I-Mab at Needham Conference: Strategic Transformation Unveiled

On Monday, 07 April 2025, I-Mab (NASDAQ: IMAB) presented its strategic transformation at the 24th Annual Needham Virtual Healthcare Conference. The company, led by CEO Sean Fu, highlighted its focus on capital efficiency and clinical pipeline progress. While the divestiture of China assets marked a significant shift, I-Mab's emphasis on three clinical-stage assets in the US aims to extend its cash runway into 2027.

Key Takeaways

• I-Mab's strategic shift in 2024 included divesting China assets and reducing its workforce from over 200 to 24 employees in the US.
• The lead asset, Giva, showed promising efficacy in gastric cancer treatment, with expansion studies underway.
• Uleledlimab's development awaits data from TJ Bio's study in China, expected in 2026.
• Raji's ongoing studies focus on optimizing dosing for solid tumors resistant to IO therapies.
• The company's cash runway is projected to extend into 2027, driven by capital-efficient operations.

Financial Results

• I-Mab guides its cash runway into 2027 due to a focus on clinical operations and capital efficiency.
• The strategic transformation in 2024, including the divestiture of China assets, contributed to this financial outlook.

Operational Updates

• Company Transformation:

- Significant changes in 2024 included the divestiture of China assets and a shift to a leaner operating model with 24 full-time employees in the US.

- Focus is now on three clinical-stage assets: Giva, Uleledlimab, and Raji.

• Pipeline:

- Giva (Claudin 18.2 x 4-1BB bispecific antibody) is being developed for first-line gastric cancer, with expansion studies involving 40 patients.

- Uleledlimab (anti-CD73 mAb) development in the US awaits data from TJ Bio's study in China, with Sanofi holding China rights.

- Raji (PD-L1 x 4-1BB bispecific) is in ongoing studies to optimize dosing for solid tumors resistant to IO therapies.

Future Outlook

• Giva:

- Dose escalation data expected in the second half of this year, with dose expansion data in the first half of next year.

• Uleledlimab:

- Data from TJ Bio's study anticipated in 2026 to inform US development strategy.

• Raji:

- Amended Phase 1 trial data expected by the end of this year.

• Expansion Plans:

- I-Mab aims to explore other gastrointestinal malignancies, such as pancreatic cancer, where Claudin 18.2 expression is prevalent.

Q&A Highlights

• Tariffs:

- The divestiture of China assets was a strategic move to mitigate potential geopolitical tensions and tariffs.

• Giva Prioritization:

- Driven by its unique efficacy and safety profile, Giva's development is prioritized.

• Uleledlimab Strategy:

- A capital-efficient approach is employed by awaiting data from ongoing studies to de-risk further development.

• Business Development:

- The company remains focused on executing its current pipeline, with Giva as the lead asset, while also considering future growth opportunities.

In conclusion, I-Mab's strategic transformation and clinical pipeline progress were key highlights at the conference. For further details, refer to the full transcript.

Full transcript - 24th Annual Needham Virtual Healthcare Conference:

Ethan Markowski, Member of the Biotech Research Team, Needham and Company: Good morning, everyone, and thank you for joining us at Needham and Company's twenty fourth Annual Healthcare Conference. My name is Ethan Markowski, and I'm a member of the biotech research team here at Needham. Joining me today from I Mab are Sean Fu, CEO, Joseph Skelton, CFO, and Philip Dennis, CMO, who will provide a presentation on the company followed by a q and a session with the remaining time. And with that, I'll go ahead and turn it over to Sean.

Sean Fu, CEO, I-Mab: Good morning. Thanks for the opportunity. We're very excited to share the latest strategy and pipeline progress of IMAP. Alright. Next slides, please.

During the presentation, we will are making forward looking statements, And the viewers should consult a forward looking statement disclaimer for more details. Next, please. So I'll be, giving a high level summary of the company's status before I invite Philip Dennis to walk you through more details about the pipeline. IMAP went through significant transformation in, 2024, and that transformation continues as you will see. Last year, we announced the divestiture, from China assets.

Next slide, please. Really change the operating model and the strategy and the focus of the company from a comp from an old IMAP, which at one point had over 200 employees, significant significantly broader pipeline and capabilities, including discovery, development, regulatory, even manufacturing, very broad, very capital heavy. And to one that it is today, we are very focused. We are operating in US with only 24 full time employees. All of them are onshore in United States.

And we are focusing on three clinical stage assets. And all of them, all of them are clinically active. This is very different from what what was before. And by doing that, by focusing on clinical operations, by focusing on translational clinical development, we are much more capital efficient, and we are guiding our cash runway into 2027. And you will see that works really well when when when we think about the data, flip in the next one to two years, some critical and exciting data readouts, and we have sufficient capital to see through those data flows.

So we are well positioned to see the next phase of a growth, and we've completed the transformation in 2024 through divestiture. So now we are focusing on the pipeline. Talking about the pipeline, let me give you a overview. The lead asset we have here is a Clouding 18.241 bb bispecific antibody. And this is one we are developing as a bolt on to standard of care in first line gastric cancer, which is biochemo.

This asset is active in monotherapy in heavily pretreated patients and showed good safety and exciting promising efficacy signals in combination studies with IO chemo in frontline gastric cancer. And based on what we saw in the escalation study of seventeen patients through three different doses. We are now conducting expansion studies for 40 patients in total across two doses to substantiate the value we saw in these assets through clinical studies was more data. And this is a very exciting asset we believe is a best in class 18.241 bb bispecific that has a active clinical development program in frontline gastric cancer. Very exciting.

The second asset we have is a CD 73 monoclonal antibody. We call it uleledlimab. This is another potential best in class assets. And through the divestiture, which I mentioned earlier, the China rights went to TJ Bile, one of our business partners, and they had a license deal with Sanofi last year in which the greater China rights of this very molecule went to Sanofi. They did two things to this asset.

One, it is a strong validation of the molecule, and, we're excited about that. And second, it give us a front row seats to the clinical development programs that's ongoing in China that we believe will give us valuable input in guiding our next phase clinical development programs. Specifically, they are looking at uilaladlimab or YULI plus IO versus IO in a randomized study in CD73 high populations. And this, if readout positive, we believe will significantly de risk the asset, will give us green light to go forward full speed with our own development programs in US. Third assets is a PD L1-four-1BB bispecific.

This one showed significant activities in monotherapy setting in heavily pretreated population. And we are running clinical studies to optimize the therapeutic window. And we believe this asset has potential to help patients that suffer from solid tumors and they are resistant to prior line of IO therapies. This is significant unmet medical need and we're very excited about the potential of these assets as well. So you can see that we have a pipeline consisting of three clinically active assets.

We're focused on advancing, these pipeline going forward. And with that, I wanted to turn it over to Philip to give you more color around those exciting molecules. Philip?

Philip Dennis, CMO, I-Mab: Thanks, Sean. Next slide, please. So I'm going to focus first on our lead program, Jeeva Stomach or Jeeva, and really emphasize that that the elevation of Jeeva as our lead asset is a reflection of data that's emerged in the last several months. And in no way reflects a lack of confidence in the other two assets that Sean gave an introduction to. Jeeva is a potential best in class 18.2 four-1BB bispecific.

It has design features I'll go over in the next slide, but it has very high affinity for 18.2. It has clinical activity in our monotherapy phase one study, again, I'll go over that in a second, in a very low level of 18.2 expression. And this leads to localized T cell activation in the tumor microenvironment that is intended to minimize four-1BB mediated liver toxicity as well as systemic immune responses. And our asset is the first to be tested in The United States, in combination with, immuno chemotherapy as a standard of care in frontline gastric cancer. Next slide please.

This slide shows the mechanism of action. If we focus on the left, the bispecific is designed that if the bispecific through its four-1BB domain encounters a T cell in the circulation because of a lack of clustering due to the fact that there's no tumor cell there, that in fact that T cell will not become activated. In contrast in the right side of that diagram on the left, if you see a tumor antigen 18.2 you see several molecules, agivastomic, interacting with the tumor cell, interacting with four-1BB on a localized T cell, you can see that that leads to T cell activation. Moreover, if we get into some details of the molecule, again, if you look at the 18.2 binding domain, it has a much higher affinity, a log higher affinity in terms of for 18.2 than the lead acid in the class of obetuximab. It has a silenced Fc portion, so there's no ADC or CDC.

This minimizes unintended systemic immune activation. And finally, has a four one bb agonist. The SCFE domains at the bottom there lead to localized T cell activation in the microenvironment, leading to potent tumor cell killing and minimal liver toxicity and systemic immune response. Next slide, please. So this is a comparison.

We know that the four-1BB, sorry, the clot 18.2 class is very crowded, especially in gastric cancer. And so what we've done here is to try to highlight some of the mechanisms of action of the leading competitors and to show how Jeeva compares very favorably. So the Jeeva mechanism of action that I just described is at the top, with number one there. There are, t cell engagers such as the Innovent t cell engager, and these typically engage, especially if they use CD3, induces tumor cell killing by T cell dependent cellular cytotoxicity and bystander killing via activation of the T cell co receptor CD3. This leads to typically a very high rate of cytokine release syndrome, and I'm going to show that data again in second.

But importantly, there are other assets such as antibody drug conjugates such as from AstraZeneca AZD zero nine zero one that leads to, killing by cytotoxicity due to delivery of the payload and bystander killing, inducing ADCC ADCP and CDC. So here there's a high risk of on target GI toxicity and off target systemic toxicity, especially, with premature release of the payload. And finally, the lead acid in the class, again, zolbutuximab or zolby, kills cells by ADC and CDC, and it has a very high risk of on target GI toxicity. Next slide please. This is a snapshot of our phase one data presented last year.

The swimmer plot is shown on the left. Without getting into too much detail, what we can see is that of the responders in this graph, there are very several long lived responses in heavily pretreated patients. In fact, that patient in orange, about the seventh one down, had been on study for about two years at this point. And why is this important? This is important because these patients had received a median prior lines, three prior lines of therapy.

And again, this represents forty three eight claud and eighteen point two positive patients. Importantly, we use a cutoff of one percent of cells at one plus or greater intensity. Of these responses, we observed seven of them for an ORR of sixteen percent. And responders range from a claudin 18.2 expression of a hundred all the way down to eleven percent. In addition of those seven responders, five had received prior, IO.

Next slide, please. Well, in addition to the efficacy, the tolerability was quite notable. We did not encounter dose limiting toxicity and we did not reach an MTD. The chart to the left shows that in terms of treatment related adverse there were virtually no grade four or five. The one exception is a grade four thrombocytopenia that was not associated with bleeding, arguably suggesting that this is not clinically meaningful.

Moreover, if we look at the rates of clinically meaningful adverse events such as nausea and vomiting, we're at two percent, one out of forty three patients at grade three. So this has really suggested that Giva has a very special place in terms of having monotherapy activity in a very highly pretreated population with gastric cancer. Moreover, it was very well tolerated as monotherapy. Next slide, please. And in fact, if we compare Giva against the early phase one data of zolbituximab, which is again a naked antibody, we can look at the first row that shows the cutoff for 18.2.

Again, ours is the minimal really that one can think of, which is one percent of cells, one plus or greater. At the same cutoff zolbituximab had a zero percent ORR, zero out of fifteen patients. And when they tightened the threshold to fifty percent of cells, two plus or greater, they had an ORR of nine percent suggesting again that Jeeva had greater efficacy in the same group of patients, although it is a cross trial comparison. Moreover, if we look at important toxicities such as nausea and vomiting, we have a much better safety profile, which again will be shown in just a second. Next slide please.

So this is a comparison of Gvastomib on the left, zolmituximab the second to the left and then the lead ADC arguably, CMG nine zero one and the lead T cell engager from Innovent IBI-three eighty nine. And what this slide is very detailed and I already went over the differential mechanisms of action. But importantly, this is data from the monotherapy phase one data. You can see that the threshold is very different for these assets, right? So with us being the broadest inclusion criteria, arguably we offer the greatest benefit to most patients.

We can see that the ORR is below that, but importantly the safety profile is what I want to talk about, which is in fact the if we look at treatment related adverse events, I've highlighted this in red. And what this shows is that if we look across the board at grade three or greater treatment related adverse events, overall Giva leads led to a thirty three percent incidence. This was not reported in zolbituximab, but for the ADC and T cell engager, we're talking almost double the rates of grade three or greater adverse events that were treatment related. And then if we look at other important adverse events such as nausea and vomiting, we can see again how we are several fold less than zobetuximab in terms of grade three or greater nausea and vomiting. And importantly, we included CRS in here because of the T cell engager.

Again, although the majority of them were grade one or grade two, each of these grades leads to patients being admitted into the hospital overnight. So this is an important distinguishing fact. And in fact, if we look at the profiles of these assets, and as someone who used to lead a major ADC program a big pharma, I can tell you that that the t cell engager and ADCs do have a profile that's quite typical and quite favorable for development in second and third line settings. However, one can look at their profile and say they are not well suited to be combined with standard of care for gastric cancer, which is IO plus chemotherapy. In contrast, Gvastomic has a really interesting profile, well tolerated with notable monotherapy activity.

And so that's what we tested. And the next slide please will show our phase one design. So this is a phase one study designed, and in fact the blue part is completed now with 17 patients, where we simply added Gvastoma get three different doses to standard of care nivolumab and FOLFOX. This is in frontline unresectable patients HER2 negative with again a minimal level of 18.2 expression at one percent. In the dose escalation, we observed no dose limiting toxicity.

We did not reach a maximum tolerated dose because we did not dose escalate beyond the point at which our biomarker plateaued. When we looked at the efficacy, what we noticed, especially in dose level two and three, is that almost all of the patients had a response. In fact, if you total the objective response rates for this cohort and compare across study at the two studies that led to the approval of nivolumab plus chemotherapy or zolbituximab in chemotherapy, our objective response rates were far in excess of those numbers reported in those phase three studies. This led us to look at the plans for dose expansion and to amend the study to include more patients because we were so impressed with this data that we really wanted to validate it. And in fact, our recruitment for the dose expansion part shown on the right, we dose expansion part shown on the right, we are far ahead of schedule.

We're months ahead of schedule in terms of recruitment. And to date, when we look at the early data coming in from dose level one in terms of the expansion cohort, the objective response rate is in fact being corroborated in the expansion cohort that was first established in the dose escalation cohort. So we're very encouraged by this data. And in fact, the dose escalation data will be presented at a major meeting in the second half of this year. And the dose expansion data is planned to be presented at a meeting in the first half of next year.

Next slide please. This slide shows both the market opportunity and really the clinical opportunity shown on the right. In terms of the market opportunity of the two hundred and fifty thousand cases of gastric cancer, about one hundred and thirty seven thousand or eighteen point two positive. So it's a very large market. But if you look at the place that zolbituximab occupies, given its indication with chemotherapy only, this is actually this rectangle is drawn to scale.

And in fact, it represents about eight percent of the total gastric cancer market. And that is that's because of the fact that Zolbe's indication is at seventy five percent or greater claudin 18.2 expression. And because its indication is with chemotherapy alone, the use of that is really predominantly in the PD L1 less than one percent that shown on the y axis. So this leaves a lot of space for Jeeva. Jeeva is potentially first in class in that purple area because the odds of Zolpi ever getting less than seventy five percent are quite low because when the claudine 18.2 expression falls off, the the activity of zolbetuximab drops precipitously.

But even if zolbetuximab moves into the IO plus chemo space shown in blue above the Zolbe rectangle, what this shows is in fact that, Jeeva still has a great chance to be best in class there because again, in the phase one monotherapy data, Jeeva had better efficacy and was better tolerated. So we think the potential for Jeeva is quite, the upside is tremendous here. But the opportunity doesn't exist in gastric cancer. And we haven't even listed other stages of gastric cancer such as locally advanced and but resectable, but in fact other tumor types as well. Next slide, please.

So if we establish proof of concept, which it certainly looks like we're on that track, with gastric cancer by combining Giva with IO and chemotherapy, why not move into other GI malignancies where Cloud 18.2 expression is quite prevalent, especially in tumor types with high unmet medical needs such as pancreatic cancer and cholangiocarcinoma, shown on this slide. The market opportunity is large here with $6,000,000,000 and $3,000,000,000 respectively for each of these tumor types. And again, most of these tumors express Claudine 18.2. For pancreatic cancer, the standard of care is a chemotherapy doublet. Why not combine Giva with the chemotherapy doublet if we know that we can add it to IO and chemo safely and improve efficacy?

Well, the standard of care in cholangiocarcinoma is in fact IO plus chemo, so why not do that experiment as well? So the upside here is tremendous. Now the development of Jeeva, next slide, please, is also secured by intellectual protection, and that's just listed here in terms of the patents in The US that have been granted for composition of matter and method of use that extend protection to twenty forty. But importantly, are other patents that are pending both in The US and globally related to method of use and the combinations that extend the protection through 02/1943 and 02/1945. Next slide, please.

So in summary, Giva is a very high affinity eighteen point two bispecific with conditional four-1BB activation. I didn't point out, but in fact we have again minimal liver toxicity, no cytokine release syndrome. So we're getting really controlled activation of T cells in the microenvironment. It is designed for long lasting immune responses across a wide range of clotting expression. And our response rate and tolerability stand out amongst other assets in the class that that really points out the the potential to to combine Jeeva with an IO chemo backbone in frontline therapy.

And again, we have important, catalysts with our escalation data being presented in the second half of this year and the dose expansion data being presented in the first half of next year. Next slide please. So I will touch on uililumab. In the interest of time, I'll be a little bit brief here. Uilililumab is arguably the best CD73 antibody out there and I will show reasons why in a second.

But CD 73 is the best target in the adenosine pathway. Why target adenosine? Because it's an immunosuppressive metabolite. And in fact, uilevelimab, especially compared to the lead antibody in the class, aleclumab that's being developed by AstraZeneca, we have better in vitro inhibition of c d seventy three. But as as Sean mentioned, we are awaiting data to emerge from our collaborator in China, TJ Bio, that is doing prospective randomized study in CD73 selected patients of Euli plus IO in frontline non small cell lung cancer.

So our development is being paused until this data emerges. But next slide, I want to point out that the really the characteristics that make us excited about this asset. In the interest of time, there are several ways to target the adenosine pathway. CD 73 is arguably the best point to inhibit the pathway because it is a point of convergence. There's no bypass around it.

It is the only enzyme that converts AMP into adenosine, and it is a rate limiting step. Next slide, please. Now the advantages of Yuli compared to aleclomib have to do with how Yuli interacts with c d seventy three, which is a dimer. Yuli acts in a way to form an intradimer binding mode, which leads to dose dependent inhibition as shown on the upper right. In contrast, aleclomab forms inter dimer binding modes which leads to this concept called the hook effect.

I can point that out to you in the next slide what that looks like if you do an enzymatic assay. Next slide please. So on the left is the ability of Yuli to inhibit CD73 enzymatic activity in an in vitro experiment. So different doses of Yuli are shown in blue. As you dose escalate, you can see that the percent of enzymatic activity falls to zero.

Complete inhibition of CD73. In contrast, when aleclomab is dose escalated at the same dose ranges, what you can see is that there is inhibition initially, but then the inhibition is paradoxically lost as you increase aleclomab concentrations. So this is what's called the hook effect. And I'll also point out that aleclomab never leads to complete CD73 inhibition, again suggesting that Euli is a better inhibitor of CD73. Next slide, please.

Does a hook effect exist exist in a model system? The answer is yes. Next slide please. So this slide shows that Oops, I'm sorry, too fast, I apologize. So this simply shows that if you in a mouse model, if you dose escalate ULE shown on the left in the shades of blue or aleclimab shown on the right, that in a dose dependent manner, you get dose dependent inhibition of CD73 as well as dose dependent tumor inhibition.

In contrast with aleclimab, you get neither. Next slide, please. And this is a data, the clinical data, single arm data, that showed, that really got us excited about our concept, which is really differentiated in the field of CD 73 assets, which is we think we can identify patients who will respond better to Euli by measure CD73. And that's shown very simply in this slide, which shows that in a frontline non small cell lung cancer cohort, if you divide the patients by CD 73 and PD L1, this slide shows that for CD 73 high, the ORR two, Yuli plus a checkpoint inhibitor that's used in China, Toripalumab, that the ORR is approximately twice of the CD73 low patients in the row below. And in fact, if you look across trial at KEYNOTE-forty two, which is a landmark study with pembrolizumab, the ORR in that study in the same PD L1 group of greater than or equal to one percent was twenty seven percent versus sixty three in the c d seventy three high group, again, that was being tested in combination with Yuli.

So I will say that that the obvious that in fact that Yuli and Tory were very well tolerated. So we anxiously await the development of the data from TJ Bio, with their randomized prospective data. Next slide, please. And let's go to the slide on Raji, and I'm conscious of time. So Raji is a really interesting four-1BB bispecific.

It leads to conditional activation of T cells whenever there's a tumor cell that expresses PD L1. And in fact, the implications here are to mitigate liver toxicity as well as systemic immune response. Next slide, please. And I want to point out some of the phase one data, which is really interesting. So this is phase one data that was presented at ASCO last year.

Forty four evaluable patients. And again, most of them had at least three prior lines of therapy. If we look at data at the three and five milligram per kilogram cohort, which we think are clinically really the clinically minimally clinically active doses, we saw an objective response rate of twenty seven percent. And this included one complete response and six confirmed partial responses. The complete response was observed in ovarian cancer patient who had received seven prior lines of therapy.

And almost three quarters of them had received prior PD L1 inhibitors. So this is really exciting to us. And I think that this is very exciting as monotherapy data, right, in IO refractory patients. Next slide, please. But what we encountered was that we did encounter an MTD at seven mgs per kg every q week.

But our most common treatment related adverse events were increased ALT and ALT, which are signs of liver toxicity, which is quite common in the four one b b class. And in fact, if we look next slide, please. If we look at the comparison with ocasunlimab being developed by Genmab in their phase one data, it's clear that we have a far superior ORR at twenty seven percent compared to seven or thirteen percent depending on which cohort you look at for ocasimlimab. But importantly, their AST and ALT rate of grade three or greater was a ten percent compared to ours at twenty five percent. So this has led us in our development of Raji in collaboration, with with ABO Bio.

What we're doing is actually amending the ongoing phase one to test lower doses and less frequent doses because we think by doing that, we will actually increase the therapeutic index, we'll minimize T cell exhaustion, and we eagerly await that data. Next slide please. So in summary of our key readouts, I'll mention we have a financial runway into 2027 to complete the trials that I've mentioned to you today. We have important readouts for Jeeva in the second half of this year for the dose escalation data in combination of frontline gastric cancer. We have the dose expansion data that will be presented at a major meeting in the first half of next year.

The prospective data of uililumab should be available in 2026, and we expect the Raji data with a different dose and schedule cohorts to be available by the end of this year. So with that, I'll stop and, take any questions.

Ethan Markowski, Member of the Biotech Research Team, Needham and Company: Great. Great. Thank you guys for the presentation. At this time, you anyone attending the call is welcome to post their question, the question using the question and answer feature, and I will be keeping an eye on that. But maybe a couple from me to start.

So kind of a broader question. It's very hot topic right now, which would be tariffs. And I know in the very beginning, you did a nice job of illustrating the changes structure in the recent years and divestment out of China. But wanted to know if there is any impact or expected impact from tariffs, or do you think that's largely mitigated, with the way IMAD is currently set up? I think you're muted potentially.

Sean Fu, CEO, I-Mab: Hope this is better. Thank you for the question. Yeah. I think the, divestiture was a strategic move that proved to be smart, to to get ahead of the curve, so to speak, to avoid any of the potential issues, from the geopolitical tension as well as the tariff, which is more recent topic. For us, I don't see the tariff gonna have an immediate impact.

Our escalation study and expansion study for givastomic, our lead assets are conducted in US. And all the data that Philip mentioned were US based studies. And our supplies of clinical materials are in place for the next phase of clinical development. So overall, I don't see tariff being a significant impact going forward. That position us, and we have enough cash to seed through some of those data flips.

So I think we're positioned in a enviable position with the pipeline being active and differentiated and with the resources to see through. So I think we can really focus on execution without having to worry about outside exogenous variables that we don't have in, immediate control.

Ethan Markowski, Member of the Biotech Research Team, Needham and Company: Great. No. Thank you for that input. So another question that we get quite frequently, and and you did touch on in the beginning, is kind of if you can maybe walk us through a little more the decision making to prioritize Jiva. I know you hit on it, but is it mostly the data, competitive reasons, combination of different variables.

Any thoughts you have there?

Sean Fu, CEO, I-Mab: No. I think those are really the important points feeding into our consideration. It really is the data coming out of Jiva and its unique position of this molecule amongst competitors. If you look at the holistic profile of the molecule, Giva thread a needle with very nice combination of pronounced efficacy and very benign safety profile, especially in combination with standard of care without changing any of the components of the standard of care. That make the clinical practice and the later phase clinical development that much straightforward.

And it's favored by, regulatory agencies if you don't change the standard of care. So that is a unique profile when you look at other modalities, be it ADC or by specific c d three engagers or monoclonal antibodies, the ability to combine with standard of care unchanged, it is quite an advantage, for for GBA. Now with Yuli, I think it's still a very strong molecule in potentially best in class. What we are doing is not to say that, you know, Yuli is going to be delayed. In fact, we're gonna say, hey.

We're gonna look at this molecule in a capital efficient way. And there is a ongoing clinical study that will significantly derisk our next phase development. Why don't we give it some time for data to mature before we put down our own capital to develop the asset in US? And it's a free option that we wanted to take advantage of. It's the exact same molecule.

So I think that's the right thing to do. And we're thinking, we're looking at a data readout from that study sometime in 2026, and we're comfortable with that timeline. To add to that, we have an FDA approved IND study plan in our hands. So once that data comes back positive, we're ready to go.

Philip Dennis, CMO, I-Mab: If and, Sean, if I could just add, again, we all are enthusiastic about the pipeline as well as especially Yuli as a best in class CD73 antibody. But I want to go back to Jeeva. One thing I did not mention that I intended to is that it's based on data, the emerging data. And the data that I mentioned, it's not just the objective response rate that is far in excess of what's been reported in the phase three studies that I mentioned. It's the fact that patients were seeing responders in the dose escalation study that are PD L1 negative or Claudine eighteen point two at one percent, bare minimums.

So these patients would not be expected to respond to either nivo fulphoxolone or Zol fulphoxolone in the study called Spotlight. So this was really part of the exciting data that emerged. And I just want to reinforce that that it's not only the data in seventeen patients with the overall objective response rate, it's the fact within that response rate, there are really outliers, anecdotes that really suggest that there's something going on here that's worth that's why we're exploring it more fully in the dose expansion cohorts.

Ethan Markowski, Member of the Biotech Research Team, Needham and Company: Great. Great. Thank you for those responses. Maybe highlighting or, you know, double clicking a little on the on the Jeeva safety data. You you showed a nice chart, kind of a cross study comparison and and how it appeared better tolerated than some of the other lead programs.

I was wondering yeah. Because I didn't see it. I was wondering if these, reduced safety events translated into lower discontinuation rates at all, or if those were pretty comparable Just so you remember.

Philip Dennis, CMO, I-Mab: Yeah. The the discontinuation rates, we don't have that on the slide. The the the easiest thing to state is that they were they were comparable. But, again, if you think about it, the idea here is not we're not trying to make the case that Jeeva is a better monotherapy than an ADC or T cell engager. It's a better monotherapy to be combined with frontline therapy.

Right? So that's you know, when you take any of these assets that you're looking at in the slide and you combine it with IO and chemo that already has a very high rate of treatment related adverse events, that you have to be very careful with what you add, especially if you're not modify the dose or schedule. So to me, you know, the discontinuation rates in the monotherapy are are, you know, again, it's slightly better with with Giva, but that's not really the message. The message is that this improved toxicity profile translates into the ability to be combined with other agents. No.

That that makes

Ethan Markowski, Member of the Biotech Research Team, Needham and Company: a lot of sense. I am monitoring questions from chat, but maybe one more for me in the meantime. So I know at IMAB, business development has always been a consideration, especially maybe for a later stage asset. Talks of in licensing a program in the past. Is that something that's still open or or in focus or less of a priority now and and more focused on really clinical development of Chiva at the moment?

Sean Fu, CEO, I-Mab: We're razor focused on the execution of the current pipeline. We see value in every molecule, especially Jeeva, our lead assets. And, we're putting our resources and our energies behind this molecule to advance it as fast as possible. Having said that, we have our years on the ground when thinking about growth potential beyond the current three pipeline assets. So we are paying attention.

We're having conversation. We're we're looking into future growth opportunities. But that is complementing to the execution efforts behind those three assets. These are our priorities.

Ethan Markowski, Member of the Biotech Research Team, Needham and Company: Great. Great. And I'm taking a look, and I don't see any further questions from the chat at this time. So just wanted to thank three of you for coming on and talking a little a little bit more about IMAD, and, thank you for attending our conference.

Sean Fu, CEO, I-Mab: Thank you very much, Ethan.

Ethan Markowski, Member of the Biotech Research Team, Needham and Company: Thank you.

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