F-Star Therapeutics Inc (FSTX) 2021 Q1 法說會逐字稿

Good morning, ladies and gentlemen. Thank you for standing by. Welcome to the F-star Therapeutic, Inc. First Quarter 2021 Earnings Call and Corporate Update. (Operator Instructions) As a reminder, this conference will be recorded and available for replay. I would now like to introduce to you, Lindsey Trickett, VP of Investor Relations for F-star. Please go ahead.

Good morning, everyone. Thank you for joining us. With me today is Eliot Forster, CEO; and Darlene Deptula-Hicks, our CFO.

We announced financial results premarket today for the quarter ending March 31, 2021. You can access the press release on the Investor Relations page of our website at fstar.com.

Before we get started, let's quickly run through the forward-looking statements. Please note that as a part of our discussion today, management will be making forward-looking statements. These statements are not guarantees of future performance, and therefore, you should not place undue reliance on them. Investors are also cautioned that statements that are not strictly historical constitute forward-looking statements. Such forward-looking statements are subject to a number of risks and uncertainties that could cause the actual results to differ materially from those anticipated. These risks include risks and uncertainties detailed in F-star's filings with the SEC.

The company undertakes no obligation to update any forward-looking statements in order to reflect events or circumstances that may arise after the date of this conference call.

With that, let me hand the call over to Eliot.

Thanks, Lindsey. Welcome, everyone, to our first quarter 2021 earnings call. It's a pleasure to provide an update on our achievements during what's been a very busy few months. So continuing our momentum from last year, we successfully raised $65 million in an underwritten public offering. This includes a group of top-tier investors and means that the company is very well capitalized with a runway into the second half of 2023. This strengthened financial position ensures delivery of the future milestones we've laid out previously and which I'll detail again here in a moment.

On the clinical side, we've seen a surge of excitement around FS118. This is driven by our internal data and external validation of LAG-3 in a pivotal clinical trial. In our view, LAG-3 is rightfully earning its reputation as the next significant checkpoint inhibitor pathway in immuno-oncology.

Protecting our assets and unique platform continues to be a priority, and we further expanded our comprehensive patent portfolio during the period. We're increasingly confident that FS222 is a potential best-in-class CD137 PD-L1 bispecific. We outlined the differentiated way that we make these tetravalent bispecifics with the publication of additional data at AACR.

In relation to our STING agonist, SB 11285, we highlighted an exciting finding relating to the synergy between radiation and the STING pathway in an article in nature.

Our partnerships continue to develop positively. Merck KGaA exercised 1/3 of 4 options in our ongoing collaboration. Following positive preliminary Phase I/II data, Denali Therapeutics have been granted fast track designation by the FDA for DNL310 derived from F-star's Fcab technology. This is hugely encouraging. Not least for patients with Hunter syndrome. And of course, we've continued to progress an exciting portfolio of 4 clinical stage assets.

Moving to Slide 5. Let me remind you of the F-star platform technology. We're the only company developing tetravalent bispecific antibodies with a 2 plus 2 binding functionality and the ability to simultaneously cross link immune cells to tumors, cluster immune receptors and conditionally activate the immune sign-ups only when both targets are engaged.

As you can see, we adapt the natural binding site of the antibody in blue and add 2 new binding sites in dark green, with only a small number of changes. This is a unique way to make bispecific antibodies, and we're the only company that can do this. And it's based and protected by our extensive IP portfolio.

Finally, the natural IgG1 antibody format makes our bispecifics easy to manufacture with monoclonal like production levels, good stability and low levels of antidrug antibodies in the clinic. The F-star platform continues to deliver with the expert guidance of our Chief Scientific Officer, Neil Brewis, and we'll have more projects to be taken forward in the future.

Here on Slide 6, I'd like to take the opportunity to remind you of our 4 clinical-stage programs, led by our Chief Medical Officer, Louis Kayitalire. We believe each has the potential to be transformative for patients. The most advanced of F-star bispecific antibodies is FS118, topping PD-L1 and LAG-3.

Again, LAG-3, has recently been validated as a checkpoint target in immuno-oncology in a late-stage clinical melanoma trial, showing superior efficacy over PD-1 monotherapy. We're very encouraged by these recent data. We believe LAG-3 will become an incredibly important pathway in patients with advanced cancer, and we look forward to seeing additional data supporting that belief.

FS118 is currently in a Phase II proof-of-concept study focused on patients with advanced head and neck cancer, who are positive for PD-L1 and LAG-3 and who have become resistant to previous checkpoint therapy.

The next program in our pipeline is FS222, the CD137 and PD-L1 targeting bispecific. As I mentioned earlier, we shared data on FS222's differentiated approach at this year's AACR. Those data demonstrated how specifically tuned affinity and avidity of both targets provides conditional binding, avoiding what others have seen as a hook effect. We believe FS222 can become best-in-class medicine.

The third clinical stage program from our platform is FS120, the CD137 and OX40 targeting bispecific. This first-in-class program causes a coordinated activation of the immune system in the tumor, which we term triple immune activation. Uniquely, it brings together the combined properties of conditional pharmacology with cross-linking and clustering of the stimulatory targets of OX40 and CD137. The Phase I clinical trial for FS120 started in late 2020, and the study is progressing. We'll share initial data later this year. We also have plan to begin a combination study with FS120 and an approved PD-1 inhibitor.

And finally, F-star's fourth clinical asset is SB 11285, a second-generation STING agonist. It can be delivered via an intravenous infusion with the potential for significant improvements over first generation STING programs. We plan to share data on SB 11285 later this year.

Before we leave Slide 6, I want to mention really positive ongoing collaborations we have with Denali Therapeutics and Merck KGaA. Denali continues to develop its blood-brain barrier transport vehicles in the neuroscience space. And as mentioned, Merck KGaA, Darmstadt, Germany, recently exercised their third or 4 options in our long-standing and valued partnership.

Turning to Slide 7. You can see the multiple value inflection points and clinical data readouts we're anticipating in the near term. As I mentioned, over the course of this year, we'll share data on SB 11285 and FS120 as well as data from the ongoing Phase I study with FS222. We also anticipate sharing data on the FS118 proof-of-concept trial around this time next year. And of course, we'll be attending and presenting data at upcoming medical and scientific conferences, where we'll share our progress.

So looking ahead to the next quarter and beyond. The company's financial outlook is strong, and we're incredibly pleased by the success of our first follow-on financing. This will power the delivery of our milestones over the next 2 years. I'm grateful for the support of our new and existing investors who are with us on this journey to create a paradigm shift for patients with cancer. I'd also like to thank the team at F-star, who continue to deliver day-by-day to develop life-changing medicines and create value for shareholders.

And now I'll hand over to Darlene to give you an update on our financials. Darlene?

Great. Thank you, Eliot, and good morning, everyone. As Eliot has highlighted, it's been a very busy quarter. We're extremely pleased with our recent equity financing and the top-tier investors who have joined us. I'll now go through the financial results for the first quarter ended March 31, 2021, which we believe provides a solid platform for the company's strategy that Eliot has just outlined. We'll be happy to take questions at the end. F-star has 4 programs in the clinic now and continues to work with our 2 long-term collaboration partners.

Our revenue consists of collaboration revenue from Merck KGaA and our license and collaboration agreement with Denali Therapeutics. Revenue typically includes amounts that relate to upfront payments, milestone payments, option exercise payments and/or amounts due to us for research and development services.

Revenue for the first quarter ended March 31, 2021, was $3 million as compared to $1.4 million in the prior year first quarter, for a quarter-over-quarter comparative increase of approximately $1.6 million. This quarter increase -- this quarterly increase in revenue was due primarily to the exercising of the third option in our collaboration agreement with Merck KGaA, as Eliot mentioned, offset by lower research and development services revenue.

Total research and development expenses were $7.3 million for the first quarter of 2021 compared to $3.4 million for the prior year first quarter. This $3.9 million increase in R&D expenses is primarily due to increased manufacturing costs and clinical trial costs with Q1 '21 being the first full quarter with 4 programs in the clinic. Q1 2021 R&D expense also included $0.4 million in noncash stock-based compensation expense.

Total G&A expenses were $6.4 million for the quarter ended March 31, 2021, compared to $3.2 million for the comparable first quarter of 2020. This $3.2 million increase in G&A expense was primarily due to increased stock-based compensation expense, professional fees and insurance costs associated with being a public company now, and rent expense associated with building leases assumed in the share exchange agreement with Spring Bank last November. Q1 2021 G&A expense also included $1.8 million in noncash stock-based compensation expense.

Net loss for the first quarter of 2021 was $9.9 million or $1.08 per basic and diluted share compared to a net loss of $7.2 million or $3.92 per basic and diluted share for the first quarter of 2020.

Now turning to the balance sheet. Cash and cash equivalents totaled $3.7 million for the quarter ending March 31, 2021, compared to $18.5 million at December 31, 2020. The $14.8 million decrease in cash was primarily driven by the company's operational needs during the quarter, but also included some Spring Bank-related items. During the quarter, we paid $776,000 of severance to former Spring Bank employees. This severance will continue through November of this year. During the quarter, we also settled the Spring Bank vendor-related dispute totaling approximately $300,000, both of these items were included in the net cash adjustment at the transaction close of the merger last November.

Also with 2 new programs entering the clinic in Q4 2020, we had approximately $5.8 million of disbursements in Q1 for clinical CRO costs, manufacturing setup costs, raw materials and batch fees.

We are very pleased to report that we strengthened our balance sheet considerably in early Q2 this year through the successful closing of our $65 million public offering of common stock in May, and the use of our at-the-market or ATM equity offering program in April, netting a combined $70.3 million after fees and expenses.

During this time, we also entered into a $10 million debt facility with Horizon Technology Finance Corp. and have drawn down $5 million on that facility. We believe that our current cash and equivalents will be sufficient to fund our projected operating plans, as Eliot discussed, well into the second half of 2023.

I continue to be encouraged by the positive sentiment we have from our analysts with 5 analysts now covering us and the investor community interest in our programs and platforms -- platform. We look forward to continuing conversations at investor and healthcare conferences this year, and hopefully, some of these meetings will be in person.

So in summary, our strengthened financial position ensures the cash runway for delivery of our future milestones. We have a new and additional group of top-tier investors joining our mission to deliver for patients with cancer. I look forward to sharing with -- sharing information with you over the course of 2021 and going forward.

With that, thank you, and operator, we can open the call up for questions.

(Operator Instructions) Our first question comes from the line of Hartaj Singh with Oppenheimer & Company.

This is Jackie for Hartaj. Congrats on securing (inaudible) financing, a lot of progress. So first, for FS118, if you could comment on the timing of that facility and assets you will do. And therefore, 120 and 222, if you could give some color, I guess, just around which of those levels are you right now based on the upcoming milestone timings you just provided here?

And then last, generally speaking, have you seen any impact from COVID on progress or not really?

Great. Thanks very much for the questions. So FS118, we expect the timing of the release of those data in the first half of next year, so the first half of 2022, and we continue to make good progress with that ongoing trial. With respect to 222, and I think you also asked about FS120. Both of those trials, again, in Phase I ascending dose design they're going very well, but we haven't disclosed the dose levels at this time. And clearly, as we update we will be able to give more details around those programs.

And then finally, in terms of COVID-19, there have been some operational impacts. Of course, we continue to work hard to minimize those. In particular, given we have research and clinical operations based out of the U.K., the U.K., as you may know, is only just emerging from a 5 months lockdown. We've worked hard to minimize any impact there, and those impacts are reflected in the timings we've disclosed.

Got it. And then second question, can you maybe discuss which programs across the pipeline you believe are aligned to have a fast path to market given the online need for those particular indications?

Yes. I mean, we're particularly excited about FS118 and the possibility there. So our first proof-of-concept program with FS118 as I mentioned in the call, is with patients who have had a refractory response to a prior checkpoint inhibitor. These patients typically have nowhere else to turn palliation or a difficult course of chemotherapy. And certainly, as we expect and as we show data emerging in the first half of next year, we'd be excited to look for potential fast track options with with that program. And so that's certainly a possible route forward.

In addition to that, FS222, which we believe has the potential to be best-in-class therapy is designed in a highly adaptive way in its first Phase I study. And clearly, as we begin to see signals of biological activity with that program, then we can rapidly accelerate into development in a way in which could take us on a fast track to the market.

Yes. Got it. Super helpful. And then last question, just on your preclinical efforts using surrogate molecule for (inaudible). I mean, as far as I've seen seems like not all antibody platforms can actually do a murine surrogate molecule. If you could just talk more on that aspect and how your platform enable or differentiate in that aspect? That would be great.

Yes. So I mean, one of the real advantages we have with our plug-and-play technology is that Neil and his team can both develop the human as well as the surrogate molecules in parallel. And of course, it's only a few changes, important changes from that natural human IgG1 format. And I think what you can see maybe even in the FS222 data that we published at AACR is the ability to tune for affinity and avidity is also a measure of us being able to translate those early signals in the nonclinical space into clinically effective molecules. And it's a measure of the 10 years we spent developing the platform that we have such utility within it.

And our next question comes from the line of Matt Phipps with William Blair.

This is Rob Andrew here on for Matt Phipps. So some nice data at the AACR meeting from the FS222 program, I think as you mentioned in the prepared comments, one of the interesting pieces was the data appearing to show FS222 kind of avoids the hook effect seen for the heterodimeric antibodies at least in vitro. So challenging for -- to do a dose response in vivo, but I'm wondering if you've kind of compared the (inaudible) and the heterodimeric formats in vivo and kind of how these might compare from a T cell activation perspective in vivo?

And then one of the questions we've been getting is around the kind of relative affinities for PD-L1 and 4-1BB, for the -- for your FS222 and for the other molecules that are in development and how this could matter from both a safety and efficacy perspective. We've seen some of the other programs have similar affinity for both targets, some have higher affinity for PD-L1 compared to 4-1BB. Perhaps if you could just kind of run over a little bit more the design of FS222 briefly in terms of the kind of high PD-L1 affinity and how the 4-1BB binding relies more on avidity, lower monovalent affinity? And what you think the implications are of those design aspects in terms of the clinical development, I think that would be helpful.

Great, rob. So certainly, those comparisons that you've talked about, we haven't yet published on. And clearly, we have a body of work that we'll continue to publish on during the course of this year. And well, it's just not the public domain. So with respect to the affinity versus avidity, so as you may recall, Rob, this sits at the very heart of our technology. So this plug-and-play platform enables us to pre tune the molecules, really seeking optimized avidity for the cross-linking and clustering of the target receptors.

And certainly, with respect to FS222, it very much plays into that. So what we have got in terms of the PD-L1 component is probably best-in-class, if not similar binding PD-L1 antagonist. And that really, in the setting of the tumor microenvironment causes a constant blockade of that pathway. But of course, in order to avoid that self competition, so the sort of thing that one might see in the clinic with other molecules. We've modulated that CD137 binding. And in terms of affinity, it's actually relatively low compared to the PD-L1.

However, when you look at avidity, so those protein-protein interactions across that immune sign-ups, and it's got very high avidity. So it enables us to continue up that dose response curve, continue a permanent blockade of PD-L1 and recruit those CD137 or 4-1BB containing immune cells and create that sign uptick -- sorry, that immune signups in order to create apoptosis. So in the clinic, the benefits of this, this means we can go after patients who, for example, have low PD-L1 expression. And as you know, those are patients who don't have a great opportunity from the first generation of checkpoint inhibitors. And we do believe that will distinguish us from some of the other FS222 like molecules in the clinic.

Great. And then if I could just ask -- just thinking about the midyear updates for FS120 and 11285 programs. Just what's the kind of thinking at the moment on the kind of means of disseminating those results? Should we expect a [Scientific Congress]? Or are you thinking it's going to be more of a kind of PR disclosure or what's the plan there?

Yes. We, of course, always would have a preference to go to scientific conferences. However, the timing as you know, is such that one-off needs weeks, if not months of lead time on that. So it's more than likely that 11285 and FS120 during the course of the summer will be by the way of press releases, giving updates on the ongoing Phase I studies.

And our next question comes from the line of Patrick Trucchio with H.C. Wainwright.

Just a follow-up on the relativity trial that evaluated the anti LAG-3 antibody in melanoma. The trial minutes primary endpoint of progression-free survival. And at the time of the announcement in March, follow-up for overall survival, the secondary endpoint was ongoing.

So I have a few questions. First, during the prepared remarks, it was noted that additional data on relativity is expected. And assuming this update is possible in the near term, I'm wondering what PFS or OS do you believe could provide increased confidence in the LAG-3 mechanism? And how we should think about the potential read-through from a more granular update from relativity to the FS118 program with the understanding of differences in mechanism, study design, et cetera?

And then secondly, should we anticipate FS118 have advantages on efficacy or safety and tolerability? Or all of the above is compared to combining 2 antibodies as it's being done in the relativity program?

And then separately, can you discuss the advantages of FS118 over the other bispecific approaches in clinical development that are also targeting LAG-3?

Yes. Pat, thanks for the question. So look, we were delighted, I think, along with the whole sector and obviously, patients who will benefit from the BMS, the high level data from the relativity trial. We look forward to seeing the data emerge from there and encouraged by the fact that the primary endpoint has been hit. Obviously, we only have the same amount of information as everyone else in the public domain.

I think the key, as I pointed out in my remarks, is that it's becoming clear that LAG-3 really is the next checkpoint pathway that will bring benefits to patients. We believe, and this is certainly demonstrated in our ongoing Phase II proof-of-concept study, not having a LAG-3 expression in the tumor microenvironment is really important to get that benefit. And certainly, as a consequence, you would expect that those patients would benefit more greatly. And we're looking to see if that indication occurs in those data as well.

With respect to 2 antibodies versus a bispecific. And clearly, FS118 is a 2 plus 2, so tetravalent bispecific anti PD-L1 and LAG-3. I mean what we can achieve mechanistically, and we published some of this at [Citi] last year is a shedding of LAG-3 from those exhausted immune cells in the tumor microenvironment. And that's brought about by the way in which we cross link, in particular, cluster, the LAG-3 and causing an enzymic-driven shedding of LAG-3 and obviously, an activation of those immune cells.

We -- although we don't think that the combinations won't do this. We don't think the extent to which they'll be able to achieve it is anything like that which we'd achieve with our bispecific and with the bispecific. And as a consequence, it may well be the case that the depth and durability of the responses with the combination would not be able to match that with bispecific mechanism. And it's why we obviously favor that bispecific approach.

Got it. That's helpful. And then just a follow-up on the study published recently that showed SB 11285 in combination with radiation is more effective than either as monotherapy in a mouse model.

I'm just wondering if you can discuss the conclusions from the piece in a bit more detail and what learnings, if any, from this preclinical work, however, could be applied to the ongoing Phase Ia/Ib trial or could be applied in future studies in the development program?

Yes, sure. So clearly, the ongoing 11285 study is -- both is a monotherapy and in combination with atezolizumab, so Roche's PD-L1 antagonist. We will, of course, look at those data as they emerge over the summer and the rest of this year. I think what was really important about the nature paper was that the 11285 pathway, so the STING pathway in turn is -- needs to be present in the tumor. And we see a synergy between 11285 and radiation.

So in fact, we're enabled. They were able to see changes in a low radiation setting. And of course, it is the case that, that may impact on future development pathways. What we would -- what we'll continue to do is explore the activation of that STING pathway by 11285 and see how we can begin, in further development plans begin to bring together radiation checkpoint inhibition and who knows what other modalities may play.

I think what that indicates sitting alongside the data around STING is what a potentially important pathway the STING pathway is in certain tumor types. And I guess, of course, notably, we have much greater flexibility because 11285 can be given by the intravenous route rather than intratumorally as many of the predecessors were limited to.

Right. And just 1 last one on the corporate announcements, including with Merck KGaA and Denali. I'm just wondering if you can remind us if the 3 targets that Merck has option have been disclosed? And if so, what are they?

And separately, what if any milestones would be due to F-star on naming or advancing those targets? And then secondly, regarding Denali. Can you give us some background on DNL310 and how success in that program could provide a read through, if any, to F-star's programs and as well if there are any milestones at F-star for program success on DNL310.

Yes. So again, we were really excited and always delighted to have Merck take one of their options as another 1/3 of 4. Ms. Darlene mentioned in her report, that does trigger a small milestone payment. Beyond that, unfortunately, the economics are not disclosed. And we don't disclose at all the targets in those programs.

With respect to Denali, we're, again, thrilled with the progress of Denali, who are excellent partners and have been over many years. And we're delighted for them. And obviously, for Hunter syndrome patients who have few other options. The read-through really is back to something I mentioned in an earlier question, which is the plug-and-play technology, we've got real flexibility and adaptability of that modified FC region, just a few amino acid changes to give, in our case, that bivalent binding for immuno-oncology. And obviously, the blood-brain barrier transporter for Denali.

So I think there's a very good read-through from the technology, and of course, Denali progressing a long way into the clinic now. It gives us confidence about the in vivo pharmacology in the target species [being man] and of course, some of the safety read through as well.

And our next question comes from the line of Wangzhi Li with Ladenburg.

Just 2, 1 on FS120. The upcoming updates for the accelerated dose titration data. Could you provide any color possible on how many single patient accelerated dose cohorts are -- or a level are tested in the trial? And for the upcoming data updates, what should we expect just single patient dose escalation for safety, PK type information or any potential for activity, any color on the upcoming data will be helpful.

And then for the 11285, similarly, with the upcoming data update, where -- should we expect efficacy data or mostly safety and PK type of data?

Yes. Thanks, Wangzhi, and thanks for the questions. Nice to talk to you again. Let me take those in reverse order, if you don't mind. Because that's likely the order of appearance of the data. So 11285. Just as a reminder, we have a 2-part Phase I study ongoing. So monotherapy and combination in the second part with atezolizumab. We gave an update at Citi last year on the overall dose design. So I shan't work through that right now.

But with that, we're exploring a number of avenues. Clearly, safety PK. And we're also looking to see if there are any biological signals in the data set and also to indicate to the market what it is that we anticipate doing next with 11285. And we'll report those data out over the coming couple of months or so.

For FS120, which will come we'll pace -- we'll stagger them. We're not at this time giving any updates on the details of that from the dose level and so on. But I can certainly tell you that we're interested in a couple of things, obviously, safety and PK and tolerability of this really potent dual agonist. And obviously, from a biological perspective. And as you know, this is a a slightly different approach with a Phase I study than we all typically do, and we've done for years and years in oncology in that we're not just looking for that safety, tolerability and ultimately dose-limiting toxicity in order to trigger the Phase II, what we're looking for are the first signs and a dose in which we get that triple activation of the immune response that I mentioned in my remarks. And that will then trigger for us that move -- rapid move to a combination with PD-1. And we'll give -- and it will be a trial in progress update and give some signals as to where we are with respect to those outputs.

And our last question comes from the line of I-Eh Jen with Laidlaw & Company.

The first question is regarding 118. Given that the recent reporting about 222, you have a strong binding to PD-1 before so to create the safety situations. And regarding 118 do you also have the ability to bind strongly to the PD-L1 even potentially in the -- some of the resistant patient, the expression level will be -- potentially will be low. So you'll be able to engage the 2 molecules to produce the therapeutic effect.

Nice to speak with you. And thanks for the question. So for 118. We -- again, through tuning, we've got a slightly different ratio with respect to affinities in that both PD-L1 and LAG-3 are actually pretty high affinity and of course, in a sense for an antagonist coupling, one would look for that because our key is to drive that cross-linking between the PD-L1 expressing cancer cells and the LAG-3, the exhausted LAG-3 expressing immune cells.

So we've driven with a kind of high, high relatively in terms of affinity. The low PD-L1 expressing tumors is a good question. We would certainly have the capability of picking those off. And what we've done in the ongoing proof-of-concept study in head and neck patients has ensured that all of those patients are both LAG-3 and PD-L1 positive.

And clearly, we have a semi quantitative view of that for the purposes of assessment. But of course, we'll be able to get more quantitative once we've got that study run out. And it will be an interesting hypothetical question as to where the PD-L1 cutoff will be where we see benefits.

Okay. Great. Very helpful. And maybe 2 quick ones. First 1 is on 222 that given that the patient recruitments are exclusively in Europe, I assume, is the current situation in Europe, particularly the COVID situation has had a further impact? Or you see some alleviation of that patient recruitment?

Yes. So yes, 222 currently is, in Spain, recruiting. Spain, unfortunately, but I guess, fortunately, for our trial, had a very early second wave of COVID and the oncology centers there who are world leading, have continued to operate functionally. And I would say 222 is going very well in the clinic, and we're encouraged by what we see. And we're in active communication.

It's likely that in the next phase for 222 we'll expand globally and bring recruitment of -- sorry, a further development across not just out of Europe, but also into the U.S. under an IND.

And maybe the last question is a housekeeping one, which is probably for Darlene. In terms of R&D expenses of this quarter or the first quarter of this year increased significantly compared to the prior quarters. So should we anticipate the first quarter R&D expenditure will be basis for the remaining of the year? Or that's just a 1 quarter or so the uptakes?

Yes. Sure. So I think you should think about the normalized or maybe slightly high, but more normalized now that this is the first quarter that we have 4 full programs in the clinic, and we will continue to have that going forward. So I would think of it as pretty realistic going forward.

Great. And congrats for the order progresses.

Great, thank you.

Thank, I-Eh.

It this concludes our question-and-answer session. And I would like to turn the conference back over to Eliot Forster for any further remarks.

Great. Well, thanks very much, everyone, for joining, and grateful for the questions. And I hope you'll agree that momentum is with us, and we've had a productive first full quarter as a listed company. In particular, our strengthened financial position ensures we've delivery of our future milestones. I'd like to thank, again, our new and existing investors, all our colleagues who show unwavering dedication to our mission from the lab to the clinic, and of course, the patients and health care professionals who contribute daily to the progress of our clinical trials.

F-star will continue to work to bring medicines to the market that will truly transform the lives of patients with cancer, and we look forward to updating you again in the summer. And with that, thank you very much.

This concludes today's conference call. Thank you for participating. You may now disconnect. Everyone, have a great day.