ChemoCentryx, Inc.
Q1 2018 Earnings Call Transcript

Published: 10 May 2018

[Operator:]

Good afternoon. And welcome to the ChemoCentryx First Quarter 2018 Financial Results Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session. As a reminder, this conference call will be recorded. I would now like to turn the call over to Steve Klass, Vice President with Burns McClellan. Mr. Klass, please go ahead.

[Steve Klass:]

Thanks, Chris. Good morning and welcome to the ChemoCentryx first quarter 2018 financial results conference call. Earlier this afternoon, the Company issued a press release providing an overview of its financial results for the first quarter ending March 31, 2018. This press along with a few slides that you may find helpful while you listen to this call are available on the Investor Relations section of the Company’s website at www.chemocentryx.com. Joining me on the call today is Dr. Thomas Schall, President and Chief Executive Officer of ChemoCentryx who will review the Company’s recent business and clinical progress. Following his comments, Susan Kanaya, Executive Vice President, Chief Financial and Administrative Officer of ChemoCentryx will provide an overview of the Company’s financial results for the first quarter before turning the call back over to Tom for closing remarks. During today’s call, we will be making certain forward-looking statements. These forward-looking statements are based on current information, assumptions and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. These risks are described in the Company’s filings made with the Securities and Exchange Commission including the Company’s annual report on Form 10-K filed on March 12, 2018. You are cautioned not to place undue reliance on these forward-looking statements and ChemoCentryx disclaims any obligation to update such statements. In addition, this conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, May 9, 2018. ChemoCentryx undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this live conference call. I will now turn the call over to Tom Schall.

[Dr. Thomas Schall:]

Thank you, Steve. And good afternoon to everyone listening. Thank you for joining us on our first quarter 2018 conference call. It’s been a scant two months exactly since we reported to you on our fourth quarter results. So, I will keep my remarks today brief. But, even in that time, we have continued to make significant progress across our programs. Specifically, we are nearing completion of patient enrollment in the ADVOCATE trial, which is our global Phase 3 pivotal trial of avacopan for the treatment of ANCA-associated vasculitis. Also, our second trial of avacopan in C3 glomerulopathy or C3G, a disease with no FDA approved therapies is also performing extremely well. Avacopan is enjoying an increasing awareness in the clinical and patient communities of how it is a highly differentiated, highly precise approach to inhibiting the complement cascade and disease settings and one where avacopan quite unlike other drug candidates -- is quite unlike other drug candidates in the growing complement intervention space. Accordingly, today, [ph] I’ll touch upon how our planning continues to pace to launch our next clinical trials of avacopan in hidradenitis suppurativa or HS as the Company expands into orphan dermatological diseases as well and where we intend to make a major innovative push. Separately, we continue to advance our CCR2 inhibitor CCX140 with trials in two subpopulations of primary focal segmental glomerulosclerosis or FSGS, the second asset in our CCXI orphan renal franchise. Let me start with avacopan for the treatment of ANCA-associated vasculitis. Our ADVOCATE Phase 3 pivotal trial is progressing superbly. The first patients enrolled have now completed their 52 weeks of treatment and we are now nearing full enrollment. Indeed today, we approached nearly 90% enrollment, the exact number is 262 patients enrolled out of the 300 total patients needed, as shown in slide three, for those of you who are following our slides. In addition to showing the effect of avacopan and improving active anti-neutrophil cytoplasmic auto-antibody-associated vasculitis or ANCA-vasculitis, the ADVOCATE trial will also test avacopan’s durable clinical benefit, which is one of the major limitations of the current standards of care. Why and how is this possible? For those of you following the slides online, I will now refer to slide four, which depicts how avacopan selectively targets the C5a receptor, C5aR, which is sometimes also called C5aR1 or even alternatively CD88 in the medical literature, for those of you who are looking up some of the references. Through its unique and highly precise mechanism of action, avacopan blocks the activation of destructive, disease causing C5a simulated neutrophils, while preserving intact the rest of the complement system and accordingly preserving the rest of complements function in tissue maintenance and in immune defense. And avacopan does so as an orally administered capsule. Importantly, avacopan’s mode of action is so precise that, and this is by our actively designing it this way, we leave entirely untouched the protective actions of a second C5a responsive pathway, those that occur when C5a activates the beneficial C5L2 receptor. In short, our doctrine, precise mechanism leads to precision medicine, leads to better clinical outcomes. At last month’s meetings of the National Kidney Foundation, NKF, we discussed the data underlying the optimism that clinical leaders have for success in the ADVOCATE Phase 3 pivotal trial in ANCA-vasculitis. The Phase 3 ADVOCATE pivotal trial is modeled overwhelmingly under proceeding Phase 2 trial designs with avacopan and ANCA-vasculitis. The Phase 3 ADVOCATE trial targets the same patient population as previously treated, it measures the same clinical effects and endpoints, and it draws on the marked benefits previously seen with avacopan in Phase 2. Our data shows that avacopan in trials to-date provides rapid and marked control of ANCA-vasculitis and to-date with excellent safety profiles while importantly, also markedly reducing the total burden of this devastating disease by reducing toxicities associated with the previous standard-of-care including the high chronic doses of noxious steroids that have been in the previous standards of care. And avacopan treatment significantly enhanced patient quality of life, all of this in a convenient, orally administered capsule. Just to reflect on that point. As many of you know, the current standard-of-care regimen for ANCA-associated vasculitis is a source itself of much of the total burden of disease for ANCA-vasculitis patients, and this is especially true from the effects of the chronic high doses of steroids such as prednisone or methylprednisolone that are the standard-of-care in this disease. We aim to make such standard regimens simply obsolete in ANCA-vasculitis. The time has come, patients need a new, safer standard-of-care for ANCA-associated vasculitis. And clinical data suggests avacopan may be just such a way forward. We look forward to the completion of the ADVOCATE Phase 3 pivotal trial and we expect results from that trial as successful, will form the basis of a new drug application NDA to be complied late next year and submitted to the U.S. FDA sometime in the first half of 2020. In the meantime, as you may know, we have a conditional marketing authorization application or CMA application, based mainly on the Phase 2 clinical data so far, in front of the EMA at present. This application is going through its normal review process, and we expect the final opinion on that application sometime early in the next year. Avacopan is clearly differentiated in its mechanism of action. It also has the convenience and benefits of an orally taken small molecule. We believe avacopan may represent an unprecedented solution for those who and now for far too long have been infected with devastating diseases such as ANCA vasculitis and its inadequate traditional treatment regimen. There is good news too in our second indication for avacopan. This refers to our clinical trial of avacopan in the rare, though severe kidney disease of C3 glomerulopathy. C3G is a terrible malady for which no FDA approved therapy exists. It is very gratifying to report today that our randomized, controlled clinical study of avacopan and C3G is now nearly 30% enrolled. So, the trial is making very good progress. As can be seen on slide five, the trial is a six-month primary endpoint study comparing avacopan and a cohort of 22 patients with the control group of 22 patients who will receive placebo for six months and then the placebo patients will cross over to avacopan. The primary endpoint is the percentage change in the C3 histological index after six months of treatment. Other standard kidney function endpoints will be assessed as well. As mentioned, C3G is a kidney disorder which often and certainly ultimately is life-threatening, and for which there is no approved effective treatment. C3G typically strikes young people who are treated with dialysis and sometimes kidney transplant. Half of all people with C3G experience kidney failure. And even with kidney transplants, the transplants often fail to halt the progression of the disease. Complement deposition in the glomeruli of the kidney disrupts kidney function. And C3G is characterized not only by C3 protein deposits, as you would expect from its name, but also frequently by the presence and deposition in the kidney of those downstream proteins in the complement system C5 and C5a proteins making this disease an excellent target for avacopan. By blocking the C5a receptor, avacopan could inhibit the activation of the destructive cells that cause the inflammation and tissue destruction and ultimate organ failure in C3 glomerulopathy. Now, turning to our second drug candidate, at least for today’s discussion, CCX140. CCX140 comprises the second part of our new armamentarium of innovative indeed unique therapies for orphan renal diseases. Our indication for CCX140 is the disorder known as focal segmental glomerulosclerosis or FSGS. FSGS is another debilitating chronic kidney disorder with no approved treatment option, as shown in slide six. In March, in the journal PLOS ONE, we published our peer-reviewed results of in vivo studies, examining the efficacy of inhibiting the chemokine receptor known as CCR2 which is target of CCX140 in the treatment of FSGS in model systems. Our published data show that blocking CCR2 provides marked renal protection in two well-established models of FSGS with rapid and sustained large reductions in proteinuria as well as improved histological changes including increased podocyte density. There will be a further presentation of these data at the upcoming European Renal Association - European Dialysis and Transplant Association or Era-Edta meeting in Copenhagen later this month. These findings support our approach in FSGS. We are conducting two clinical studies with our CCR2 inhibitor CCX140, one in patients with primary FSGS, with nephrotic syndrome and another in sub-nephrotic primary FSGS patients. We are in the process currently of actively recruiting these FSGS patients to these studies. FDA has indicated that especially for nephrotic syndrome FSGS patients, a significant lowering of proteinuria may well constitute itself the endpoint for registration. And importantly, recall that we have a good degree of clinical experience with CCX140 in the renal disease setting. CCX140 in a one year long, large Phase 2 trial in patients with diabetic nephropathy that is chronic kidney disease that occurs as a consequence of Type 2 diabetes, met its primary endpoint of a durable, one-year, significant reduction in proteinuria. Finally, I would like to touch upon our exciting expansion with avacopan into orphan dermatological diseases. As avacopan lives up to its description as a pipeline in a drug, we are working on our plans to initiate clinical development of avacopan in a new disease area, hidradenitis suppurativa or HS. As you can see on slide seven, HS represents a very, very significant unmet clinical need. We have received a great deal of interest from the dermatological and rheumatological investigational clinical communities in this disease. They are fascinated as we at CCXI are that HS is a neutrophil-mediated disease where C5a plays an important role in driving the disruptive path of physiology of neutrophils in this disease. There is a great potential demand in HS. The only incumbent approved therapy is an antibody therapy. And room for therapeutic improvement seems to be the consensus in the HS community. Nevertheless that incumbent appears to have sales approaching $1 billion in HS. Our belief is that avacopan could be a more effective and very valuable remedy in this important dermatological indication. In the near-term, we will update you and the details of our development plan that will move swiftly and that scale in the development of avacopan in HS. Make no mistake, this could mark another era of ChemoCentryx as we move avacopan into a second important area of chronic need that is orphan dermatological diseases. On this topic, I will just preview that this new era in orphan dermatological diseases will certainly be an anchored by avacopan and HS but ultimately may in addition be extended with a new asset coming out of our discovery pipeline platform. Specifically, an orally administered small molecule inhibitor of the chemokine receptor known as CCR6 could play a unique and key therapy role in the orphan disease of say study pustular psoriasis or GPP. GPP is a rare inflammatory skin disorder and extremely high unmet clinical need, and in area for large potential value creation. In fact, we recently presented a poster two days ago at the American Institute of Immunologists meeting in Austin and another poster will be presented at the International Investigative Dermatology meeting that takes place next week in Orlando on the properties of molecules inhibiting CCR6 in disease models including those for generalized pustular psoriasis. I will discuss this exciting new asset in more detail in future calls. As I turn the call over to Susan to review our financials, I will remind you that we have a very healthy balance sheet. Capital efficiency being a long-standing and proud tradition here at CCXI. We believe for example we have sufficient funds to advance avacopan to top-line data from our Phase 3 ADVOCATE pivotal trial and into potential registration signings in the U.S. and EU. Susan?

[Susan Kanaya:]

Thank you, Tom. Our first quarter 2018 financial results were included in our press release today and are summarized on slide eight. Revenue was $9.5 million for the first quarter compared to $8.2 million in the first quarter of 2017. The increase in revenue was primarily due to the Company’s adoption of Accounting Standards Codification Topic 606, effective January 1, 2018. Research and development expenses were $14.7 million for the first quarter compared to $10 million for the same quarter in 2017. The increase in 2017 to 2018 was primarily attributable to continued patient enrollment in the avacopan ADVOCATE Phase 3 pivotal trial in ANCA-associated vasculitis and expenses related to the avacopan and CCX140 Phase 2 clinical trial in patients with C3G and FSGS respectively. General and administrative expense were $4.7 million for the first quarter compared to $4.6 million for the same period in 2017. The increase was primarily due to higher employee-related expenses, partly offset by a decrease in professional and legal fees. We recorded net losses for the quarter of $9.4 million compared to $6 million in the first quarter of 2017. Total shares outstanding at March 31, 2018 were approximately 49.1 million shares. Lastly, we ended the quarter with $177.1 million in cash and investments, and we continue to expect to utilize cash and investments between $65 million and $75 million in the calendar year 2018. Tom?

[Dr. Thomas Schall:]

Thank you, Susan. As you can see on our final slide, slide eight, there are a few key takeaways. In the first quarter of 2018, we continued the momentum we had generated throughout 2017. We are close to completing patient enrollment in our landmark Phase 3 ADVOCATE pivotal trial of avacopan for the treatment of ANCA-associated vasculitis, demonstrating our capability to run sophisticated, multi-centered trial across several continents, indeed across the globe. Positive data from the ADVOCATE trial will allow us to begin to compile full MAA and NDA dossiers late next year. We are making excellent progress too in our second trial of avacopan that is in C3G, another disease with no approved therapy and in which patients could benefit from avacopan’s unique mechanism of action. Trials of our second renal disease asset, the CCR2 inhibitor CCX140 are ongoing in two patient populations at primary FSGS. And we will update you soon on our plans to expand energetically and markedly in the value creation with avacopan beyond kidney disease into the very exciting realm of treating hidradenitis suppurativa. Strong momentum continues and I believe future prospects are very bright indeed. With that, I will now turn the call back over to the operator and we look forward to your questions. Operator?

[Operator:]

[Operator Instructions] And our first question comes from the line of Anupam Rama from JP Morgan. Your line is now open.

[Tessa Romero:]

Hi. Thanks for taking the question. This is Tessa on for Anupam today. Thank you for the update here and all the progress. Want comment on the Phase 3 ADVOCATE trial. With the update that you’re now at 85% of target enrollment, how should we think about timing of a Phase 3 top-line readout? And then, secondly, if you could walk us through the primary endpoint here, which is a dual endpoint, as I’m sure everyone is aware of, BVAS remission at weeks 26 and 52. Maybe walk us through what the trial is powered to detect with respect to difference in BVAS response and what constitutes the clinically meaningful win? And then, one more related question, if I could. Realizing that ADVOCATE allows for combination treatment with either cyclophosphamide or rituximab background therapy, how should we be thinking about the proportion of patients to be treated with either background therapy, now that the trial is 85% enrolled?

[Dr. Thomas Schall:]

Thank you. All excellent questions. So, first the top-line readout. As I mentioned, the ADVOCATE trial is enrolling at almost an unprecedented pace, certainly for a pharmacologic agent in a blinded trial in ANCA vasculitis. We’ve been projecting all along that our optimistic rates of enrollment would take us to a full enrollment by midyear. And I think you can see from the figures that I gave today, we’re well on track to hit full enrollment by the middle of this year. We will -- as you also rightly pointed out, we treat for a total of 52 weeks. So, the last patient out will be obviously 52 weeks from that full enrollment date, and therefore will start compiling data sometime mid-2019 and will certainly be targeting a top-line data release in the second half of 2019. So that’s kind of how the timeline will work out. Going back to the clinical endpoints. So, BVAS or Birmingham Vasculitis Activity Score BVAS is the validated endpoint, in fact, it’s the lone regulatory endpoint that has a precedence. It measures a variety of signs and symptoms of active vasculitis. And that is the endpoint we are using, a BVAS score of zero, which means BVAS remission. We saw very encouraging BVAS zero scores in the Phase 2 trial, and those seem to be achieved in a rapid and durable fashion in the absence of the traditional need for high chronic doses of glucocorticosteroids. So that really was the basis by which ADVOCATE was designed. It is larger and it is longer, so that we may also test for the durable effects of benefit. Durable effects of benefit are one of the limitations of the current standard of care as you probably know, because both steroids and certainly cyclophosphamide have very bad effects on their own and must be tapered or used in intermittently. I will come back to BVAS in just one moment, but there are other measures of the burden of this disease, which regulatory agencies in both Europe and the United States will be paying close attention too, since BVAS only specifically talks about signs and symptoms of active vasculitis. It doesn’t capture other important metrics including for example, safety, and most particularly safety that might be associated with high doses of glucocorticoids. Accordingly, we have built in a glucocorticoid toxicity index and that will be something that we monitor very carefully as well. We are -- we actually had a significantly fewer number of traditional glucocorticoid-associated severe adverse events in the Phase 2 studies than the standard of core. So that’s also encouraging. We are building in also quality of life indices validated metrics such as SF-36 and EuroQOL-5D-5L, those were also significantly improved in the Phase 2 data and there will be a lot of attention paid to those. And naturally, we will be looking at other key secondary endpoints including not just the primary endpoints of BVAS at week 26 and week 52 which I’ll come back to in response to your previous question, but at other time points including early time points in this trial. Objective outputs of renal functions and ANCA vasculitis affects the kidney very commonly, will also be assessed as they were in Phase 2. So, this is going to be a very rich data package with which we can bring forward a dossier to both FDA and EMA and with which we will be able to inform how the drug is used ultimately in clinical practice. The primary endpoints are based solely on regulatory precedent, to be honest with you. There is a BVAS remission score at week 26 that means we want to test the proportion of people with a BVAS score of zero at essentially six months in the trial and want to see how they are in -- how they compare between the two arms. The clinical data and the published literature and there is only one good study using BVAS at week 26 and that is the so called RAVE trial where cyclophosphamide was tested against rituximab in the presence of high doses of chronic steroids. That tells us that people should be in remission, BVAS remission on the standard-of-care at least in the RAVE trial which was 200 patients approximately, 100 per arm, the glucocorticoid plus cyclophosphamide arm was about 54% BVAS zero at month six. The rituximab plus glucocorticoid arm, the comparator arm was about 10 points higher, about 64% BVAS remission at month six. Those are quite significant results. It’s interesting that BVAS though is actually set up to basically quantitate how well people were doing on the traditionally derived standard-of-care. In other words, BVAS is kind of designed to score high with background therapy. So to match or exceed the background therapy arm is considered clinical success by the agencies, if your drug is thought to have other positive attributes, especially if your drug is thought to have other positive attributes as well. Why I tell you all that is because you asked me about powering. And to understand powering, you have to understand that the statistical null hypothesis at week 26 is the proportion of individuals in BVAS remission in the two arms where the therapy arm is statistically at least no worse than the standard-of-care arm. So it’s statistically non-inferiority as it was in the one precedent that we have for Phase 3 trials where rituximab was awarded a label for use in ANCA-vasculitis. So, we are highly powered at week 26 to show statistical non-inferiority. Our expectation and our preference is that we will be as in the rituximab RAVE trial, statistically non-inferior and numerically superior to standard-of-care. Both those -- the endpoint of week 26 BVAS remission under those conditions is considered to be significant clinically and I think most clinicians will certainly agree with that; and from a regulatory standpoint, as I mentioned clearly constitutes the lone regulatory precedent for a license in ANCA-vasculitis for a pharmacologic agent. And so, especially in Europe, it’s quite accepted that clinical success would be achieved with BVAS, the BVAS primary endpoint at 26 weeks. We wanted to do something a little bit more in this trial, so we went another 26 weeks of therapy and we asked the question “What will BVAS remission look like at week 52 or 12 months?” There again, we have really high power to be at minimum statistically non-inferior and we have very good power to actually see statistical superiority between the new treatment group of avacopan versus the standard of care. So, there that minimum being non-inferior again will be a win in some parts of the world but being statistically superior at week 52 in BVAS remission will be a big win all over the world, and that’s what we’re aiming to do. So, we have, you’re quite right, two primary endpoints. They are independently assessed, because what we will do is a statistical hierarchical analysis, testing, will run all the data for 52 weeks, we won’t look early at a 26-week endpoint and then say then later at 52-week. We’ll run all the patients. We’ll first statically analyze BVAS remission, non-inferior at week 26. If yes, we will ask the question BVAS remission non-inferior at week 52; if yes, we will then ask the question BVAS superior statistically at week 52; if yes, we’ll actually go back to week 26 and ask the question BVAS superior week 52. So, I know that’s a bit of a complicated, but I hope thorough response to your question. We are certainly well over 90% powered for the non-inferiority endpoint at week 26. And we have quite good power even for superiority at week 52. We assume frankly because the way medical practice exists in this area, because by definition you are forced to take steroids, and by definition you are forced also to have pulsatile treatment with such things as cyclophosphamide that in fact the BVAS remission rate that are durable will be fewer or that rate will be less at week 52 than in the active therapy group of avacopan. And so that’s the way the trial is designed and it really eliminates the medical need, if you will in this indication. So, we didn’t design the trial with anything but standard clinical practice in mind in the standard of care arm. You asked too about the background rituximab and cyclophosphamide. We have been agnostic as to what the background therapy is. That agnosticism is based on two things, one is our own experience in the Phase 2 clinical development plan where there really was no difference in the response rates on avacopan whether the patient was on cyclophosphamide, which is the historical standard of care and still that which is used by the majority of folks outside the U.S. or rituximab, which is more popular here in the U.S. They seemed all to have both BVAS response and BVAS remission rates at fairly equivalent levels and the rest of the objective markers, the decrease in protein proteinuria, stabilization of EGFR and the like, those two seemed mostly just attract with the presence of absence of avacopan and not on the background therapy. We anticipate now you asked about -- now that we have lots of enrollment, we don’t -- I don’t have the unblinding, if you will, of the background therapy, even in statistical form at this point. But I do know that the geographical distribution of the patient population enrolled to date will suggest that we’re going to have about the same background therapy proportion between rituximab and cyclophosphamide as we did in the Phase 2 studies. So, we feel that everything is quite predictable and we’re drawing upon our own experience from our Phase 2 studies. And lastly, we’re drawing upon the data from again that lone Phase 3 published study, the RAVE trial where again the rates between remission at week 26 were statistically similar, certainly that new therapy was non-inferior and even the numerical rates were only different by about 10%. So, we’ve modeled all of that into our assumptions in this trial to come up with the numbers that we are working with.

[Operator:]

[Operator Instructions] And our next question comes from the line of Ed White from H.C. Wainwright. Your line is now open.

[Ed White:]

So just a question on aHUS. You didn’t mention on the call. I am just wondering if you can maybe mention your plans for development for avacopan in that setting.

[Dr. Thomas Schall:]

Thank you, Ed. I am glad you brought up that question. As you know, we also talked a lot about a new indication outside the kidney space, HS. And I will tell you, we’ve been working in aHUS for a little while now, trying both to protocolize a trial with avacopan as well as actively in the context of compassionate use setting. I will tell you frankly that we’ve had increasing difficulties with the availability of patients for protocolized clinical trials. There are a lot of new entrants into the aHUS space. And recent, very recent developments in data really show that clinical practice is probably changing and frankly reinforcing the position of the incumbent eculizumab. So, I think all of those folks have done a very good job, and it’s been very difficult for new folks like us to break into that space. Currently, we decided to deprioritize aHUS a little bit in order to much more aggressively pursue the clinical development of avacopan in HS. So, as I said, I can send you some very recent studies indeed where I think eculizumab and how people are modifying the use of eculizumab over time really are entrenching that molecule as ever more thoroughly as ongoing standard-of-care for both control and essentially long-term control of aHUS. So for that reason, candidly, we are deprioritizing that program at the moment in deference to investing our energies in a very big way in the HS area. We may well also be announcing in not too distant point in the future whether or not we will pick up another orphan real indication but I will have more to say about that at the appropriate time.

[Ed White:]

And just a question on CCX140. What is the development plan for diabetic nephropathy going forward? Are you interested in that indication or is that more for Vifor and you will take a backseat on that one?

[Dr. Thomas Schall:]

Thank you, Ed. Very, very perceptive question as well. As you know CCX140 met its primary endpoint in the Phase 2 trial in diabetic nephropathy. It really is a vast under-met need in the world and will continue to be I think for many, many years to come. The issue is the challenge of development in Phase 3, many thousands of people, many hundreds of millions of dollars and probably a good five-year development plan in Phase 3. And still the FDA and EMA are a little bit not entirely clear on the registration endpoint. So, we and others have decided to delay any kind of development in that very expensive and difficult path. And we pivoted, as you know, to another chronic kidney disease in the orphan space, FSGS. That is no to say that there will never be a development of CCX140 in diabetic nephropathy. Again, there is a vast need. And Vifor Pharma, our commercial partner on both avacopan and CCX140 does have the right in the contract at a very defined point in the future to opt to be able to develop in chronic kidney disease and diabetes or diabetic nephropathy totally at their expense. And if they were to do that and they were successful, it might actually extend very effectively, the lifecycle of CCX140 as it comes out of its orphan drug protection time, if you will. And certainly, we would benefit ultimately because we would still derive revenues off the top-line based on our royalty scheme with Vifor Pharma. And moreover, we would be able to cultivate [ph] that molecule in the United States. So, it’s all to the good. It’s a nice option to have in the contract. For the moment, we are focusing very, very heavily, however, on the orphan kidney space of CCX140 and specifically in FSGS.

[Operator:]

At this time, I’m showing no further questions. I’d like to turn the call back over to Tom for any closing remarks.

[Dr. Thomas Schall:]

Well, thank you, and thanks for everyone for joining our call today. We look forward to updating you as we execute on our plans. We’ll also see many of you next month at the Jefferies and JMP Securities healthcare conferences in New York. So, I look forward to further discussions as well there. Thanks again all of you. And you may now disconnect.

[Operator:]

Ladies and gentlemen, thank you for your participation in today’s conference. This does conclude the program. And you may all disconnect. Everyone, have a great day.