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Edited Transcript of RETA earnings conference call or presentation 8-Aug-18 8:30pm GMT

Q2 2018 Reata Pharmaceuticals Inc Earnings Call

IRVING Aug 22, 2018 (Thomson StreetEvents) -- Edited Transcript of Reata Pharmaceuticals Inc earnings conference call or presentation Wednesday, August 8, 2018 at 8:30:00pm GMT

TEXT version of Transcript

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Corporate Participants

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* Colin J. Meyer

Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development

* J. Warren Huff

Reata Pharmaceuticals, Inc. - Chairman, CEO & President

* Jason D. Wilson

Reata Pharmaceuticals, Inc. - CFO & VP of Strategy

* Vineet R. Jindal

Reata Pharmaceuticals, Inc. - VP of Strategy

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Conference Call Participants

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* Adam Anderson Walsh

Stifel, Nicolaus & Company, Incorporated, Research Division - MD & Senior Analyst

* Joseph Patrick Schwartz

Leerink Partners LLC, Research Division - MD, Biotechnology

* Matthew Lee Kaplan

Ladenburg Thalmann & Co. Inc., Research Division - MD & Head of Healthcare Equity Research

* Maurice Thomas Raycroft

Jefferies LLC, Research Division - Equity Analyst

* Yigal Dov Nochomovitz

Citigroup Inc, Research Division - Director

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Presentation

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Operator [1]

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Good day, ladies and gentlemen, and welcome to the Reata call -- Reata management call to discuss second quarter financial results and an update on development programs. (Operator Instructions)

Before the company proceeds with its remarks, please note the forward-looking statement disclosure in the company's press release. The company will be making forward-looking statements on today's call. There are many factors that could cause results to differ from expectations, included those noted in the company's SEC filings. Today's statements are not guarantees of future outcomes. Please also note that any comments made on today's call speak only as of today, August 8, 2018, and may no longer be accurate at the time of any webcast replay or transcript rereading.

An audio recording of today's webcast will be available shortly after the call today on Reata's website at reatapharma.com in the Investor and News section. Following the prepared remarks, we will open up the call for questions. (Operator Instructions)

I would now like to introduce your host, for today's conference, Vinny Jindal, Vice President of Strategy. Please go ahead.

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Vineet R. Jindal, Reata Pharmaceuticals, Inc. - VP of Strategy [2]

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Thank you. Hello, and welcome to Reata management's call to discuss Reata's second quarter financial results and to provide a review of our development programs. This afternoon, we issued a press release with the summary of these results, and the press release can be found on the Investor and News section of our website at reatapharma.com. I'm joined today by our Chief Executive Officer, Warren Huff; our Chief Medical Officer, Colin Myer; and our Chief Financial Officer, Jason Wilson. I'll now turn the call over to Warren.

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J. Warren Huff, Reata Pharmaceuticals, Inc. - Chairman, CEO & President [3]

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Thanks, Vinny. Good afternoon, everyone, and thank you for joining us for our quarterly call. As most of you know, we're developing bardoxolone for the treatment of severe and rare forms of chronic kidney disease, where renal inflammation and fibrosis are key drivers of kidney function loss and kidney failure. Our lead program is in Alport syndrome patients in our CARDINAL Phase II/III study. Additionally, we're conducting the PHOENIX trial, an open label Phase II study, enrolling patients with 4 additional rare forms of CKD, including ADPKD, IgA nephropathy, FSGS and CKD caused by type 1 diabetes.

In July, we announced 1-year data from the Phase II portion of CARDINAL as well as the full data for the ADPKD cohort of the PHOENIX trial. Data from CARDINAL demonstrated that bardoxolone produced long-term improvements in kidney function in Alport syndrome patients, who were actively declining while on standard of care. Furthermore, the significant retained eGFR benefit observed in this trial underscores the point that kidney function improvements produced by bardoxolone have the potential to delay or prevent dialysis in these patients. These data also suggest that the Phase III portion of CARDINAL is conservatively powered to show a statistically significant improvement in retained eGFR benefit compared to placebo, which is the key endpoint for approval by the FDA. We continue to expect top line data in the Phase III portion of CARDINAL to be available in the second half of 2019.

During July, we also announced that ADPKD patients in our PHOENIX trial experienced significant improvements from baseline in eGFR after 12 weeks of treatment with bardoxolone. In diabetic CKD and now Alport syndrome, 12-week eGFR improvements from bardoxolone treatment correlated with long-term kidney function improvements. As a result, the 12-week eGFR improvements observed in ADPKD patients suggest that the long-term eGFR improvements observed in other forms of CKD may translate to patients with ADPKD. In light of this finding, we're developing plans to advance bardoxolone into a pivotal clinical program in ADPKD.

With respect to our other CKD studies, we completed enrollment in the IgA nephropathy type 1 diabetic CKD cohorts of PHOENIX in the second quarter. And we expect full primary endpoint data from these cohorts to be available during the third quarter of this year. Full primary endpoint data from the FSGS cohort are expected to be available in the first half of 2019.

Turning to our second registrational program, we're studying omaveloxolone, our second generation Nrf2 activator, in the ongoing pivotal MOXIe trial for the treatment of Friedreich's ataxia. The MOXIe study is proceeding as planned, and we continue to expect top line pivotal data from this study to be available in the second half next year. Based on the results observed in Part 1 of MOXIe and the design of the pivotal Part 2 of MOXIe, we're optimistic that omav will become the first approved therapy for patients with FA.

Our third pivotal study is the CATALYST trial of bardoxolone in connective tissue disease associated pulmonary arterial hypertension, or CTD-PAH. The study is also proceeding as planned, and we continue to expect top line data from this study to be available in the first half of 2020. Based on the results observed in our Phase II LARIAT trial and the design of the CATALYST trial, we're optimistic that bardoxolone will become the first therapy approved specifically for patients with CTD-PAH.

With that overview, I'll now turn the call over to Jason to provide a summary of our financials for the quarter.

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Jason D. Wilson, Reata Pharmaceuticals, Inc. - CFO & VP of Strategy [4]

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Thanks, Warren. As mentioned earlier, this afternoon, we reported financial results for the second quarter of 2018. Our net loss for the quarter was $28.2 million or $1.08 per share compared to a net loss of $11.6 million or $0.52 per share for the same quarter last year. The increased net loss for the 3-month period is primarily driven by 4 factors. On the revenue side, there was a decrease in revenue due to a previously deferred revenue related to a license agreement being fully recognized in 2017. On the expense side, we saw an increase in research and development expenses related to clinical and manufacturing activities. In this quarter, we also had general and administrative expenses and fees specifically related to the milestone receivable that we recorded, which increased our G&A expense. And due to the change to our debt agreement, we recorded an extinguishment of debt in this quarter as well.

At June 30, 2018, we had a little under $139 million in cash. And in July, of course, we closed an equity offering with the net proceeds of approximately $233 million. Based on our current cash, we believe that cash and cash equivalents and unexpected milestone payment from KHK, our Japanese partner, will be sufficient to fund our operating expenses and capital expenditure requirements into 2021.

And with that, I'll turn the call back over to Warren.

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J. Warren Huff, Reata Pharmaceuticals, Inc. - Chairman, CEO & President [5]

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Thanks, Jason. At Reata, our mission is to develop small molecule therapeutics with novel mechanisms of action for severe orphan diseases with no effective therapies. We conduct a battery of Phase II studies looking for meaningful improvements in clinical parameters, and we set a high bar for advancing programs in the pivotal studies. This approach has produced our current pipeline of 3 promising registrational programs in Alport syndrome, Friedreich's ataxia and CTD-PAH. A fourth program in PKD, this is transitioning to a pivotal Phase III study, and a series of additional Phase II proof-of-concept studies that provide expansion opportunities in our key therapeutic areas of nephrology in neurodegenerative disease.

Over the course of the next 18 months, we expect to generate significant news flow, including the full results from the IgA nephropathy and type 1 diabetic CKD cohorts of the PHOENIX trial this quarter, the full results from the FSGS cohort of PHOENIX in the first half of 2019 and top line pivotal data from our registrational studies in Alport syndrome and Friedreich's ataxia in the second half of 2019.

With a strong balance sheet and a portfolio of ongoing pivotal programs, the company is well positioned to produce positive Phase III data and commercialize one or more groundbreaking therapies for underserved orphan diseases in the coming years. We look forward to updating you soon on our progress.

That concludes our prepared remarks, and I'll now turn the call over to the operator for questions.

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Questions and Answers

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Operator [1]

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(Operator Instructions) Our first question comes from Maury Raycroft with Jefferies.

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Maurice Thomas Raycroft, Jefferies LLC, Research Division - Equity Analyst [2]

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My first question is just in trying to pin down differences between the rare kidney diseases you're pursuing with bardoxolone. I'm wondering if you could talk about different types of collagen IV mutations, which are found in Alport syndrome in males and females and, I believe, in FSGS too. And how these mutations may influence the spectrum of kidney disease? And also any thoughts on prevalence?

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [3]

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Hey, Maury. It's Colin. So yes, there's a spectrum of mutation of type IV collagen that result in Alport syndrome that occur in both males and females. There are several different inheritance patterns, and that defines the rate of progression. What's now known is that females are affected just as much and likely more so than males, even though Alport syndrome is thought to be by some just a male-only disease. And so males may be affected earlier in their life, and males with X-linked disease are -- reach end-stage renal disease by a median age of 25. Importantly, patients with autosomal recessive disease, which is equal in males and females, reach it at a similar time frame. Females with X-linked disease are actually more common than males with X-linked disease, and they tend to reach ESRD in their 60s, so that still obviously affects their life. And so as far as numbers of patients and so that we estimate with Alport syndrome Foundation, that there are 30,000 to 60,000 patients who have Alport syndrome in the U.S. The Alport syndrome Foundation believes that perhaps up to 1/3 of patients with FSGS actually have Alport syndrome. Furthermore, many of the Alport syndrome key opinion leaders have published recently that there's likely a fairly large set of patients, who have Alport syndrome but are misdiagnosed as having thin basal membrane disease. And so that's -- we're trying to explore that right now to figure out how big that population may be, but that would provide a potential substantial increase in the numbers.

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Maurice Thomas Raycroft, Jefferies LLC, Research Division - Equity Analyst [4]

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Helpful. And any thoughts on how that could influence trial design? I guess, are these patients in the current Phase III? And could they be included into an FSGS trial?

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [5]

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So if patients have a type IV collagen mutation, they're allowed in our trial. And so if they're misdiagnosed as having something else such as thin basement membrane disease or FSGS, if their genotype have been found to have a type IV collagen mutation, they're allowed in our trial. And so our trial does contemplate those patients. And so we've had a campaign recently with several of our top-enrolling sites to investigate patients who may have suspected Alport syndrome, and there's a common phenotype. Oftentimes, young male with blood in the urine who looks like an Alport syndrome patient but just do not have the genetic workup. And so as I mentioned, we're exploring to figure out how common those patients may be but [the lurch] estimate suggest it's a meaningful increase in the numbers that I've mentioned of 30,000 to 60,000 patients in the U.S.

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Operator [6]

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Our next question comes from Adam Walsh with Stifel.

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Adam Anderson Walsh, Stifel, Nicolaus & Company, Incorporated, Research Division - MD & Senior Analyst [7]

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Appreciate you guys taking my questions, and just a follow-up to Maury's question a moment ago. In looking at the reclassification potential for these collagen disorders as potentially Alport syndrome, that could be obviously very meaningful in terms of the size of the thin basement pathology, if that's reclassified obviously as Alport, that greatly expands the market. There's been some talk amongst KOLs about trying to reclassify these thin basement membrane patients as Alports. Is that just talk right now, Colin? Or is there some kind of push in guidelines or diagnostic push in order to kind of -- to get this reclassification done? Or is this just really kind of conversations amongst KOLs at this point?

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [8]

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It's clearly more than simply conversations amongst KOLs. And there are some, I would say, kind of formal guidelines in the academic community, where they are suggesting that these patients, in fact, do have Alport syndrome. And I think there's -- we need to differentiate between 2 distinct patient populations. One, these patients who are diagnosed on the basis of a clinical diagnosis with a, basically, histological finding that appears to be thin basement membrane disease. But there's -- many of those these patients actually have type IV collagen mutations and therefore have Alport syndrome. It's not really a reclassification. It's just a proper diagnosis now that there's the molecular genotyping tools in order to actually correctly diagnose those patients. There is a second set of patients who have mutations in other proteins that are not type IV collagen but also important for integrity in the filtration barrier in the kidney. And so I think there is some suggestion and some work to determine if those patients should be formally reclassified as having Alport syndrome. That's probably a smaller component. But based upon the prevalence of the mutations in type IV collagen, it appears likely to be much more common in part because these patients simply aren't diagnosed correctly.

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Adam Anderson Walsh, Stifel, Nicolaus & Company, Incorporated, Research Division - MD & Senior Analyst [9]

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And then if we could just get any more granularity, if you had it, on the timing design and kind of duration of the Phase III ADPKD trial launch?

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [10]

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Yes, so I think as we mentioned when we announced the PHOENIX data recently, we're actively planning to move that program into a pivotal Phase III trial. And so we're undergoing a process right now. We'll provide more formal guidance in the next few months. And I think an important consideration is data from the rest of the PHOENIX cohorts. And as we've stated, we'll have data from the IgA nephropathy and type 1 diabetic CKD cohorts this quarter. And so I think we'll have more guidance once we have those data and have a little bit more time to plan.

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Operator [11]

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Our next question comes from Yigal Nochomovitz with Citigroup.

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Yigal Dov Nochomovitz, Citigroup Inc, Research Division - Director [12]

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Recently, the FDA had issued some documents related to surrogate endpoints for ADPKD, which I'm sure you're familiar with. And one of those was kidney volume. I'm just wondering if that's something that you would consider in your design sort of a Phase III to potentially get accelerated approval.

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [13]

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So that could be, Yigal, if surrogate. But FDA has already also said they'll take eGFR as an endpoint for full approval. And so the only precedent in the U.S. for an approved product is from Otsuka's tolvaptan, which was approved in April of this year. That company conducted 2 Phase III trials. Their first trial, the TEMPO 3:4 trial, actually had total kidney volume as the primary endpoint, and FDA did not accept that data for registration in the U.S. And they required the company conduct a second trial, the REPRISE trial. That was 12 months in duration and then had a 2-week off-treatment eGFR assessment for full approval. That's the same endpoint that we were given for Alport syndrome in the CARDINAL trial. FDA gave us that endpoint for accelerated approval at 1 year and full approval for 2 years. And so we think that for us, based upon the powering assumptions, it's much easier to show a difference in eGFR. We've already seen it. And really the total kidney volume is more of a surrogate of a surrogate. And so the eGFR data are much stronger and, I think, are already clearly more important to the regulators, especially here in the U.S.

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Yigal Dov Nochomovitz, Citigroup Inc, Research Division - Director [14]

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And is there anything on the biology related to ADPKD that would suggest that the retained benefit that you might observe in that setting would be different, either better or worse than what you've just shown in the Alport study?

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [15]

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No, I think there's a few reasons to suggest why we think it would be similar. Number one, if you simply look at the literature and the role of inflammation in Alport syndrome and PKD, there's actually stronger data demonstrating that inflammation is important in PKD versus Alport syndrome.

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J. Warren Huff, Reata Pharmaceuticals, Inc. - Chairman, CEO & President [16]

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And in particular, the Rel/NF-kappaB, which is suppressed by our -- by bardoxolone's activity.

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [17]

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So the biology is actually stronger, oncology and in PKD. And then furthermore just a clinical data, so we clearly see acute improvement in kidney function in patients of PKD that are similar magnitude in absolute and relative terms to Alport syndrome as well as the diabetic data we've generated as well as the interim IgA data. And so we think that it's likely that we'd see a similar fact. And so from our perspective, the CARDINAL-like design should be palatable to FDA for registration for 2 reasons. Number one, because that's a design that they required for tolvaptan, and it's a design they gave us for CARDINAL.

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Yigal Dov Nochomovitz, Citigroup Inc, Research Division - Director [18]

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And then just pressing on some of the themes from the earlier questions regarding the size of the market you're going into such as in Alport. Obviously, one that's much, much bigger than any of those is type 2 diabetes CKD, and maybe you haven't done that because of just the pricing dynamic in that setting. But is that something that is on your long-range plan? Or you're not going there?

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J. Warren Huff, Reata Pharmaceuticals, Inc. - Chairman, CEO & President [19]

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This is Warren. I'll address that. It's obviously a target indication. The 2 prior studies were quite validating in terms of the effects of the drug in that patient population. Of course, as you know, our partner, Kyowa Hakko Kirin in Japan, is conducting a Phase III registrational study in type 2 diabetic CKD. And they've adopted in that study the kind of newly validated or standardized guidelines for margin end trials so that the data from that study would -- has endpoints that would likely be adopted outside of Japan both by the FDA and by Europe. And so at this point, we're going to execute our plan to work through these rare renal diseases and launch the product into these rare forms of the disease, which collectively represent a very significant market opportunity. And then at some point, we will decide whether it makes sense to develop the product for the broader type 2 diabetic CKD, or for that matter even broader markets, for example, for hypertension-induced CKD.

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Operator [20]

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Our next question comes from Joseph Schwartz with Leerink Partners.

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Joseph Patrick Schwartz, Leerink Partners LLC, Research Division - MD, Biotechnology [21]

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A couple financial questions that we hear a lot first, and then a clinical question. So how much do you expect each of your Phase III kidney programs for bardoxolone to cost? And how many would you expect to pursue?

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Jason D. Wilson, Reata Pharmaceuticals, Inc. - CFO & VP of Strategy [22]

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Well, we haven't really ever given specific guidance on the cost of the trials, but I can say that they're extremely cost-efficient. These are rare disease trials and come with small patient populations and efficient trial designs. In terms of how many we might pursue, that's something that we would be announcing as the data for the various trials come in.

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J. Warren Huff, Reata Pharmaceuticals, Inc. - Chairman, CEO & President [23]

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Right. But as we have said, we're now planning to pursue a trial in ADPKD. And we'll give guidance late this year or next year on the timing of that study after we get -- after we have an opportunity to go through the regulatory interactions. I'd just add to Jason's comment. These are not expensive on a per-patient basis. There's not the complicated and expensive imaging, for example, involved in the studies. It's pretty much routine clinical visits and clinical chemistry-based endpoints. So they're really just driven by the numbers, and they're not a large impact.

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Joseph Patrick Schwartz, Leerink Partners LLC, Research Division - MD, Biotechnology [24]

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That's very helpful. And then how do you think about pricing across so many different sized markets, which when you add them together get quite large and outside the realm of orphan?

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J. Warren Huff, Reata Pharmaceuticals, Inc. - Chairman, CEO & President [25]

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Sure. Of course, the 5 additional rare -- out of the 5 rare forms of CKD that we're conducting the programs in, the lead, Alport syndrome, is probably the least prevalent of the group. It's also one of the most severe forms. So it would obviously -- if that were the only thing we were doing, it would support probably the highest price. PKD, among the rare forms, probably at the other end of that spectrum, with a prevalence of 400,000 to 600,000, diagnosed population of approximately 120,000 patients in the U.S. And so you can think of a range of pricing for -- and by the way, I would add, so the endpoints given to us by FDA for Alport syndrome would reflect disease-modifying activity. And so in Alport, there's no approved therapy and it's a deadly disease. So you can imagine pricing would be consistent for the first approved therapy with disease-modifying activity in a rare, deadly disease. And then as we expand the label, I would expect over time, frankly, have the pricing fall in line with the expanded opportunities.

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Joseph Patrick Schwartz, Leerink Partners LLC, Research Division - MD, Biotechnology [26]

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Okay, great. And then does GFR progress or decline linearly?

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J. Warren Huff, Reata Pharmaceuticals, Inc. - Chairman, CEO & President [27]

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And by the way, before -- one -- just one last thing. Just in case -- you may or may not be aware, the tolvaptan for PKD is kind of one benchmark. They just priced it at, I believe, $170,000 annually in the U.S.

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Joseph Patrick Schwartz, Leerink Partners LLC, Research Division - MD, Biotechnology [28]

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Right, okay, it's super helpful. My last one is just clinically, does GFR decline linearly throughout all these diseases? Or is there a point where it tends to accelerate or fall off a cliff? And can you show that you're able to prevent patients from declining below certain thresholds such as that which is -- indicates dialysis is necessary? Like a responder analysis?

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [29]

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Yes, so across these different forms of CKD, there are different rates of progression. They're typically between 1 to 5 or 6 mil per minute on average. In those that we're studying, I'd say probably between 2 to 4 primarily. We've already, of course, released data showing that in Alport syndrome, the annual loss prior to entry in our trial was 4.2 mil per minute per year. Those patients typically start losing kidney function very early on in their life, and it's fairly linear for PKD in the 3 years prior to the patients entering our PHOENIX trial. They often average 4.8. It's not exactly linear in PKD. It's usually patients have fairly stable kidney function for perhaps the first few decades of life. And then there's fairly linear decline. [Importantly], it's not like they fall off a cliff and lose extreme amounts in a very short period of time. It's this range of 4, 4 to 5. Prior studies have shown 3 to 5. And then for IgA and type 1, we'd expect it to be slightly lower but still fairly meaningful. And so I think our trials are adequately powered to show [not only] improvement in kidney function at 12 weeks in the PHOENIX program by [doing any kind of] 1- or 2-year trial. We would expect to show separation from placebo whatever the rate of decline is. And as far as showing differences in certain thresholds, it really depends upon the trial design, which I think what's the most important to FDA is showing for us disease-modifying activity, showing improvement off-treatment. The most important threshold is obviously a patient going onto a kidney transplant or dialysis and so with a GFR of less than 15. And in rare forms of CKD, those trials are not feasible. They typically require a couple thousand patients minimum to show a difference, and so that's why FDA has worked to adopt these eGFR-based endpoints for approval.

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Operator [30]

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Our next question comes from Brian Skorney with Baird.

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Unidentified Analyst, [31]

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This is [Trevor] on for Brian. I'm just wondering if you would lay out the time line for AbbVie to opt-in. And what are your current thoughts on getting back the ex-U. S. rights from them, and whether AbbVie's rights are transferable to another company?

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Jason D. Wilson, Reata Pharmaceuticals, Inc. - CFO & VP of Strategy [32]

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Yes, so we've just kind of summarized where the commercialization rights are. We've obviously retained all of the commercial and economic rights in the United States. Our partner, Kyowa Hakko Kirin, has commercialization rights in Japan and Southeast Asia. And then AbbVie has an option to commercialize the product outside of the U.S. in the Kirin territories, and they have an opportunity to elect to commercialize the product as late as the availability of the Phase III data from the Alport syndrome trial. And so they will have an opportunity to elect in at that time. We expect that 1 or 3 things will happen. Either they will elect in and will launch product in the rest of world territories that I mentioned. We will -- the rights will -- we will make arrangements for either ourselves to launch in those territories or place the rights with a substitute partner for AbbVie.

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Operator [33]

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(Operator Instructions) Our next question in queue comes from Matt Kaplan with Ladenburg Thalmann.

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Matthew Lee Kaplan, Ladenburg Thalmann & Co. Inc., Research Division - MD & Head of Healthcare Equity Research [34]

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Just wanted to zero in a little bit on the IgA nephropathy and type 1 diabetes CKD data from the PHOENIX study coming out soon given the kind of consistency of the results that we've seen. Can you just help us to get a sense in terms of what we should look for or expect in terms of change in eGFR in those 2 ideologies of CKD?

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Colin J. Meyer, Reata Pharmaceuticals, Inc. - Chief Medical Officer & VP of Product Development [35]

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Sure, Matt. So I think we're looking to see improvements in kidney function that look real and clinically meaningful. And so as I mentioned, there's going to be differing historical rates of decline across these indications, but all will be meaningful, we believe. And then we may see different magnitudes of increase. But I think our threshold have always been if we see more than a few point increase in GFR, that to us demonstrates the drug is affecting the underlying inflammation, is improving kidney function. And obviously, the value proposition for patients is that if we can increase kidney functions, stabilize it, patients may never need dialysis or a kidney transplant if their kidney function isn't falling. And so it's less about the absolute increase and more about is there any increase that would be clinically meaningful. And so that's what we're looking for, and we wouldn't expect the exact same number, and we just want to see an increase that appears real and meaningful.

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Operator [36]

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I'm not showing any further questions in the queue at this time. This does conclude our Q&A session. I would now like to turn the call back over to Vinny Jindal for any closing remarks.

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Vineet R. Jindal, Reata Pharmaceuticals, Inc. - VP of Strategy [37]

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Thanks, David, and thanks to everyone for dialing in today. We look forward to updating you again soon. Take care.

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Operator [38]

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Ladies and gentlemen, thank you for participating in today's conference. This does conclude today's program. There will be an audio recording available shortly after this conference call on Reata's website at reatapharma.com in the Investor News section. You may all disconnect. Everyone, have a great day.