Michael Mitchell – VP, IR
Clive Meanwell – Chairman and CEO
Simona Skerjanec – SVP, Innovation Leader, Antiplatelet Therapies
Sameer Mehta – Chairperson, Lumen Foundation
Dominick Angiolillo – Author; and Professor, University of Florida
Adnan Butt – RBC Capital Markets
Jason Kantor – Credit Suisse
Cory Kasimov – JP Morgan
Joe Schwartz – Leerink Swann
Jon Eckard – Citi
Umer Raffat – ISI Group
Steve Byrne – Bank of America
Biren Amin – Jefferies
The Medicines Company (MDCO) Discussion on Phase 3 Cangrelor CHAMPION PHOENIX Trial Results and Outlook Conference Call March 10, 2013 2:00 PM ET
Welcome, ladies and gentlemen to The Medicines Company Conference Call to discuss Phase 3 Cangrelor CHAMPION PHOENIX Trial Results and Outlook. Your host for today’s call is Mr. Michael Mitchell. Please proceed, sir.
Thanks, Ethan, and good morning from San Francisco at the American College of Cardiology’s 62nd Annual Scientific Session and Expo. Today, we will review the results of cangrelor’s CHAMPION PHOENIX trial and the outlook for cangrelor. I would like to remind you that this call will contain forward-looking statements about The Medicines Company that are not purely historical and all statements that are not purely historical may be deemed to be forward-looking statements, which involve a number of risks and uncertainties.
Without limiting the foregoing, the words believes, anticipates, plans, expects, estimates, aim and similar expressions are intended to identify forward-looking statements. Important factors that could cause actual results to differ materially from those indicated by such forward-looking statements are identified in the company’s SEC filings, including a Form 10-K filed with the SEC on March 1, 2013. Copies of our SEC filings can be obtained from the SEC or by visiting the Investor Relations section of our website.
Clive Meanwell, Chairman and Chief Executive Officer, will provide his perspective; and Simona Skerjanec, Senior Vice President, Innovation Leader, Antiplatelet Therapies, will lead our discussion of the results. Then Clive will moderate our Q&A session and available with us on the Q&A session is Brent Furse, our Chief Customer Officer and cardiology experts from the world that Clive will introduce before the Q&A.
So with that, I’ll turn it over to Clive.
Well Michael, thanks very much, and welcome to everybody to our call from sunny San Francisco. Earlier this year, I indicated that we started 2013 with an established base business, which is growing robustly; an exciting portfolio of high-value assets in acute and intensive care medicine; the superb team of people here at the company who are ready, willing, and able to drive growth; and momentum in pretty much all aspects of our business.
Today, we’re pleased to be on the report and comment on the late-breaking news from ACC, namely the publication of the CHAMPION PHOENIX trial of our investigational compound, cangrelor. New data validate one potential high value product from our exciting portfolio. The work, led by my colleague, Dr. Simona Skerjanec, who is with us here for the call, demonstrates our abilities to work at the highest levels of scientific endeavor. And the news adds another element of lift to our growth as we enter the spring time.
So without further ado, let me hand it over to Simona to describe the new data, the context, and the outlook.
Thanks, Clive. My name is Simona Skerjanec and I’ve been working on cangrelor and Angiomax for 10 years. Therefore, it gives me great pleasure to describe the important results, which were presented earlier today by Professor Deepak Bhatt here at ACC. In addition, I would like to provide some context for the trial and a roadmap for the rest of the year.
Let’s start with the essential results of PHOENIX trial reported earlier today. And for this, I’d like to refer you to the online publication of The New England Journal of Medicine posted this morning. The PHOENIX trial is the third of a three major studies in PCI. These trials have studied a wide range of patients ranging from stable angina treated electively to major heart attacks treated emergently.
The total number of patients studied exceeds 25,000. PHOENIX reported 10,942 modified intent-to-treat patients for the primary analysis of effectiveness. Importantly, the population included 56% of stable angina patients, 25% NSTEMI patients, and 18% STEMI patients; and therefore, covers the full spectrum of patients that require PCI.
The trial was global with 37% of patients from the U.S. and 63% of patients, ex-U.S. Patients displayed the usual range of medical history, comorbidities, and concomitant treatments associated with ischemic heart disease.
As you may have already – heard already, the PHOENIX trial met all of its pre-specified goals as following: First, cangrelor significantly reduced the rate of ischemic events, including stent thrombosis during PCI. Specifically, the primary endpoint was reduced by 22% with a p-value better than James Bond of 0.005.
Second, there was no significant increase in severe bleeding. And third, intravenous cangrelor given for two hours was associated with a predictable and easily manageable adverse event profile which, overall, was not different from oral clopidogrel. Consistent with previous trials, there was an increased, but low incidence of transient breathlessness in patients treated with cangrelor.
All of these results were both clinically and statistically robust and consistent across all analyzed subgroup populations.
I am not going to describe the details of the study design today, but refer you to both, The New England Journal article and the methodology paper published in the American Heart Journal last year. But for transparency, the most important issues of the design and results, which are being discussed by the academic community this weekend relate to; dose and timing of the clopidogrel comparator, transition from intravenous cangrelor to oral antiplatelet therapy, ascertainment and definition of myocardial infarction following PCI and definition of stent thrombosis. I would deal with each of these in turn.
First, the PHOENIX protocol requires clopidogrel to be given according to institutional preference. The result of this was that 74% of patients were given 600 milligrams. Furthermore, the majority of patients were given clopidogrel upfront. This means that the comparator drug administration not only reflected current treatment practices, but also gave cangrelor a stiff test. Among the subgroup of 8,136 patients, in which the comparison of cangrelor to 600 milligrams of clopidogrel was studied, cangrelor significantly reduced the primary endpoint by 23%. It is inferred from this and previous studies that IV cangrelor demonstrated greater effect than a 600-milligram loading dose of clopidogrel.
Improvement in ischemic results was consistent irrespective of timing of clopidogrel administration. Cangrelor was associated with 20% pure ischemic events compared to pre-loaded clopidogrel and 21% pure ischemic events compared to clopidogrel given during or immediately after PCI. Taken together, these two observations support the conclusion reached by the investigators that the dose and timing of clopidogrel comparator did not confound the study. Cangrelor was more effective than clopidogrel given at any dose or at any time.
Patients were smoothly transitioned from intravenous cangrelor to oral clopidogrel without an apparent gap in protection. We also plan to study transition of intravenous cangrelor to new oral drug such as ticagrelor and prasugrel and we anticipate similar results.
The ascertainment of myocardial infarction associated with PCI has been challenging scientific question for many years. In the PHOENIX trial, we used the universal definition of MI. This definition takes account of ongoing elevated cardiac markers of ischemia before PCI to avoid inaccurate over-counting of MI. We encountered that issue in the two previous CHAMPION trials and we addressed it successfully in the PHOENIX trial. Consequently, the CHAMPION PHOENIX investigators were able to demonstrate clear and consistent reductions in myocardial infarction consistent with the mode of action of cangrelor and the primary hypothesis of the trial.
An editorial accompanying the PHOENIX trial publication today questioned the methodology of classifying and reporting stent thrombosis. In a supplement to the paper itself, the detailed definition of stent thrombosis is given. The supplement also describes the universal application of the adjudication process included blinded use of core laboratory for all patients to determine whether stent thrombosis occurred. So this is a non-issue in the view of the authors of the paper and other experts here at ACC.
Also, here at ACC, Professor Deepak Bhatt, the co-primary investigator commented on the efficacy results including the 38% reduction in the odds of the key secondary endpoint, the incidence of stent thrombosis and the low statistically comparable incidence for the safety endpoint of severe bleeding at 48 hours. Professor Bhatt commented in the press release issued by American College of Cardiology that these endpoints are – we worry about a lot in interventional cardiology and cardiology in general.
The study examined a very wide spectrum of patients, which means the result really do apply to a substantial percentage of patients undergoing stent procedures around the world. We concur with Professor Bhatt’s comments and look forward to moving cangrelor forward. In the years to come, we believe that cangrelor has the potential just like Angiomax has been able to do to protect millions of patients against the disastrous and costly consequences of acute coronary thrombosis associated with PCI.
Now, let me provide a roadmap for the rest of the year. First, regulatory discussions have been underway for some time in both the U.S. and Europe. We anticipate submitting an NDA in the U.S. in the second quarter and in the European Union by the end of this year. The reason for later filing with European regulators is to accommodate their need for complete validation date on manufacturing batches at the time of filing, which is a condition not required in the United States.
The regulatory submission will now rest on four major clinical trials treating more than 25,000 patients. Those four trials are CHAMPION PLATFORM, CHAMPION PCI, CHAMPION PHOENIX and the BRIDGE trial, all of which have been published in either The New England Journal of Medicine or JAMA.
We intend to ask for product indications both for PCI and all subgroups of patients and in patients, who require bridging from oral antiplatelet therapy before surgery. In addition, we expect to submit a series of publications both from CHAMPION PHOENIX and from the pooled analysis of the CHAMPION program in collaboration with investigators.
We will continue to analyze CHAMPION PHOENIX and other data and generate information to support rational value-based pricing strategies for cangrelor. We believe it will be possible to offer economic dominance in several patient segments around the world and we will apprise you of our progress.
Assuming regulatory approval, we look forward to adding cangrelor to the bag of our existing products carried by our frontline organization as early as 2014. In view of its clinical performance in trials and potential, we believe cangrelor can address a substantial market with significant unmet medical needs. We believe that the results of PHOENIX further support at least our prior projections in which we estimated peak annual sales of $450 million, which is expected to drive significant value growth for our shareholders.
We also believe that introducing – introduction of cangrelor into the worldwide market will bring us closer to our purpose, which includes alleviating patient suffering and improving the economic efficiency of the world’s leading acute and intensive care hospital.
With that, I’ll turn it back to Clive.
Well, thanks, Simona, for that excellent review. For a firm like ours committed to innovation in acute and intensive care medicines, few, if any, announcements could be more exciting than this one. The new intravenous antithrombotic – excuse me, the last new intravenous antithrombotic introduced for use in PCI was our very own Angiomax sometime ago. Before then, it was way back in the 1990s that the family of intravenous drugs acting on the GP IIb/IIIa platelet receptor, ReoPro, Aggrastat and Integrilin were introduced. Those drugs moved the field forward, so will this one.
Developing innovative drugs is not easy, but we are gratified by the results now in hand based on CHAMPION PHOENIX, indeed, based on the totality of data now available for cangrelor, our understanding of antithrombin and antiplatelet therapies and considering our productive relationships with leading hospitals around the world. Subject to regulatory review, we’ve reached a highly promising point of operating leverage in this field.
We and our investigating partners believe that these data support our long-held view of the clinical promise of cangrelor. Our approach to development of the compound has been consistent and we’re able to perform CHAMPION PHOENIX efficiently with the help of many, many people.
We welcome the customary transparent academic review process, which has been stimulating during preparation of The New England Journal of Medicine article and the presentation made by Professor Bhatt here at ACC today. We actually relish the chance to take on the excellent scientific and medical questions arising from that review and we’re confident in the robustness of our underlying logic, the data and our interpretations. In particular, we look forward to publishing the pooled CHAMPION program data around 25,000 patients.
Above all, at times like this, we’re energized by our potential ability to make a difference. And we’re, therefore, keen to support investigators, regulators and later on reimbursement experts, payers and caregivers to ensure that cangrelor finds its appropriate place in the care armamentarium of acute and intensive care hospitals around the world.
So with that in mind, we invite you to join us today three well-renowned interventional cardiologists. Here at the ACC, we are joined by Dr. Sameer Mehta, an interventional cardiologist based in Miami, who’s also chairperson of the Lumen Foundation, which does global work in the advancements of acute myocardial infarction and of course, he’s the author of many publications and perhaps the definitive book on acute myocardial infarction management in the cath lab.
Also with us, from the University of Caen in France is Professor Dr. Martial Hamon, who, among other things, is well-renowned for his work in arterial access particularly driving this option of radial access around the world. And third and not least, Dr. Dominick Angiolillo, who, as you may recall, was the first author on the BRIDGE paper that was published in JAMA and Professor Angiolillo is at the University of Florida in addition to being a highly active interventional cardiologist.
So with those three colleagues, plus Brent Furse here and Simona, we’ll be happy to take on questions internationally, in addition to working with them, we want to support the information needed to the financial communities.
So with that, let’s open it up for some questions and back to the operator.
(Operator Instructions) Our first question comes from the line of Adnan Butt with RBC Capital Markets. Please proceed, sir.
Adnan Butt – RBC Capital Markets
First, congrats to the company for the positive data shown today. And my first question, Clive, you can distribute it as you like, but it’s geared towards the investigators, can they independently comment on how they view the risk benefit of cangrelor and where they expect to use it specifically and in what patient populations?
Adnan, I’m happy to direct that to our three experts. Let’s start, Dr. Mehta with you, maybe so – first of all, a view on the risk benefit that Dr. Bhatt described this morning, the balance perhaps between thrombosis and the bleeding, I don’t know what your thoughts were.
Well, it – cangrelor appears to be almost perfect in the spectrum that you want to achieve in the cardiac cath lab by taking care of most patients with PCI. I tend to believe that the maximum benefit will accrue to the patients with ACS including STEMI. I think the dramatic reductions in the stent thrombosis is going to probably provide us the agent, which is remarkable and – the real key is going to be whether it completely eliminates the use of IIb/IIIa, because despite their efficacy, we have always been concerned about the increased bleeding. And to me, of course, this is a drug, which is not only good for the interventional cardiologists, but also for the cardiac surgeons, as it advances the care of the patients, who need to be moved to probably IV therapy and get them across surgery.
Dr. Mehta, thank you. Let me turn to Dr. Angiolillo for really an extension of the same question from Adnan. So Dr. Angiolillo, you did the BRIDGE study. Perhaps you could comment on that and what kind of patients those represent. And then also, talk about other settings in the cath lab for stable angina, for unstable angina so that you think this may be able to play a part?
Perfect. So I’ll start off with the potential of the drug and the huge unmet need for bridging therapy. We have a large number of patients, who are coming with an acute coronary syndrome or treated with stents and they rely on their dual antiplatelet therapy, standard of care with aspirin plus clopidogrel, prasugrel, for example, and do require surgery. And this is something which has emerged even more with the introduction of drug-eluting stents, where we need to have these patients on adequate antiplatelet protection.
The issue has been – well, if we send these patients to surgery while on an antiplatelet therapy, they have a high risk of bleeding. But the problem is if we stop it to prevent bleeding, they have a higher risk of recurrent ischemic events.
So to date, cangrelor has been the only agent that has been specifically studied in a prospective randomized fashion as a bridging strategy and the uniqueness of the drug is its pharmacological properties of having a very fast onset and offset of action and specifically, targets the P2Y12 receptor, which is being inhibited by the agents that we know to provide ischemic protection.
The other advantage is within the BRIDGE trial, it’s the only study with an intravenous agent, where we did a dose finding, so to tailor the antiplatelet effect, which is necessary for that specific patient. So there are many, many scenarios, because we know that the incidence of surgery can vary between 10% to 20% within the first year of having acute coronary syndrome or undergoing coronary stenting, so a very clear unmet clinical need.
And we do know that our patients with coronary disease also have progression of their disease and may require a bypass surgery in addition to any other type of surgery. So again, this is the setting of a classical BRIDGE scenario.
Let’s go to the PCI setting, and the trial replicates, really, what’s happening in the real world. In the real world, patients come to the hospital as an inpatient or as an outpatient and they’re on a cath lab table; we proceed directly with PCI in the vast majority of patients. And the timing to go to the cath lab is short and we do not see a broad uptake of pre-treatment because of the concerns of patients going to surgery. So again, bring up the concept of BRIDGE.
Here we have an opportunity to obtain immediate, so, when I say immediate, within seconds, blockade of the P2Y12 receptor, which has been shown over the course of the past almost two decades to be the key target in preventing recurrent ischemic events and this was fully supported as discussed from the PHOENIX trial.
And one other thing that was in Adnan’s question, the risk benefit. I mean, what you saw the data today for really doing its complete form perhaps for the first time, what was your impression?
Yeah, so definitely, when we are dealing with any antiplatelet agent, we want to find a fine balance between the reduction of ischemic events and minimizing bleeding complications. And so what we saw in this trial and the way it was designed, providing the drug during the procedure, we were able to get the best of both worlds. So using – only using a very sensitive definition of bleeding was there some signal which was the – essentially the hematomas, which is something that we expect in our patients, so a net clinical benefit, which is indeed very, very favorable.
Let me turn to Dr. Martial Hamon for a perspective, perhaps from more of a European viewpoint, Martial the dual antiplatelet therapy has been widely adopted in Europe. It’s even a little more progressive perhaps than the U.S. in some sense. How do you see this trial impacting your colleagues in Europe and in France and so on?
This is obvious, just in terms of the presentation two minutes ago, one hour or two hour – one hour ago, so it’s a new data for me. I’m very impressed by the result and clearly, I see the advantages of this drug especially in STEMI patients in Europe. So you address more – most of the concern you may have in this clinical setting and which is high risk PCI, we need to have a really effective drug on board immediately and for sure, cangrelor is the ideal drug to address this – all these ischemic events in the few hours after stenting and this is clearly very, very impressive for me.
Looking at the subgroup analysis, I’m also very impressed that in all subgroups analysis, all the consistency of the results are really going in the good direction for the primary endpoint, including high-risk PCI and all STEMI patients.
So again, I will stress that in the setting of the STEMI on primary PCI, this is really the ideal drug. We’re really waiting for such a drug, because the new gen pyridines including prasugrel, ticagrelor are not so effective in the setting of a STEMI that was delaying the absorption of the drugs and effectiveness has been proven to be not so important in this setting.
So clearly, in the setting of the STEMI, we are really eager to jump on this type of drug. For all the subgroup, especially elective PCI, probably we will need to look at those data more deeply in the future. But clearly the other strategy, which is loading dose, for example, of prasugrel in the setting on non-STEMI has failed, as you know, in Sankyo’s trial, which has been prematurely stopped.
So, again here in high risk non-STEMI patients probably we will find another group of patients, where the drug would be very, very effective. They are eager to adopt this strategy for showing the picture.
We’ll come to the other questions on the line in just a moment. I wanted to just stay with the point, Dr. Angiolillo, you could – another comment you wanted to add.
Yes, I wanted to add, because when we speak about high risk patients with STEMI and the introduction of the concept of intestinal absorption, we now have data from a study dealing with the more potent agents, not just with clopidogrel that there are several hours of time delay to achieve the effects. And this is just the nature of the Bs of how human beings are made, oral drugs just need to be absorbed and sometimes metabolized before they achieve the effects.
Another component is in the high-risk cases, which is being performed more in Europe are cooling strategies in STEMI patients. Cooling strategies have clearly shown to be associated, will reduce absorption and increase risk of stent thrombosis, which is something that has emerged over the course of past several years and now even published. And so, this is a further reason why we need a way to get effective and immediate P2Y12 inhibition not being concerned about the absorption process.
So, Dr. Mehta, just to build on this, there are lot of choices now and there are the IV II beta inhibitors, which have been going down a little bit, but nevertheless still around and available, then we have this new generation of oral antiplatelet agents, we ourselves, of course, promoting BRILINTA happily in the U.S. with our colleagues at AZ. So we’re very comfortable with the positive nature of these oral agents. But there are basic pharmacological differences between cangrelor and those IIb/IIIa groups and the oral agents. Can you help summarize the basic facts that underpin what clinically people affect?
Well, one of the aspects to understand is when you look at the pharmacokinetics, particularly when you are looking at the oral agents clopidogrel, prasugrel and ticagrelor, you’ve got issues both with the plasma concentration and then you are achieving the maximum and the steady state and with all of them, there is a pattern with – particularly with clopidogrel, you also have the issue of the Plavix non-responders, which can be a very high percentage of people.
And when you’re looking across the spectrum, you’re looking at the plasma concentration is achieved with the clopidogrel, you don’t even know exactly. Prasugrel takes about 30 minutes to 40 minutes, ticagrelor almost 2.5 hours than the cangrelor achieves that instantaneously and within a minute.
At one hour, when you’re looking at it, clopidogrel is inhibiting 25%; prasugrel improved it to 50%, and ticagrelor is a little better at 78%, and 100% of these are achieved with cangrelor. Maximum state when you’re looking at the drug, once again, about 50% to 55% with clopidogrel, 80% with prasugrel, a little better at 88% with ticagrelor and once again 100% with cangrelor, and these are exactly the similar issues, which you are reaching with the IV IIb/IIIa.
The big difference is not only that. I think the popular perception that you need to knock out platelets completely, platelets can be your friends too, and that is exactly the benefit where you see in that there is immediate recovery; as soon as you’re able to stop cangrelor, they resume their function.
If you are looking particularly, Clive, going back into what Dr. Hamon had mentioned on the STEMI subset, I think there instantaneously, you’re recognizing that globally, in the United States, Europe, all over Asia, we have the new terms, which are known as door-to-balloon time, where you’re trying to immediately open the infarct-related vessel, and why would you want to use the agent, which is not going to inhibit the platelets for three hours to four hours when you’re trying to do a procedure within 90 minutes. So I think IV cangrelor will receive almost immediate use for a very burgeoning night and now how much are these primary PCI or the STEMI cases, which we talk about. It could be as high as 27% of procedures across the globe.
Okay. Adnan, I think we’ve sort of talked around your question. I hope that’s sufficient. Would you mind going back into the line and we’ll get the next question please?
Adnan Butt – RBC Capital Markets
Sure, Clive. Thanks. Thanks.
I think I hope that was at least partly helpful. Very comprehensive answers. We could take the next question, please, operator.
The next question comes from the line of Jason Kantor from Credit Suisse. Please proceed.
Jason Kantor – Credit Suisse
Congratulations, as well, really great execution to the trial and in terms of data. I wanted to kind of ask some of the details here. There were some subgroups, where there were some remarkable activity. I’m just wondering if that – if there are some mechanistic reasons, for example, patients with – 5% to 10% of patients with peripheral artery disease, very big benefit there. I’m wondering if something underlies that.
And also, when you look at U.S. versus ex-U.S., ex-U.S. was about two-thirds of the patients, but it looked like overall, U.S. patients better and I’m wondering if there’s some aspect of the data that explains that, and do we have any information on the patient that went to CABG, did they do better having been on the short-acting drugs? And I’ll just step back.
Jason, thank you. Thanks to your PhD. You know well that subgroup analyses are somewhat hazardous and well, I think the whisker plot for peripheral artery disease does sort of jump out and look rather exotic. I think it would be a mistake to read too much into that. Even though there is an interaction p-value of 0.003 on that, I think, our view is when you examine 20 subgroups, 30 subgroups, 50 subgroups, you’re going to get one or two jumping out like that. So we don’t have any biologically plausible explanations. And I think at the moment, we feel that the overall consistency is quite astonishing actually. You’ve called out one of the ones that jumps out, but I don’t think we would over-interpret that.
Regarding the ex-U.S., U.S. as well, I mean obviously working with our colleagues at AZ, we’ve been helping them under the clinical community to appreciate with oral ticagrelor so that U.S., ex-U.S. interaction wasn’t terribly important either and that the best estimate of the results of the trial is its overall estimate. And I think we feel the same way here that it’s good to see that this class of drug, it seems to be affirmed that there’s no geographic interaction. And also by the way, there was no interaction with aspirin, which was an important question, which has been discussed in other setting.
So I think overall, the sub-population data are consistent and other than one or two blips of the kind you mentioned, I think we are very comfortable that we should interpret the trial in the same way the overall point estimate does.
As far as CABG is concerned, there are a handful of patients who went under CABG and Simona, I don’t know if you want to comment on that, but I think the CABG-related bleeding, which was not part of the primary bleeding endpoint was certainly not increased.
Yeah, I want to comment the primary analysis was conducted on the so-called modified intent-to-treat population, which included patients, who received drugs and underwent PCI. So that’s one part that reduced the potential number of patients undergoing CABG included in this analysis.
But the other aspect that’s important was design of the study was to identify patients and randomize patients after the anatomy was known. As you know, most of these decisions, whether or not a patient undergoes CABG or not, are made at that point. So those patients were not included in the study. So we have very limited data in bleeding in patients undergoing CABG. I do think there were about 12 patients or 13, I think, patients and there was nothing important to report on those patients.
I’m going to hand it back to Dr. Angiolillo in a moment to comment on the BRIDGE data on bleeding in CAB – in patients undergoing cardiac surgery. But I want to clarify the study analysis populations for our colleagues on the phone.
Obviously, you randomize all the patients. And then at that point, you have an intent-to-treat population. But the modified intent-to-treat population, who was pre-specified for analysis, included patients who not only received some drug – some study drug, but also underwent PCI. Well, you could say, what did happen to the people who didn’t? And in fact the ITT population, which includes the other patients, otherwise excluded, had exactly the same efficacy result.
Now, the safety population, which is usually looked at in these trials, is anybody who received any of the study drugs at any time, irrespective of whether or not they then went on to get PCI. And so, when we report the safety data here and in The New England Journal and to the regulatory agencies, the safety population is everyone who got any drug.
And then finally, there is another patient population called the per protocol population, where we studied patients who received all aspects of the protocol as exactly as laid out in the protocol, which is obviously a smaller number of patients, maybe 5% of patients who don’t. Every single one of these patient population showed the same results with the same – approximately the same point estimates about the bleeding and ischemia and essentially the same p-values for any differences.
So I think we can say it’s pretty robust. And with a trial of 11,000 patients you would really expect that. But let me come back to you, Dr. Angiolillo and just talk about those surgery patients in the BRIDGE trial, what was your experience there with regard to stopping the drug and then them going to surgery.
Very good. So the question that was actually, previously asked couldn’t have been better addressed than in the trial – the first trial, where patients went to bypass surgery. And one thing that sometimes people tend to forget from the BRIDGE trial is that cangrelor infusion within the trial was prolonged up to seven days with a median duration of around 3.5 days, so a very prolonged infusion out of specific editorial dose.
And the trial was specifically designed to measure at – on a daily basis, platelet reactivity and then surrounding the surgical period, this was also performed in a very meticulous way, really to show how at the time of surgical incision, did platelet reactivity have that gone backed down to baseline and which was nicely achieved.
And so in turn, the clinical finding was that there were no differences in the study-defined bleeding between the two groups, so again, very reassuring data, and again, despite a very prolonged treatment with cangrelor in the BRIDGE trial.
Okay. Jason, I hope that’s satisfactory for you. Maybe I could go on to the next questioner, please.
Jason Kantor – Credit Suisse
Thank you very much.
The next question comes from the line of Cory Kasimov, JP Morgan. Please proceed.
Cory, can you hear us?
Cory Kasimov – JP Morgan
Hello. Are you there?
Yes. Hi, Cory.
Cory Kasimov – JP Morgan
Hi. Sorry about that. So, thanks for taking the question. Let me add my congratulations as well. Two questions for you, Clive. I guess the first one’s for the cardiologists, and I’m just wondering, in their opinion, whether or not it matters that the primary – the positive primary endpoint here was driven by MIs and stent thrombosis as opposed to that being of the harder endpoint by death.
And then secondly, Clive, for you, now that the data had been presented and published and we gained a better understanding of the clinical utility of cangrelor, is there anything further that you could share with us with regard to your IP strategy or should we simply assume a five-year life cycle in the U.S.? Thanks.
Yeah, thank you. We’ll deal with those exactly in the order you gave them, if you don’t mind. So the composite endpoint, no significant reduction in death, the death rate, 0.3% in both arms, but what do you feel about that, gentlemen, Dr. Mehta, starting with you, perhaps?
Great. When you’re looking at PCI, the events you’re looking are exactly the acute MI, the death and more meaningfully, the stent thrombosis. Those are the endpoints which are making the big difference. And when you’re trying to evaluate the risk, whether the drug possesses a risk benefit analysis, the downside of it has to be that these benefits have to be countered by the bleeding. So now you have a drug, which reduces the ischemic endpoints across the spectrum than the ones which are most relevant to us, death and MI, without causing bleeding I think is extremely favorable.
Yes. So I think when we do clinical trials, we need to be always – always keep in mind that we’re not targeted to reduce mortality and – because the trials were just not designed that way and quite frankly, with the very low event rates as this real world clinical trial shows, we will probably need a 100,000 patient trial at a minimum to show that.
So we always have to keep in mind the – why we’re conducting these trials and the definition of the endpoints.
Yes, I agree with my colleagues for sure and with the follow-up of 48 hours, which was – here as a time point of our study, stent thrombosis and MI are very, very important endpoints to look at and there is no excess of bleeding. And we stress this point that without excessive bleeding, the results are really impressive for me in this clinical setting.
And again, in the setting of high-risk STEMI patients, that makes a lot of sense for me to be combined especially with a direct thrombin inhibitor bivalirudin and of course, having a regular access in all those patients as a different access line.
Clive, another, I think, distinction here is if you look at the subset of the patients, it was found equally beneficial across the spectrum of what we do in the cath lab, PCI with the stable patient, unstable patient, ACS, non-STEMI and the STEMI. So I think it has a favorable disposition across just about everything we do in the cath lab.
All right, good, and Cory, I’d add something that Simona had mentioned. We will be ourselves presenting to the regulators the combined analysis of all the CHAMPION trials, which is approximately 25,000 patients now and there you probably do have enough deaths to at least get a bit more comfort about what direction it’s going in and I think that having already looked at that, we’re pretty comfortable with the fact that deaths are numerically reduced, albeit non-statistically significantly. And I think people find that very reassuring that it goes in the same direction as does the other endpoint. So I think that’s very consistent.
Now, as far as the IP strategy is concerned, Cory, I think today we’re going to restrict most of our comments to the trial itself and the data. As you would imagine, we have thought about that a lot. We’re, especially now, so excited with the data. We’re going to pull out all the stuffs and make sure that we get as longer period of runway on the exclusivity with this drug as we can. And you’ll be hearing, as Simona said, more about that through the years.
So, today we want to focus on the PHOENIX trial. But you’re absolutely right and that’s something we’ll be pushing very hard.
Cory Kasimov – JP Morgan
All right, fair enough. Thank you.
Thanks, Cory. I think we can go to the next question. I think it may even be from Joe Schwartz.
The next question comes from the line of Joseph Schwartz with Leerink Swan. Please proceed.
Joe Schwartz – Leerink Swann
Hi, everyone. Thanks for taking the question. Congrats. I wanted to ask how the physicians saw cangrelor fitting into or changing the antiplatelet treatment algorithm in terms of where it is best used in the hospital. And as they think about patient flows, can antiplatelet therapy be given earlier now, in the ER even, without as much pressure to determine anatomy first in case of patient requires surgery later. How do they see things evolving with cangrelor available?
Again, let’s go straight to them. I’m going to do it backwards this time. We’ll start with Dr. Hamon, your perspective on Joe’s question?
Yes, it’s a very important question. You know that in France in Europe, we have a lot of pre-hospital ambulance, et cetera, with physician on board, so we can imagine for STEMI patient, for example, having this drug started as soon as possible to have an excellent projection of primary PCI.
In all of those cases, probably in the cath lab will be (inaudible) that we need to think about it. And that for sure, in Europe, we are trying to start as early as possible for the drugs and we are probably talking about it.
Joe, I think one of the messages that I’ve got from experts over the years is as much as the onset speed of the drug is interesting, and it certainly is it’s the offset. It’s the no regrets that if you start it, you can’t stop and it’s going to go away. And as Sameer Mehta mentioned a moment ago, you get your platelets back quickly. Nowhere more demonstrated I think Dr. Angiolillo than in the BRIDGE trial, how do you react to Joe’s question?
So it’s an interesting question, and typically, in clinical practice, we try to apply the use of the drug the way it was done in the clinical trial, but then once we have the drug in our hands as clinicians, we try to use it in ways that maybe was not conducted in the trial, because we think of benefits for the patient. And so we already alluded to the STEMI population. And this represents actually the only cohort where we know that an option treatment reduces mortality. So clearly, there is an opportunity there as well as an opportunity in those settings where you believe that you need to get a drug on board as soon as possible, but again due to the very fast offset of action, you’re not concerned about surgery.
Another population, which was briefly alluded to this morning, but again, as a practicing interventionist working at a bigger pro hospital, is for our incubated patients now. These are – were not patients obviously that we would consent to be part of a clinical trial, but do represent in big volume centers, where we get a lot of sick patients, where you want to make sure that the drug works.
We have an opportunity for the first time to have an IV P2Y12 receptor antagonist and also without having all the problems that we’ve had with oral agents where they need to be crushed, put down on nasogastric tube, problems of absorptions, and I do believe that this represents another window of opportunity in addition to how the drug was studied specifically in the trials.
Okay. I’m going to turn to Dr. Mehta in a minute. Where else do you think this may or may not be applicable?
Clive, I can – I’m going to answer that question in another way, in which case today that the data which is available to us today, where would you not use cangrelor. That’s another innovative way of looking it. I think the only subset, where you may not want to use this drug would be an elective PCI patient, where the anatomy is known.
For most other patients, where you do not know the anatomy, and the patient is in an emergent condition, now let’s explore that. Where you don’t need the anatomy, that makes such a big difference, because whenever you are blindly starting on even the most potent antiplatelet, you have condemned the patient to a PCI option only. You have virtually eliminated the surgical options, because now you are going to wait five days to seven days and the patients whose anatomy you don’t know was coming to you crashing with the STEMI or ACS, that to me is going to – it gives you the spectrum of predictability and control over your patient’s outcome in a hospital whether he needs PCI or surgery.
The other patient you are looking at is this aspect of knowing the anatomy, I think, is going to play a very critical role. So to me, as I predict out, I think as soon as this drug is going to become available, you’ll see immediate pickup in the STEMI cases, probably also in the ACS non-STEMI and some patients with the elective, where the anatomy is not known, because you would rather use a drug which couldn’t be turned off.
Now, one of the other questions, which had come off, which probably did not get fully explained, is the comparison with the IIb/IIIa. And when you are looking at the pharmacology and your understanding, one of the problems that the IIb/IIIa which probably leads to their bleeding, is the prolonged duration of infusion, which is needed.
So now, you are going to be using the duration of 12 hours with the abciximag and up to 24 hours and 36 hours with the Integrilin and Tirofiban. Tirofiban, of course, is virtually out of the U.S., but it is still relevant in parts of Europe and hugely in Asia. So as opposed to this, you’re going to have cangrelor, which you can turn off, I think, the median duration of infusion is about two hours, and you’ve got your platelets back.
Okay. Joe, we’re going to move on, if you don’t mind. I think there’s another question behind you.
Joe Schwartz – Leerink Swann
Thanks very much.
The next question comes from the line of Jonathan Eckard with Citi.
Jon Eckard – Citi
Hello. Thanks for taking the question and also congratulations on the data. My question is kind of, I guess, a continuation of Joe’s question, where, if I’m not mistaken, the current practice, both in Europe and U.S., would be kind of initial treatment maybe with an oral agent like clopidogrel and before the patient reaches the cath lab, what kind of interaction studies have been done with cangrelor and some of these other agents that would provide comfort in doctors, who – to use cangrelor in a patient who may have already received an oral agent before reaching cath lab?
Yeah, I think that’s a really good question, actually. And you may recall that in the CHAMPION PCI trial that preceded this one, 30% of patients entered and randomized on clopidogrel already. So that’s a very important subset of data, so it gives us a lot of confidence that we are adding substantially. Remember that those people probably are on a 75 milligram maintenance dose, hopefully, and their level of platelet inhibition at the time they arrive at the hospital, assuming they’re responsive, is going to be in the 40% to 55% inhibition range.
I think what we’ve demonstrated in this trial is that that’s not enough. I think that we also demonstrated in our previous trials that stent thrombosis will happen in patients who are under-inhibited. And so, therefore, even in those situations, there may be some physicians, who would choose to take a sort of belts and suspenders approach and add the IV provided they don’t believe they’re having bleeding and certainly in CHAMPION PCI, the bleeding results were no different to the ones we talked about today. So I think that’s going to be quite important.
I also want to comment again on BRIDGE, because the other situation where patients did come in on Plavix. Dr. Angiolillo, would you comment on that one?
Yeah so, definitely actually it was the criteria for being included in the trial to have been exposed to a kind of pyridine either clopidogrel or prasugrel.
And so, sometimes with cangrelor, there’s a little bit of confusion on the concept of interaction. So if a patient is on – has been exposed to clopidogrel or to P2Y12 inhibitor, already arm the P2Y12 receptor, cangrelor comes on and inhibits the unblocked receptors. And we have a series of beautiful PD studies performed by some of our European colleagues nicely demonstrating that additional antiplatelet effect coming to near complete P2Y12 receptor blockade and there is an interaction for the patients for a – on treatment. So hopefully that addresses the interaction question. And again, we already alluded to the data from the prior CHAMPION trials.
And regards to the concern of the upstream treatment, again this – I think my question – my response to those answers is what happens when you give the drug on top of, but there are – supporting on the score there’s a lot of profound regional differences in practice patterns across the globe on the value – on pre-treatment. And so, yes, this does occur, but I can say that in our practice, we do not re-treat for two reasons: Time to the cath lab is quick. You want to know coronary anatomy first before you start giving your blood-thinning medications and two, if the patient does need to go to surgery, it does become an issue.
Jon, as well I think, when we originally started working with these transition studies a few years ago, we did a trial in Kentucky, which frankly, confused us as well at the time, which was looking at the way oral clopidogrel did or didn’t interact with IV cangrelor. I think we’ve updated – we’ve done a lot more studies since then, which I think have really cleaned this area up now and exactly what Dr. Angiolillo is saying. I would say, though, that we will continue to do studies of transitioning on and off oral agents. I think the more we know about this, the better.
The good news is we have a very nice set of assays we could use to demonstrate all these. And so far they saw that they did show a very smooth transition, both on and off the oral agents, the modern oral agents that we hope will be increasingly used including BRILINTA. So I think we’re making progress there. We’re looking forward to that being pretty cleaned up in the next year or two. Jon, I hope that’s satisfactory for now. Let’s turn to the next question, if we may.
The next question comes from the line of Umer Raffat with ISI Group. Please proceed.
Umer Raffat – ISI Group
Hi, guys. Thanks for taking my question. Congratulations again. I had a few quick questions. First one was just want to dig a little more into the lower risk patients. So I wanted to understand what’s the time between randomization and the PCI procedure instable angina patients in this trial, because I’m trying to understand the implications for patients that are scheduled for PCIs in the following weeks. So that’s number one.
Number two, I didn’t see stroke endpoint broken out in The New England Journal paper or in the presentation. So I just wanted to understand the performance there. And then finally what are your thoughts on The New England Journal editorial that was published this morning as well? Thank you.
Well, thanks a lot for asking me those questions. I really appreciate it. I’ll deal with The New England Journal editorial in just a moment, hopefully, respectfully as we always would. But Simona, you’ve really worked hard on these data. What – how would you give, Umer, his insights there?
Yeah, so for the stable angina patients, 56% of stable angina patients from around the world, we required more as an inclusion criteria for the anatomy to be known. So therefore, these are the patients that get diagnosed on the table and they immediately proceed to PCI. So the time between randomization treatment is we’re saying about 30 minutes which was required by the protocol.
And just to add to that, in the United States, there’s data that suggest that what’s called a same-day PCI is on an increase. These are the outpatient procedures and they’re rising and they are – probably 30% of the stable procedures are the so-called same-day PCIs, where you diagnose a patient on the table and then you needed to be proceeded to PCI and those were the patients included in PHOENIX trial.
That’s great. Now, turning to the editorial, look, I think we – this is a great process. You – the academic review process, Umer, is rigorous and the idea that everybody agrees on anything – agrees on everything, we wouldn’t make any progress whatsoever in science. So that’s the first thing to say.
We recognized the issues. In fact, I think that the issues raised in the editorial are the very issues we expect to discuss with regulators and with the doctors and caregivers around the world. Where we highlight 75% of the patients had 600 milligrams of clopidogrel to compare? An editorial might reasonably highlight the fact that means that 25% didn’t and contrast and compare the viewpoints. I think that stand in a very healthy and respectful way all around.
Similarly, questions about how endpoints were defined or adjudicated are important questions and perhaps because of the way The New England Journal sets things up, all of the absolute details of this are put into supplementary tables and protocols, which are not necessarily held in the main paper. And I believe that the questions that the editorial raises regarding, for example, stent thrombosis are all answered there very explicitly.
I want to say that every patient in this trial had core lab review of their angiograms and all stent thrombosis in this trial were adjudicated at CRF. In fact that was highlighted in the conversations after the – in the review by the panel after Dr. Bhatt’s presentation earlier today.
So I think that might be a fact that the editorial missed in the actual data and the actual conduct of the trial. But in all respects, the editorial that – that’s been witnessed is very healthy, very reasonable and we’re happy to take on the debate.
Umer Raffat – ISI Group
Great. And then the stroke endpoint?
Well, the stroke, I think, there was like one-on-one. I think they want to be two strokes a trial. Simona, do you remember?
It’s absolutely no signal at all. Fortunately, very, very few patients in this trial had a hemorrhagic stroke and I think it was a non-event. Well – no, it was clearly an important event for those patients, but it’s not different between the two groups.
Umer Raffat – ISI Group
Great. Thank you very much.
Thank you. Let’s go to the next question if we may, please.
Your next question comes from the line of Steve Byrne with Bank of America. Please proceed.
Steve Byrne – Bank of America
Hi, thank you. It appears that the incremental benefit of the cangrelor was roughly the same whether the clopidogrel was 400 mgs or 600 mgs. And so my question for the panel here is, is that logical that you could have a similar incremental benefit, but at a different level of thrombotic events depending on whether on the dose of clopidogrel and at the higher dose, you have an overall lower level of events, is that logical and do you see the study as maybe changing the conversation from one versus the other or perhaps both is better?
Interesting question. Martial, you’re a trial meson. What do you think?
I think when you look at the data in the subgroup analysis the primary endpoint is going in the same direction in both groups. And in fact, it’s a little bit better with 600 milligram of clopidogrel. And I – in the OASIS-7 trials or CURRENT trial comparing different dose of clopidogrel, the magnitude of the effect was not so huge. So in such a trial, I think it’s very reensuring that there is no interaction at all between the two doses anyway, because you have 60% of the patients who are inactive or stable patients. I don’t expect any drastic impact on this specific subgroup.
I think, as well Steve, one of the limitations of these univariate analyses is that there could be other – there could be multiple factors at play. For example, we know that the 300 milligram dose was more frequently given to stable angina patients, whereas the 600 milligram dose was more frequently given to ACS patients. And so, there may be things to discover in multivariate analysis to iron all this out. I think when we’ve done those multivariate looks including the analysis of the primary endpoints stratified by 600 milligram by 300 milligram it comes out as a similar effect irrespective of these multiple interaction factors.
So I think the important question it’ll be continued to be debated by the academics and we’ll keep working within the market. I don’t think, from a product adoption point of view, it’s going to make much of a difference.
Steve, any other questions for you right now?
Steve Byrne – Bank of America
No, that’s good. Thank you.
Yeah, thank you. Let’s go to the next question, please.
The next question comes from the line of Biren Amin with Jefferies.
Biren Amin – Jefferies
Yes. Hi, guys. Thanks for taking my questions and congrats on the data. I guess first off, Clive, in that clinical benefit, I think Dr. Bhatt reported odds ratio of about 0.80 when you’re incorporating major bleeding into the primary composite. So was this based on GUSTO severe major bleeding or did you also look at ACUITY major bleeding in which I think you reported significantly higher major bleeds for cangrelor? Thanks.
I’m going to let Simona answer that one, Biren. Good question.
Yeah, so it was – so the primary safety endpoint was successfully declining the protocol and that was the GUSTO-defined severe bleeding. So, net clinical event includes all the ischemic events plus GUSTO severe bleeding. We have combined GUSTO severe/moderate, which is more sensitive tail and the results remain significant. We did not include ACUITY into (inaudible).
Yes. I think the net benefit equation, although was post hoc as Dr. Bhatt pointed out, it has become of great interest. I think that we can take some credit for putting that on the map with Angiomax since they look pretty good for this. Second question, Biren, I think you had two points, maybe.
Biren Amin – Jefferies
Yeah. And I do have a question on ACUITY major bleeding. I think it was as we mentioned, it was driven by groin hematoma. So I wanted to understand how many of the patients had femoral access versus radial access, which appears to be a growing trend in the U.S.? Thanks.
Yes. And we have one of the world experts in the room, so we have to talk about that. I think about 20% radial, if that was right. Is that correct? And really, I think for the – obviously, we know that radial reduces access-site bleeding, but we also know that radial doesn’t reduce the important bleeding associated with the organ bleeds and I don’t think that trial results were different between the two groups.
Martial, do you want to comment on that? I know it’s your interest.
Yes. Yes, of course. It’s very important, because it’s really the different exit time now more and more trials in Europe and I know that in the United States it will be seen in two years for sure. And in the trial here, you had the subgroup analysis showing that you have identical result in this subgroup of radial access compared to the femoral – to the patient explored and treated by femoral access.
So I think, as expected, the most important thing for the patient is clinical endpoint. You cannot imagine to have different result in this subgroup, especially with a drug which is not increasing bleeding too. And it is a stressed point again that bleeding is very similar between the – it’s very low and no excessive bleeding using cangrelor. So in the two groups, femoral access or radial access again here you have the same result. And of course, it is a smaller group. It’s around 3,000 patients compared to 8,000 patients treated by femoral access, but again, as you can see, the subgroup analysis is you have similar trends between the two groups.
Okay. We’ve been on better now in 10 minutes, I’m going to suggest we take one more question and then, maybe break for lunch. Operator, are there any more questions left?
There is a follow-up question from Adnan Butt.
Okay, let’s go. Adnan?
Adnan Butt – RBC Capital Markets
Thanks. Thanks for cutting me off earlier.
Oh, sorry, did I? I’m sorry.
Adnan Butt – RBC Capital Markets
So, here’s my question. Let’s – well, first, what’s the general view of using clopidogrel as a comparator versus either BRILINTA or Effient? And secondly, in terms of switching data, what’s the strategy there, when might that be available? And for the physicians, how comfortable would they be switching patients to either BRILINTA or Effient versus clopidogrel?
Right. Well – I’ll deal with the first one; then I’ll leave the last one for Sameer Mehta and Martial Hamon. Well, first of all, as a comparator drug for clinical trials when the study started, I think it was a no-brainer to have preempted the entry of ticagrelor into market would have been, I think, a mistake given that they haven’t even finished the trials when we started this trial. And then although prasugrel was, by this time, I think on the market when we started this trial, I think the experience with it was very little and I think we would have been heavily criticized for not taking on clopidogrel 600 milligram.
Remember that in our prior trials, the 600 milligram dose of clopidogrel, which is the global standard, was required in our previous trials, so we already had a lot of data regarding 600 milligrams of Plavix and we were comfortable in this trial to let it be according to institutional preference. And as you see, 74% of hospitals and the trialists in this trial did use the 600 milligram.
So I think we have tens of thousands of patients with the comparative data against the worldwide gold standard of therapy which is clopidogrel. The prasugrel and BRILINTA adoption so far is, I would say, generally modest, but of course increases. Going forward, I’m sure people will want to study these drugs, either in tandem or in series, and we obviously are going to continue investigating those issues.
So, BRILINTA, we’re in partnership with AstraZeneca. We’re very happy with our partnership. We stated some months ago that it was our intention to work in partnership with AZ with BRILINTA. If you remember, it’s called the ABC strategy which is Angiomax, BRILINTA, and cangrelor, and here we are now at a point where perhaps some of those studies can go forward. Similarly with our colleagues at Lilly and Daiichi Sankyo, there’s a lot of interest in working together to make sure we can provide, from both sides, the right information for physicians to look at transitioning from and to oral therapy. This is a key issue.
So, I’ll leave the last word, though to Professor Mehta and Professor Hamon on the matters of your view of switching and how important this is going to be going forward.
I think several important points were raised. Most have been answered. As the interventional cardiologist, if you look at what you want as the most desirable aspects, as you start to proceed the PCI procedure, there is no doubt irrespective whether you are in the stable patient and definitely more on the unstable and STEMI, you want maximal inhibition of platelets without paying a price for it. That’s all. So, as far as if you understand that as – you bring up an excellent point that this data is comparing it to clopidogrel, but once you have this basic understanding, you can extrapolate the data also to prasugrel and ticagrelor.
There was a recently done Italian study of 155 patients. For them going to the cath lab, they realized that this is the proof to verify now assay that there’s only with the best in group ticagrelor, there was a 55% inhibition, so you are taking these patients without maximally inhibiting.
One of the points in the conference call, which didn’t come up today, I was a little surprised, is that already in parts of the world there is a release of the bioresorbable stents. So you’re going to be putting in a $6,000 stent without inhibiting the platelets, doesn’t make any sense. I think this is going to be extremely critical. You want a drug, which can immediately turn off the platelets and have an ability to restore the same platelets which can be your friend immediately after the procedure.
So I think overall, it’s a fantastic trial. It has covered most of the relevant aspects. The two ones, which I think are unknown, you picked up one of them is the one how it compares with the newer antiplatelet agents. And of course, we’ll have to figure out how exactly does it compare with the IIb/IIIa agents. It’s just that historically we know that blocking a P2Y receptor is more effective and a better strategy without paying the price of excessive bleeding.
And briefly Martial any additional comments?
No, I think – I agree completely with Sameer on this specific point. For sure, it’s maybe a drug to be used in PCI overall especially in acute coronary syndrome management and we stressed the point again that the STEMI patient really needs a clinical setting while you really need to be – to have a rapid onset of platelet inhibition. So it’s a fantastic drug in this specific subgroup. I’m sure of that.
Regarding the switching strategy, of course, here we have clopidogrel and we know that now especially in some trials in Europe, we move them with new gen operations using prasugrel more and more effectively in STEMI patients, for example, and ticagrelor in the future for sure. But anyway, we had to follow the context on registry for sure to look at that, but right now, cangrelor and IV ADP receptor blockade like this is – and given the results of the CHAMPION PHOENIX trial, it’s really long much trial I think.
Well, thank you very much everybody. Adnan, I hope – I apologize for cutting you off earlier. I’m so sorry. I hope that has addressed that question. We will, of course, as a company, be continuing to study these switching strategies. Regulators will find them interesting just as we all do. So, more work to come as outlined in Simona’s view for the rest of the year.
I think we’ll call it a day here. I want to thank everybody for joining us. I want to congratulate Dr. Skerjanec and her team. Thanks, of course, the literally hundreds of people, investigators, study coordinators in the hospitals, monitors, pharmacists who get involved in doing these global trials, it really is an amazing it takes a village as they say and really this one was done in an excellent way and the quality of the results and of the conducts of the trial does everybody know it’s credit.
So thank you to all of those people and also, of course, thank you for your interest today dialing in on a Sunday and we look forward to speaking again soon.
Thanks a lot. Bye-bye.
Ladies and gentlemen that conclude today’s conference. Thank you for your participation. You may now disconnect.
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