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# GSK plc GSK plc - Special Call - GSK plc

Monday, June 17, 2024 8:00 AM

#### Event Participants

Executives 5 Nick Stone, Luke Miels, Tony Wood, Nina Mojas, Hesham Abdullah

#### Attendees 2

Evangelos Terpos, Andrea Cercek

#### Analysts 8

Mark Purcell, James Gordon, Matthew Weston, Peter Verdult, Emmanuel Papadakis, Graham Parry, Unknown Analyst, Peter Welford

#### Nick Stone Executive

Hello, everyone. Welcome to our next meet GSK management's event, getting ahead of cancer. This is an interactive event with the presentation sent to our distribution list by e-mail, and you can also !nd this on gsk.com. Please turn to Slide 2. This is the usual safe harbor statement.

Please turn to Slide 3, and let me now hand the call over to Luke to share today's focus.

#### Luke Miels Executive

Thanks, Nick. So today, we hope you gain a better understanding of our material growth opportunities across our key areas of focus in oncology, hematology, gynecologic cancers and other tumor types....

# GSK plc GSK plc - Special Call - GSK plc

Monday, June 17, 2024 8:00 AM

#### Event Participants

Executives 5 Nick Stone, Luke Miels, Tony Wood, Nina Mojas, Hesham Abdullah

#### Attendees 2

Evangelos Terpos, Andrea Cercek

#### Analysts 8

Mark Purcell, James Gordon, Matthew Weston, Peter Verdult, Emmanuel Papadakis, Graham Parry, Unknown Analyst, Peter Welford

#### Nick Stone Executive

Hello, everyone. Welcome to our next meet GSK management's event, getting ahead of cancer. This is an interactive event with the presentation sent to our distribution list by e-mail, and you can also !nd this on gsk.com. Please turn to Slide 2. This is the usual safe harbor statement.

Please turn to Slide 3, and let me now hand the call over to Luke to share today's focus.

#### Luke Miels Executive

Thanks, Nick. So today, we hope you gain a better understanding of our material growth opportunities across our key areas of focus in oncology, hematology, gynecologic cancers and other tumor types. We'll highlight the future potential of Blenrep, we anticipate to be a multi blockbuster asset that delivers a favorable bene!t risk pro!le for multiple myeloma patients in need. We will also discuss our di"erentiated immuno-oncology combinations, primarily anchored to anti-PD-1 Jemperli as the backbone. And given our recent in-licensing of 2 ADCs from Hansoh we will detail our future opportunity across solid tumors.

And !nally, we'll walk you through the near-term catalysts that will help us to achieve our stated growth ambitions. If we can go to Slide 4, please. You'll hear from myself, along with Tony Wood, our CSO; and Dr. Evangelos Terpos to walk us through the most recent Blenrep data. And for Q&A, we'll also be joined by Nina Mojas, Hesham Abdullah and Mondher Mahjoubi.

So if we just go to Slide 5 now. As a reminder, GSK focuses on preventing and treating disease in 4 therapy areas. We most recently spoke to you about our progress in respiratory. And today, we will cover the emerging oncology portfolio. Slide 6, please.

Now I don't think I need to tell people on this call that oncology is an exciting area. We are con!dent that our oncology strategy, which we'll cover shortly, will contribute to our previously committed 2031 GSK ambition. And it has the opportunity to deliver transformative medicines for patients and value for shareholders. The growth of our competitive portfolio stems from the potential to achieve clinical outcomes in de!ned cell populations.

And in the near term from 2024 to 2026, we expect our in-line medicines to continue growth. We also anticipate a potential market entry of Blenrep in second-line multiple myeloma, and this represents upside to our current ambitions. In the latter part of this decade through to 2031, we expect a shift in cells composition to re#ect potential Blenrep expansion, the emergence of immuno-oncology combinations and the entry of our two ADCs across tumors. In a moment, Tony will begin our medicines spotlights with Blenrep and the recent practice-changing data presented at ASCO.

Please now turn to Slide 7. So GSK Oncology is focused and focused across 3 core areas: hematology, gynecologic cancers and other growth opportunities in solid tumors. We've got several modalities, whether they are antibody-drug conjugates, immunotherapy or targeted small molecules that span these disease areas. Hematology portfolio includes Ojjaara in myelo!brosis and belantamab mafodotin or Blenrep in multiple myeloma o"ering signi!cant growth opportunity. Gynecologic cancers will continue to be a cornerstone of our portfolio with Jemperli in endometrial cancer and Zejula in ovarian.

We also have a strong opportunity to strengthen our gynecological impact with our recently in-licensed B7-H4 ADC from Hansoh. And lastly, we're gearing investment decisions to maximize these medicines in additional solid tumor types where they could deliver transformational e\$cacy, such as with colorectal, lung and head and neck. I'll now hand it over to Tony on Slide 8.

## Tony Wood Executive

Thanks, Luke. Please turn to the next slide. Multiple myeloma is a complex disease with new combination treatment options continuing to emerge. With each line of treatment comes accumulating toxicity and decreasing time until the next relapse. What's more, novel modalities often necessitate hospitalization or inpatient care, particularly for anti-BCMA agents.

Importantly, for the 70% of !rst-line patients who receive lenalidomide, they only bene!t from 12 to 28 months progression-free survival in second line and beyond. With this in mind, future treatment options need to address unmet need, namely extending overall survival and time in remission, lowering toxicity, broadening eligibility and treatment accessibility across sites of care. We're grateful that Dr. Evangelos Terpos, Professor of Hematology at the National and Kapodistrian University of Athens and a DREAMM-8 Principal Investigator is able to join us to walk us through recent Blenrep data. Welcome, Dr.

Terpos. Please turn to Slide 10.

## Evangelos Terpos Attendee

I'm Evangelos Terpos, Professor of Hematology and Director of the Stem Cell Transplantation Unit in the University of Athens in Greece, and I'm going to present to you the data of the novel studies, DREAMM-7 and DREAMM-8 and the newly diagnosed transplant ineligible patients with multiple myeloma who received the combination of BRd, an investigatorinitiated study. Next slide, please. This is the study design of the DREAMM-7 which included patients with 1 prior line of therapy and relapsed refractory multiple myeloma and the treatment schedule included the combination of bortezomib and dexamethasone potential at the standard schedule and in the !rst trial we had the addition of belantamab mafodotin at a dose of 2.5 milligram/kilogram every 3 weeks followed by after 9 cycles by 2.5 milligram/ kilogram every 3 weeks alone. Or in the ARM B, the addition of daratumumab at the dose of 16 milligram/kilogram weekly for cycles 1 till 3, then every 3 weeks for cycles 4 to 8, and then after cycle 9, we had Daratumumab monotherapy. So we had a direct comparison between belantamab mafodotin and daratumumab as monotherapy after the 8 cycles so from cycle 9 and afterwards.

The primary endpoint was PFS, key secondary endpoints, overall survival, duration of response and MRD. We had Strati!cation for prior lines of therapy, revised ISS and prior bortezomib use. Next slide, please. Regarding PFS, you can see that the combination of belantamab, Velcade and dexamethasone produced an impressive more than 3 years median PFS of 36.6 months versus 13.4 months of daratumumab, Velcade and dexamethasone with a hazard ratio of 0.41. So BVd demonstrated a statistically signi!cant and clinically meaningful PFS bene!t with a median PFS that was 23 months longer than that of DVd.

Next slide, please. Regarding overall survival, even with this medium follow-up of 28 months, you can see that we have a median overall survival that has not been reached in both arms, but the proportion of patients who are alive at 18 months was 84% in BVd and 73% in DVd o"ering a hazard ratio of 0.57 that was statistically signi!cant. So overall survival, so the nearly strong and clinically meaningful trend favored BVd, and of course, additional survival follow-up is ongoing. Next slide, please. And this is mainly because of the impressive overall response rate, which was 82.7% in BVd and 71.3% in DVd.

But if we see the quality of the responses was much more impressive with BVd with at least a complete response in 35% versus 17% of DVd and the MRD negativity rate in complete responders was 25% versus 9.6% in BVd and DVd, respectively, and the VGPR MRD negativity 38.7% versus 17% in the 2 arms, respectively. Next slide, please. The PFS bene!t was consistent favor BVd versus DVd across all the prespeci!ed subgroups, including patients with lenalidomide refractory or high risk cytogenetic and especially for those patients who are lenalidomide refractory, and this is a big number of patients now and an unmet need you can see. Next slide, please. BVd o"ering median PFS of 25 months versus 8.6 months of DVd in the non-lenalidomide refractory patients, the median is more than 3 years and 18 months in BVd and DVd, respectively, but you have also to appreciate that patients who are lenalidomide refractory were more heavily pretreated with 3 or more prior lines of therapy in 42% of the patients in BVd compared to 19% in the same arm for those who were not lenalidomide refractory.

Next slide, please. Regarding high risk also, if you can appreciate that BVd o"ered the hazard ratio of 0.31 those with high risk cytogenetic o"ering a median PFS of 33.2 months versus 10.5 only in DVd. For the standard risk patients, also BVd continues to have a median PFS, which has -- which is 36.6 months versus 15.3 months in the DVd with a hazard ratio of 0.44. Next slide, please. The DREAMM-8 study was a study that included relapsed refractory patients with 1 prior line of therapy, but all of them have been exposed to lenalidomide, so a more focused study on lenalidomide explored in refractory patient.

In that study, Bortezomib, Pomalidomide and Dexamethasone which is one of the standard of care was compared to belantamab mafodotin, pomalidomide and dexamethasone. Pomalidomide and dexamethasone was given at the standard dose like Bortezomib in ARM B, while in belantamab, we had a very nice schedule with a dose of 2.5 milligram per kilogram given at cycle 1 only every 4 weeks now, and then followed by 1.9 milligram per kilogram every 4 weeks from cycle 2 and onward.

And there was Strati!cation for prior lines of therapy, Prior bortezomib and Prior anti-CD38 therapy while the primary endpoint was PFS and key secondary endpoints included overall survival, MRD negativity and duration of response. Next slide, please. The Median PFS has not been reached for the belantamab, pomalidomide and dexamethasone arm, while the 12 month probability of progression-free 71% versus 51% in PVd. In PVd the median PFS is 12.7 months that is expected also based on the OPTIMISMM study that gave approval to this combination, the hazard ratio is 0.52. Next slide, please.

Regarding the di"erent prespeci!ed subgroups in the PFS we have seen bene!t with BPd in all these Prespeci!ed subgroups including patients with high risk cytogenetic as you can see, here, with a hazard ratio of 0.57, but especially to patients who are refractory to lenalidomide with the hazard ratio of 0.45. Next slide, please. And patients who are refractory to anti-CD38 monoclonal antibody and daratumumab with a hazard ratio of 0.65. Next slide please. The response rate was almost similar between the 2 arms.

However, the quality of response was much better with BPd versus PVd so CR or better was 40% versus 16% and VGPR or better 64% versus 38% in the 2 arms, respectively. Next slide, please. The MRD negativity was much higher, almost 7x better or 5x better with BPd versus PVd. The CR negativity MRD rate was 24% versus 5% in the PVd and the VGPR MRD negativity activity rate 32% versus 5% for the 2 arms, respectively. Next slide, please.

The overall survival showed a trend in favor of BPd with 12 month probability of survival of 83% versus 76% in PVd and of course, the data are not matured yet. Next slide, please. How about ocular adverse events which is the most important side e"ect. And I would say one of the very few side e"ects of belantamab you can see that we are about the worsening of best corrected visual acuity because this is something that can impact the daily activity of the patients. And you can see that 20 to 50 best corrected visual acuity reduction happened with 34% of the patients versus only 2% who had 22 to 100 or worse.

The time to onset for the !rst event was 73 and 105 days, respectively. And the improvement of the !rst event happened in 98% and 100% of the patients, respectively. First event result in 94% and 80% of the 2 groups of the side e"ects, respectively. Next, slide please. The Median time between the doses increased the longer patients were on treatment and the

dose delays did not have any impact on the PFS.

BVd patients with at least 1 dose delay of more than 12 weeks, the median PFS was exactly 36.6 months. 23% of the patients experienced 20 to 50 or worst events in the !rst 3 months, and the prevalence decreased thereafter, as you can see in the graph. Rate of treatment, discontinuation due to ocular events were very low. Next slide, please. In the DREAMM-8, the respective number of patients with best corrected visual acuity reduction to 20 to 50 and 20 to 200 was 34% and 1%, respectively.

The !rst event resolved to normal baseline, happened in 84% and 50% of the patients, but you can recognize that it was only 1 out of the 2 patients in the 20 to 200 group. And the !rst event improved in 92% in all patients respectively. So visual acuity change that could a"ect activities of daily living were reversible in most patients for both studies. Next slide, please. So in summary, I would say that in DREAMM-7 the combination of belantamab, Velcade and dexamethasone was 36.6 months compared to 13.4 months in patients who received daratumumab, Velcade and dexamethasone after a median follow up of 28 months.

The PFS was consistent across subgroups associated with poor prognosis, including patients with lenalidomide refractory or high risk cytogenetics. We have a strong and clinically meaningful overall survival and more quality overall response rate and durability of response with BVd. In the DREAMM-8 study, the median PFS has not been reached yet with belantamab, pomalidomide and dexamethasone versus pomalidomide, Velcade and dexamethasone, which the median was 12.7 months after a median follow-up of 22 months.

All the patients in this study who had been exposed to lenalidomide, and the PFS consistent across all prespeci!ed subgroups, including patients with high risk cytogenetics or lenalidomide or anti-CD38 refractory patients. We had greater response rates, including MRD negativity with BPd versus PVd and an early signal for overall survival advantage. Regarding safety and tolerability of BVd and BPd regimen to the DREAMM-7 and DREAMM-8 studies, this was consistent with the known safety pro!le of the individual agents with dose modi!cations that were e"ective in enabling patients with ocular adverse event to achieve PFS outcomes and low treatment discontinuation rates consistent with that of the overall study population. Next slide, please. This study gave us the rationale to go to a Phase I/II study in the newly diagnosed patients who are not eligible for transplant.

And these patients were intermediate, !t or frail. We randomized the patients to receive either 1.4 mg, 1.9 mg or 2.5 milligram per kilogram but given every 8 weeks or every 2 months in combination with lenalidomide and dexamethasone and primary endpoint was the safety, tolerability and the dose that we are going to go for the Phase II study and secondary endpoints which is a lot of data as you can see here.

Next slide, please. The overall response rate was 100% in all the subgroups. And we've that we had a slightly higher number of patients with complete response in the Cohort 1 of the 2.5 milligram per kilogram, but we have very good responses in the 2 others, 2 other arms also. And the progression-free survival was extremely good as no patients after median follow up of 24.8 months has progressed. However, we had some deaths because the study was run especially at the time of the delta strain of the subgroup 2.

That's why we have 4 patients who died because of COVID-19 and also we had 2 patients who died because of pneumonia, 1 because of intracranial hemorrhage and 1 sudden death. Don't forget that these patients were intermediate, !t or frail and the median age is 74-year of age. Next slide, please. Regarding the ocular adverse events, you can see that the vast majority of the patients had no or Grade 1 adverse events and Grade 3 or more adverse events happened in a very low number of patients. As you can see, for example, keratopathy was for the Cohort 2 of the 1.9 milligram per kilogram every 8 weeks, which was the dose that we have chosen to go to the part 2 of the study was only 0.3%.

Importantly, the time to resolution of keratopathy was only 1 month, the time to resolution of the best corrected visual acuity change from baseline was almost 2 months in all the groups. And the time to resolution of meaningful BCVA decline with more than 3 lines drop in better seeing eye was between 1 and 1.5 months. The frequency, and clinically relevant vision impairments happened in 10% in the Cohort 1 with more than or equal to 3 lines drop in the better seeing eye to up to 13.4% in Cohort 1 and 7.7% in Cohort 3. Next slide, please. Regarding Ocular symptoms who have impact on the activities of daily living and you can see in the second part of the !gure, you can see that in the group of patients who received 1.9 milligram per kilogram every 8 weeks who had only 5.7% of the patients who had almost most or half of the time symptoms that impaired their clinical, their daily activity of living, while the 93% of the patients had not such symptoms.

Next slide, please. And in order to achieve that, we had a schedule of, as we call it, appropriate belantamab dose administration. So if you see within red color B, we call it inappropriate belantamab administration is when the substantial ocular symptoms are present, and this can impact the quality of life of the patient and their daily living of the patients.

So if we don't give belantamab at that time, then we avoid these side e"ects. Well, in the contrary, as you can see on the left, we have an appropriate dose administration will have a dramatic reduction in the visual acuity. On the contrary, if you see on the right, the appropriate dose administration diminished the visual acuity reduction based on this snellen chart. Next slide, please. So in summary, the extension of belantamab doses to every 8 weeks or even 12 weeks if we had any symptom, did not lead to reduced e\$cacy compared to previous study implementing the every 3-week schedule.

This is also that the e\$cacy of belantamab is maintained even when administered in extending time intervals as we've seen also in the DREAMM-8 study. Furthermore, the extended dosing schedule had only a minimal impact on vision-related functioning with all or most of the time in the activity of daily living responses recording less than 2.5% of assessments. Furthermore, the frequency of clinically relevant impairment in vision was low as meaningful BCVA decline was observed in less than 10% of assessment with a rapid time to resolution.

So thank you so much for your attention, and we're going to the next presentation now.

## Luke Miels Executive

Thank you very much, Dr. Terpos. We greatly appreciate your time and expertise in sharing the potentially transformative DREAMM-7 and DREAMM-8 second-line data, as well as

insights from your clinical experience with your !rst-line data. As you just showed that management of eye related side e"ects is important to help patients achieve design outcomes. So let's -- we're just going to have a patient here who has experienced and managed eye related side e"ects whilst on Blenrep treatment.

Please, if we go to Slide 35.

[Presentation]

## Luke Miels Executive

So with the information you just heard from Dr. Terpos and the patient who has received Blenrep treatment. You can get a sense that Blenrep has the potential to meet unmet needs in second-line multiple myeloma across both standard and heavily pre-treated populations. You can see on this chart, which provides information for each regimen regarding lenalidomide exposure, PFS within the intention-to-treat population, regimen constraints and frequency of administration for both the standard and heavily pretreated populations in second-line multiple myeloma. The Blenrep triplet regimens have the greatest or equal lenalidomide exposure associated with the greatest PFS bene!t.

And the most convenient frequency of administration. So when we look at this, it's anticipated that Blenrep in both academic and community settings will be di"erentiated among the anti-BCMA class. And we expect !lings in all major markets by the end of this year. So if we now go to Slide 37.

Given the complexity of the multiple myeloma market, patient treatment eligibility can be broadly mapped along a scale of age and !tness from young and !t to old and frail. On the left-hand side of the chart, you can see side of care breakdowns, which are listed across our current standard of care as well as future anti-BCMA agents with the bene!t risk pro!le of Blenrep it's anticipated that Blenrep would serve patients regardless of age and !tness levels as well as being available in both academic and community settings. And it's this con!dence in this broad applicability that's given us the insight to further our Blenrep development program in earlier settings, which Tony will discuss on the next slide.

# Tony Wood Executive

We've just discussed Dr. Terpos' data in !rst-line myeloma and data from DREAMM-7 and 8 that showed Blenrep combinations outperformed daratumumab. These compelling data and broad patient eligibility support our investment decision to initiate DREAMM-10, a Phase III study of Blenrep in !rst line multiple myeloma. Please turn to the next slide. Now moving to Ojjaara, which was recently approved for the treatment of myelo!brosis with anemia.

Please turn to Slide 40. Myelo!brosis patients experienced disease hallmarks of splenomegaly, constitutional systems, anemia and thrombocytopenia. Nearly all patients become anemic over time with worsening of anemia associated with decreased overall survival. 1 year after diagnosis, around 50% of patients require red blood cell transfusion, that severely impacts their quality of life. These patients need treatments that extend overall survival and address the spectrum of myelo!brosis manifestations.

Ojjaara is the only JAK inhibitor to address symptoms, spleen response and anemia, and Luke will share with us the recent launch success.

### Luke Miels Executive

Now following the acquisition of Sierra Oncology in 2022, we accelerated commercialization and launched Ojjaara in the U.S. and EU with line agnostic labels. Ojjaara performance has been outstanding, I'm very please to say, delivering the fastest U.S. launch uptake by JAK inhibitor in myelo!brosis out of the !rst 2 quarters post launch. U.S.

share has been signi!cant across both !rst line and second line with market research indicating about 60% of U.S. ACPs anticipating that they'll increase their use within the next 6 months. EU launches have also been successful in the U.K. and Germany, and Japanese approval is anticipated in the second half of 2024. And we're also exploring further indications of the overlap of oncology and in#ammation, with this target and continue to believe in the blockbuster potential of Ojjaara.

Next slide, please. We're now going to talk about Zejula and the impact in ovarian cancer outcomes and promising new data in glioblastoma, which we're very excited about. Next slide, please. Zejula is another one of our key medicines and continues to deliver sustained growth in the !rst-line maintenance setting in ovarian. And we've been able to more than double total sales over the last 5 years in a very competitive environment.

Active surveillance in !rst-line maintenance of ovarian cancer remains high despite evidence supporting the use of PARP inhibition in this setting, particularly within the BRCA wild type population who respond well to chemo. Additionally, alongside anticipated readouts in endometrial, which is RUBY 2 and non-small cell lung cancer, which is the COSTAR lung study. Zejula is also being explored in unmethylated MGMT glioblastoma in which no meaningful treatment improvement has been seen in over 40 years. Clearly, this is very important because with a high unmet need, which is indicated by an alarming 2% 5-year survival rate for glioblastoma patients. Zejula has the properties and the potential to demonstrating full improvement.

And Tony will now take you through the new data. Next slide, please.

### Tony Wood Executive

Zejula has a di"erentiated opportunity in glioblastoma. Unlike other PARP inhibitors, Zejula crosses the blood brain barrier in preclinical studies, indicating a favorable brain tumor penetration. Phase II data just presented at ASCO showed promising improvement in a single-arm study, which showed approximately a 15-month median PFS versus 5 months for historical standard of care. These data give us con!dence to imminently initiate a Phase III supported collaborative study with the Ivy Brain Institute in newly diagnosed MGMT glioblastoma. Zejula will be studied against temozolomide as a standard of care.

Study primary completion is anticipated in 2027.

## Luke Miels Executive

Next, we'll now cover Jemperli and the CD226 axis slides, so if I can go to that slide, please.

While Jemperli's strong foundation is anchored in dMMR endometrial cancer, it's also being explored in colorectal and head and neck cancers. Immuno-oncology has shown transformative outcomes for dMMR endometrial cancers, whilst signi!cant unmet need still remains for the MMRp, the patient subgroup. In colorectal, chemotherapy as a standard of care signi!cantly impacts patients' quality of life. So new treatment options are needed to deliver greater clinical bene!t and the dMMR strati!cation is of clinical signi!cance.

The head and neck cancer clinical improvement is also needed and has not been seen in more than 20 years in the locally advanced setting, while about 85% of patients are PD-L1 positive, the bene!t of an anti PD-1 or PD-L1 therapeutic has not been seen in the earlystage disease. The development of Jemperli across endometrial, colorectal and head and neck gives us con!dence on the potential of this product. If we move to Slide 47. Jemperli's foundation is in !rst-line dMMR endometrial cancer. And the -- in the !rst-line dMMR endometrial cancer, the statistically signi!cant PFS bene!ts in the dMMR MSI high population of the RUBY trial was not reached at 30 months versus 7.7 months of standard of care.

And this is what led to U.S. and EU approval in 2023. If we look on our revenue sense, Jemperli has delivered more than 250% growth year-on-year '23 versus 2024. This has been driven by the unprecedented data, coupled with strong execution on the ground. If we look at the uptake of Jemperli, it's achieved about a 33% new patient share in the U.S.

and more than 35% new patient share in Germany with a strong U.K. performance since the launch in March of this year.

Building upon that !rst-line dMMR success, the RUBY 1 trial is also the only trial to show statistically signi!cant overall survival in an all-comer population with 44.8 months median overall survival versus 28.2 months. The !rst-line indication for all-comers in endometrial has been accepted to FDA priority review with an August PDUFA date, and GSK will also be imminently !ling with the EMA. The impressive data for Jemperli gives us further con!dence in the future combination potential of Jemperli and our B7-H4 ADC endometrial. Jemperli is also being developed in other dMMR tumors, and Tony will walk you through our plans. Next slide, please.

# Tony Wood Executive

Jemperli has indeed been shown to have clinical bene!t in other dMMR-driven tumors, such as rectal cancer. Recent ASCO data from a supported collaborative study with Dr. Cercek from MSK show unprecedented 100% complete clinical response in the 42 patients treated with Jemperli monotherapy. These responses are durable with no evidence of progression. Data from this study provide continued con!dence in our AZUR program in colorectal cancer.

AZUR-1 exposed Jemperli monotherapy and locally advanced unresected setting for dMMR rectal cancer. The study is designed to inform if Jemperli monotherapy could potentially replace chemo and surgery as a standard of care. AZUR-2 exposed Jemperli monotherapy in a Perioperative setting for dMMR colon cancer. This study also lends to Jemperli potentially replacing chemo as a standard of care. Data from AZUR-1 and AZUR-2 are expected beyond 2026 contributing to the more than GBP 2 billion asset ambition for Jemperli.

Let's hear more from Dr. Cercek on the unprecedented !ndings serving as the foundation for

Jemperli development in colorectal cancer.

#### Andrea Cercek Attendee

The idea of the study was to see if we could use dostarlimab alone to potentially replace all 3 treatments that were considered standard of care, so chemotherapy, radiation and surgery. We now have 42 consecutive patients treated with dostarlimab that have had a clinical complete response. So every single person that we've treated, the tumors disappeared completely with just 6 months of dostarlimab. Maybe even the more exciting part of the presentation this year is that we're reporting the durability of responses. And so now we have 24 patients who have had a complete response for more than a year after completing treatment.

It's really never been seen before where just 1 biomarker was measured for de!ciency and 1 drug, dostarlimab, really leads to these types of responses.

So the potential of dostarlimab in Mismatch repair de!cient early stage rectal cancer for our patients is huge. Standard treatments would have signi!cantly altered their quality of life in fertility, sexual dysfunction, bowel and bladder dysfunction, potential for permanent colostomy. None of our patients on trial have needed any of those interventions. This data has really contributed to the AZUR program, both AZUR-1 and AZUR-2 are based on the e\$cacy of dostarlimab in early stage mismatch-repair-de!cient colon and rectal cancer. The most impressive thing here on behalf of GSK is that this study is designed thoughtfully based on our trial, thinking about the patients and the patient outcomes with an endpoint of a clinical complete response and not simply taking patients to surgery because that gets you the answer right away, and that shows how good the drug works.

I think for science, it's incredible and it's rewarding and it's amazing to see these types of responses. But for the patients, it's absolutely life-changing.

#### Tony Wood Executive

These are truly impressive data, and we hope that patients continue to bene!t from Jemperli monotherapy. Beyond dMMR tumors, Jemperli is also being investigated in locally advanced head and neck cancer. JADE-3 is a Phase III trial that builds on development lessons in head and neck cancer and explores Jemperli monotherapy as a new standard of care in a postchemoradiotherapy setting. Two notable trial design elements are important here. Firstly, the selection of a speci!c, newly diagnosed and treatment-naive patient population.

And secondly, a post-cisplatin-based CRT setting, allowing optimal potential for PD-L1 bene!t. Jemperli is additionally being studied in non-small cell lung cancer combination with belrestotug. The Phase III program span for belrestotug was gated and dependent on preliminary, interim and safety data from the Phase II GALAXIES study.

Consistent with the recent iTeos disclosure, interim analysis from this study found that the combination of Jemperli and belrestotug exceeded prede!ned e\$cacy criteria with clinically meaningful tumor reduction in each dose. Data also indicated an acceptable safety pro!le. We expect to present these data in the second half of 2024. As such, GSK and iTeos will imminently initiate the Phase III GALAXIES LUNG-301 study in previously untreated PD-L1

high current or former smokers, with locally advanced unresectable or metastatic non-small cell lung cancer. This is the !rst registrational study for the belrestotug-Jemperli combination.

Several elements provide con!dence in belrestotug in this competitive setting. These are the molecules optimized Fc engagement, greater potency, clinically proven Treg depletion and the proven anti-PD-1 pro!le of dostarlimab as evidenced in our PERLA trial.

Please turn to the next slide. In summary, our Jemperli development program spans multiple solid tumors as either monotherapy or as combination backbone, where we envisage di"erentiated outcomes relative to the class. We are con!dent in Jemperli as an IO backbone and will develop Jemperli proprietary combinations across our portfolio. Moving now to ADCs on the next slide. Please turn to the next slide.

GSK584 is our ADC with best-in-class potential in gynecological malignancies. B7-H4 protein is highly expressed across these malignancies and serves as a key immune checkpoint. Hansoh presented clinical data at ESMO in 2023 showing an ORR of 33% and 27% at 2 di"erent doses in triple negative breast cancer patients in China for this molecule. GSK will develop 584 in novel combinations with proof-of-concept studies initiating later this year. Please turn to the next slide.

GSK227 targeting B7-H3 is our second in-licensed ADC from Hansoh. Antigen expression is broad across numerous tumors with high unmet need and presents exciting development opportunities. Clinical activity disclosed at ASCO in 2023 in small cell lung cancer patents shows a 63.6% ORR for this molecule. This broad clinical activity provides con!dence in monotherapy use in relapsed and refractory disease as well as combinations in earlier settings, particularly with dostarlimab. We believe 227 has the potential to be !rst to market in several solid tumors.

Now handing back to Luke to conclude on Slide 56.

#### Luke Miels Executive

Next slide, please. To conclude, this slide shows peak sales potential for key assets and the material contribution oncology can have to GSK even before we add we hope the relaunch of Blenrep. Ojjaara continues to deliver strong performance with physicians indicating a switch to Ojjaara treatment within the next 6 months, and we will continue with geographic expansion in the near term. Jemperli is a critical backbone of our immuno-oncology development programs and further growth in endometrial cancer with pending regulatory decisions and development beyond dMMR-driven tumors will drive growth. Belrestotug, our TIGIT inhibitor and nelistotug our CD96 inhibitor, and our PVRIG inhibitor can also contribute with doublet and triplet combinations focused in non-small cell and head and neck.

We will also initiate GSK-sponsored clinical trials for our 2 ADCs, GSK227, which is the asset targeting B7-H3, and GSK584, which is the one targeting B7-H4 and our clinical development programs will combine each ADC with proprietary combinations with enormous potential. Finally, Dr. Terpos walked us through the impactful Blenrep data to showcase this important medicine has potential to bene!t patients signi!cantly. And we've excluded Blenrep from our long-term ambitions, but it clearly represents a signi!cant upside opportunity for us, and we

look forward to keeping you updated on the progress of this asset. Turning to the last slide.

As a reminder, here are the forthcoming catalysts that you should monitor to track our progress. Overall, we're very con!dent in delivering our 3 core disease areas in oncology, hematology, gynecologic cancers and emerging tumor types, whether they're through the antibody drug conjugates, immunotherapy or targeted small molecule modalities, these medicines will signi!cantly contribute to delivery of our long-term ambition and continued momentum. So with that, thank you. We'll go back to Nick, and we'll open up to Q&A.

## Nick Stone Executive

Thanks, Luke. So as we move into the broader Q&A session with the team, I just want to remind everyone, if you want to ask a question on Zoom, please raise your hand using the icon in the menu bar and then we'll open your line so that you can ask the question. [Operator Instructions] And we're going to take our !rst question, please, from Mark Purcell at Morgan Stanley. So over to you, please, Mark.

## Mark Purcell Analyst

Yes. So just 2 questions. The !rst one, could you help us understand the competitive landscape for BCMA targeted medicines. There are a number of other approaches out there, which I guess you highlighted in the slides, but if you can compare any other ADCs in development but also CARs, bispeci!cs, et cetera, and just provide some color where Blenrep sits relative to those? And then secondly, in terms of the greater than GBP 3 billion setting, peak sales potential and risk adjusted for Blenrep.

Can you help us understand how signi!cant the second line setting in isolation is relative to the !rst-line ambitions?

## Luke Miels Executive

Thanks, Mark. So I think on the !rst question, if we can go to Nina to cover the competitive landscape, and then I'll comment on the GBP 3 billion-plus ambition.

# Nina Mojas Executive

Yes, sure. Just checking if you can hear me, okay?

Tony Wood Executive

We can hear, Nina.

### Nina Mojas Executive

Yes. Perfect. Okay. I will start. I would also probably ask Dr.

Terpos. I think he's on the call to add his perspective. From the landscape perspective, I think this is something that we continue to remind people. For U.S. speci!c, majority of the patients, about 70% of all the patients are treated in the community setting.

And this is Mark, where your question -- this is relevant for your question, comparing to other BCMA agents. So if we look at bispeci!cs in particularly CAR-Ts these are agents or assets

that are administered in the hospital setting, largely in the academic centers, both because of the administration, but also because of the management of adverse events. So that's the !rst part of the question.

How does it compete, keep in mind, community setting, physicians, it's community physicians who like to keep their patients. These are second line relapsed patients who do not prefer to be sent -- or spend signi!cant amount of time in the hospital and then particularly are not very keen on managing those adverse events through delivering the drugs or supportive care that requires hospitalizations. That's just on the convenience. On the e\$cacy, we have seen the data for CAR-Ts and in second-line setting for bispeci!cs, we have still -- we still haven't seen the data in second line. So we will need to see where it goes.

But comparing the e\$cacy of, BC of Blenrep versus CAR-Ts, we are actually not too far. And then once we see the bispeci!cs, we will see if the e\$cacy that they deliver is going to be worth the process of hospital administration, signi!cant infection risk and management of other adverse events that again requires hospitalizations. I don't know if Dr. Terpos wants to add something as well from his own experience.

#### Evangelos Terpos Executive

I don't know if you hear me also.

#### Nick Stone Executive

We can, Dr. Terpos. Very clearly.

### Evangelos Terpos Executive

Okay. So the anti-BCMA treatment seems to be the fourth pillar of multiple myeloma therapy. And for patients, who have been exposed to both daratumumab and lenalidomide upfront, which is the vast majority of patients in both the U.S. and Europe. We can say that in second line, we don't have a lot of available options, for example, for now if we talk for now what it is available, not o" label, of course.

What it is available in Europe, for example, for a patient who progressed on daratumumab and lenalidomide in the MAYA regimen, then you can see that the only reimbursed let's say, regimens, includes the old fashioned PVd, CellVd, Kd and only in a very, very few countries, including in my opinion, only Germany and with speci!c, let's say, speci!cations in Switzerland and Austria, the cilta-cel can be given. So I think that we have an unmet need here. And the 2 studies, especially that of the belantamab with pomalidomide and dexamethasone seems to cover this unmet need. Just to let you know that especially in Europe, the cilta-cel is available in a vast minority of the patients who are eligible to receive it, even in countries like Germany that is the most in use in Europe country for cilta-cel. And from what I've heard, the vast majority of patients also in United States do not have the possibility to have the CAR-T because they are treated in the -- outside of academic centers.

This is the one thing. But on the other hand, even if you see the e\$cacy, as Nina mentioned, of the belantamab and you compare it with the cilta-cel, which is the second line option that can be given to the patient is not far away. On the other hand, it is much more convenient. It

can be given to intermediate, !t and frail patients that de!nitely is the majority of patients with myeloma, who have not to forget what is the median age of myeloma at diagnosis in our center, for example, is 69 years, in other countries, it's 71 or 72. So the standard myeloma patient at !rst relapse is not the patient that we see several times in clinical study so de!nitely he is not 62 years of age or 64-year of age he is much let's say, more elderly and not eligible for receiving a CAR-T in the vast majority of cases, not only because of age, but mainly because of co-morbidities and frailty.

So I believe that the both combinations will give the opportunity to our patients to have very good therapies. BVd has given the best e\$cacy in patients who have been exposed and are refractory to lenalidomide and also BPd to me o"er a special attention for patients who have been given daratumumab, bear in mind it's especially for those who are refractory to 1 or both of these agents.

I don't say anything about the bis because I want to talk about evidence. I am one of the authors of the guidelines of EHA, for example, for the treatment in myeloma. So I want to talk only based on evidence. We have no data at all for the patients for 1 till 3 paradigms of therapy with bispeci!c targeting BCMA. Although I have to say that from some of the data that are reported during ASCO and EHA for !rst-line therapy seems not to be to me, extremely encouraging, especially for the side e"ect and the safety pro!le and especially the infection rate.

# Luke Miels Executive

Thanks, Dr. Terpos, and Mark I'll just cover your second question very quickly. Look, I think you should see that GBP 3 billion-plus that we communicated a couple of years ago as a base. The bulk of that is the second line setting. And I think what hopefully is coming very clear to you from the experience that Dr.

Terpos has discussed and Nina is after the analogue that we're looking at is CD38 Darzalex in that second-line setting. So you can start to model the scale there. Of course, it's always subject to regulatory interactions and the ultimate !rst-line design that we go through.

# Nick Stone Executive

Thanks, Mark and thanks, Luke. So our next question is going to come from James Gordon at JPMorgan.

# James Gordon Analyst

James Gordon, JPMorgan. First question was just noting you've reintroduced a peak sales forecast, but it isn't yet part of the guidance. The guidance does include some assets that are quite a lot earlier. So just why is that or where might you have the con!dence to add it back in? Is it that you still need more mature OS from DREAMM-8 or more tolerability or something like that.

Why being a bit cautious than some of the other assets where we seem to have quite a lot less data but seem less [Technical Di\$culty]. And then the second question was I have been long a competition of other approaches. So clearly bullish on the TIGIT.

How does this compare in terms of your excitement to other approaches, both your own and competitor approaches. And I know for instance, you've got a TIM3 that I think reports next year that wasn't on the guide or catalyst list. And there's also other people doing it's not just mono-therapies but bispeci!c or even bispeci!c TIGITs combined with TROP-2 ADCs. So could it be that -- if it's a good approach, but actually a bispeci!c approach experts or even combining a bispeci!c with a TROP-2 ADC, it could be even more e\$cacious?

### Luke Miels Executive

Sure, James. Thanks. And I think on the !rst question, essentially, we want to have a few more regulatory interactions, but I hope you get the sense of the amount of time that we've allocated the thoughtfulness that we have spent around how to manage the bene!t risk of Blenrep. So we'll update in the future, all in good time. Hesham, maybe if you could cover James' second question, please.

## Hesham Abdullah Executive

Yes. No, happy to do that. And James, thank you very much for the thoughtful question. I think probably, !rst and foremost, it's important to highlight that we have a number of di"erent immuno-oncology assets that we're currently evaluating or assessing across di"erent tumor types. And you touched on, of course, TIGIT, but also dostarlimab which is our PD-1 inhibitor and then, of course, TIM-3 nivolumab as well.

With that in mind, I'd also like to highlight that there's 2 other assets in that CD22 6Xs beyond TIGIT, which includes CD96, but also, of course, our -- so TIGIT, CD96, and PVRIG as well, AZUR-2. With that in mind, what I would like to highlight is for TIGIT, it is probably when compared to other assets. It is a bit more unique. Of course, it's Fc-enabled. That's one.

Two, we're actually looking at, of course, in this instance, combining it with PD-1 inhibitor dostarlimab which we've actually benchmarked quite well to other leading PD-1s in the class. You may recall, of course, we had the Phase II data from the PERLA study. This was a head-tohead study of dostarlimab plus chemotherapy versus pembro plus chemotherapy in !rst-line non-small cell lung cancer, and it actually demonstrated what appear to be similar levels of clinical activity in the context of response rates, but also encouraging trends for key secondary endpoints that include progression-free survival and overall survival AZUR-2. And the data was previously presented at ESMO most recently in 2023.

With that in mind as AZUR-2, we feel, of course, having us certainly, a TIGIT that is Fc-enabled a really strong PD-1 backbone and then, of course, some preliminary data that's emerging from our Phase II platform study, where we've actually looked to explore di"erent dose levels of TIGIT, speci!cally 3 di"erent dose levels AZUR-2 relative to the benchmark of a PD-1 inhibitor, our own dostarlimab which again has behaved, performed consistently as pembrolizumab that certainly at least at this stage, the data is encouraging. It warrants us moving forward with Phase III investment. But beyond that, we're also thinking more holistically across our portfolio. So you may have heard from the presentation that we also have access to -- now our own B7-H3 antibody drug conjugate, B7-H3 is expressed in nonsmall cancer and we expect to actually be evaluating that as part of di"erent combination regimens.

So you talked about the whole [indiscernible] ADCs may have to play along. I think B7-H3 will also be a key asset in that capacity as AZUR-2. And we'll actually be looking to combine it with these with our TIGIT and our PD-1 inhibitor as well, looking at that relative to, for example, what other competitors may be considering they're evaluating as well. TIM3, we're really positioned, of course, in this post-IO setting. So we have our ongoing Phase III study, which is called COSTAR, looking at the combination of dostarlimab, plus cobolimab, plus docetaxel versus docetaxel plus dostarlimab versus docetaxel.

It's a 3-arm study. It initially began as a Phase II/III trial graduated from Phase II into Phase III based on some prespeci!ed thresholds for clinical activity that were met on certain key surrogate endpoints and the Phase III study is currently ongoing. Again, you may be aware, of course, that TIM3 is expressed in non-small cell lung cancer and certainly is a key primary resistance mechanism to checkpoint blockade and speci!cally PD-1.

And so we think the rationale makes sense from that perspective. And we know that the study graduated from Phase II to Phase III because it met some of the key, at least e\$cacy criteria at that time point. So all in all, what I would say is we're looking at di"erent ways to at least evaluate, assess a number of di"erent agents that we have across our portfolio. They include di"erent IO assets. They include sequencing.

They include combinations with other therapeutic modalities such as antibody drug conjugates, and may include potentially looking at earlier stage of disease, again, all based on data as it continues to emerge and outcomes as well at that point in time.

# Luke Miels Executive

Thanks, Hesham. And I think, James, you've seen with the approach on TIGIT internally that we're very disciplined in terms -- and Hesham made this point several times, very disciplined in terms of looking at clinical pro!le and the evidence before moving. But when we do make a decision to move, we're going to move in a very focused way, but we're going to move with speed when we see what we like. Next question, please, Nick.

# Nick Stone Executive

So our next question is going to be from Matt Weston at UBS.

## Matthew Weston Analyst

Two questions, please. The !rst is on DREAMM-10. And now based on the readout using MRD, approximately when would you expect we'll see a readout of that trial? And then my second question is to Dr. Terpos.

It's about sequencing of drugs. So we now have some great data from Blenrep in second line from DREAMM-7 and DREAMM-8 And now the proposal is take Blenrep into the frontline. But really, we've got no idea what to do with the Blenrep patient after it's been used in the frontline setting. So as a clinician, I'd be really interested as to whether or not if it were positive in frontline, you'd be prepared to use the drug, not knowing what to use next or whether really we should wait for overall survival data from DREAMM-10 before we can really understand the sequencing bene!t of Blenrep in the earlier?

### Can you hear me?

## Tony Wood Executive

Yes, I think we've Dr. Terpos I think what Mark was saying is the [indiscernible]. Over to you, and then we'll come to you Hesham.

# Evangelos Terpos Executive

Can I start? Okay. Matt you are right that if -- and the BCMA agent, especially Belantamab is approved in the !rst line, we don't know exactly what will be the sequencing. But what we discussed previously, it was exactly is happening in the treatment of myeloma, all the drugs are approved in that way. They are going !rst to the 1,000% unmet need, which is the very end of myeloma.

Then they go to the early relapses, 1 to 3 prior lines of therapy, and then they go to !rst line. See what we are talking about today, we are talking for patients who are refractory to daratumumab !rst line, and the options that I o"ered or at least the options that are o"ered to physicians include outside of the U.S., mainly Pom/Vd, the OPTIMISMM study that included no patient who have been exposed, not on refractory, had been exposed to dara CellVd no patient, I think it's 11 patients who have been exposed to dara in the CellVd arm. KD, no patients have been exposed to dara. And of course, we have also the cilta-cel that has now been approved and includes mainly lenalidomide refractory patients and very few who were exposed to dara. So it is di\$cult.

And now we are having the !rst, let's say, very good regimen like [ Bela, Pom, Dex ] which to me, it would be the second-line therapy outside of cilta-cel when it's going to be available, and it's going to be for a minority of my patients. Bela, Pom, Dex which is going to be for these patients, and there are data for these speci!c patients. So unfortunately, it is the same with all the drugs. You see that T cell engagers were licensed in the very end myeloma after the fourth line of therapy and now that we are having studies in !rst line. So what's going to happen next after that we will be obliged to have either the older regimens, dara or isatuximab-based therapies or the CAR-Ts or the bis while we know, for example, the CAR-T cells are not doing so well after BCMA, but this happens at the very end.

Will it be the same if we give Belantamab upfront using it every 2 or 3 months and to give Cilta-cel second line. We don't know if the results will be similar to Belantamab N2+ refractory patients and Cilta-cel. So your question is extremely important, but I don't think that will be any physicians who can give you an answer because, unfortunately, what you described is exactly what we are facing in our clinical prognosis where all the drugs are !rst approved in the very late myeloma and then go slowly to 1 to 3 prior lines of therapy and then to !rst line. And at the time that they are approved at !rst line, the available options at second line, all these data are based on studies that they have not had any patients who have been exposed to the drug that now is on !rst line.

I don't know if I -- I tried to answer your question. I know how di\$cult it is. We don't have any data. The data that we have in the very end-stage myeloma, I don't think that they will be con!rmed in the !rst or second line. So then every time we need to create new data for what's happening with a speci!c combination after a new approved indication.

# Tony Wood Executive

Thanks, Dr. Terpos. Hesham DREAMM-10, please.

# Hesham Abdullah Executive

Yes. No, absolutely. And if it's okay, maybe we'll just to kind of touch on what Dr. Terpos was highlighting AZUR-2 in the question early on, should we wait for survival data before we start moving drugs into frontline. Well, what's interesting is probably, as we look at the existing data for CAR-Ts in second line, we haven't necessarily seen neither of the CAR-Ts actually demonstrated pretty signi!cant improvement in overall survival.

What we have seen, at least in DREAMM-7, is a very narrow miss to demonstrate stat sig OS at the time of the interim PFS analysis, which was positive, of course. So the narrow miss was 5.00012. And so we feel very con!dent that at the time of the next prespeci!ed interim OS analysis for DREAMM-7, we'll be able to demonstrate stat sig OS bene!t. So that's the !rst point. The second, of course, for DREAMM-8.

You see the hazard ratio is 0.77. I expect that to actually get better over time, especially given the duration of response that this drug can demonstrate, Blenrep that is.

And so with more maturity of data and more follow-up, I think you'll see that change over time AZUR-2. Getting back to the question around DREAMM-10, I think everyone is well aware, of course, that there has been a recent advisory committee meeting that was held and convened by the FDA in the U.S. whereby there was overwhelming support, of course, for the adoption, the use of MRD negativity as a surrogate endpoint in multiple myeloma. So with that in mind and with the data and the meta-analysis that were generated on the correlation of MRD to long-term outcomes, we're planning on incorporating this as a co-primary or dual primary end point in DREAMM-10. So both MRD negativity and as well PFS.

I think I would probably also call everyone's attention to the data that Dr. Terpos presented during the presentation, which actually showed at least both in DREAMM-7 and DREAMM-8. In DREAMM-7, more than a twofold increase in MRD negativity rates.

And then in DREAMM-8 actually a !vefold increase in MRD negativity rates. So that certainly gives us a lot of con!dence, hope as we think about DREAMM-10, and the potential for demonstrating that type of improvement. Now again, I'd just like to highlight 2 things. One is we're going to continue, of course, to progress with our current !ling plans globally for the second-line indications, including DREAMM-7 and 8. As Luke had alluded to in the presentation, those !lings are planned for the second half of this year, and we will have !led in all major markets regions by the end of the year as well.

Of course, we've been in ongoing dialogue with health authorities, regulators, and we'll continue to at least get additional updates as we move into, of course, the latter part of this year, and that will certainly also continue to support our evaluation, our assessment of DREAMM-10.

In terms of timings for MRD negativity and when it could potentially readout, again, these are all of course, time to event end types of end points, -- and really depend on extent to follow

up. But what I would say is maybe there is a range in the year probably in the possibility of 2.5 to 3 years that we could be looking at. So by late 2027 or 2028, but again, we'd have to look at and assess and evaluate where the thresholds are set for demonstrating in getting a meaningful improvement in MRD negativity.

### Tony Wood Executive

Great. Thanks, Nick, next question, please.

### Nina Mojas Executive

Yes. So our next question is going to come from Peter Verdult from Citi.

#### Peter Verdult Analyst

Peter Verdult from Citi. Just a few questions, please. Just a follow-on on Matt's question about timelines. I think Hesham at ASCO, you said 3 years, so we're looking at probably a launch of '28, '29. Could you remind us the IP situation on Blenrep given the full start so far, when do you expect or the GSK view, the timelines in terms of major LOEs?

And then just for Dr. Terpos and maybe the GSK team themselves. I mean the discussions at ASCO were almost saying less is more and urging the company to almost explore lower doses given how durable responses have been. And although you've ameliorated the ocular tox, it's still bothersome. So I'll be interested in Dr.

Terpos view about exploring longer dosing intervals, lower doses still, whether there's any appetite to do that GSK?

And then 1 cheeky follow-up just for Tony on the ADCs. I mean, it was clearly a massive theme at ASCO, there's now hundreds in development. [indiscernible] 74 and 73 are clearly hot targets. Every man, woman, dog seems to have one. So can you help just triangulate for us whether you feel you're in the vanguard on these ADC targets or the rear guard?

Is there any indications where GSK could be !rst to market?

### Luke Miels Executive

Thanks, Pete. I'll answer your !rst question very quickly. So 2032 for the primary patent in the U.S., the primary patent. Dr. Terpos, if we can turn to you and then once you've concluded Tony, I'll hand it over to you.

#### Evangelos Terpos Executive

Thank you, Peter. I think that what you mentioned is what I'm investigated. I mean in the !rstline therapy as we have seen my study in combination with lenalidomide and dexamethasone, I checked lower doses like 1.4 and 1.9 milligrams per kilogram given every 8 weeks, as long as the standard dose of 2.5 mg per kilogram, but again, every 8 weeks. So we'll start with that. And we have now 66 patients with a median follow-up of more than 24 months.

I can tell you that we have not only 1 progression. And the majority, if not all the patients, if I am right correct now all the patients receiving now 1.9 milligrams per kilogram every 12

weeks or every 3 months, which -- and the e\$cacy is extremely good, all patients have responded to treatment. Of course, we talk about newly diagnosed patients, but I have to tell you that all my patients in this study have intermediate !t or frail according to the IMWG frailty score.

So there are patients that they -- I mean, they are really -- they are not the !t ones. So we have extremely good results, suggesting that the drug is very well tolerated. The ocular problems that we have with this schedule is very low and the e\$cacy is very high. I think that based on some of the preliminary data that I had, GSK used a di"erent schedule in the DREAMM-8 that to me, it was extremely important, starting from a higher dose 2.5 milligram per kilogram and then 1.9 milligram per kilogram the second site. So they lowered immediately the dose, and they give it every 4 weeks instead of every 3 weeks in the DREAMM-7 because they have recognized early that the e\$cacy probably is the same given the drug every 4 weeks or even every 8 weeks because a good number of patients, I'm not in the position to say how many of them in the DREAMM-8 are in the every 8-week schedule and the e\$cacy is very good.

So I believe that it is a very e\$cacious drug. One thing also that has not been published yet, but I can tell you from the analysis that we've seen is that the higher the dose, the higher the ocular toxicity, the higher probably the response rate. So I think for the relapsed refractory setting, I like the schedule of starting with the 2.5 milligram per kilogram and then to immediately go in lower the dose 1.9 every 4 weeks and then to go from the 1.9 every 8 weeks if the patient has ocular toxicity. And I believe that, Peter, you have right that in the real world, I believe that the majority of the relapsed/refractory patients are going to have after an initial dose having the drug every 8 weeks, for example, if it is with Pom/Dex for every 6 weeks, it is with Velcade and dexamethasone. And in the real world, the drug is going to be given every 2 or 3 months, o"ering very good results to these patients.

# Peter Verdult Analyst

Helpful.

Nick Stone Executive

Tony.

Tony Wood Executive

Can you hear me?

Nick Stone Executive

Yes, clearly.

#### Tony Wood Executive

Great. So just a sort of headline -- as far as the 2 ADCs are concerned, I'd say in the context of H4, very much competitive and in the leading pack for H3, as Luke mentioned earlier, what we're focusing on there is generating di"erentiated data through the platform studies. And then when we have those data in hand, moving aggressively and quickly recognizing the

competitive environment. A couple of things to stress on top of that. Obviously, unlikely that these agents will be administered in the context of a regimen outside of on immunotherapy.

And we're very competitive in the PD-1 and TIGIT spaces as you've already heard and having individual assets, which will allow dose titration to achieve optimal e"ects there as well as potentially optimize pro!les and the cost of growing on position and understanding of Jemperli as a backbone therapy, not only in gynecological cancers, but in lung.

Probably the other thing to sort of emphasize since you asked the question to me is, of course, we'll continue to allocate capital across the portfolio in terms of the principles that you've heard before from Luke and myself, and I was very much focusing on return on investment and the potential to drive long-term growth. So I think we're in great shape. We're certainly in a good position and the decisions we'll take will be on the basis of di"erentiated data in the context of platform and building out on the strength of position we've got in gynecological cancers.

# Nick Stone Executive

Hesham, do you want to add?

# Hesham Abdullah Executive

I just a quick build on what Tony highlighted as AZUR-2. I think !rst and foremost, I would just highlight that one of the elements, of course, that's really important for antibody drug conjugates is really the -- not only the target, but the linker and the payload. And one of the things that we've done at least in terms of looking at B7-H3 and B7-H4 is evaluate and assess our belief in the behavior of the platform itself that we've gotten access to now through HNSCC. And we believe that it behaves very consistently with the leading platforms and the likes of Daiichi Sankyo. So that's one.

Two, actually, combinations are going to be really important. They're going to be very critical for the development of these types of ADCs. And certainly, that includes combinations with in-house assets like dostarlimab, PD-1 combinations with other targeted therapies that may synergize with [indiscernible] the summaries were head and those might include other agents that target DNA damage response.

And then three, of course, existing standard of care. And then three, I would say we built capabilities. We've recruited a lot of great talent that has had experience with antibody drug conjugates, whether it be Daiichi, whether it be at AstraZeneca or other certainly big biopharma, but then also moving with pace. Moving with pace and continuing to assess any potential opportunities as they emerge.

And then !nally, what I would say is strategy matters. I think if everyone recalls, of course, what happened with the PD-1, PD-L1 class, it wasn't always about being !rst. And it's the right strategy, the right development strategy, the right tumor types, the right combinations, the right approach and the right patient segments and biomarkers that will be really critical to the success of antibody drug conjugates. So I just want to highlight that and then just say that stay tuned. Stay tuned.

I think for anyone that knows me knows what I do try to just note things and then you guys can look at them in hindsight and re#ect on whether or not I was right or wrong.

## Tony Wood Executive

Thanks, Hesham. As I need to say some days when I come to work, I think I might have walked into my old Swiss employer or another U.K. company where I spent some time. So -- but I think critically, we've been able to assemble a group of people on the back of this collection of products, as Hesham has said, that have a track record of picking opportunities. And there's a recognition that operating in oncology is di"erent.

Again, the theme of focus, discipline and speed, and that balance is something that we are very quick to emphasize. And again, it's just the tip of the iceberg with the people that you see on the call today in terms of the people that we've been able to assemble to support these assets. So that's very, very exciting. Should we go to the next question, Nick, please?

### Nick Stone Executive

So I'm trying to introduce -- I might have misheard you Tony.

### Tony Wood Executive

One very quick comment to cap o" on Hesham's point there. We've also built signi!cant manufacturing capability associated with Blenrep. And that's going to be an important aspect of indication expansion in this area.

## Luke Miels Executive

Absolutely. Thanks, Tony.

#### Nick Stone Executive

Thanks both. So Emmanuel Papadakis at Deutsche Bank.

#### Emmanuel Papadakis Analyst

Maybe a question on Blenrep. Just you thinking about the sophisticated complexity of Blenrep on the dosing algorithm. One of the virtues of Blenrep's applicability is its ease of use in the community setting. Presumably, you need a well-de!ned dosing algorithm to avoid immunity docs getting lost on complexities and worry about trading over e\$cacy or safety. So if DREAMM-7 and 8 are approved, what are you expecting to be labeled in terms of how they manage those levels and frequency?

And then in DREAMM-10, what are you planning to actually use as the dose regimen? And a quick one on Ojjaara. You don't seem to have any additional clinical development plans. Are you planning or considering a bit combination study? How much of an impact do you think that's going to have on the treatment landscape in the frontline if that combination is approved?

### Luke Miels Executive

Thanks, Emmanuel. I think, Hesham if we can cover the expected label and there's probably a

lead question to that, that will come up, which is pricing. One of the, I guess, the positives of withdrawal is that we can reset pricing in U.S. and Europe. So we'll need to think through that, but it's a nice problem to have.

So Hesham, over to you for dosing expected label.

## Hesham Abdullah Executive

Yes. No, thank you very much, Luke. Emmanuel, a good question. What I would start with and say is that I think what we've probably seen at least from some of the additional analyses that we continue to generate as it's really important to start with the 2.5-milligram dose. So that is really important and critical, especially in the context of a second-line setting where patients are coming in, they have existing disease and getting that depth of response early on for the !rst one to two cycles is quite important.

With that in mind, I think everyone is well aware, of course, that the drug was used at a 2.5 milligram every 3-week schedule at least per protocol within both studies. So I think that will be probably the starting point, right? But there are also toxicity management guidelines that were implemented in each study AZUR-2.

And we're hoping, of course, that at least as we engage the regulators and we share the data, of course, within our submission that being able to manage each individual patient based on those toxicity management guidelines and using the dose reductions the interruptions as a means of guidance will be important. This is not new. It's not new to Blenrep, it's not new in oncology. It's been done across multiple assets before where you dose each individual patient based on their level of tolerability to the drug. And you use, of course, the side e"ects that they're experiencing as a means of actually titrating the dose down, delaying it and so forth.

So again, based on some of the data that we're seeing within the study, I think -- and use probably observed from the patient AZUR-2, dosing it every 6 weeks, dosing it every 8 weeks. Those are things, certainly, again, guided by the individual patient experience, are things to think about or consider in that context.

# Tony Wood Executive

Thanks, Hesham. And Nina, if you could just cover the LCM thoughts for Ojjaara quickly, and we'll go to the next question.

### Nina Mojas Executive

Yes, de!nitely. So when we licensed the asset, we actually had some plans for combination therapies and combination assets that have been in development in myelo!brosis. Unfortunately, as for the last 10 years, it has been graveyard of drug development and many of those potential partners fell o". So navitoclax is not a candidate anymore. We still have to see what's going to happen with the BET inhibitor pelabresib.

Is this going to cross the regulatory line or not. If it does, there potentially is a space for the combination because both ruxolitinib and pelabresib are myelosuppressive. So potentially causing even more anemia and thrombocytopenia than the individual agents on their own

and momelotinib would be a very good combination partner. But we !rst need to see what happens with pelabresib. Beyond myelo!brosis, we are looking at additional indications where momelotinib could have a very interesting role and mode of action would !t that gap, but we will announce once we initiate those studies, we will start talking about it at that point.

## Tony Wood Executive

Super. Thanks, Nina. Nick?

## Nick Stone Executive

So we're going to take our next question from Graham Parry at Bank of America.

## Graham Parry Analyst

So a quick question on DREAMM-10. It looks from the slide that, that's powered for superiority. I just wondered, is there a non-inferiority test in the design. There was like just going to be a straight shoot out where you need to show superiority?

And then secondly, just regarding the opportunity for Blenrep and most KOL feedback has been that they would prefer CAR-T if it's available in a large treatment center, but to your point, 70% of patients around in the community setting. So could you just talk there to the practical management of liaising with ophthalmologists for managing the eye toxicity? And within that setting, do you still think it's going to be more frail patients that would be getting this. So perhaps just help sort of narrow down that target population even more roughly what percentage of the second-line myeloma patients we're talking about that.

# Nick Stone Executive

Great. Thanks, Graham. Hesham, if you could please take the DREAMM-10. And then Nina, you've done a lot of work in terms of the pathways in the U.S. And then, Graham, if I could just add, if you cover that, Graham, I might just build on your question.

If we get asked Dr. Terpos at the end, if you had a patient in front of you that you were looking to initiate on this treatment and they raised ocular complications, how would you explain that in layman's language to that individual around your treatment strategy and how you're going to manage that? So on Hesham you !rst and Nina and then if we could as Dr. Terpos.

## Hesham Abdullah Executive

No, happy to. Thank you, Luke. So !rst and foremost, just in terms of what the potential design of DREAMM-10 could look like from a statistical analysis perspective, I would just start o" by saying it's been great to see, of course, the emergence of a number of di"erent therapeutic modalities recently in multiple myeloma for patients. That is important. I think we have to acknowledge that just in terms of providing treatment options.

But with that in mind, in order to meet the -- to move -- continue to move the !eld forward, we have to also take into account that we need to provide at least potential therapeutic options that actually provide patients with a step-change in treatment outcomes and the potential for better therapeutic bene!t. So if anything, the DREAMM-10 study design will be directly certainly looking at or focusing on demonstrating superiority to an existing standard of care

regimen in frontline multiple myeloma.

I think the DREAMM-7 data gives us a lot of con!dence in that, I think if you look at all of the di"erent outcomes in the study, whether it be the primary outcome of the study PFS, with a median of a little over 36 months versus 13 months on the daratumumab based arm. If you look at the key secondary outcomes, duration of response, depth at response and certainly also, of course, overall survival, which is still preliminary at this point in time. They all give us a lot of con!dence in what the DREAMM-10 outcome could look like, but more speci!cally, of course, in demonstrating superiority in that regard. And we have to certainly acknowledge that as you look at the number of di"erent at least existing therapeutic modalities that are available to patients that target BCMA, some have limitations in terms of their side e"ect pro!le. We've talked about, of course, the CAR-Ts, the potential for risk of early death, especially with bridging therapies and so forth.

And there was even an advisory committee meeting that was held around that for both assets. We see the infection rates. Nina spoke to those as well, too, with bispeci!cs. Both, of course, require hospitalization, and they're not available to patients in the community setting. So that's actually where 70% to 80% of multiple myeloma patients go, and hence, that's where the unmet need currently exists as well, AZUR-2.

And of course, that's beyond what Tony had around the investments that we're making in manufacturing, but we have, of course, CAR-Ts limited by manufacturing and supply chain challenges as well, too.

The other piece I just want to touch on was actually around the patient -- the types of patients and Dr. Terpos will touch on this better than I can, of course. But I would just like to highlight that we've seen it at ASCO data on subgroups presented from DREAMM-7 and DREAMM-8. So if we wanted to talk about how this drug works in which subgroup of patients, this drug works, actually works in everyone. And thankfully, it's able to provide a bene!t, meaningful bene!t to patients that are higher risk, patients that are standard risk, patients with extramedullary disease, patients that have received prior lenalidomide, lenalidomide refractory, patients that have received prior dara and DREAMM-8 AZUR-2.

And I think that's really important. There was one slide that Luke presented during the presentation that shows which types of patients to actually Blenrep would actually be good for.

And certainly, what you can see is probably all types of second-line patients, irrespective of number of prior lines of therapy, irrespective of risk and irrespective of !tness as well, too.

## Nick Stone Executive

Nina, and then we'll come to Dr. Terpos.

# Nina Mojas Executive

Yes. So very brie#y, a lot will really depend on the label and the REMS or no REMS or REMS requirements. If you remember our !rst Blenrep launch in the U.S., the REMS requirement was quite stringent and challenging de!nitely. So what will be the requirement in the end will

determine to which extent and how physicians hematologists need to engage with eye care professional. Is it going to be ophthalmology speci!cally or it's going to be potentially optometrist?

How frequently and for how many infusions that interaction needs to happen? All of that will be quite critical and will determine to which -- how much of pain or e"ort physician will need to go through to initiate patients successfully.

What we do know in the meantime, because now we are talking after having hundreds and thousands of patients treated versus 3, 4 years ago when we launched when it was dozens patients of treated is -- what we know is that no patient went blind, no patient lost their eyes, no patient died because of ocular adverse events unlike many of the other therapies that you are talking about. And what we do know also is that many physicians after treating more than one patient, they start to recognize how to treat the patients and they start to be able to manage those ocular eye-related side e"ects on their own. And I'm not sure that there is anyone better to describe that than Dr. Terpos, who has a lot of experience with that. So I will ask him to also answer the question.

# Evangelos Terpos Executive

Yes. Thank you. I think that you touch now one of the most important aspects of belantamab. I believe that the ocular toxicity, although as Nina mentioned, is something that cannot kill you or nobody was blinded because of belantamab mafodotin. It is a toxicity that may create some problems only when the patient hear that you may have some eye problems.

So when you have a patient in front of you, because that was the question, you have to explain to him what he has to -- let's say, to expect from belantamab, not only of the e\$cacy, of course, that we all know, it's very easy to understand, but also of the safety. And the ocular problems are also severe in the majority of the patients. The majority of the patients may have a gritty dye, a sore eye maybe some pain sometimes. But I mainly focus on the number of patients that they may have a problem in their daily activities.

If the patient cannot treat, cannot see the tablet or the smartphone, cannot drive or they have problems in seeing television, especially at night, these are real important problems. And that's why one of my main intention is to manage to make the drug ophthalmology free, let's say, if possible. And in order to do that, in our study, we have a randomization between the reduction and the handling of the drug based only in the ophthalmology assessment. And in the Group B, we have both the ophthalmology assessment and the OSDI questionnaire, the !rst 5 questions are describing symptoms while the other 4, they describe activities of daily living like reading, watching the television or reading the tablet and the smartphone or driving. And I can tell you that in the dose that we used in the newly diagnosed multiplemyeloma with the 1.9 milligrams per kilogram every 8 weeks, there was less than 5% of grade of more than 4 hours, as we said, during the last 5 days, problems in the daily activities.

And this is the time that you have to stop the drug and then to restart when this has totally recovered. I want to tell you that we have several patients with the ophthalmology grading to keratopathy, then they have almost no problems at all. And until now, we -- according to this evaluation, we had to reduce or to stop the drug administration. So I believe that we will be

very soon in the position that we can say that for the vast majority of the physicians possibly for -- 1, 2 or 3 cycles, the most we may have an ophthalmology evaluation because the physicians needs to be secure for what they are doing.

And then based on the questionnaire, we are going to provide a very good tool, the anamnestic tool in order to drive the decisions. Don't forget that we had initially bortezomib, for example, many years before with the peripheral neuropathy that we gave it twice per week, and then we ended up with once per week and the patients had electromyograms and everything, going to neurologist for the peripheral neuropathy. And now, of course, this peripheral neuropathy is very well managed by the hematologist. And I believe that this is also one of my tasks to provide the tool in the hematologist in order not to need the ophthalmologist or at least to need it -- to need the ophthalmologist very rarely. One more thing that I want to focus on is that seen -- now than 300 patients under belantamab, one, especially the newly diagnosed patients, we have seen that there is ophthalmology - ophthalmological problems in a very high frequency in these patients.

And they're talking about newly diagnosed because someone can tell you that the relapsed refractory patients have received probably a lot of dexamethasone that create these problems. And this main problem is cataract. So initially, I have seen that almost all my patients, I mean, the elderly patients had cataract in the study. And I wanted to check, let's say, what is the incidence of cataract in the real -- I mean, in the healthy individuals. And we've seen that above the age of 70, it was like between 65% to 75%, the majority of the epidemiological studies.

And the cataract is a problem because why it is a problem because with keratopathy Grade 1, if you have cataract Grade 1 or 2, you may have no problems. You have no blurred vision, nothing there. But if you have keratopathy Grade 1 in a cataract Grade 3 and 4, then you may have blurred vision and reduction in your vision acuity.

And I think that this is something that we have to take into consideration when we talk about ophthalmological toxicity. The toxicity that the Blenrep is creating is reversible in more than 90% of the patients within 1 month of treatment. That's why given the drug every 8 weeks, for example, or even every 6 weeks after the initial, but then you can have very good results. Another thing -- another important issue is that we are doing in our study in the newly diagnosed, but I didn't see it yet in the DREAMM-7 and 8 is that when we describe the number of patients they have an event especially ocular adverse event, then even if the patient had a keratopathy of Grade 2 or 3, let's say, during the !rst site, another in the future, then this is described as one event. I would like to see what we are having in our newly diagnosed studies, the number of ophthalmology visits with problems, then you can realize there but the number of patients who continue to have a problem probably after 1 event may be 0 after or it is may be extremely less.

So in order to conclude, I believe that we have ophthalmology toxicity of belantamab mafodotin which is totally manageable, is totally reversible, very fast. And that's why the administration every 6 to 8 weeks is extremely easy to happen. And my task, one of the my task now is to provide anamnestic tool to the physicians in order to make them ophthalmology free. And I believe that we will make it, and we will transform belantamab, like bortezomib that the physicians can do it after some time, of course, they do all the reductions and the alterations in the administration of the drug by themselves.

## Tony Wood Executive

Fantastic. Thanks, Dr. Terpos. I think a very practical outline and something that's going to be utilized by community-based physicians. Nick, go to the next question, please.

## Nick Stone Executive

Yes, so we've got 3 questions left. So I'm going to come to Richard Parkes at BNP Paribas.

## Tony Wood Executive

So over to you, please. We don't have Richard. Maybe come back to Richard.

## Nick Stone Executive

So we'll take that -- so we'll take Navid Malik from TLSD.

## Unknown Analyst Analyst

Yes, Navid Malik from Life Sciences Division. Quick couple of questions. On Zejula in unmethylated MGMT GBM patients. Can you tell us in the Phase II study, how many IDH1 mutations that were in treatment versus the historical control? And I'm kind of intrigued as to why you're not necessarily looking right now anyway at the MGMT methylated patients who could be evaluated in a separate trial?

And the second question on the Blenrep, for intermittent and low dosing, do you think that there's a possibility, although I don't think this is seen right now, but is there a possibility you could introduce some degree of resistance or refractory to elements because obviously you're not giving the dose that consistent where you're taking the patients o" once they see these ocular side e"ects.

#### Tony Wood Executive

Sure. Thanks, Navid. I think on the Zejula unmethylated population, Hesham, if you cover that. And then Dr. Terpos, if we can just come back to you in terms of your thoughts of this, again, this resistance question.

## Hesham Abdullah Executive

Well, yes, let me start o" !rst just about the -- going after the unmethylated patient population and speci!cally of course I think everyone's well aware that this is an area of key unmet medical need and typically outcomes tend to be even worse in terms of prognosis. So why did we evaluate this patient population? That's really the reason, of course, that Dr. [indiscernible] and I had actually assessed them in their study. So that's one.

Two, I think probably also just highlight that IDH mutations are typically of quite low prevalence even in GBM as AZUR-2. So with that in mind, we could certainly look into how many patients there may have been, but expect to be very few, if any, that were part of this cohort that was treated in the investigator-sponsored trial AZUR-2. One thing to just highlight speci!cally regarding your second question around resistance, of course, and Dr. Terpos will probably touch on this a little bit.

I think as of now, at least and based on the data that currently exists in the !eld, we're not necessarily seeing that there's any BCMA antigen loss that's happening. Actually, that's not the case. And what I would also highlight is the discontinuation rate actually due to the eyerelated side e"ects is actually rather low in both DREAMM-7 and 8. So it's actually less than 10% in both studies AZUR-2. So it's not necessarily why the patients are coming o" treatment.

But Dr. Terpos could certainly touch on the resistance question.

# Evangelos Terpos Executive

The recent BCMA seems to be extremely interesting. I mean in general, the resistant has 2 important pathways. The one pathway is the reduction in the BCMA expression in the surface of the plasma cell that we believe that it was the main. But it seems that this is not the main and the critical point of the resistance. The critical point seems to be the BCMA, let's say, the change in the form of the BCMA in the surface of the myeloma cell in order the antibody cannot bind to its binding position.

So there is a mutation there that makes the antibody not to bind in its position, and that's why we have the resistance. And this is not only with the belantamab, it is with teclistamab, with elranatamab it has been shown, especially by the work of Nizar Bahlis from Calgary several times.

So I don't think that if you give the drug every 6 or every 8 months, this is going to increase the resistance on the contrary. And even the clinical data suggest if this happened as the majority of the patients will have, let's say, a bigger interval between the administration, they would have worse results, which is not happening. So I believe that -- and that's why you also when you go from the one anti-BCMA agent to the other, the other can work that's why I don't believe that it is lower expression of the BCMA that creates the -- that makes the di"erence. So probably, they are the mutation stage that creates the di"erence. And that's why probably after belantamab, another anti-BCMA based regimen for example, teclistamab may work as we have seen that it can work at a lower, of course rate of response, but it can work.

So to me, I don't believe that if we give the drug at intervals of 6 or 8 weeks, this will create any problems in the refractoriness of the disease or the resistance to that, maybe even the opposite.

# Tony Wood Executive

Thank you Okay. So I think we're up to the last question, do we just Peter Welford.

# Peter Welford Analyst

Just 2 quick ones. Firstly, just coming back to the DREAMM-10 design, if I can. I know you say plus together with standard of care. Just curious on your thoughts, and I imagine you've not yet determined this, but what the standard of care would be? And I guess most relevant is DARZALEX potentially being considered, i.e., a second, I guess, antibody-based?

Or will this most de!nitely not be combined with the DARZALEX regimen in the !rst line?

And then secondly, just coming to TIGIT. You've talked about the Phase II, obviously triggering the go decision for Phase III and being very disciplined on this. I wonder if you can just give us a bit more insights in terms of, !rstly, is it based on response rates? Or do you have any sort of measure of long-term sort of follow-up in terms of duration of response and then early survival curves in the Phase II? And secondly, is there any with regards to toxicity, I think there's some in the !eld who have seen incremental toxicity when they're combining the 2 IO agents.

Just if you could give any sort of comment at all on what you see with regards to the tolerability of your Jemperli-belrestotug, that would be great.

# Tony Wood Executive

Fantastic. Thanks, Peter. I think, Hesham, both of those to you and then we'll go to...

# Hesham Abdullah Executive

Thank you. So I'll start o" maybe with the !rst question really around the choice of the control arm, regimen and DREAMM-10. And what I would say is we're -- like I mentioned this or touched on it earlier, we're planning on looking at or evaluating what is a CD38-based regimen in frontline as a control arm. So you look at, for example, the MAIA study, which included, of course, DRD, but you also look at, for example, some of the recent data that's been emerging, including data from the MRAS study with isatuximab as well. Again, I would say that there's maybe di"erent patient populations.

We know that the triplet versus quadruplet kind of based approach also has di"erent tradeo"s at least for such a control arm with regards to potentially toxicity as well, AZUR-2. But what I would say is we're de!nitely going to be looking at a CD38-based regimen. And based on the DREAMM-7 data, I think you can get a sense that certainly a DAR-based regimen, at least for a sponsored GSK study, would potentially be a key one to consider as a control arm.

It's not to say that we wouldn't evaluate at least through other mechanisms, generating data with quadruplets or generating data that compares us to quadruplets. That is also an option that we will consider and evaluate and assess as well, too.

The second question, speci!cally around TIGIT and the data that we've used at this time, preliminary data that we've used from an interim analysis from our ongoing randomized platform study. It's actually, I would say, probably a combination of di"erent surrogates that we're evaluating. We're assessing. Of course, the data is continuing to mature over time. But it is certainly looking at a combination of response rates, looking at also preliminary at least duration of response data but also depth of response through molecular response and circulating tumor DNA data AZUR-2.

So it's a combination of all 3. And again, we're going to continue to follow that data over time as it matures. And I would just highlight that, of course, we anticipate presenting that data at a future scienti!c congress as well, AZUR-2.

And to note, at least for the Phase III study, we have appropriate gating criteria that we've built

into it to make sure that we continually assess, of course, the data that's emerging from the platform trial relative to also any measures that we've included in the Phase III study as well, AZUR-2.

# Tony Wood Executive

Thanks, Richard. Look, I think with that, we'll conclude. I think if you look at this from a specialist perspective, or a generous perspective, the sense of progress that we're making in this very focused and disciplined fashion, hopefully, is apparent and justi!ed your time today in joining us, and also a sense of the team behind this collection of assets. I'd also like to thank Dr. Terpos for joining us today out of his busy schedule.

We're very grateful for the time that you've taken to inform people with an interest in the company.

So thank you, and thank you to everyone who today and appreciate the thoughtfulness of your questions in the time. Thank you.