Bayer Aktiengesellschaft (BAYN) Earnings Call Transcript & Summary

Good afternoon, and good morning. It's a great pleasure to be with you today, and I welcome you to our 2021 Investor Webinar for Pharma. As announced in October, at the Crop Science webinar, we are planning a series of these events in an effort to keep you appraised of the key developments and milestones across the group. Today, we are showcasing one of the most important launch assets from our pharma pipeline, brand name KERENDIA or finerenone. We will be sharing today 4 things: First, details of the clinical profile; second, then the differentiated nature of KERENDIA; third, how it fits into the treatment landscape; and fourth, our current plans for life cycle management. With me on the webinar today are Christian Rommel, our Head of R&D at Pharma; and Sebastian Guth, Head of Commercial Operations, Americas in our Pharmaceutical division. We will begin the webinar with some prepared remarks from Christian and Sebastian, followed by about roughly ballpark 30 minutes of Q&A. So pretty much the same setup as we've had in the last webinar with Crop Science. You'll find instructions for participation in the Q&A in the Zoom chat, and I will remind you of those again later on. As always, before we begin, I would bring your attention to the forward-looking statements included in the materials today and currently on the screen. And with that, the floor is yours Christian.

Thank you, Oliver, for your introduction, and welcome, everybody, to today's webinar about our key launch as at KERENDIA. As we outlined at our Capital Markets Day in March, a key task for the new executive team at Pharma is to drive the Pharma top line during the loss of exclusivity phase for Xarelto and EYLEA and to return to business to sustainable growth thereafter. Among others, a key building block to achieve this task is KERENDIA or finerenone. KERENDIA is a nonsteroidal selective antagonist of the mineralocorticoid receptor or referred to as MR, which is activated by aldosterone and cortisol in regulated gene transcription. KERENDIA blocks MR overactivation in both epithelial, for example, kidney; and non-epithelial for example, heart and blood vessel tissues. Overactivation of the mineralocorticoid receptor, again, MR, is sought to contribute to inflammation in fibrosis. KERENDIA has a high potency and selectivity for the mineralocorticoid receptor and has no relevant affinity for androgen, progesterone, estrogen and glucocorticoid receptors. The selectivity profile of our molecule is not only important for the mechanism of action, but also as it relates to safety. The first approved indication for KERENDIA as chronic kidney disease in patients with type 2 diabetes. This is an underrecognized chronic silently progressing life-threatening condition. Globally, around 160 million patients are affected when it comes with a high disease burden which shortens life expectancy by 16 years on average compared to those living with neither of the diseases. To help you to put this into context, the prevalence of atrial fibrillation, which is the main indication for Xarelto is about 45 million patients globally. Patients with chronic kidney disease, or CKD, and type 2 diabetes, have residual cardiorenal morbidity and mortality despite current therapies. The risks of progression towards kidney failure and cardiovascular events increased the severity and stage of CKD. In patients with less advanced CKD, cardiovasculars is most pertinent whereas the risk of progression to kidney failure events is higher with more advanced CKD. When we listen to patients who face CKD progression, we often hear the following: Diabetes wasn't a big deal to me. The problem was that it killed my kidneys, and I did not know. This tells us exactly how we can support patients with chronic kidney disease in type 2 diabetes. It is not only about making KERENDIA available to patients, it is also about diagnosing the disease to intervene earlier and to educate about the renal and cardiovascular risk these patients are facing. In fact, these patients face a threefold risk of cardiovascular death and 50% of CKD patients progress to later this stage of the disease, which often end up into end-stage renal disease and need for dialysis. There is an urgent need for more treatments to protect kidney function and avoid dialysis for as long as possible as well as to prevent cardiovascular events. The majority of physicians demand better treatment options beyond current standard of care. Those new options should provide a dual kidney and cardiovascular benefit and have clinical utility across a broad spectrum of patients including those at earlier stages of the disease and in this context, we continue to guide our development strategy. Next slide, please. We executed the largest CKD Phase III trial program in patients with type 2 diabetes to date with more than 13,000 patients enrolled. The aim was to investigate the efficacy and safety of finerenone on top of maximally tolerated [indiscernible] and systems inhibition on kidney and cardiovascular outcomes. The program included 2 Phase III trials, FIDELIA-DKD and FIGARO-DKD, which are complementary in nature due to the features such as their near identical designs and endpoints. FIDELIA-DKD enrolled late-stage patients with type 2 diabetes and Stage 3 to 4 CKD and moderately-to-severely elevated albuminuria. FIGARO-DKD builds on FIDELIA-DKD and that it expands the patient population to those with earlier stages of chronic kidney disease, CKD. Both trials met their primary endpoints. Data represented at last year's ASN Congress and at this year's ESC Congress. Both trials are complemented by Fidelity and integrated analysis with the aim to pull the complementary studies for more robust estimates of finerenone's efficacy and safety across the spectrum of patients. The patient's characteristics are depicted in the heat map shown here from the kidney disease, improving global outcomes organization, overly with the eGFR estimated glomerule filtration rate, urinary albumin to creatinine ratio profiles of patients included in this analysis. As you can see, Fidelity study, a broad spectrum of patients across the continuum of the disease. Eligible patients with type 2 diabetes in CKD treated with maximum tolerated label dose of an ACE inhibitor or an ARB inhibitor included in the trial. Patients had to have serum potassium concentration at or below 4.8 millimolar per liter at screening. Other key exclusion criteria included clinical diagnosis of symptomatic chronic heart failure with reduced ejection fraction due to a Class 1a recommendation of MRAs. A differentiating feature of the clinical program for finerenone is the fact that it enrolled more early-stage patients than other contemporary trials in CKD with type 2 diabetes. More than 4,000 patients, including those on drug substance and those on placebo had moderately increased albuminuria, which is characterized by UACR of less than 300 milligrams per gram. This number of patients should allow for robust data generation in this particular subgroup. Credence and DAPA-CKD 2 trials that investigated SGLT2 inhibitors in CKD with sub-2 diabetes and will substantially less early-stage patients. The press of patient population that was enrolled in the finerenone trials is further exemplified by the fact that also a high number of late-stage patients were included. These are characterized by severely increased albuminuria within UACR of greater than 300-milligram per gram. Why is this important to have robust data generation in earlier-stage patients with CKD in type 2 diabetes? Well, first, these patients represent the majority of the prevalent patient population. And secondly, positive clinical outcomes include this population should support treatment intervention early in the disease to delay progression and to avoid adverse outcomes for the patients. So let's now have a look at the FIDELITY data. In this patient population with CKD was moderate to severely elevated albuminuria and type 2 diabetes, finerenone led to 14% reduction of the risk of cardiovascular morbidity and mortality and a 23% reduction of the risk of CKD progression, including a 20% relatively risk reduction in the development of end-stage kidney disease and dialysis. The requirement for dialysis is one of the most dreaded complications of CKD progression. It is associated with substantial morbidity and costs a significant reduction of this outcome, which is of great relevance to both patients and payers is therefore notable. Importantly, these outcomes are achieved on top of standard of care treatment to control blood pressure and HbA1c. All patients were treated with maximum tolerated dose of an ACE inhibitor or ARB. Owing to its mechanism of action, finerenone treatment is expected to increase serum potassium concentration through MR antagonism. In FIDELITY, hyperkalemia was indeed more frequent with finerenone versus placebo. However, the incidence of hyperkalemia-related adverse events, this clinical impact was low, in fact, very low. Hyperkalemia related permanent treatment discontinuations occurred only in about 1% of patients when adjusted for placebo over a median follow-up of 3 years. This combined analysis of 2 complementary trials provides robust evidence of both cardiovascular and kidney protection with finerenone versus placebo. The FIDELITY analysis suggests a strong effect of MR over-activation in the pathogenesis of both cardiovascular disease and CKD progression in patients with CKD and type 2 diabetes. Cardiovascular and kidney risk can be reduced with phenomenon even in patients with less severe CKD and type 2 diabetes, which highlights the importance of initiating treatment before CKD has progressed. Since the design of the FIGARO-DKD and FIDELIO-DKD studies, SGLT2 inhibitors have emerged as a therapeutic option for patients with CKD and type 2 diabetes. In an effort to make results from different studies more comparable, we use data collected in the FIDELIO-DKD trial and the methodology is similar to that of CREDENCE, which investigated the use of clinically -- versus placebo in these patients. The post-hoc analysis of FIDELIO-DKD included patients with meeting the CKD inclusion criteria of the CREDENCE trial. In addition, the cardiorenal composite endpoint was equivalent to the CREDENCE primary end points. In this analysis, the cardiorenal endpoint risk was significantly reduced by 26% with finerenone versus placebo. After adjusting for history of heart failure of the patient, the risk was reduced by 28%. In CREDENCE, the cardiorenal endpoint with reduction of 30% with canagliflozin versus placebo. Thus, both the FIDELIO-DKD and CREDENCE studies demonstrate cardiorenal endpoint risk reduction of a comparable magnitude when trial differences are still considered. From a physician perspective, KERENDIA comes with the advantage to build on a known well-established mode of action, inhibition of the renin angiotensin aldosterone systems are referred to as RAAS. RAAS over-activation is associated with kidney and cardiovascular diseases, which often coexist as a cardiorenal disease. Thus, RAAS inhibition by angiotensin-converting enzyme inhibition or by angiotensin receptor blockage has become the gold standard for treatment of CKD in patients with type 2 diabetes since decades. KERENDIA builds on this mechanism, and that it extends the RAAS inhibition to the minimal corticoid receptor pathway integrated part. Also there is a rich history of RAAS inhibition starting some 60 years ago and innovation get evolved over the last 25 years with limited clinical progress to address significant residual unmet medical need. Higher attempts to identify the RAAS blockade have failed, either there was no clinical benefit obtained or side effects have reached unacceptable levels. KERENDIA now opens the door for an extended RAAS inhibition option, and it is thus continuous the long-RAAS-centric treatment history for cardiorenal diseases. This extended RAAS inhibition via mineralocorticoid receptor inhibition on top of ACE and ARB was not accessible until today. Steroidal MR antagonists like or are not indicated in the U.S. for the treatment of CKD due to their clinical limitation and side effect profiles. KERENDIA builds on a passive physiological pathway with known positive treatment outcomes that is well established among physicians. Against the backdrop, we believe that the clinical profile the wells established and intensified mode of action and its familiarity among physicians may put KERENDIA in a position to become an established treatment option for CKD and type 2 diabetes on top of existing therapies. Along with this comes the clarity of the U.S. label, which will be explained by my colleague to you now, Sebastian Guth. Sebastian, take it here.

Thank you, Christian, and a very warm welcome also from my side. Now as Christian has mentioned, the FDA label largely recognizes the clinical benefits that were demonstrated in the FIDELIA-DKD trial. KERENDIA in the United States is indicated to reduce the risk of sustained eGFR decline of end-stage kidney disease, of cardiovascular death, of nonfatal myocardial infarction and of hospitalization due to heart failure in adult patients with chronic kidney disease associated with type 2 diabetes. Also noteworthy is the fact that the U.S. label includes just the risk of hyperkalemia in the warnings and precaution section. This is a common characteristic for any RAAS inhibition therapy and as said, as such, also well entrenched. A prominent U.S. thought leader recently described the safety profile and label of KERENDIA and I quote "as pristine," which to me is a good articulation of the label in the United States. KERENDIA is safe, efficacious and easy to use as it has minimal unwanted effects in plays well with other drugs making it an ideal foundational treatment for this population of patients. Now as you can see on this next slide, we're committed to a global launch of KERENDIA. In addition to the United States, where we launched a product in August, we filed in Europe, in China and in other markets. Assuming standard review times, we would assume a potential approval in Europe early next year. And in China, KERENDIA may come to the market already next year, which is much earlier than originally planned. Now let's focus on the U.S. In the United States, we significantly invested to cover both the relevant specialists and tap into a targeted portion of the U.S. primary care market with KERENDIA. As our initial launch focus based on FIDELIA, is on later-stage CKD patients, with an early focus on nephrologists, endocrinologists, select cardiologists and a targeted general -- and targeted general physicians that largely behave like specialists. As we expand into earlier patient segments over time, we see ourselves continuing to expand the target audience. To approach today's audience, we built a commercial field organization that is more than 500 colleagues strong. Now it is worth mentioning that we received more than 30,000 applications for these new positions. Applicants came from some of the leading players in the cardiorenal field, which allowed us to build an organization with significant expertise and established relationships in this therapeutic area right from the get-go. The activities of our medical representatives are complemented by strong digital and medical education engagement particularly during this time of COVID. We achieved early pay events and have coverage with some of the key plans. Two of the largest PBMs already covered KERENDIA in their commercial formularies and several national health plans, many regional health plans and Medicaid plans are also already covering KERENDIA. Additionally, access programs like a co-pay card program and a free trial program are in place to support early access. Our commitment to KERENDIA goes beyond chronic kidney disease in patients with type 2 diabetes. We're building on an extensive clinical program for KERENDIA under the umbrella brand of [indiscernible]. Just recently, we announced the initiation of the FIND CKD study in a placebo-controlled Phase III trial to investigate the efficacy and safety of finerenone on the progression of chronic kidney disease in patients with nondiabetic CKD. A primary objective of the study is to demonstrate superiority of finerenone over placebo in delaying the progression of kidney disease in these patients. Although diabetes is well recognized as a leading cause of chronic kidney disease globally, a substantial proportion of the global burden is nondiabetic in origin and attributable to other causes such as hypertension and chronic kidney inflammation. A FINE CKD study, will enroll more than 1,500 patients, and we expect a primary study completion for 2025. Already last year, we initiated the FINE ARMS-HF study, a placebo-controlled Phase III study to evaluate the efficacy and safety of finerenone on morbidity and mortality in patients suffering from symptomatic heart failure with a left ventricular ejection fraction of equal or greater 40%. The primary objective of the study is to demonstrate superiority of finerenone over placebo and reducing the rate of the composite endpoint of cardiovascular death and total heart failure events. of the mineralocorticoid receptor system has been shown to be of benefit in the treatment of heart failure. Considering the reduction in the risk of hospitalization for heart failure that was demonstrated in FIGARO-DKD, there's probably much more to learn about the potential of finerenone in the setting where only limited treatment of these exist today. The trial will enroll more than 5,500 patients and is currently expected to be completed in 2024. Now in summary, we believe that KERENDIA has the potential to become a foundational cardiorenal disease modifier with a strong scientific and clinical base. Starting from today, with the approved indication of CKD and type 2 diabetes, we believe that the potential for KERENDIA goes beyond this indication. It may well expand as I've alluded to, into heart failure and nondiabetic CKD. Our huge investments in life cycle management is testimony to our beliefs. We continue to see significant commercial potential for KERENDIA and reiterate our peak sales estimate of more than EUR 1 billion. We hope that you share our excitement about KERENDIA and that you will closely follow the developments here to come. The journey has just begun. Thank you. With this, I hand it back over to Oliver to open our Q&A session.

Thank you so much, Sebastian. Thank you, Christian, for your remarks and the presentation. Very much appreciate it. And I think with that, we will move to the Q&A. Before we start, as last time, some housekeeping items on the Q&A from my end. [Operator Instructions]

I see the first hands going up, which is great. [Operator Instructions] And I think the first question comes from Pete Verdult from Citi. It doesn't seem that -- Pete has got lost, again, I think. So next question comes from Sebastian Bray from Berenberg.

Hello, can you hear me?

Yes, absolutely.

Well, thank you very much for taking the time to have a chat and show us for data from the seminar. I'm wondering, let's say we get to 2024, and the data on the heart failure with preserved ejection fraction turns out to be promising. How would you think about the relative market size of the chronic kidney failure, which is the core products of the -- chronic kidney disease pardon me, which is the core market for this product versus heart failure. Could heart failure be a bigger market than chronic kidney disease?

Sebastian, I will take that question and first and foremost, obviously, thank you for the question. Now we have, at this present moment, not communicated a specific commercial potential for KERENDIA in either heart failure or nondiabetic chronic kidney disease. As you know, we've communicated peak sales potential of EUR 1 billion which pertains to the indication of chronic kidney disease and type 2 diabetes are known. And to be honest, we're not prepared at this present moment to guide more specifically to the peak sales potential in our life cycle management indications. I will prefer to wait for the data to then talk about the peak sales potential at the appropriate time.

That's understood. So just to clarify, the data that you have presented today with the greater or equal to the EUR 1 billion -- greater than, pardon me, that does not make any provision for this product being successful in heart failure with preserved ejection fraction, is this fair?

That is correct. So the peak sales potential we've communicated today of greater than EUR 1 billion pertains to the indication of chronic kidney disease and type 2 diabetes alone. And we will update the peak sales potential at the appropriate time predicated upon the results of our life cycle management studies.

Next one, I think Pete is back online. I think he made it back, Pete, you would be next.

Just 2 questions. Just on the original Phase II data for finerenone in heart failure, just remind us how you pick that apart to justify moving into Phase III? So I just want to get your better sense to your level of confidence and the data you're using to support that to push that into Phase III? And then just to play devil's advocate, and I think you've mentioned this during your prepared remarks, a lot of docs will say, if I've on an early stage kidney disease patient, why would I consider finerenone. I've got a patient with lots of co-pays, why don't just give them an SGLT2 or a GLP-1. I get cardiorenal benefits along with glycemic control and weight loss. So how are you going to push back against that pushback?

Christian, do you want to answer first to the question of heart failure, then I'll dive in and answer Pete's second question.

Yes. Certainly. Happy to support the second one, too. But first, studies, FIDELIA and finerenone. We met our predefined primary and secondary endpoints. So let me remind you that -- when we look at the composite endpoints of the FIDELITY study and the cardiovascular outcome and the components for hospitalization for heart failure, cardiovascular deaths and non-fatal MI, the KERENDIA was led to a reduced risk reduction of 40% of the primary endpoint from heart failure hospitalization and cardiovascular deaths. While if you look at RRR, it was 23% with the components to renal deaths. And the -- basically, when we had met our top line on the Phase II studies, we decided to go ahead. It was a predefined endpoints, and we thought that the efficacy data along the, I think, a stellar safety profile, in particular to potassium elevation mandated us, excited us to go forward. And I think the outcome now with FIDELIA and FIGARO on the Phase III and the composite analysis of FIDELITY. And as we mentioned, even when you do the [indiscernible] to CREDENCE, I think is extremely encouraging. On the second question, I'll quickly start. Remember that we have a very novel mechanism of action here, which is independent of interference with hyperglycemia and insulin metabolic profile. But I'm sure that Sebastian would love to build on that. Before it gets again lost on us, we have an anti-inflammatory and potentially anti-fibrotic which is the underlying pathology of chronic kidney disease. And Sebastian, maybe you want to take it from here from the treatment management this glucose-lowering agent.

Yes. No, thank you, Christian. And Pete, great question, great to reconnect on top of that. So I would say 4 quick thoughts. The first one, as Christian has demonstrated in the prepared remarks, if you simply look at the robustness of the evidence, you will note that we have studied KERENDIA in a substantially larger number of early-stage patients than SGLT2 inhibitors. For example, so the robustness and scale of the evidence in it by itself is very significant and obviously important for physicians that consider the appropriate treatment choice. Second thought, and again, Christian has spoken to that is that KERENDIA's provides mechanistical continuity on top of the well-established RAAS inhibition with ACE and ARB's inhibitors for the treatment of cardiorenal disease. And in many ways, physicians have for a long time tried the dual RAAS therapy and studies to date have failed, that is changing with the arrival of KERENDIA. Third thought is that KERENDIA can be combined with any other standard of care, and Christian has spoken to that as it works independent and is, in fact, complementary to other RAAS inhibitors and does not require physicians to adopt diabetes background therapies, which for many of them in daily clinical practice is actually important. So in many ways, it provides a dual benefit. And that's what speaks to physicians. I myself have spent a lot of time out in the field. And I can tell you that it does resonate, and it's a very relevant offering that we're bringing forward with KERENDIA.

Next question comes from James. James Quigley from Morgan Stanley.

So a couple sort of short ones really. So for the half year trial and the nondiabetic CKD trial. Do you have interim analyses built into those trials? And if so, sort of around about what point? That's question number one. Then question number two, you mentioned that the label is based on the FIDELIO data to the later-stage trials -- patients, sorry. What's the process and the timing for increasing -- for bringing the data on bigger or for the earlier-stage patients? And does that really matter in terms of use or patients who already looking at the early stage patients as well? I think I will leave there.

All right to the final study. As you know, we are recruiting, and we are in for this. I think unless you correct me, the primary completion will be Q1 2024. That's our current estimate. The nondiabetic kidney study is also going forward, and there I would need help from Juergen on the time line. You may want to look that up, and if you please.

Going to or with James on that one, Christian. No problem.

Okay. And then the other question was first thing I can take. So the other question?

Sorry, James, I interrupted you. Go ahead. I think your second question was on the update of -- potential update of the label to include the FIGARO data in the United States? Is that the correct understanding?

Yes.

Absolutely. So we filed the FIGARO data with the FDA. We actually filed on the 5th of November and are expecting the label to be updated. As I alluded to in my earlier remarks, our initial launch focus is on the FIDELIA population, which is later-stage patients, and we're then expanding in our commercial efforts as we see the label getting updated and as we continue to gain traction in those later-stage patients. So it's a very well planned out launch and commercial strategy that supports the launch of KERENDIA in the United States and beyond.

Next question comes from Florent Cespedes from SocGen. And then next is Michael Lassen from UBS, just heads up, Michael.

Can you hear me?

Yes. Very good.

A quick question on the trial FINE-CKD. Could you elaborate a bit on the challenges of this population because the nondiabetic CDK patients, it's quite heterogeneous population, and the size of the trial looks not extremely big. So I just like to your thoughts on the challenges on the -- and why you are so confident to address this population, even the rationality of the population. That's my main point.

Yes. So we acknowledge that the disease -- basically molecular understanding, heterogeneity. We'll learn more about as we progress with the trial. In terms of the size of the trial, you can imagine that our clinical statistician and how planning this and design and be confident that with the trial of the design that -- we will have the statistical power to deliver the for the predefined endpoints. Why are we confident? It's based on our experience in the FIGARO and FIDELIA trials, of course. Please remember that we have a large safety database that helps when you now do the life cycle management, expand into other indications, like the earlier patients. We also started pediatric as you might have recognized and now the nondiabetic. So we have a large data set. We know the molecule, the therapy. And that has given us the confidence and we'll update you as we progress. But I want to acknowledge that the nondiabetic is more heterogenic [indiscernible] thing.

And maybe a quick follow-up. I suspect that you have some prespecified subgroup some populations in the trial that could at some point, depending on the results give you an indication on what is the -- what are the patients who are the best responders to the treatment?

Yes, that we will look, but I don't think we want to share much about it right now on this call, but this is our common practice in pursuing those developments.

Next one comes from Michael Leuchten from UBS.

One question for Sebastian, one for Christian. Sebastian, just going back to the launch plan strategy. I think the nephrologist audience is relatively clear. But I think it's going to be a little bit tougher into the endo, maybe the PCP. So with the 500 reps that you referred to, should we expect this to be scaled into the label expansion as you just discussed? Or is that actually going to be scaled on the readout of the FINEARTS study that would give you a heart failures and indication, something that the SGLT2s can currently already promote? And a question for Christian. You referred to this as a potential anti-fibrotic. When do you think you can demonstrate that.

Michael, great question, and let me address the first one and then Christian will address the second one. So to your question, at this present moment, as you highlighted, our initial focus is on nephrologists and on a select group of GPs that in many ways, behave somewhat like specialists, and we see those as the primary prescribers for KERENDIA. And as we then expand -- as we expand the population we cover, you can also expect us to continue to expand our sales organization to cover a greater number of, in particular, primary care physicians. In addition, we are -- as I look at our early experiences, encouraged by the response of endocrinologists and see cardiologists playing a more important role in future strategies. So these are target audiences we will continue to look at and appropriately cover as the note progresses.

Yes. And then to your to your question of the mechanism of action, it's probably fair to say if you just come from the science side that it's a very strong or valid hypothesis that overreaction on the mineralocorticoid receptor leads to inflammation, reactive oxygen, which is a key mediate messenger that causes fibrosis and those underlying inflammation and fibrotic events drive chronic kidney disease and cardiovascular disease progressions. So we think that this is part of the ultimately mechanism of action, the overaction of the MR signaling system and the outcome of transcriptional changes then I would refer for now to a good body of evidence in preclinical kidney and cardiovascular disease models. Not only there is an unbiased because it's not only generated by ourselves, and in the nondiabetic clinical trial, we will look in experimental exploratory evidence for anti-fibrotic mechanism of action. There is more data to come. But if I think about what's known, what has been shown in [indiscernible] pharmacology, I think it's been holding up. And as we talk to -- this is the unmet need when you think about the unmet need in disease biology, anti-inflammatory, anti-fibrotic for this disease as we then can combine with other therapies.

I think the next question comes from Sachin. Sachin Jain from Bank of America.

I've just got a few actually, and they're all hopefully quite short. So firstly, U.S. pricing strategy. I think you've priced at a decent premium to SGLT2s, if I'm correct. Can you just talk through the rationale for that given the data seems similar when you present the equalizer trial composition? That's the first one. Secondly, in the introductory comments, you mentioned you've got some payers online. Wonder if you can just quantify what percentage of addressable patients are currently covered? And how we should think about that progressing in the next 6, 12, 18 months? A similar question for your initial focus on specialists and nephrologists, cardiologists, et cetera. Just to get a sense. I think you mentioned this in the introductory comments, but I missed it, but what percentage of patients are managed by specialists versus PCPs? And how important is that PCP expansion? And then the last one sort of pulls together the 2 prior questions. The reason for those questions, I'm just trying to get a sense of how you think this product will be sequenced versus SGLT2s, which obviously, at the moment, have much broader labels with the nondiabetic and heart failure population. So again, similar to a prior question, what's the reality probability of your payer pricing and sort of specialist strategy relegating this to a second-line agent post SGLT2?

Sachin, thank you for the question. That's all questions, I should say. So let me address the first one, pricing. So we have priced KERENDIA at a WAC price of $569.10 per 30-day script or $18.97 per day prior to discounts. Now if you look at the net price that is in line with our expectations, and as you know, the industry has experienced net price erosion over the last couple of years. If you reflect -- if I reflect on the discussions with payers and then give you some color on that, we clearly see payers recognizing the need for diagnosis and treatment of chronic kidney disease associated with type 2 diabetes and to prevent the progression of end-stage kidney disease and/or dialysis and cardiovascular complications. In the discussions, the payers acknowledge that KERENDIA is safe, effective and very easy to use. And we, as you can imagine, in active discussions with commercial and Medicare plans at both the national and regional levels. And I must say we're really encouraged by the early coverage decisions and I'll see coverage expanding in line with our plans. Now you asked specifically whether we can give you guidance on the exact size of the population that is covered today and we're, in fact, not prepared to provide specific guidance. But what I can tell you is that at this moment, both commercial and Medicare access are progressing in line with plans, as I said. And we're expecting peak coverage by July of 2023. So we see coverage building up to its peak in July 2023, which is in consideration of both commercial processes and Medicare bid cycles. The next question you had is -- was around the role of PCPs and whether or not we cover PCPs already today? And I just want to give you a little more color on that. So at this present moment, as I said before, we cover both nephrologists and primary care physicians that, in many ways, behaved like specialists and take a more active role in managing also later stage patients. These are typically patients of Stage III, Stage IV disease. And that's not an insignificant number of primary care physicians here in the United States. So we are covering, as of today, already nephrologists, other key specialists and a fairly significant number of primary care physicians, which we're then expanding over time. To your question of sequencing with SGLT2s. I think as we look at the clinical evidence and Christian spoke to it, we clearly see that KERENDIA is a foundational treatment for patients with chronic kidney disease and type 2 diabetes. And if I look at the data at this present moment, just to give you a little bit of color, about 85% of the patients that have been initiated on KERENDIA to date are initiated on KERENDIA alone and not sequenced in any shape or form through, for example, an SGLT2. So that speaks to the robustness of the evidence and what we're bringing and the importance of what we're bringing to this patient population.

-- we also have preliminary right or limited evidence that from the FIDELITY trial that from a safety perspective, we can combine, it's a limited set of data, it's about 7% of patients at baseline with SGLT2 inhibitors. From a safety perspective, we can combine. And from a mechanistic understanding, I do think it's fair to say that SGLT2 inhibitors may require the ACE and ARB's inhibitors in order to see their full potential, which we think is not the case for finerenone being on the last pathway. So you can think of that of going forward, the potential and combinations.

I think we have time for one more question, looking at the time and I skew the last question coming from Damien from Morningstar.

Great. Can you hear me okay?

Yes.

I just wanted to follow up on that last question. And try to understand how well positioned KERENDIA is versus the SGLT2s. If you look at cross-trial comparisons, you could arguably say some of the SGLT2s look like they performed a little bit better. But in the FIDELIO study, there was the allowance of using SGLT2s. And I guess the question is, how prevalent was the usage of SGLT2s. And if you were to exclude that, could you talk at all about the strength of KERENDIA maybe on a more apples-to-apples cross-trial comparison. And I get there's a lot of challenges with this question. And statistically, it doesn't always work. But what I'm trying to get at is just how strong is KERENDIA versus SGLT2s in a more level playing field?

Maybe I take the lead -- maybe I'll take the lead and then Christian chimes in, because I think it's really important to recognize, and we've spoken about this before, that KERENDIA is a foundational treatment for patients with chronic kidney disease and type 2 diabetes. And we clearly see that resonating as we engage with physicians across the United States. And I've spoken to it earlier, but just a very quick recap. It's really the mechanistical continuity on top of well-established RAAS inhibition that is -- that sort of makes intuitively a ton of sense to physicians. It's the fact that it can be well combined with any other standard of care as it works independent and complementary to other RAAS inhibitors. And it's the fact that it provides a specific treatment and does not interfere with any diabetes medication and does not require physicians to adjust and play around with the diabetes background therapy, which, again, in daily clinical practice is obviously very important to them. So we see that clearly resonating with the physician audiences here across the United States. And if you then look at the data in combination with SGLT2 for those that are interested in doing so, as Christian has alluded to, we do have a pretty robust 7% of patients of such a large trial in absolute terms is actually a pretty substantial data set. So we do have a substantial data set in Christian can speak to that best. That gives us a clear indication of both safety and I think early indicators also on the efficacy of a combination of physicians choose to go there.

Thanks, Sebastian, 2 or 3 yes -- 2 or 3 points to add. One is in our study, we enrolled patients at an earlier stage compared to any of these SGLT2 inhibitors. So there are some trial differences, of course. And then we did, what you suggested and if you may go back to -- after the meeting, you can look at Slide 12 again, of our presentation of CREDENCE like post-hoc analysis, what we concluded when we analyze this, the data are rather comparable more than they are different. Yet they have very different mechanism of action. So by the robustness of the data of both FIDELIA and FIGARO, understanding the patient population in earlier-stage patients and then this analysis of CREDENCE like analysis, I think that we feel strong again, like Sebastian says that when referring to finerenone as a foundation therapy for chronic kidney disease.

And Christian, maybe or Damian, one aspect that we haven't spelled out, but that is important to recognize is that when you look at the results of FIDELITY, you see that the cardiovascular benefits of KERENDIA that were demonstrated in FIDELITY were consistent regardless of the baseline use of SGLT2s, which again is a strong signal that all patients should be on KERENDIA, as we've alluded to earlier.

Thank you, Damian. I think that concludes program for today. Thank you so much, Sebastian. Thank you so much, Christian, for taking the time today. I also like to thank the team behind the scenes, everybody involved making this happen. It always seems flawless, but it's a lot of work behind it. So we hope you enjoyed this event. And we would appreciate, obviously, your feedback on the performance as we intend to keep that performance also going forward. We like to improve where we can at any point in time. I'd like to thank all of you for your continued interest and hope you stay safe. Thank you so much. Talk to you guys soon. If there are any follow-ups, please don't hesitate to get in touch with me over. Thank you, guys. Stay safe.

Thank you.