Basilea Pharmaceutica AG (BSLN) Earnings Call Transcript & Summary

Ladies and gentlemen, welcome to Basilea Pharmaceutica's Full Year Results 2019 Conference Call and Live Webcast. I'm Alice, the Chorus Call operator. [Operator Instructions]. And the conference is being recorded. The presentation will be followed by a Q&A session. [Operator Instructions]. The conference must not be recorded for publication or broadcast. At this time, it's my pleasure to hand over to David Veitch, Chief Executive Officer. Please go ahead, sir.

Thank you. Hello. This is David Veitch, CEO of Basilea. I would like to welcome you all to our conference call and webcast, reviewing our financial results and key achievements for 2019 and discussing our upcoming milestones and financial guidance for 2020. I would like also to mention that this call contains forward-looking statements. Joining me on our call today are Adesh Kaul, our Chief Financial Officer; and Dr. Marc Engelhardt, our Chief Medical Officer. This morning, we issued a press release and our financial report on the results for the financial year 2019. These documents are available on our website at basilea.com. For those on the call who are less familiar with Basilea, we focus on the research, development and commercialization of innovative medicines that address the medical challenges in the therapeutic areas of oncology and infectious diseases. We have a proven track record of progressing brands from research through clinical development to the market. We have successfully brought 2 anti-infective brands to the market: our antifungal, Cresemba; and Zevtera, our broad spectrum MRSA active antibiotic. We have oncology assets in clinical development, and we have a number of oncology and anti-infective assets in preclinical development. I would first like to provide a brief summary of our key achievements in 2019. We had a strong year in 2019. We achieved important financial goals, and we continue to make great progress launching our 2 marketed brands, Cresemba and Zevtera, around the world. During 2019, our commercial partners doubled the number of Cresemba launched countries. Cresemba is now marketed in more than 40 countries worldwide. Our total revenue increased CHF 134.4 million. This includes a significant revenue increase from Cresemba and Zevtera by 39% year-on-year to CHF 114.3 million. This largely reflects the end market sales growth we're seeing around the world. Due to the increase in revenues and management of our operating expenses, we improved our operating results for 2019 by 29% compared to 2018. As a result of increasing cash flow from our revenues and the management of our cost base, we continued to reduce our net cash consumption year-on-year, resulting in a solid year-end cash position of CHF 161 million. This provides us with the necessary flexibility to continue moving forward to our next potential value inflection milestones in 2020 and beyond. We also made significant progress in our clinical stage assets. For our FGFR kinase inhibitor, derazantinib, we initiated a Phase I/II study in patients with urothelial cancer, atezolizumab therapy in combination with immunotherapy. This study is called FIDES-02. Early in 2019, we reported positive interim results from the FIDES-01 study, a potentially registrational Phase II study with derazantinib in patients with iCCA, or intrahepatic cholangiocarcinoma, and these tumors harbor FGFR2 gene fusions. We subsequently expanded FIDES-01 into iCCA patients with other FGFR2 genetic aberrations with the aim of further strengthening the differentiation of a compound. For our tumor checkpoint controller, lisavanbulin, based on data readouts on 2 early stage studies with the IV and oral formulation in patients with glioblastoma, we decided to move into a targeted biomarker-driven Phase II study with the oral formulation of lisavanbulin in patients with recurrent glioblastoma. Finally, we reported positive top line results from our antibiotic ceftobiprole from a Phase III study in patients with complicated bacterial skin infections, or ABSSSI. This is the first of 2 Phase III studies required for potentially gaining regulatory approval in the U.S., which is commercially the most important market for ceftobiprole. Adesh is now going to give an update on our commercial progress and present more detailed financial highlights for the financial year 2019 as well as provide our financial guidance for 2020. And then Marc will provide you with more detailed information on the progress of our most advanced development programs. I'll now hand over to Adesh.

Thank you, David. In 2019, together with our partners, we continued to make significant progress in the commercialization of our 2 hospital anti-infective brands, Cresemba and Zevtera. The most current in-market sales numbers available for Cresemba show that in the 12-month period ending September 2019, the global in-market sales of Cresemba grew by 32% year-on-year to approximately USD 190 million. In the U.S., our partner Astellas reported Cresemba sales for January to December 2019 of USD 146 million, which is a 28% growth year-on-year. The sales performance is not only driven by a continued strong sales uptake in the U.S., but also by strong sales in markets outside of the U.S. The Cresemba sales in Europe were particularly positive, which was reflected by 2 sales milestones in the total amount of USD 12 million being triggered in 2019. The strong growth of Cresemba sales is expected to continue over the coming years as we expect our partners to launch Cresemba in more and more countries. At year-end 2021, we anticipate that Cresemba will have been launched in about 60 countries. Partnerships continue to play an important role in the execution of our global commercialization strategy and provide a strong basis for future revenue growth. Our partners for Cresemba include Pfizer for most of Europe, China and Asia Pacific, and Astellas for the U.S. In addition, we have strong regional partners for Zevtera and Cresemba in other territories. All in all, our partnerships for Cresemba and Zevtera cover more than 100 countries worldwide. In 2019, new important Cresemba launch countries included Canada, for instance, and Singapore as the first country in the Asia Pacific region. Basilea participates in the commercial success of Cresemba and Zevtera through royalties or a transfer price structure. In addition, we already received around USD 250 million in upfront and milestone payments, and could realize up to an additional USD 1.1 billion in potential future regulatory and sales milestone payments from our partnerships. Moving on to financials. I will highlight some of the key financial figures that were published in today's press release and in more detail in the full year report. I'd like to mention that all the figures that I will refer to are in Swiss francs. We are very pleased with our financial performance in 2019. We did beat our guidance, both on revenues and operating results. Deferred and non-deferred revenue contributions from our 2 marketed brands, Cresemba and Zevtera, together increased by 39% to CHF 114.3 million in 2019. Most importantly, non-deferred revenue from Cresemba and Zevtera increased by 36% to CHF 68.8 million, reflecting the strong in-market sales performance reported by our partners. Other revenue, mainly consisting of R&D reimbursements from BARDA, decreased CHF 6.7 million, in line with the lower expenses for the ceftobiprole development program as the first of 2 Phase III studies were successfully completed in 2019. We completed the Toctino-related deferred revenue recognition in 2018, which is why there is no corresponding revenue contribution reported in 2019. In spite of the approximately CHF 30 million reduction from lower Toctino-related revenue and other reimbursements, total revenue increased from CHF 132.6 million to CHF 134.4 million in 2019. For 2020, we anticipate that the non-deferred revenue contributions from Cresemba and Zevtera will continue to grow at a healthy double-digit rate to CHF 77 million to CHF 87 million, in line with the anticipated strong commoditization progress of our partners, especially related to Cresemba. Deferred revenue contributions from Cresemba and Zevtera are expected to decrease to CHF 33 million as we complete, in the course of 2020, the deferred revenue recognition of the Pfizer upfront payment and the Astellas upfront development and regulatory milestone payments received in previous years. In other words, our Cresemba and Zevtera related revenue mix is moving increasingly to its non-deferred revenues, which more directly correlate with the in-market sales and provide near-term cash flows. Non-deferred revenues are expected to reach between 70% to 72% of total Cresemba and Zevtera related revenues in 2020. For the breakdown of the deferred revenue in 2020, about CHF 21 million are expected to be booked in product revenue and about CHF 12 million in contract revenue. We continue to carefully manage our expenses. This is reflected in our flat operating expenses, that means R&D and SG&A expenses, 2019 versus 2018. We expect to keep our R&D and SG&A expenses at a stable level also in 2020. Cost of products sold are influenced by a number of factors. Generally, it correlates with the volume of product that we delivered to our partners. However, as we are still in the launch phase, and at the same time, transitioning stepwise responsibility for supply to Pfizer for their territory, there are some one-off effects that impact our cost of products sold. Once the transfer is completed in 2020 or 2021, our Cresemba revenue mix is expected to move more to its royalties and milestones. This and increasing economies of scale will result in increasing gross profit margins forward-looking. Summarizing our guidance for 2020, we anticipate a continued strong double-digit growth of the non-deferred revenue contributions of Cresemba and Zevtera to CHF 77 million to CHF 87 million, as a result of the expected strong in-market sales growth. The total deferred and non-deferred Cresemba and Zevtera related revenues are expected at CHF 110 million to CHF 120 million. As we continue to carefully manage our expenses, we expect to further reduce our net cash consumption and to report a strong cash position of CHF 100 million to CHF 110 million at the end of 2020. I will now hand over to Marc for the clinical development update.

Thank you, Adesh. Let me continue further with our antibiotic ceftobiprole. In Europe and several markets outside of Europe, ceftobiprole's approved for the treatment of community and hospital acquired pneumonia, as marketed in most countries under the brand name Zevtera. One of our key priorities for ceftobiprole is to gain access to the U.S. market, which is by far the most important country for the commercialization of branded hospital antibiotics and is estimated to account for up to 90% for anti-MRSA treatment such as [indiscernible]. Based on special protocol assessment agreements with the U.S. FDA, 2 successful cross-supportive Phase III studies are necessary for registration in the U.S. Our Phase III program for ceftobiprole into its 1 study in acute bacterial skin and skin structure infections, and 1 study in Staphylococcus aureus bacteremia or blood stream infections. The program is funded up to approximately 70% by BARDA. This allows us to advance the development of ceftobiprole for the U.S. market in a cost-effective way. In 2019, we reported positive top line results from the first of the 2 studies, the so-called target study or Phase III study in patients with skin infections. The second Phase III study in Staphylococcus aureus bacteremia is called ERADICATE. It is well on track and is expected to report top line results as planned in the second half of 2021. If the bacteremia study is also positive, Basilea planned to submit a new drug application to the U.S. FDA. As ceftobiprole designated a Qualified Infectious Disease Product by the FDA for these indications. If approved, ceftobiprole will be eligible to receive 10 years of market exclusivity in the U.S. from the date of approval. TARGET was a randomized double-blind Phase III non-inferiority study and enrolled 679 patients. Patients received either ceftobiprole, given intravenously 3 times daily, or the comparator regimen of twice-daily intravenous vancomycin plus aztreonam. In summary, ceftobiprole was non-inferior to vancomycin plus aztreonam in this study. And the key endpoints for the FDA and Europe were both met. Ceftobiprole met the prespecified primary endpoint of early clinical response at 48 to 72 hours after start of study drug administration in the intent-to-treat population, which is the key endpoint according to the FDA guidance for the U.S. Ceftobiprole also met the prespecified secondary endpoints of investigator-assessed clinical success at the test-of-cure visit, 15 to 22 days after randomization. This is the key endpoint for the EMA in Europe. Now moving on to oncology. Our lead oncology drug candidate is derazantinib, which we in-licensed from ArQule, which is now a wholly-owned subsidiary of Merck. Derazantinib is a targeted, only available small molecule inhibitor of the fibroblast growth factor receptor, or FGFR, family of kinases. FGFR genetic aberrations, for example, gene fusions, mutations or amplifications, has been identified as potentially important therapeutic targets for various concepts, including intrahepatic cholangiocarcinoma or iCCA, and urothelial, gastric, breast and lung cancers. Derazantinib also inhibits the colony-stimulating factor-1-receptor, or CSF1R, and the vast [ land of fuel ] growth factor receptor 2 of FGFR2 kinases. CSF1R is an important target in the modulation of the tumor-immune microenvironment. The inhibition of CSF1R by derazantinib seems to be a unique feature for derazantinib compared to other FGFR inhibitors. FGFR2 is known as a therapeutic target in the anti-angiogenic treatment in multiple cancers including gastric cancer. Our development strategy focuses on achieving differentiation over other FGFR kinase inhibitors by leveraging the unique properties of derazantinib. Key differentiation factors for derazantinib included unique kinase inhibition profile and its clinical safety profile. [indiscernible] clinical development program for derazantinib currently comprises 3 studies. 2 of them, FIDES-01 and FIDES-02, are ongoing in iCCA and in urothelial cancer. And we are planning to start a third study, FIDES-03 in gastric cancer, in the third quarter of 2020. Crystal structures indicated that the improved CSF1R inhibition activity of derazantinib versus other FGFR kinase inhibitors can be explained by a better fit of derazantinib into the active side of CSF1R. Other FGFR kinase inhibitors, such as the approved FGFR kinase inhibitor, erdafitinib, have different chemical structures and may not fit as well into the active site. The CSF1R inhibition may have been important in the treatment of urothelial cancer, but may also have a broader utility to support combination studies with immunotherapy and other cancer types. Preclinical data has shown that tumor macrophage modulation through CSF1R blockade may render tumors more responsive to T-cell checkpoint immunotherapy, including approaches targeting PD-L1 and PD-1. CSF1R kinase inhibition may thereby improve the susceptibility of tumors to immunotherapy. Experiments with mouse bone marrow derived macrophage support that derazantinib modulates CSF1R kinase activity and clinically achieved the concentrations in vivo. Basilea has entered into a clinical supply agreement with Roche for atezolizumab, or Tecentriq, a PD-L1 checkpoint inhibitor, to explore this immunotherapy combination in patients with urothelial cancer and gastric cancer. In urothelial cancer, patients' FGFR genomic abnormalities sweetly show low PD-L1 expression, which has been associated with reduced response to immunotherapy; therefore, derazantinib as a single agent and combined with PD-L1 inhibitors may address several oncogenic mechanisms and provide a new treatment paradigm. Another pillar in our differentiation strategy of derazantinib to other FGFR kinase inhibitors is the safety profile, where derazantinib shows some of the FGFR kinase inhibitor class effects, but also clear differences with a low occurrence of retinal events neurotoxicity, hand-foot syndrome and stomatitis. Such differences are relevant for patients, as these side effects may compromise the patient's quality of life and have been shown a result in treatment discontinuation. In January 2019, we reported encouraging interim results from the registrational Phase II study called FIDES-01 in the second-line treatment of FGFR2 fusion positive iCCA. Top line results for this cohort are expected in the second half of 2020. In addition, we have expanded the FIDES-01 study in June 2019 with a new cohort of ICCA patients with FGFR2 gene mutations or amplifications in their tumors. Through this new cohort, we intend to further define the full therapeutic potential of derazantinib in patients with iCCA. Interim data from the second cohort are also expected in the second half of 2020. In the third quarter of 2019, we have started FIDES-02, a Phase II study with derazantinib as monotherapy and in combination with Roche's PD-L1 checkpoint inhibitor, atezolizumab. This is a biomarker-driven multi-cohort clinical study in patients with advanced urothelial cancer expressing FGFR genetic aberrations, and first interim results are anticipated for the second half of 2020. In the third quarter of 2020, we are planning to start FIDES-03. This study will explore derazantinib in patients with gastric cancer and FGFR genetic aberrations, and will also include a cohort in which derazantinib is combined with atezolizumab. We've decided to investigate derazantinib in gastric cancer based on derazantinib's unique kinase inhibition profile, convincing preclinical in vivo data and the high medical need in this indication. Moving to our tumor checkpoint control in lisavanbulin, or BAL101553. We're focusing our clinical development activities with lisavanbulin on glioblastoma, the most common and aggressive form of primary malignant brain tumors and an area of high unmet medical need with very few treatment options available. Lisavanbulin is a novel microtubule targeting small molecules. It can be administered oral and IV, crosses the blood-brain barrier and has shown potent activity in brain tumor models in monotherapy and combination therapy. In line with our approach to involve biomarkers early in clinical development, we have been evaluating a panel of biomarkers. One of those is end-binding protein 1 or EB1, which was previously identified in preclinical models as a response-predictive biomarker for glioblastoma. In our Phase I glioblastoma clinical study with daily oral dosing of lisavanbulin, we have observed a profound and exceptional objective response in a glioblastoma patient whose tumor tissue was EB1 positive. This patient continues on treatments with lisavanbulin for more than 20 months now and shows a more than 80% area of reduction of the brain tumor. As non-responding patients did not show this pattern of strong EB1 expression, and based on additional biomarker work, we are therefore assessing the potential utility of EB1 in a biomarker-driven clinical study in glioblastoma and are planning to start this Phase II study mid-2020. We also continue with our Phase I study in newly-diagnosed glioblastoma patients of lisavanbulin in combination with standard radiotherapy in the U.S., which is conducted by the Adult Brain Tumor Consortium. I will now turn over to David.

Thank you, Marc. So in summary, we are on track with the execution of our strategy, in terms of both significantly increasing cash flows from our marketed brands, Cresemba and Zevtera, and advancing our R&D portfolio towards the next milestones. In particular, the clinical milestones in 2020 and beyond are as follows: We will progress the Phase III ceftobiprole study in Staphylococcus aureus bacteremia with the aim of having top line results in the second half of 2021 in order to file in the important U.S. market at the end of 2021. In the first half of 2020, we anticipate to complete enrollment into the Phase II registrational study in derazantinib in iCCA patients, FIDES-01, and expect then top line results for the cohort with FGFR2 fusions to be available in the second half of this year. In the second half of this year, we also expect interim data from the iCCA FIDES-01 cohort with other FGFR2 genetic aberrations. And finally, on derazantinib, we also expect the first interim data from the FIDES-02 study in urothelial cancer in the second half of 2020. We have already amended the clinical supply agreement with Roche for their PD-L1 checkpoint inhibitor, Tecentriq, their plan to explore the combination with derazantinib as well as derazantinib's monotherapy in gastric cancer. And this gastric cancer Phase I/II FIDES-03 study is anticipated to start in Q3 this year. For lisavanbulin, we are planning to start a biomarker-driven Phase II study in glioblastoma, mid-2020. And finally, we expect completion of patient enrollment into the ongoing Phase I study for lisavanbulin in patients with newly-diagnosed glioblastoma by mid-2020. We'll now open the line to any of your questions.

[Operator Instructions]. First question comes from the line of Louise Chen from Cantor.

So my 3 questions are as follows. First question is, just curious if you could provide more color on your competitive advantage for derazantinib in urothelial cancer and gastric cancer? And then second question is what supports the use of derazantinib in gastric cancer? I know you talked a little bit about it on the call, but just maybe if you could elaborate more, that will be helpful? And then the last question I have for you is on lisavanbulin. Can you provide more color on your biomarker and the type of patients that can be best treated with your drug?

Okay. Thank you, Louise. David here. Actually, they're probably best -- all those questions are best answered by probably Marc. So Marc, why don't you kick off, and then Adesh and I can jump in. But in terms of the competitive advantage of derazantinib in urothelial gastric and then the data supporting gastric cancer and why gastric cancer, and then the EB1 lisavanbulin.

Yes, Louise. Thanks a lot. So for the urothelial cancer, the key differentiation is, as we've outlined also in our presentation today, the activity of derazantinib against colony-stimulating factor-1-receptor, which was kinase on macrophages and is involved in the modulation of the tumor-immune microenvironment. And we have done comparative kinase screen versus all competitors in clinical development. And that's a unique feature of derazantinib. And we believe that this might contribute to potential improved efficacy when combined with an immune checkpoint inhibitor. So I think this is clearly the differentiation we have. And we have done some more work into this. We have looked at the crystal structures which explained by derazantinib and, for example, are not erdafitinib fit into the finding profit of CSF1R. And we've also done in vivo experiments now in actual macrophages to confirm that CSF1R inhibition really happens. So that's, I think, the key differentiation for urothelial. In addition, I think for any combination it looks like that derazantinib is differentiated by the safety profile. I mentioned during the call that this is related to retinal toxicity, nail, hand-foot syndrome, stomatitis, so it may be easier to combine it. Gastric, I guess where we were coming from was a large screen in patient-derived xenograft models where we looked across a large number of tumors and different tumor types to just see where we have the most consistent best efficacy, and that was gastric. From a kind of biology perspective, we also have seen that in addition to the CSF1R, in addition, it does under -- inhibits [indiscernible] [ co ] factor receptor 2. There are compounds approved for this -- is a compound approved for this target in gastric cancers. So this may contribute or may really be an underlying biologic rationale, but the primary kind of both for gastric cancer came from convincing the data in a series of non-clinical models.

Then the lease of lisavanbulin and the EB1, the type of patients.

So for lisavanbulin, I think we would -- initially a Phase II study that we're planning to start mid of this year would be in a recurrent setting. This is where we've seen this exceptional responder in the study in the U.K. with daily oral lisavanbulin. We have done quite substantial nonclinical work and also looked into tissue banks, and have a relatively good idea on how to do the biomarker selection. These data will be published later this year. But I think it's premature to detail on them, but we basically have prevalence estimates and also have, I think, identified how to do the patient selection in that trial.

Yes. In order to start the study in Q3 this year, which is the -- what we -- I think we said during the presentation. Is that answer your questions, Louise?

Yes.

Next question comes from the line of Raghuram Selvaraju, H.C. Wainwright.

This is Edward Marks on for Ram. I appreciate you guys taking the questions. I have 2 financial questions and 1 clinical question. Just a little clarification. I was wondering how you plan to get to the projected year-end 2020 cash flows or cash position of CHF 100 million to CHF 110 million, if you had CHF 161 million at the end of 2019 and the operating loss is only projected to be CHF 20 million to CHF 30 million. I was wondering if there are some nonoperating items contributing to this cash decrease?

Adesh, do you want to take that?

Yes, sure. Thanks for the question. So as you have seen probably in our guidance, we're looking at CHF 30 million non-deferred -- [ basic ] deferred revenue contribution to the top line. So these are noncash items. This is noncash revenue. And hence, that's sort of the difference. There are also noncash items with regard to expenses, but in essence, really the big difference comes from deferred revenues, which are all noncash relevant. Does this answer your question?

Yes, yes, absolutely. And then when -- or might profitability or maybe at least cash flow breakeven be attainable by the end of next year?

Yes, that's a good question. The way we would answer that is that, obviously, clearly, our model in the past has been to -- we take compounds to the end of Phase II. And then we partner the Phase III like we did -- we're doing currently with ceftobiprole with BARDA, and we did with Astellas with isavuconazole. The caveat, I would say, is that assuming that we would partner one or both of the compounds in development in Phase II, which for lisavanbulin and derazantinib. So if we partner either of those compounds during the course of 2021 then -- and we keep on maintaining our stable cost base that Adesh talked about and our cash generative revenues keep going in the direction they're going in, then we can foresee the possibility of us breaking even in 2021.

Excellent. That's good to know. And then finally, on the clinical side, just when you outlined a lot of your time lines there, which I really appreciate. But looking at top line data, I was just wondering when we might see the top line data for the Phase II study of lisavanbulin in glioblastoma? And would the Phase I study in the newly diagnosed patients yield data before the end of this year?

Yes. So we expect for the Phase II study in recurrent glioblastoma that's -- will be [ far ] market-driven to have data available that are meaningful in the first half of 2021. And for the -- I think you asked for the Phase I study in the U.S. with ABTC. This is basically, from a readout perspective, it requires survival data, because it's newly-diagnosed to the end studies. So these patients, by definition, they do not respond. They are kind of followed for progression during overall survival. So these data, we would expect somewhat later, more towards 2022, the readout.

The next question comes from the line of Victor Floc'h, Bryan Garnier.

I have a couple of questions regarding derazantinib. So first one, I just wanted to understand why did you prefer to start a study in gastric cancer rather than in the breast. So I understand that you have great confidence about your derazantinib in gastric cancer, but in the meantime, the frequency of FGFR variations seems to be quite high in breast. So I just wanted to understand what drove you to want gastric? And my second question is about the competition from the antibody, monoclonal antibody targeting FGFR, such as atezolizumab and [indiscernible]? I just wanted to hear your views about those 2 assets in terms of competition?

Marc, you're probably best placed to comment on why gastric rather than breast?

Well, as said, we've done a quite comprehensive screen through various models. And gastric just was -- the gastric cancer models were quite consistently responding to derazantinib, so that was our main rationale. I forgot to mention before that there's biologically, we've seen in the FGFR2 activity of derazantinib, and that for gastric cancer population maybe really indicate utility. We -- I think from a differentiation perspective, this to us just seemed the best move. And also, the -- it is -- gastric cancer has not really explored. I -- other FGFR -- a small molecule of FGFR inhibitors and the high medical need would probably also allow a quite rapid access to market if the interim results turn out to be positive.

And then the comment about the antibodies in development, how do we see those in vis-a-vis derazantinib, the antibodies with -- targeting FGFR?

I think this is to be seen. As in other areas, FGFR inhibitors, I think there is utility for antibodies, but there's also utility for small molecules. And the -- I think the difference -- the differentiation we have with derazantinib really is that we have profiled this molecule in terms of its kind inhibition profile and it affects more than just the FGFR1, 2, 3 kinase. It also inhibits CSF1R, which is -- provides the differentiation for combining derazantinib with immunotherapy, with FGFR2 maybe another differentiator for our approach in gastric cancer, whereas the antibodies, they will just work against one very specific target.

The next question comes from the line of Brian White with Cantor.

I'm going to ask actually another variant on a question that's just been asked actually on derazantinib. And just thinking about the comprehensive preclinical model experience. And I just wondered, did actually derazantinib show activity in other cancer settings in addition to gastric? Or was it only gastric? And then secondly, thinking about the combination with Tecentriq, and I get the differentiation and the mechanism behind why it might work well with that checkpoint inhibition. And I wondered if you thought about other classes, for example, the path inhibitors or DNA damage repair pathways in particular? And then just thinking about more generally on oncology assets and bringing some of these programs into Basilea, I guess that these could be quite expensive if they were one late-stage oncology assets, and there will be a reasonable degree of competition for these programs also. But I wondered if there were -- if you thought about core development structures that could perhaps facilitate Basilea's involvement, while still preserving cash for these programs?

Yes. Okay. We'll come back -- thanks for the questions, Brian. We'll come back to the in-licensing and the -- but the -- in terms of the derazantinib questions, Marc, again, any color on that?

If it was coming on [indiscernible] to the previous question, why did we choose gastric, what have we seen?

It wasn't the question, sorry. The question was, did -- I get why you chose gastric. Was there any activity in any other cancers, or is that it?

Yes, I think I know -- answer that this implied, that, yes, we have -- as we have looked across a large range of different tumor types, and we have seen signals beyond iCCA urothelial and gastric cancer. It's, I think as said, we've explained why we said gastric, I think the data we've seen and the signals we're seeing in the other cancer types, they will need some further consolidation. It's too early at this point in time to make this close to making firm statement about our plans for additional clinical studies in cancer types beyond, I should say, urothelial cancer and gastric cancer. But there's clearly potential there. And I guess, it's -- somehow we've considered as derazantinib as a pipeline and drug in this context where we have the ability to expand into various indications, and the first 3 we have disclosed. We may move on to additional indications once we've consolidated the present signals. And the other question, I think, was about the combination. And currently, I think we're focusing on combination with immunotherapy. But we are also looking at combination approaches with other compounds, including chemotherapy, anti-androgenic treatments, a number of other combination partners, which could also include path inhibitors. But I think from a -- realizing this clinically, we -- I mean we are there with the atezolizumab combination of PD-L1 inhibitor combination. And we will be disclosing in the first half of 2020 or later in 2020 our detailed combination approach in the gastric cancer study, which is atezolizumab, and also we'll include other combination approaches.

And then the in-licensing strategy in terms of ...