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CymaBay Therapeutics Inc (CBAY 0.03%)
Q1Â 2020 Earnings Call
May 11, 2020, 4:30 p.m. ET
Contents:
- Prepared Remarks
- Questions and Answers
- Call Participants
Prepared Remarks:
Operator
Welcome to the CymaBay Therapeutics' First Quarter 2020 Earnings Conference Call. [Operator Instructions]
I would now like to turn the conference over to Mr. Dan Menold, Vice President of Finance. Please go ahead, sir.
Dan Menold -- Vice President, Finance
Thank you, operator, and good afternoon, everyone. I hope that you've had a chance to review the press release we issued announcing our first quarter 2020 financial results and business update. You can access that release on our website under the Investors tab.
Joining me on the call today are Sujal Shah, Chief Executive Officer, and Dr. Chuck McWherter, Chief Scientific Officer; Klara Dickinson, Chief Regulatory and Compliance Officer; our Principal Investigators in our PBC and NASH Program, Dr. Gideon Hirschfield and Dr. Stephen Harrison and the Chair of our Expert Review Panel Dr. Paul Watkins. Sujal and I will provide an update on the review of our seladelpar investigation and financial position before we open-up the call for Q&A.
Before we begin, I'd like to remind everyone that statements made during this conference call, including the Q&A session, relating to CymaBay's expected future performance, business prospects, events or plans, including clinical plans and in particular for this call regulatory approvals and anticipated timelines and data release dates, and cash runway are all forward-looking statements as defined under the Private Securities Litigation Reform Act of 1995. Although the company believes that the expectations reflected in such forward-looking statements are based upon reasonable assumptions, actual outcomes and results are subject to risks and uncertainties and could differ materially from those forecast due to the impact of many factors.
The company assumes no obligation to update or supplement any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by applicable law Participants are directed to the cautionary statements set forth in today's press release, as well as the risk factors set forth in CymaBay's quarterly and annual reports filed with the SEC, for factors that could cause actual results to differ materially from those anticipated in the forward-looking statements. This conference call is the property of CymaBay review panel, and any recording or rebroadcast is expressly prohibited without the written consent of CymaBay.
At this time, I'd like to turn the call over to Sujal.
Sujal Shah -- President and Chief Executive Officer
Good afternoon and thank you for joining us. During our last quarterly update call in March, we discussed our continued focus on completing the ongoing investigation of the unexpected histological findings identified by study pathologists in our Phase 2b study of seladelpar in patients with NASH. I'm pleased today to announce that we have good news on that front. Although it will take more time to gather and analyze all of the data that we intend to share with the FDA, we have now successfully cleared a key step in our process. At the end of last week, a panel of eight of the world's foremost expert liver pathologists and hepatologists, bringing together extensive knowledge in drug-induced liver injury, NASH and cholestatic liver diseases completed a four-day independent and in-depth review that analyzed the findings from our NASH Phase 2b study.
At the conclusion of the meeting, the panel unanimously agreed with the following statement, "the features noted by study pathologists at end of treatment were confirmed on this review. However, these did not differ qualitatively between baseline and end of treatment. We suspect these histologic features are underreported. However, in the experience of the pathology review subcommittee, these features may be observed in patients with NASH. The panel unanimously concluded that the data in aggregate, including the complete absence of clinical and biochemical evidence of drug-induced liver injury and the lack of significant differences in histologic features or their changes across the placebo and treatment groups do not support injury related to seladelpar.
The panel also unanimously supported lifting of the clinical hold and the reinitiation of clinical development". It was extraordinary to have assembled this distinguished group of liver experts with the depth of their experience and their outstanding reputations in clinical science and drug safety. The committee was chaired by Dr. Paul Watkins of UNC, Chapel Hill, a leading hepatologist in the area of drug-induced liver injury, who is joined by two leading hepatologists in liver injury, Dr. Neil Kaplowitz of USC and Dr. Willis Maddrey of UC Southwestern.
Joining the committee where three influential figures in liver pathology. Dr. David Kleiner, Head of the Drug-Induced Liver Injury Network at the NIH; Dr. Pierre Bedossa from the University of Paris; and Dr. Zach Goodman, from Inova Health Services. The committee was rounded out with prominent clinical hepatologists in NASH and PBC. Dr. Michael Charlton of the University of Chicago; and Dr. John Vierling of the Baylor College of Medicine.
Before describing the basic steps of the investigation, I want to emphasize that we have not yet discussed full results from our investigation nor any of the panels conclusions with the FDA. Despite the favorable review by the expert panel, there is no guarantee that the FDA will agree to lift the clinical hold and allow us to continue the development of seladelpar We are planning to reengage with the agency as quickly as possible, but the submission of a complete response to the formal clinical hold and their review of all the data gathered will be necessary before the FDA can make a decision that will allow us to restart clinical development of seladelpar.
In order to provide context for the expert panel review, I'll first provide a thorough recap of our NASH Phase 2b study design. The study results and histologic findings identified by study pathologists last November that led to halting the development program for seladelpar. The study was a randomized double-blind, placebo-controlled dose ranging Phase 2b study of seladelpar, which enrolled 181 patients with biopsy, confirmed NASH The primary efficacy outcome was the change from baseline in liver fat content at 12 weeks, and a key secondary measure included evaluation of histological improvement in NASH and fibrosis, as assessed by comparing the scoring of liver biopsies at 52 weeks with baseline.
In June 2019, we reported minimal reductions in liver fat, but robust and clinically meaningful reductions in markers of liver inflammation and injury, including ALT, AST, Gamma GT and alkaline phosphatase at 12 weeks. The study remained blinded and was planned to continue to the 52-week end point to evaluate the effects of seladelpar and histological improvement of NASH and fibrosis. We remained optimistic at that time because of published studies that had correlated reductions in liver enzymes, namely ALT, with improvements in NASH histology.
In March of this year, we reported dose ordered improvements in NASH resolution without worsening of fibrosis. And in one point or greater improvement in fibrosis stage without worsening of NASH in Seladelpar treatment groups versus placebo at week 52 or end of treatment. The present responders with resolution of NASH and no worsening in fibrosis were eight, 10.3, 19 and 26.1% in the placebo 10, 20 and 50 milligram seladelpar groups respectively. The corresponding responder rates for at least a one stage improvement in fibrosis with no worsening in NASH were 23.1%, 23.8% and 37%. The percentages of patients meeting both end points were eight 5.1, 11.9 and 19.6%. For the placebo, 10%, 20% and 50% milligram seladelpar groups, respectively. With most of the patients having completed 52 weeks of treatment last November, the study pathologists began their blinded assessment of the 52-week liver biopsies.
Our plan had been for them to conclude the biopsy review in February for the final group of patients still active in the study as they finished their 52 weeks of treatment. As events unfolded during the review of the first batch of slides, they identified a subset of patients with what they described to be an unexpected pattern of histological findings overlaid on NASH pathology. In order to protect the integrity of the investigation by our experts, including the blinded pathology review of all paired biopsies, We've not previously shared additional details on the original findings. Now that the review panel's work is complete, we are able to provide additional information. Out of 181 subjects enrolled, 152 or 84% had an end of treatment biopsy, which is comparable in percentage to other NASH biopsy studies.
The study pathologists identified 42 of the 150 to end of treatment biopsies as having atypical histology with a total of six of 24 or 25% in the placebo group, eight of 39 or 21% in the seladelpar 10 milligram group, 10 of 42 or 24% in the seladelpar 20 milligram group and 18 of 46 or 39% in the seladelpar 50 milligram group. Thus the incidence of cases flagged appeared similar between placebo and seladelpar 10 and 20 milligrams, but was higher in the seladelpar 50 milligram group. The study pathologists described these findings as unexpected or atypical in NASH pathology and potentially concerning for drug-induced liver injury. The findings were predominantly characterized as an interface hepatitis with or without bile duct injury or cholangitis, presence of plasma cells and eosinophils and in some cases vascular lesions.
It's important here for me to highlight that these atypical features are not usually examined in NASH clinical studies where the intent is to establish eligibility and evaluate endpoints by scoring for steatosis, lobular inflammation, hepatocellular ballooning and fibrosis. Another element important to mention is that the baseline biopsies were read at least 12 months before the end of treatment biopsies. And like many studies, were not reread as part of the end of study protocol. Also to remind you of how the situation unfolded, there was no clinical correlate with these findings. Patients with and without these findings had either improving or stable levels of biochemical markers of inflammation and liver injury throughout the 52 weeks of treatment, which included ALT, AST, gamma GT, alkaline phosphatase, total bilirubin, direct bilirubin and high sensitivity-CRP.
In addition, there were no signals of immune or allergic reaction as reflected by changes in eosinophils, or in clinical symptoms of liver injury, nor were there other changes in markers that can be associated with progressing liver disease, such as platelets or coagulation parameters. No occurrences of liver decompensation or liver related AEs in association with peaks in liver chemistries were observed for any other patients with a paired 52-week or end of treatment biopsy. Importantly, these findings were unanticipated based on prior clinical and preclinical experience with Seladelpar.
After consulting with study pathologist and expert hepatologists and with patient safety at the forefront of our mind, the decision was made to halt development of seladelpar in all indications while committing to an in-depth review of these findings. The FDA agreed with this decision and formally placed a clinical hold on seladelpar development and subsequently provided input on necessary steps toward understanding the significance and consequence of these findings for the patients flagged in the study. Our commitment to completing the investigation reflects our responsibility to the patients in our NASH study, as well as to those who took part in our global PBC studies. The discordant picture between the existence of unexpected liver histology in a subset of patients and the absence of any clinical or biochemical signals of liver injury and inflammation was the key unknown we set out to better understand.
Turning to the investigation, the first step was to assemble and analyze a comprehensive profile of all study data, including patient demographics, medical history, concomitant medications, and to measure additional biochemical markers typically elevated in drug-induced and immune-mediated liver injury. This included immunoglobulins, autoimmune and tissue antibodies, cytokines and other inflammatory markers in search of any signal that may correlate with the unexpected findings. The outcome of this extensive effort was that there was no pattern of medical history concomitant medications, clinical science or laboratory or other biomarker changes that were associated with patients having the atypical histologic findings in our study. The second step in the investigation was a rigourous blinded independent review of baseline and enter treatment biopsies by the three expert pathologists, Drs. Kleiner, Goodman and Bedossa.
This time intensive process included two levels of review, a blinded review of all biopsies completely randomized from one another, and a second review of the blinded paired biopsies in which the chronological order of the biopsy pair was randomly vary. Two of the pathologists performed the first review, assessing each independently. This review blinded them to knowledge of baseline and of treatment and dose assignment and used the Ishak modified Histologic Activity Index scoring system, which has been adapted to identify histologic patterns of drug-induced liver injury.
All three pathologists independently performed the second blinded paired review, assessing better, same or worse across multiple features of histology, including interface hepatitis, portal inflammation, parenchymal inflammation, hepatocellular ballooning, steatosis and fibrosis. In addition, the pathologists noted the presence or absence of features, including eosinophils, plasma cells, bile duct injury and vascular injury. The only direction we provided to the pathologists was to highlight generally the types of histology that had been called out by the study pathologists in order to make certain nothing was overlooked. By its very nature, these reviews are very different from histology reviews conducted to score NASH in Phase II paired biopsy studies.
First, the blinded reviews of baseline and end of treatment biopsies were all done at the same time. And second, it was more comprehensive than what is usually done for NASH clinical studies because it included features that classically define NASH, steatosis, lobular inflammation, ballooning and fibrosis, as well as the specific atypical types of pathology called out by the study pathologists. Our intention was to have an objective independent analysis of histology to identify cases that raised a suspicion for drug-induced liver injury that would then be brought to the full expert review panel to discuss. What transpired from the independent pathology review was that all three pathologists were in agreement that they did not observe any histology, that on a case by case basis couldn't be seen in NASH patient biopsies.
And that they did not observe any features of histology that were alarming or would be red flagged for drug-induced liver injury. Although the features identified by study pathologists were certainly visible, the review panel, pathologists' conclusion was that the clinical significance of these did not point to evidence of drug-induced liver injury or anything otherwise alarming for these patients in the absence of any clinical or biochemical signal for liver injury. Furthermore, these underreported features that can be seen in NASH patient biopsies were observed by the panel pathologists at baseline in our study population and deemed to be qualitatively unchanged through the end of treatment.
With this view, the review pathologists agreed that having the full expert review panel adjudicate the 42 cases identified by the study pathologists would be the best course of action to confirm their overall view that there was no evidence of drug-induced liver injury based on review of biopsies from patients in the study. The third step in the investigation brought together all expert panel members to review the 42 cases flagged by the study pathologists.
To discuss the significance of any findings observed and to ultimately assess whether or not treatment with seladelpar caused drug-induced liver injury in our NASH study. Medical history, concomitant medications, patient demographics, laboratory markers and liver histology at baseline and into treatment will reviewed in detail for each of the 42 patients. None of the 42 patients were deemed to have any clinical or biochemical evidence of drug-induced liver injury.
Furthermore, 29 of the 42 patients were deemed to have no evidence of emergent or progressive unexpected liver pathology. The remaining 13 patients were deemed to have evidence of emergent or progressive unexpected liver pathology, of which 12 were deemed to be either not study drug related, or unlikely related to study drug and were equally distributed across treatment groups, including placebo. One was deemed to be possibly related to seladelpar for a patient who also had a diagnosis of systemic lupus erythematosus.
Although no patients had elevations of ALT and bilirubin to meet Hy's Law, the panel reviewed and discussed an eDISH analysis and confirmed their conclusion that there was no clinical evidence of drug-induced liver injury. The final day of discussion at the export panel centered around overall observations related to features of histology present in our baseline population, presence and progression of under reported features of NASH pathology and the clinical significance of what was observed in patients in our study.
We plan to reach out to the FDA to discuss all of the data we have collected to date and the results of the panel review meetings. Once we gather their feedback, we plan to submit a complete response to the seladelpar clinical hold. Timelines are uncertain at this moment, but this effort remains our highest priority. Although we cannot guarantee how and when the FDA will respond, whether or not they will require us to gather additional information or if they will accept the conclusions that have been made by the panel, we are confident that we have conducted a truly rigorous, independent review with the foremost leading liver experts in the world to help us definitively support the conclusion that seladelpar did not cause drug-induced liver injury in our NASH Phase II study. We have worked closely with our Board throughout the investigation and panel review and have their support for our next steps forward.
Before we open up the call for Q&A, let me turn the call over to Dan to provide you with an overview of our financial position at the end of Q1 and our projected cash balance through midyear. Dan?
Dan Menold -- Vice President, Finance
Thank you, Sujal. As a reminder, during the fourth quarter of 2019, management implemented a restructuring program following the placement of our seladelpar program on clinical hold, pending further investigation of the histologic observations noted in our NASH study and pending completion of our review of strategic options. We continue to be focused on cost containment and looking at additional steps we can take in the fiscal year 2020 in order to closely control the company's operating expenses and associated cash burn. Late in the first quarter of 2020, the need for a sustained cost containment emphasis was further underscored by the unexpected and rapid onset of the coronavirus pandemic and the associated travel restrictions and shelter-in-place orders that were issued by governmental authorities and jurisdictions where we are partners, investigators and vendors conduct operations.
In response to these measures, we have taken steps such as enabling remote operations for all our employees, which have allowed us to continue our operating activities. While our 2020 results today have not been significantly impacted and our planned clinical and strategic objectives are not currently expected to be affected, unforeseen pandemic related disruptions could occur in the future, making the full effects of the pandemic on our operating capabilities and our business uncertain. Accordingly, we will continue to closely monitor pandemic developments and their associated risks to our business. And we will take actions available to us, where possible to mitigate them. Additionally, everything we do will be guided by a commitment to taking all steps possible to ensure the health and safety of our employees.
I will now briefly turn to a review of key elements of our first quarter financial results, beginning with a current update on our fourth quarter 2019 restructuring plan. As part of this plan, we froze hiring, significantly scaled back future procurement plans, announced a 60% reduction in our workforce and scaled down or canceled many of our existing contracts for goods and services. As a result of these actions, we recorded a $5.1 million restructuring charge during the fourth quarter, which was primarily comprised of employee severance costs and to a lesser extent, costs associated with certain contract terminations. Of the total $5.1 million in restructuring charges, $3.3 million of these charges are expected to be settled in cash. We've paid out $1.6 million through the first quarter of 2020, and remaining cash payments are expected to be paid out over the course of fiscal 2020.
Moving on, I'll next provide a review of first quarter expenses. Research and development expense for the three months ended March 31, 2020 was $9.5 million as compared to $18.6 million for the same period in 2019. As a result of the clinical hold placed on the seladelpar development program in the fourth quarter of 2019, research and development expense in the first quarter of 2020 was significantly lower than the same period in 2019 due to declining clinical trial activities related to our PBC Phase III, NASH Phase 2b and PSC Phase II clinical trials and other studies as we continue our efforts to scale back and shut them down as planned.
General and administrative expense for the three months ended March 31, 2020 was $4.3 million compared to $5.7 million for the same period in 2019. General and administrative expense was lower in the first quarter of 2020, primarily as a result of lower continuing labor costs and other administrative expenses following our restructuring efforts undertaken in the fourth quarter of 2019. Overall, our net loss for the three months ended March 31, 2020 was $13.1 million, or $0.19 per diluted share. This compares to a net loss of $23.1 million, or $0.37 per diluted share for the same period in 2019. The decrease in net loss for the first quarter of 2020 compared to the prior year period was primarily due to decreases in our operating expenses, including our clinical trial and labor related expenses as discussed earlier.
Finally, I'd like to share with you our current cash position, the outlook for planned activities during the remainder of 2020 and the expected impact of those activities on our operating expenses and our cash burn. At March 31, 2020, we had $176.2 million in cash, cash equivalents and short-term investments on hand compared to $190.9 million at December 31, 2019.
As noted earlier, in 2020, management intends to fully conclude its investigation of the clinical observation seen in NASH patients, while completing a review of all strategic options. In addition, management will continue work to complete ongoing clinical study closeout and monitoring activities. These activities involve a number of key efforts, including conducting early termination visits with patients, recovering investigational drug product, caring for monitoring NASH patients with histologic observations, conducting investigators site monitoring and close up visits and quality reviewing, analyzing and reporting on clinical trial data accumulated to date.
In the first quarter, we made progress on many of these activities and objectives, despite the unexpected onset of the coronavirus pandemic and the travel restrictions and shelter-in-place orders that have impacted our operations. As mentioned earlier, we will continue to closely monitor pandemic developments and their associated risks to our business, and we will take further actions available to us where possible to address them.
Going forward, we estimate our overall cash burn for the first half of 2020 will be between $30 million to $35 million. Of this total, we expect between $20 million and $23 million will be used to fund the clinical study close out, patient monitoring and seladelpar investigation activities previously mentioned.
Let me now turn the call back to Sujal for final remarks. Sujal?
Sujal Shah -- President and Chief Executive Officer
We have not yet shared any of the data collected to date during our investigation, nor the conclusions of the expert panel with the FDA. Thus, while we will refrain from commenting on specifics that are important primarily for our discussions with regulators, we are happy to discuss our process and conclusions from the investigation.
As Dan mentioned at the opening of our call, joining me for the Q&A are our Chief Scientific Officer, Chuck McWherter, our Chief Regulatory and Compliance Officer, Klara Dickinson; Chair of the Expert Independent Review Panel. Dr. Paul Watkins; and our lead Principal investigators in PBC and NASH, Dr. Gideon Hirschfield and Dr. Stephen Harrison.
With that, I'd like to remind everyone that the purpose of today's call was to discuss our results and the update on seladelpar. We're now happy to take questions. Operator?
Questions and Answers:
Operator
Thank you. [Operator Instructions] The first question comes from Yasmeen Rahimi from ROTH Capital Partners. Please go ahead.
Yasmeen Rahimi -- ROTH Capital Partners -- Analyst
Hi, team. Thank you so much for sharing so much color with us. Very helpful. And congrats on the great progress. Couple of questions for you. The first one is directed to you Sujal. Can you share with us what could be the reason why maybe the frequency or the initial observation of the atypical lesions was seen by the two pathologists made the frequency or the initial observation of the atypical lesions were seen by the two pathologists made first and then later observed by Dr. Watkins. In the press release, it was noted that you stated that the committee concluded that these histological features are underreported. Can you share with us how often the independent committee observed those underrated and why those may have been missed in other studies? And then I have a follow-up.
Sujal Shah -- President and Chief Executive Officer
Okay. Well, thank you for the question, Yasmeen. I'll take the first question and then let Dr. Watkins address the second. First, I think it's very important for me to highlight a number of points, particularly points of differentiation between the process the study investigators conducted as part of the study protocol versus what was done in the independent panel review by the pathologists on the subcommittee. There was not a difference in incidence of the features identified by study pathologists. In fact, as was determined by the panel, the findings of the study pathologists upon their review of only the end of treatment biopsies was in fact confirmed. The real key differentiation, Yasmeen, to the procedures here is that the independent pathologists, of course, conducted two very thorough and rigorous investigations, one that was blinded to each of the study groups, as well as baseline an end of treatment in reading the biopsies specifically scoring for the modified HAI.
And a second in which they did a paired review, also in a blinded fashion in changes observed between two biopsies from each patient. So the real takeaway fundamentally from the study -- from the review pathologist had more to do with the existence of many of these features, in fact, at baseline and or the clinical significance of those features themselves relative to their implication in drug induced liver injury. And Dr. Watkins, perhaps if you have an opportunity, if you could maybe give color from the panel itself around the idea that many of these features that our review pathologists, in fact, highlighted could be seen on a case by case basis in patients with NASH. For example, interface hepatitis, bile duct injury, the conclusions around the panel relative to how these features largely may be, in fact, underreported in the setting of NASH.
Dr. Paul Watkins -- Chair of Expert Review Panel
Right. So, yes, I obviously was compensated for my work here, but I have no stake, financial or otherwise in the outcome of this drug. And first just set the background. One thing I have a lot of experience with is assessing drug-induced liver injury and spontaneous reports and large experience in clinical trials. And this was very unusual in that what brought the issue to attention was a histologic finding. And actually histology is not even part of the usual evaluation of somebody with potential drug-induced liver injury. So one of the first things that I did and the other two experts was really look at this as we would normally look at data from a clinical trial, which is looking at the routine liver chemistries, any question of liver dysfunction and by the usual ways that you approach assessing drug-induced liver injury, there really was no signal there.
And I can come back to that if you want more information. So it really came down to the pathology and the three pathologists that were selected and they know all on the phone and WebEx together are really sort of the three tenors, I would say, in terms of pathology that you want both world renowned experts in NASH, but also very importantly in drug-induced liver injury. There's no two people in the world who have more experience with histology or drug-induced liver injury than Kleiner and Goodman. And so what was done was to systematically go through those 42 cases where we presented -- the clinician presented the clinical. This is a 53-year old woman presented the clinical findings the usual way you look to assess liver injury due to drugs. And then they showed the pathology, but also on the line where the two original clinical trial pathologists who first raised the questions and in some cases they would say, well, wait, go back, look at this other part of the pie. This is what we were concerned about.
So there was no potential for confusion between what they had originally been concerned about and what was specifically looked at and evaluated by these three pathologists. And in every case, the things that they were finding that they were concerned about and there was a list of things. It wasn't a consistent pattern was looked at and evaluated and then gone back for the first time for the clinical pathologists to look at the initial biases. And in every case, there were qualitatively the same findings. And both Kleiner, Goodman and Bedossa were saying, these are things that we can see in NASH, people don't talk about them much. And that was one of the things that came out of this that there should be manuscript for the world to understand things like interface hepatitis and portal inflammation can be part of NASH.
You don't have to think of a separate process. So, just again, I think the most thoroughly histology I've ever been part of and then in addition, the clinical -- traditional clinical evaluation of drug-induced liver injury really led to a unanimous consensus that we were not seeing anything adverse that could be attributed to the study drug.
Yasmeen Rahimi -- ROTH Capital Partners -- Analyst
Thank you, Dr. Watkins for the color and Sujal my apologies for asking one last question. Can you share with us to the extent you can, what is the path forward to get clearance from the FDA? How many patients, I guess, have completed the 52-week analysis in the PBC study? Is there a chance you could run a smaller Phase III in PBC? Whatever color or content you can help us to visualize the path forward would be very helpful. Thank you.
Sujal Shah -- President and Chief Executive Officer
Yes, Yasmeen. I will have Klara, our Chief Regulatory -- oh, sorry, Dr. Kleiner.
Dr. David Kleiner -- Head of the Drug-Induced Liver Injury Network at NIH
Go ahead. No, please. I was going to just say, Dr. Watkins that I don't -- I'm not an expert at that.
Sujal Shah -- President and Chief Executive Officer
Okay. Sure, I'll -- we will ask Klara, our Chief Regulatory and Compliance Officer, to give you some color, Yasmeen, in terms of our next steps forward with the agency.
Klara Dickinson -- Chief Regulatory and Compliance Officer
Yes, our first step was -- is really going to be reaching out to the FDA to have a meeting with them to discuss the findings that are presented here today to orient them to what we've learned and our intention to submit the response to the clinical hold to assure the most efficient way in which the FDA can review the information. So during that dialogue, it'll be primarily focused on addressing their safety concerns as it pertains to liver injury. And then after the clinical hold is lifted and we're through that process, we can begin discussing with them future clinical trials as it pertains to the PBC program.
Sujal Shah -- President and Chief Executive Officer
And Yasmeen, you were asking the questions about where we were in our PBC study. I'll simply highlight that we had somewhere around 100 patients, in fact, north of six months of dosing. We'd not had a meaningful number of patients all the way through the 52-week endpoint in our ongoing Phase III study that terminated earlier this year. But we did maintain the blind in that study. That data is being -- it's been locked and its being cleaned and there will be an opportunity for us to, of course, learn a tremendous amount from what was effectively a significant number of patients through at least 6 months of dosing around both primary and key secondary endpoints. And we'll take that learning into our consideration as we think about next steps forward, particularly in PBC. Should we be successful at getting the clinical hold lifted.
Yasmeen Rahimi -- ROTH Capital Partners -- Analyst
Thank you, Sujal.
Sujal Shah -- President and Chief Executive Officer
Thank you, Yasmeen.
Operator
The next question comes from Eliana Merle from Cantor Fitzgerald. Please go ahead.
Eliana Merle -- Fitzgerald -- Analyst
Hey, guys, thanks so much for taking the question and congrats on the panel findings. It's an exciting moment for you guys. Just in terms of as you're working through the next steps, as you prepare for the FDA meeting, what exactly are you doing in terms of preparations and going through the data? Are there any final analysis that you plan to do as you look through this and sort of ask for the clinical hold to be lifted? And then just in terms of the findings themselves, I mean, in question, do you anticipate from the FDA, are there any instances where, say, there is an imbalance in something that even if it wasn't a severe safety finding or wasn't being drug related, were there any other imbalances in the higher dose arms that were seen as part of this investigation? Thanks.
Sujal Shah -- President and Chief Executive Officer
Sure. Maybe what I'll do is start off with the latter part of your question and invite any of our experts to weigh in as well in order to provide you a key summary. As I noted in my prepared remarks, in fact, around 70% of the cases flagged by study pathologists were deemed to have features of histology that were present at baseline in as much, if not more than even at the end of treatment. Of those remaining subjects, as we noted, in fact, where there was some either emergent or progressing unexpected features of histology, be it a level of portal inflammation or interface hepatitis that progressed from baseline to end of treatment, that were largely deemed to be not related or unlikely related to seladelpar. There in fact was a balance across treatment groups, including placebo 10, 20 and 50 milligrams. Yes, Klara, you want to talk a little bit about the regulatory...
Klara Dickinson -- Chief Regulatory and Compliance Officer
As it pertains to the information we'll share with the FDA, It'll be summarizing the data that was actually reviewed by the SHRC panel, expert panel and reporting out the actual results of the scoring performed by Doctors Kleiner and Bedossa and Goodman for their review. It will also include the transcripts from the meeting itself, some of the dialogue that transpired and the actual images, digitized histology images and obviously the safety data from the locked database. So does that answer the question, Elene? Okay.
Eliana Merle -- Fitzgerald -- Analyst
Yes. Yes, that's helpful. And I guess just a follow-up. In terms of thinking about sort of clinician response to this, I know obviously these are sort of new results in terms of the panel conclusions that you have. But from your initial conversations with physicians, I mean, there's what the FDA wants. But then I guess there's also what would get a physician comfortable in terms of redosing patients specifically, and diseases where it might be chronic dosing. I mean, what are some of the reactions from the physicians that you're speaking with in terms of comfort around these findings in this investigation? Thanks.
Sujal Shah -- President and Chief Executive Officer
So I think we're fortunate to have both Dr. Gideon Hirschfield and Dr. Stephen Harrison on the line. Perhaps I'll let each of them provide their context. They were observers across the panel meetings that were conducted. Perhaps. Gideon, do you want to start and then Stephen you follow?
Dr. Gideon Hirschfield -- Principal Investigators in our PBC and NASH Program
Yes, sure. It's a pleasure to listen. I mean, I think that the message is ready for me that, that's been the most rigorous analysis I think I've ever been involved in of a clinical trial of NASH. And the findings are incredibly reassuring for the patients that we had under investigation for a drug which was looked very promising and very effective in PBC. So I think the sponsor can be congratulated on doing the most incredibly difficult task and looking at great detail in histology. And what we see is very reassuring. And of course, fundamentally, it fits our experience of using this drug in all patients with PBC, which we found it to be a safe drug, and we saw promising effects so of efficacy. So all very consistent and all very positive.
Dr. Stephen Harrison -- Principal Investigator NASH Program
Yes, this is Stephen Harrison, I'll just footsteps put what Gideon said. This was a no holds barred reviewed. I mean, the sponsor had no hooks in this at all. I mean, Paul and his team had free rein to look at this however they wanted to look at it. It underwent a very thorough and rigorous review. From the clinical perspective, you have to remember, this took everybody by complete surprise. The normal way as a hepatologist, I look at patients with liver disease is I look at their labs. And there was no signal at anything negative was happening in these patients. In fact, to the counter, in a lot of these patients, they were very positive signals.
So to find this grouping of atypical findings at baseline that led to the clinical hold was really quite a surprise. And many of our patients were upset at the fact that they had to go off this medication because of the benefit they -- that they had been receiving, not just biochemically, but also symptomatically. So I think from my perspective, I think I speak for quite a few PIs that were involved with the trial. If a clinical hold were able to be lifted, I think there would be a groundswell of support to get our patients back on this drug in a study setting so it can be formally -- the formal evaluation can be complete and potentially move the drug forward.
Operator
Thank you. The next question comes from Steve Seedhouse from Raymond James. Please go ahead.
Steve Seedhouse -- Raymond James -- Analyst
Thank you. Good afternoon. My questions are for Dr. Watkins with Sujal. We welcome, obviously, your thoughts as well. The first one I have is did the panel recommend a specific clinical path forward, i.e. any preclinical or Phase I clinical studies that are necessitated by this new finding, or a specific or explicit, rather, recommendation to restart both NASH and PBC clinical development? That's question one.
Dr. Paul Watkins -- Chair of Expert Review Panel
So this is Paul Watkins. The unanimous conclusion was that there was no evidence to support this drug causing liver injury. We -- and therefore, there was no -- from our perspective, the concern that had been initially raised based on only look at the 52-week biopsies no longer existed. So there wasn't any it was putting it to bed and we were not asked whether the preclinical evaluation was sufficient or anything like that. Our mission was just to evaluate these new concerns.
Steve Seedhouse -- Raymond James -- Analyst
Okay. That's right. So the mandate was exclusive to -- and not to delay and not to anything else. Is that essentially a fair understanding?
Sujal Shah -- President and Chief Executive Officer
That's right, Steve.
Dr. Paul Watkins -- Chair of Expert Review Panel
Yes. I mean, it was -- yes, it was to evaluate the concern that had been raised. The only concern, safety concern in terms of delivery that has been addressed. Of course, there was a thorough review of everything about the biopsies, but the focus was on those 42 patients that had been singled out by the clinical trial pathologists.
Steve Seedhouse -- Raymond James -- Analyst
Okay. That's helpful. And then another point of clarification, Dr Watkins, is the conclusion of the panel that the patients with atypical findings should not have been enrolled in the study in the first place, given the baseline findings or did the panel essentially conclude that you'd be fine enrolling these patients in either this study or future studies?
Dr. Paul Watkins -- Chair of Expert Review Panel
Yes, I'm not sure that that question was ever exactly posed, but I am pretty sure I know the answer, which is the pathologist felt they see this in NASH and that it's the part of the disease, part of the spectrum of disease. And therefore, I don't believe they would say that these patients should not say going forward the included, but that the knowledge that they have needs to get out into the public domain.
Charles McWherter, Ph.D. -- Senior Vice President and Chief Scientific Officer
Yes, this is Chuck. I would agree with that statement, Dr. Watkins. In fact, the baseline population, for example, for interface hepatitis had between 60% and 70% of subject had interface. So it's very, quite common and I do remember at one point in the discussion, there was a question raised from one of the participants about whether subjects should have been excluded. And I specifically remember one of the expert pathologists, should they've not even been enrolled in the study with the question. And they said paraphrasing, the close paraphrasing is, my God, I hope not. We'd exclude 75% of our subjects in NASH studies if we did that. So I think my understanding from the comments made from both -- from all three pathologists was that they see these features.
And in fact, we even had a comment from one of them who said during that review process, he was also simultaneously screening subjects for new NASH studies. And having -- had the conversations being exposed to this issue, he was saying, in fact, yes, he's seen this in subjects that are currently being screened for other studies. So I think the message is really that it was there before. But because the field is focused on the defining characteristics of NASH, steatosis, lobular inflammation, ballooning with fibrosis. They often don't put particular attention, especially for eligibility criteria.
Steve Seedhouse -- Raymond James -- Analyst
Okay. So just let me have one more question and then -- it's perhaps a little bit long. I'm just having a hard time understanding -- it sounds to me and please correct me if I'm wrong, but it sounds like there really wasn't a failure in the trial design here. And from the standpoint of these patients will in all likelihood be the type of patient that will enroll in a Future NASH study. And really, it's just a failure of the processes in place to evaluate liver histology. And I guess it's just remarkable that this hasn't happened, or manifested in any other trials in the past. So maybe the question is for Dr. Harrison at least and maybe Dr. Watkins as well.
Just I guess what do you do going forward in reassessment of completed studies, assessment of ongoing studies, changes to enrollment criteria, If I'm wrong about the first point or screening processes, like how does this change Nash drug development for both seladelpar, but for everything really. It's not clear what these learnings will do other than obviously, revised held up or which is remarkable.
Dr. Paul Watkins -- Chair of Expert Review Panel
Well, this is Paul, I can walk -- so I can take that on. I mean, I think the key here was not looking at the 52-week biopsies in isolation, but [Technical Issues] with the initial biopsy. I think had that been done by the clinical pathologists, although they weren't asked to do this, I'm -- pretty strongly believes they would have not felt that there was a liver safety concern.
Dr. Stephen Harrison -- Principal Investigator NASH Program
Hi. This is Stephen. I completely agree with Paul's comment. I think, moving forward one bright spot besides the fact that it's great news for seladelpar is the NASH field, I think, is going to be a big winner here because, again, you had five of the world's best pathologists look at these slides. And there's kind of been an eye opening experience for them. And then for the clinical hepatologist as well, and for me in particular, living in the NASH world like I do, it was an eye opener for me. So I'm not sure we change our criteria for outcome measures based on the findings here, but clearly I can see us broadening our aperture a bit on what we call histopathology as it relates to NASH.
And clearly, I think there will be a broader understanding of some of the lesions that that maybe are here, too, for an unappreciated on a broader scale. So I think there's a learning here about what's happening relative to the underlying disease. Remember, this is a multi-factorial disease. Lots of different pathways to activation, all kind of spurred on by fatty acid toxicity, lipotoxicity. And there's an overlay of genetics and epigenetics on top of this. So not every patient looks identical to the next patient. And so it's like a bell shaped curve, I would imagine. There's very classic lesions and then there's non-classical but still associated lesions. And I think we're just learning about this. We're still, believe it or not, in the early days of really putting our hands around NASH. What this means clinically and then as we develop therapies to try to swage this disease pattern and bring health back to the liver, we're learning about these things.
So I think ultimately we're going to take away some very positive things from this that will be broadly applicable. And then we'll follow the FDA guidance on what a positive endpoint will be for drug development. It -- does it stay NAS, driven with ballooning of zero and inflammation of zero or one, with fibrosis improvement of one stage or more with no worsening of NASH, or does it change? I don't know. But I think we'll learn from this and we'll see where that goes moving forward.
Dan Menold -- Vice President, Finance
Can I just add something here?
Sujal Shah -- President and Chief Executive Officer
Yes, go ahead, Dan.
Dan Menold -- Vice President, Finance
I just wanted to add, I think it also challenges us about the supremacy of liver biopsy generally. It's a very, very difficult field of medicine and it really is actually qualitative in many regards. And really, it's why the whole field of developing drugs for chronic liver disease, NASH, PBC is trying to move away from liver biopsy precisely because, in fact, what you see is it can be very distant, depending on how people look and how people interpret. So that's the whole world is trying to move to things that are more sort of independently validated. So it's really a bronze standard when we're assessing lots of aspects of liver disease.
Sujal Shah -- President and Chief Executive Officer
And maybe I'll just add a couple of points here, Steve, because I think this question is a very important one. And so just to pause on it, perhaps giving you an example might help to illustrate what each of the experts on the call just identified. So as we looked at these biopsies and in fact, had the three review pathologists do an in-depth scoring of 300 plus biopsies, there was an appreciation for a feature of NASH that's quite well understood, despite the fact that it's not part of the -- D activity score. So portal inflammation, for example, is a feature that, in fact is well described. Now, sitting with 20, 30 plus year experts in liver pathology and hearing them comment that while it's not -- while we decided it's not part of the scoring for NASH, it's nevertheless very prominent and may, in fact, be underappreciated with a learning, I think, certainly for us as a sponsor.
But to hear that from 20, 30 plus year veterans talking about one specific feature of NASH that in fact is well understood, but perhaps underappreciated was an interesting learning from this process. And taking portal inflammation forward, for example, some of the pathologists commented that they weren't surprised that in the setting of advanced portal inflammation that you would see interface hepatitis. Now, up until this point, at least our understanding was the interface was not necessarily typical. But even as Chuck represented, the HAI scoring in a blinded fashion revealed 60% to 70% of patients had at least some level of interface. Be it largely mild, but perhaps anywhere from 20% to 25%, even having mild to moderate or even advanced interface. And once again, really as -- perhaps another complication of advanced portal inflammation was a discussion the pathologists had around bile duct injury.
And the fact that at least in some cases within NASH, perhaps as a secondary consequence of advanced portal inflammation or as one pathologist put it "collateral damage of advanced portal inflammation", you could expect to see some bile duct injury. And so, as we move from this process to first engaging with the FDA, it is certainly a key priority of ours to share as much of the learnings out of these panel review meetings. The independent pathology review to publish and to share this information with the medical community, really to advance the entire field.
Steve Seedhouse -- Raymond James -- Analyst
Yes. Thank you, Sujal. I just want to say kudos for the persistence and really the rigor of this analysis and talk to the panel and everyone involved. Thanks for taking the questions.
Sujal Shah -- President and Chief Executive Officer
Thank you, Steve.
Operator
The next question comes from Jay Olson from Oppenheimer. Please go ahead.
Jay Olson -- Oppenheimer -- Analyst
Congrats on the panel findings and thanks for taking the questions. I was wondering if you could just look into the future and assuming that the clinical hold on seladelpar is lifted. Could you talk about how you would pick up where you left off in the clinical development in NASH and then separately, how you could proceed in PBC and whether or not you might have a registrational dataset there? Or would you need to conduct additional clinical trials in PBC? And then separately, since we just learned from Genfit that the Phase III study of elafibranor failed to meet the primary endpoint. If you could just comment on any read across to either seladelpar or the NASH space in general? Thank you.
Charles McWherter, Ph.D. -- Senior Vice President and Chief Scientific Officer
Hi, Jay. This is Chuck McWhirter. I'm going to try to take on the issues that you raised there. So I think I will come to NASH shortly, but I think just to remind everyone, the Phase II data that we had in our open-label study for seladelpar has really been robust and it showed a really strong profile for reductions in cholestatic markers alkaline phosphatase and improvements in transaminases. And of course the effects that we saw on pruritus were really encouraging. So we continue to believe that this profile has clearly shown its potential to offer patients a second line treatment alternative with improved efficacy and better tolerability. So I think that interest is really reflected in -- that interest in PBC is really reflected in the fact that we had fully enrolled 265 patients into ENHANCE in about a year in spite of the availability of an approved second line treatment.
So with that in mind, our commitment really is to first work with the FDA to lift a hold and then reinitiate clinical development. And we think that PBC is likely our most attractive and derisk first entry. So we've always been very thoughtful about expanding beyond PBC. And we think that the effects that we saw on NASH resolution in fibrosis really deserve additional consideration. You've mentioned really what happened was announced with elafibranor today, that obviously has an impact on the landscape. But of course, right in front of us is obeticholic acid with REGENERATE and they're expecting a regulatory decision soon. And that's going to have a lot of important lessons for us regarding launch uptake, reimbursement, what's the measure of success and how is this being accepted into the community.
So I think just kind of recap, I think PBC is really front and center right now. The NASH results are really quite interesting. And I think we did see some encouraging results on efficacy endpoints. But there's a little bit more to understand there. And of course, we don't want to get ahead of ourselves too much. We still have to be very thoughtful about our interaction with the FDA and try to address any concerns that they might have.
Sujal Shah -- President and Chief Executive Officer
And I'll just add, Jay, you asked a specific question around differentiation with elafibranor, which is, in our minds largely a PPAR alpha, although it is a mixed PPAR alpha delta agonist. As you can see from data that we have now, both in PBC as well as in NASH, there are some differentiating features, particularly around the robustness of the anti-inflammatory benefit that we see with seladelpar, whether or not that's one of the key features leading to the efficacy we saw in our NASH study, both on NASH resolution and fibrosis, I think needs to have some continued attention. But we've always felt that a very potent selective delta agonist has the potential to provide a meaningful anti-inflammatory benefit. And even now with some of this data NASH, what appears to be a good anti fibrotic benefit in a good portion of the patients that we had enrolled.
Jay Olson -- Oppenheimer -- Analyst
Great. Thanks for taking the questions.
Sujal Shah -- President and Chief Executive Officer
Thank you, Jay.
Operator
The next question comes from Joel Beatty from Citi. Please go ahead.
Shawn Egan -- Citi -- Analyst
This is Shawn Egan calling in for Joel. Congratulations on all the progress and I appreciate you taking my questions today. I guess first on the panel, with the reassessment of all the data that the panel reassess the fibrosis improvement and NASH resolution score. And if so, will that be shared in the future? And I've a follow-up question on timing as well.
Sujal Shah -- President and Chief Executive Officer
Yes, so I can answer that first part of the question. The purpose of the panel as Dr. Watkins outlined was really to make it take a deep understanding of whether or not seladelpar caused drug-induced liver injury in the NASH study. We did not ask the panel to assess the effects of seladelpar on NASH resolution or fibrosis.
Shawn Egan -- Citi -- Analyst
Okay, great. Thank you, Sujal. And then any time on the timing and plans to share the Phase III PBC data you've gathered to date? And also any timing on the comprehensive findings of the panel?
Sujal Shah -- President and Chief Executive Officer
Yes. So I think you make a good point. As I mentioned, ENHANCE is the study that we did have to terminate early double-blind placebo controlled registration study for seladelpar in PBC. Nevertheless, we maintain the blind in that study. That study remains blinded today. The data has been locked in, is being cleaned by the CRO. It will offer us an opportunity to eventually evaluate and share that data publicly. And so we look forward to doing that at the appropriate time.
Shawn Egan -- Citi -- Analyst
Great. Thank you so much.
Sujal Shah -- President and Chief Executive Officer
Thank you.
Operator
The next question comes from Thomas Smith from SVB Leerink. Please go ahead.
John -- SVB Leerink -- Analyst
Hi. This is John [Phonetic] for Tom. Quick question. With these histology results were there more associated with NASH pathology or with fibrosis? And then do they any way foreshadow a greater risk of progression to more advanced stages of fibrosis or to cirrhosis?
Sujal Shah -- President and Chief Executive Officer
Yes. So I guess...
Dr. Paul Watkins -- Chair of Expert Review Panel
This is Paul.
Sujal Shah -- President and Chief Executive Officer
Right. Go ahead, Paul.
Dr. Paul Watkins -- Chair of Expert Review Panel
You want to -- Sujal, well I think these things tracked more with the activity of the NASH than the fibrosis. Whether or not there's any prognostic value in terms of the rate of progression for potentially response to NASH treatment, I don't know.
Sujal Shah -- President and Chief Executive Officer
Yes, I think I was going to effectively share the same sentiments. I think it's not necessarily well understood how the progression of any one of these particular features on their own plays a role in progression of NASH. But I think important, at least from our assessments to highlight a couple of things as we mentioned, almost 70% of the 42 patients called out by study pathologists, in fact, were deemed to have either as much, if not more, of some of these features of histology at baseline than they did at the end of treatment. So, we didn't view the presence or absence of these features in our population baseline or end of treatment as any sort of complicating element of what we saw in terms of some very promising effects on both NASH resolution as well as fibrosis.
Dr. Stephen Harrison -- Principal Investigator NASH Program
This is Stephen. I'll just chime in there. You bring up an excellent point and this needs to be looked at and in fact we did discuss that a future look at placebo group, looking at these baseline lesions and marching out over time to see what happens. Not just from the CymaBay trials, but REGENERATE, Resolve-It, all these big databases where we have a large placebo contingent. Going back and looking at some of these baseline findings and see if that tracks with outcomes or progression of disease. I mean, maybe this could be a predictor of a rapid fibrosis, a predictor of rapid development of disease or progression of disease. Who knows? There's just a lot of data that we could mine as a result of these -- the work that's been done here.
John -- SVB Leerink -- Analyst
Yes, I appreciate that. And then one other quick question, kind of on, I guess, some timelines. If -- let's say a couple months from now, we assume the FDA gives the best case, we're delighted to move forward with developments. Do you think you'd have to redo a Phase 2b program for NASH or do you think you can move straight to a Phase 3?
Sujal Shah -- President and Chief Executive Officer
It's a good question. I don't know that we've gone as far as projecting what the agency's response will be at this stage. But the design of our Phase 2b study and perhaps Stephen can even provide some commentary, was a design that would have, of course, allowed us to move straight into a Phase III study was a paired liver biopsy. So the agency does require a paired liver biopsy, of course, as you know, in Phase II to progress into Phase III. 152 patients that completed end of treatment biopsies, the vast majority of which actually made it through 52 weeks of dosing. As we mentioned, the study was actually powered on the primary endpoint, which was a 12-week change in liver fat content, not powered to the secondary endpoints on NASH resolution and effects on fibrosis.
Nevertheless, I think the data that we've gathered for the patients in this study that did have paired liver biopsies, I think arguably can be viewed as some of the more promising Phase II data in a paired liver biopsy that's been demonstrated, at least for an oral agent in NASH.
Dr. Stephen Harrison -- Principal Investigator NASH Program
Yes, I'll just chime in. This is Stephen again. So, I mean, when you look across the broad landscape of Phase 2b trials with paired histology that have subsequently gone in to Phase III, this is within that realm. And as Sujal mentioned, the vast majority of those patients were able to get across the 52-week finish line and get a follow-up liver biopsy. So I think it -- what we've heard today is safety biochemically, clinically, histopathologically not a concern. With that in hand, then it just really shifts, in my opinion -- it's just my opinion, it pivots to, OK then do we have a dose ranging study that with paired histology, with enough data to move in Phase III And I think if you look at what they've published previously the preliminary top line results clearly is a dose response relationship.
And as Sujal mentioned, I mean, when you're looking at seladelpar 50 and you're getting 26% resolution of NASH versus 8% for placebo, and let me just comment on placebo there. That's within what we would consider a normal "normal placebo response". That's very positive. And in the fibrosis benefit on top of that, I think puts it into a league that would be very reasonable to move into a Phase III trial. Again, that's just my opinion. But I think that's perfect. The data we have would warrant moving to Phase III.
John -- SVB Leerink -- Analyst
Great. I appreciate it. Thank you very much.
Sujal Shah -- President and Chief Executive Officer
Thanks for the question.
Operator
Thank you. This concludes the question-and-answer session. I would now like to turn the conference back over to Mr. Sujal Shah for any closing remarks.
Sujal Shah -- President and Chief Executive Officer
Thank you, operator. I want to make just a few more remarks. Since our announcements last November, every member of our remaining team at CymaBay has been tirelessly dedicated to the seladelpar investigation and our evaluation of strategic alternatives on behalf of all of our stakeholders. In the face of a suspicion for safety concerns in our NASH Phase 2b study, we took decisive action not to put patients at risk.Our commitment quickly turned toward pulling together a deep bench of liver experts to help us analyze and interpret tremendous amounts of data we have been collecting over the past five months. We took no shortcuts in our investigation. NASH is a complex, heterogeneous disease and one for which we have only seen a significant acceleration of clinical development with potential novel interventions over the past 10 years.
I believe there will be much we can share with the field to increase our understanding of the many elements of NASH that today are largely underappreciated. In the end, I firmly believe this effort will only contribute to the base of knowledge needed to continue making significant advances for patients with liver disease. We look forward to our continued role in this effort and to providing updates as we make progress in the weeks and months ahead. I'd like to thank all of the experts who participated on our review panel, several of my colleagues in the industry who aided in our efforts, everyone here at CymaBay to the patient advocacy groups who inspired us not to give up, on the effort to understand the findings from our NASH Phase II study, and of course, to the patients who have participated in our clinical studies. Thank you all again for joining us today.
Operator
[Operator Closing Remarks]
Duration: 78 minutes
Call participants:
Dan Menold -- Vice President, Finance
Sujal Shah -- President and Chief Executive Officer
Dr. Paul Watkins -- Chair of Expert Review Panel
Dr. David Kleiner -- Head of the Drug-Induced Liver Injury Network at NIH
Klara Dickinson -- Chief Regulatory and Compliance Officer
Dr. Gideon Hirschfield -- Principal Investigators in our PBC and NASH Program
Dr. Stephen Harrison -- Principal Investigator NASH Program
Charles McWherter, Ph.D. -- Senior Vice President and Chief Scientific Officer
Yasmeen Rahimi -- ROTH Capital Partners -- Analyst
Eliana Merle -- Fitzgerald -- Analyst
Steve Seedhouse -- Raymond James -- Analyst
Jay Olson -- Oppenheimer -- Analyst
Shawn Egan -- Citi -- Analyst
John -- SVB Leerink -- Analyst
