be looking for? And then, also, what do you think the profile would be that would help you capture meaningful market share in a first-line setting?

Howard Robin

Yeah. I think, good questions. I think, we haven't discussed a lot about the exact secondary endpoints at this point. I think, clearly as a novel mechanism that it was completely different approach than IL-13, I would like to see a drug that's similar in activity to Dupixent with a very different biologic profile. I'll let J

Jonathan Zalevsky

Yeah. Sure. Thanks, Jay. Yeah, so just to reiterate, as Howard said, we haven't sort of guided on the specificity of the topline. Obviously, the majority of the data, we would need to present at a medical meeting. But we would intend to focus obviously on the 16-week induction data as we have described and to give at least a minimum directional, right, understanding of the performance of the drug. I think it's a bare minimum. We can cover that more later. And then, in terms of the profile, I mean, it's pretty obvious that the greatest way to impact the share in the frontline setting is with efficacy, right? So, if we are able to replicate the Phase 1b results that were really quite marked, right, quite notable, I would say that's one of the strongest ways to impact the first-line treatment space. But even all that aside, we're a completely different mechanism. We're not another IL-13. We're not a depleting antibody like Roca is. We're really providing a completely different mechanism of action, and we're providing the data set that's already demonstrated the potential for really durable responses, which could translate into very, very low-frequency dosing regimen, which would, at minimum, be highly convenient to patients. So, we think there are really a number of ways that we can impact this market and we're very excited that being a novel Treg mechanism gives us these additional avenues for.

Howard Robin

Yeah. I think it's also important to point out that while Dupixent is certainly an excellent drug, no debate on that, there's a high percentage of patients failed Dupixent therapy over time. And as J

Jay Olson

Thank you. That's super helpful. And if I could sneak in a question on 255? Can you just talk about any updates on timing or expectations for the interim PFS results from the JAVELIN Bladder Medley study and what we should be looking for there? Thank you.

Howard Robin

We should be seeing results from that middle of this year. J

Jonathan Zalevsky

Yeah. That's exactly right. It is event-driven, right? So, you need to accumulate PFS event. Merck gave us some guidance at the middle of the year, like summertime is about the kind of time where we might expect to see that. And then, in terms of PFS events, obviously, our goal is to improve, right, on the PFS and potentially maybe even the OS of single agent Bavencio in this setting, right, in the post-chemo setting. So that's obviously the objective of the study. That's what we'd like to see, that's what Merck would like to see as well. I mean, that's how the study has been designed with Bavencio as an active comparator to directly test the combination of 255 plus Bavencio versus Bavencio alone.

Jay Olson

Thank you. Super helpful. Thanks for taking the questions.

Operator

Thank you. Our next question will come from Roger Song from Jefferies. Your line is open.

Roger Song

Great. Thanks for the update and taking all the questions. I have a quick one related to the Phase 2 atopic dermatitis. Given the enrollment you have completed, compared to the recent atopic dermatitis trial, what's your expectation in terms of the patient baseline? And then, how will that impact the -- particular on the placebo arm? What's your expectation there? Thank you.

Howard Robin

Jonathan Zalevsky

Yeah, Sure. Yeah. Thanks, Roger. So, one of the things that we'd really like to see is the baseline EASI to be in the range of, like, 25 to 30, right? Because as we've seen, like, other studies historically, those kind of baseline EASI scores for the entire population have generally been linked with lower overall placebo responses and also better studies. There's more dynamic range to measure from patients that are having higher EASI scores. So, that's one of the things that we'd like to see in the study, something in that kind of range for baseline. And then, in terms of setting expectations for placebo, I mean, we don't know. I mean, this is a blind study, but certainly, we would like to see much, much lower placebo response rates than have been reported recently for some of the studies and including the studies that were reported last December, such as from [Q32] (ph), where the placebo rate was very, very high. One of the things that we did in our study that I tried to cover earlier in our call was that we really had a number of prospective features that we built into the study, such as limiting The US footprint geographically. We only had 17% of our sites in the US. Focusing on board-certified dermatologists and immunologists that had demonstrated experience working in atopic dermatitis study as well as measuring the easy score multiple times before drug was administered and patients were randomized. And all of those things we did prospectively in order to protect the study and ensure that ideally we don't have a very, very high placebo response rate. So, when we present the results of the topline later this year in June, we'll show what that is directly. So, thanks for the question, Roger.

Roger Song

Thank you.

Operator

Thank you. And our next question will come from Mayank Mamtani from B. Riley Securities. Your line is open.

Mayank Mamtani

Yes. Good afternoon, team. Thanks for taking our questions, and glad to see the progress here. Could you touch on -- just a related question to the last comment, J

Howard Robin

Yeah, that would be the kind of information we would share in the future when we present the results of the study.

Mayank Mamtani

Okay. Got it. And then, the escape piece in the protocol how patients go on the escape arm, could you just remind me how that's kind of structured for induction and maintenance? And then lastly, just high-level read through from AD dataset to the RE

Jonathan Zalevsky

Sure. Yeah. So, in the way the study is designed, which was one of the expert pieces of advice also given to us by the standing committee is that, when patients reach the end of the 16-week induction, if they are not better than EASI-50, then they have the option to enter into an escape arm. And the escape arm is the 24 microgram per kilogram dose of RE

Mayank Mamtani

Thank you, J

Operator

Thank you. Our next question will come from Arthur He from H.C. Wainwright. Your line is open.

Arthur He

Hey. Good afternoon, Howard and team. Thanks for taking our question. So, J

Jonathan Zalevsky

Yeah. Across the clinical program, we've evaluated various doses, both weight-based dosing, such as what we're using in the study, and also flat dosing as was used in other studies like the LUFA study. And then really when you look at it, that gives you a range of different note doses that we've established. So, we've gone well above and well below. And actually, the 24 microgram per kilogram is really an optimal dose level. It gives us all the things that we want to have from a PK-PD relationship. We engage as a target very effectively. We get very robust Treg expansion, and you can dose for a very long time at that dose level without seeing any cessation or any hysteresis in any of the pharmacodynamic responses. And from the biomarker data that was asked earlier and that we published, you can also see the very robust induction of immune pathways that we see at that dose level. So that's really an optimal dose level that we're really focused on.

Arthur He

Thanks for that. So -- and the second question is also regarding probably both AD and AA study. Could you remind us how the stratification in both study in terms of the disease severity wise? How that could be decided for the stratification?

Jonathan Zalevsky

Yeah. So, we haven't shared all of the details of the full stratification for that study, but I'll share, I think, what's the most relevant and important, Arthur. So, our study is enrolling the severe and very severe population. So, severe people have a SALT score between 50 and 35, and very severe people are 95 to 100. And very severe people are almost like they're total. They're almost, if not, in all cases, completely bald, right? And so, our study has quite a high number and are in both categories. And one of the stratification is to balance that between the treatment arm, right? So, that's one key stratification. The severe and very severe patients, we want to balance across the treatment arms. And there'll be other ones as well that we'll present when we present the topline results from that study in the fourth quarter. But I think severe, very severe is probably what you were wondering about.

Arthur He

So, how about AD study?

Jonathan Zalevsky

Yeah. Again, we haven't -- we'll share all of the full details of that later when we present the topline. But just as an example of flavor, the geographic regions is one of the important things to stratify in those kind of studies, and that's one of our criteria.

Arthur He

I see. Thanks for that. Congrats on the progress.

Jonathan Zalevsky

Thank you.

Operator

Thank you. [Operator Instructions] And our next question will come from Chris Shibutani from Goldman Sachs. Your line is open.

Unidentified Analyst

Hey, good afternoon. This is Eric on for Chris Shibutani. And thank you so much for taking my question. So, just wanted to elaborate a little more on the point you made about the biomarker analysis and the AD trial. Do you have a sense of how translatable this correlation between biomarkers and clinical outcomes are and maybe the larger trial or potentially or across different patient populations? And are there plans to incorporating this biomarker in future trial designs?

Jonathan Zalevsky

Yeah. Thanks, Eric. That's a really good question. So, what we were able to do in the Phase 1b atopic derm study is what I call more like descriptive analysis. We characterize the dose dependency of biomarkers analyzed by an MMRM model against various covariates that we did in the analysis. And we could see pathways that were statistically changed both as a function of dose and as a function of time. And why consider it more of like a summary or descriptive analysis is because the study was pretty small. And actually, in this Phase 1b study, there was a high number of responders. So, it was not really the right dataset to do a lot of correlative analysis. We did try. We tried a lot of correlative analysis, but it wasn't clear from that particular study given its small size. Now, in our Phase 2b study, this atopic dermatitis study, we're doing that again, but now the study is designed, much larger. And also, we have a lot more understanding about the collection time points that we learned from the Phase 1b that are more optimized in the Phase 2. And also, we're collecting tape strips so that we can collect what's happening locally in the lesion against the serum biomarkers using the [old link] (ph) panels and the cellular analysis by flow cytometry. So, one of our objectives translationally in this Phase 2 study, in addition to all of the other normal kind of efficacy and safety endpoints, is we also want to dive very deeply into the translational sort of molecular phenotype of the patients and then understand any of these correlative analyses, whether they can be predictive, prognostic, and so on. So that'll be a very exciting dataset that we'll be excited to share in the coming -- in the future.

Unidentified Analyst

All right. Thank you very much.

Operator

Thank you. And that does conclude our question-and-answer session for today's call. I'd now like to turn the conference back over to Howard Robin for any closing remarks.

Howard Robin

Well, thank you, everyone for joining us today, and we look forward to sharing important data from our Phase 2b studies of RE

Transcript from March 12, 2025