Ladies and gentlemen, thank you for standing by, and welcome to the Gossamer Bio Q3 2020 Earnings Call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question-and-answer session. [Operator Instructions]. I would now like to hand the conference over to your moderator today, Mr. Bryan Giraudo, Chief Financial Officer. Thank you. Please go ahead, sir.

Thank you, operator, and thank you all for joining us this afternoon. I am joined on today's call by Gossamer Bio's Co-Founder and Chief Executive Officer, Dr. Sheila Gujrathi; as well as our Chief Scientific Officer, Dr. Luisa Salter-Cid. Earlier this afternoon, Gossamer Bio issued a press release announcing its financial results for the third quarter ended September 30, 2020 in addition to providing a corporate update. Please note that certain information discussed on the call today is covered under the Safe Harbor provision of the Private Securities Litigation Reform Act. We caution listeners that during this call, Gossamer management will be making forward-looking statements. Actual results may differ materially from those stated or implied by these forward-looking statements due to risks and uncertainties associated with the company's business. These forward-looking statements are qualified by the statements contained in Gossamer's news releases and SEC filings, including in the Annual Report on Form 10-K and subsequent filings. This conference call also contains time-sensitive information that may only be accurate for a limited period of time. Our ability to meet our guidance especially that related to the timely initiation and completion of clinical studies, in addition to our ability to release results from our clinical trials in a timely manner may be adversely affected by the ongoing COVID-19 pandemic. Gossamer Bio undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call. Now, I'd like to turn the call over to Sheila. Sheila?

Thank you, Bryan, and good afternoon to everyone who is joining us on today's call. We appreciate you taking the time to hear about the progress Gossamer has made. Earlier this afternoon, Gossamer Bio was pleased to announce its financial results from the third quarter 2020 in addition to several updates to the status of our pipeline of clinical product candidates. Gossamer Bio was founded as an innovative research and development engine to deliver value to the collection and development of a pipeline of multiple independent programs across the therapeutic areas of inflammation, immunology and oncology. This engine is centered around an experienced team with a history of successful and efficient execution in these closely related therapeutic areas. Each program is backed by regular preclinical and clinical work to understand and derisk the product candidate focused on areas of high unmet need and a differentiated product profile that would be meaningful for patients. We are pleased to be advancing two independent molecules targeting two different indications into Phase 2 trials. We are also excited to discuss new clinical data from our immuno-oncology candidate GB1275 as it continues to progress through its Phase 1/2 trial in solid tumors. All told, development progress for multiple candidates is a manifestation of Gossamer purpose. The continual and simultaneous advancement of multiple high potential programs through the execution of the appropriate experiments to create value for shareholders. First, I will briefly review the status of GB001, our once daily oral DP2 antagonist for the treatment of moderate-to-severe asthma. In October, we read out the top line results of our Phase 2b LEDA study. While the primary endpoint of asthma worsening was not met, GB001 did demonstrate a consistent reduction of 32% to 35% in the proportion of patients exhibiting asthma worsening across all three active…

Thank you, Sheila. We will now review the financial results for the third quarter of 2020. We ended the quarter with $555.4 million of cash and cash equivalents. We anticipate our cash, cash equivalents and marketable securities, along with access to our debt facility, will provide sufficient capital resources to fund operations and capital expenditures into the second half of 2023. Research and development expenses in the third quarter of 2020 were approximately 41.8 million as compared to R&D expenses of 40.1 million for the same period of 2019. G&A expenses were 11.4 million in the third quarter as compared to G&A expenses of 9.8 million for the same period in 2019. Our net loss for the quarter was $57.8 million, equating to $0.80 per share. For the same period in 2019, we reported a net loss of 48.5 million, which equated to $0.80 a share. The increase was primarily attributable to an increase in interest expense of $4 million and a decrease in investment income of 1.7 million. With that, I will turn the call back over to Sheila to offer some closing comments before we open the line up for Q&A. Sheila?

Thank you, Bryan. It has been an exceptionally busy quarter and year at Gossamer, especially as we advance multiple clinical and research programs during the COVID pandemic. I want to extend my personal appreciation to our patients, physicians and partners who have helped us achieve the activation of Gossamer’s third and fourth Phase 2 trials to date. I would also like to extend my sincerest gratitude to the Gossamer team who continue to bring their best selves and go beyond possible during these unprecedented times. With that, I will now turn the call over to the operator for questions. Operator?

Thank you so much. Ladies and gentlemen, we will open it up for a question-and-answer session. [Operator Instructions]. Your first question comes from the line of Tyler Van Buren. Your line is now open.

Hi, guys. Good afternoon. Thanks for taking the questions. I had a couple on GB002 and the PAH data coming up. Understand that it's more potent and selective than imatinib, but I guess I'm specifically interested in ratio of lung exposure given the route of delivery. Can you just – I guess has there been any data in terms of ratio of lung exposure with imatinib that you could speak to and how much higher you think GB002 could be when we see the data? And then can you just confirm will we see data from planned [ph] patients? And did you mention a six-week OLE as a possible we could see data from that as well?

Great. I’ll start and then I’ll ask Luisa Salter-Cid, our Chief Scientific Officer, to add anything she would like. So yes, we do have several full [indiscernible] exposure in the lung to plasma. And we have done more characterization of this pre-clinically as well as in our normal healthy volunteer study in terms of measuring peripheral, PK and then in our PAH Phase 1b trial. It's important to understand that we designed this molecule specifically to have low systemic PK concentration, because clearly what we saw with the prior imatinib experience in the clinical Phase 2 and 3 PAH trials was really substantial issues around safety and tolerability, so that if you have high imatinib PK levels that hit again a number of kinases, that they were having a significant number of adverse events, serious adverse events, including GI side effects as well as [indiscernible] events, and CNS subdural hematomas. So this is really critical that we would be able to ensure, again, low PK level systemically in the periphery. And so GB002 is rapidly cleared and never reaches high level systemically. So what you see are low levels from the CMAS perspective, but then rapid clearance. And we've shown this in our normal healthy volunteer trials and we're confirming that profile in the PAH population. So that's a really critical component to this profile, where you again want very substantial lung exposures that’s very, again, manageable systemic exposures to really improve upon the safety and tolerability. So that's critical. So, we'll continue to discuss that. And I think we can touch upon that in our webinar in December to go into more details on that. Regarding the Phase 1b experience, again, as I mentioned, this is a two-week study. We do have a six-month OLE available for these patients proportionately. We had patients in that OLE in the early part of this year. But because of COVID, they had to come out because we had to pause really the conduct of the study, given the total shutdown at the sites, especially for the PAH treating centers. So we will mainly be focused on two-week data in December. So again, focused on PK, safety, tolerability, target engagement and biomarkers, and continue to discuss the program. With that, Luisa, do you have anything else to add?

Yes. I think you've pretty much covered, but I think one another thing is, it’s not only just the exposure, but it's also the duration that really 002 has a high retention on target and because of that, we have actually sustained exposure in the lungs for a long period of time. So it's not just the PK distribution, but it's also the way that 002 binds on target. And we have data from the PD endpoints such as the MPR2 and others that really confirm this prolonged PD.

Great. Thank you.

Great. Thanks, Luisa. So I think we're going to look forward to really presenting a substantial amount of preclinical data and further characterization that we've done with our molecule to really share how we think it's truly best in class and the right molecule for PAH patients, particularly.

Your next question comes from the line of Joseph Schwartz. Your line is now open.

Hi, guys. How you doing? Thanks for taking my question. I also wanted to ask one on GB002 to start and that has to do with some comments I think I heard you say about how you might be able to look at some data from the ongoing Phase 1b in patients and gauge some potential to bridge off of the effects that you've seen in healthy volunteers, if I'm not misunderstanding. I was just wondering if that was accurate, if you could expand on that. And then since this isn't a vasodilator per se, at what point would you hope to see a signal and what would that signal be in terms of PD markers or how are you thinking about when you might start to see some interesting signs?

Yes, great. I think my points were really, Joseph, that we have a pretty substantial Phase 1 experience. When you look at our SID, our multiple ascending dose studies in normal healthy volunteers across a range of doses and now with the Phase 1b in PAH patients, so the totality of the clinical experience we have to date is great for where we are in the stage of development. I think we're taking all the right steps to make sure that we're going with the right design for the Phase 2 trial. So I think what we'll be sharing in December really is the totality of our Phase 1 experience. And so that's what I was mentioning in terms of being able to bridge. And look, it’s not only what we generated in terms of data from the PAH patients in the Phase 1b, but also bridging that information back to normal healthy volunteers and seeing consistency in PK exposures and the like. So I think that was the point I was making. And secondly, on your question on time points for efficacy readouts, I think intensively for PD, our hope would be we could follow some patients over time and be able to look at changes in peripheral clinical disease such as proBNP levels as well as potential changes on imaging such as echocardiogram. If you're asking me about timing, if you look at some of the amount of data, they were able to see effects, as you know, really even in that 12-week timeframe. But, of course, our Phase 2 study is a 24-week study. And so that's – and that's looking at PVR. So it will be also looking at imaging and some of these systemic markers as well for clinical disease as well as biomarkers. So I think it will be a pretty robust dataset coming out of the Phase 2. And again, unfortunately, just because of the COVID pandemic really impacted or ability to have the more robust Phase 1b experience we were hoping for, but nonetheless we think we got very informative and impactful data for the program.

Cool, we'll stay tuned. So then on GB001, I was wondering if you could give us your thoughts or expectations for when we might be able to look forward to learning about what biomarkers you found are associated with a better response than the LEDA trial?

Yes. I think that for us is I think we’re shooting towards that first half of next year to be able to kind of get the budgetary feedback we're seeking. We have to schedule these meetings in the same divisions that deal with COVID and other therapeutics that are out there being studied in the COVID patient population. So we’re very mindful of that. But our hope is that we're going to get that registry feedback and then we'll look forward to presenting more the detailed data in our plan forward in that first half.

Sounds good. Thanks.

Your next question comes from the line of Geoff Meacham. Your line is now open.

Hi, guys. Thanks for taking the question. I had a couple. The first one is on 002. Is there a population in PAH that you feel like you could maximize the differences in PVR resistance? I guess maybe those not well controlled on combo therapy, for example? And then what types of effect size, Sheila, would you say that you're aiming for in the study just as a proof of concept as you sort of get the – prepare for a larger study? And then I have one follow up on 001.

Yes. That's exactly the patient population we're going after, Geoff. We're looking at patients to continue to have higher PVRs and disease burden and symptomatology, despite being on at least two classes of vasodilator therapies, if not three classes of vasodilator therapies. So they are functional class II and III patients with again a pretty substantial disease burden and they are on background therapies that we're adding on to. So I think we're really enriching for kind of a higher disease activity population, which we think is the right population to be studying in this Phase 2 trial. So I think that’s a very, very compelling unmet need. In terms of the effect size, if you look at the data from imatinib from their IMPRES trial, they saw about a 32% reduction in PVR, like 30% to 32%, as well as improvement – about 30% improvement in six-minute walk distance. Now that was done a while ago in terms of when that study was conducted, how sick those patients were. And then they were also on II or III classes of vasodilator therapy. So that's similar. That was also an add-on study design to those other classes of therapy. So that's really helpful to know that they saw that level of improvement, despite being added on to vasodilators. And I think that's, again, a very compelling rationale for our program. So I think, obviously, that would be terrific to be able to show that type of similar efficacy. Again, the question is, how much are patients improved since then with their level of disease control? And so we're going to be talking – thinking more about that and talking more about that as we get our study off the ground.

Got you. Okay. That's helpful, Sheila. And then maybe one for you or for Bryan. I know you're still getting feedback on 001 on next steps. But when you think about strategic options here or partnering, is it a parallel process or do you have to have absolute clarity on Phase 3 design as sort of a first step to negotiations? Thank you.

Yes. I would say both, right, because we engage in discussions. It’s, of course, a very critical piece for us to understand what is the regulatory and development path forward. So I think those are obviously very natural things that we have to get information on. Bryan, do you want to provide any commentary?

Yes. Thanks for the question, Geoff. I think our practical challenges that while we have ideas around what a Phase 3 program could look like, really hard to engage in substantive discussions until we let regulators weigh in. And that obviously has a direct read through to the investment that any partner would have to make in Phase 3 and then what the really potential commercial presentation could be. So it is a little bit of a chicken and the egg conversation, and we're working diligently to be able to get those answers. Because right now, the only real reference point the strategic market has as to what a Phase 3 with a DP2 antagonist looks like is what our friends at Novartis did. And so we're obviously trying to see if we can have a more streamlined and efficient plan. But until we have regulators weigh in on that, it's really hard to talk about what that financial as well as infrastructure commitment any partner would have to make.

Okay. Thanks, guys.

Thanks, Geoff.

Thanks.

Your next question comes from the line of Josh Schimmer. Your line is now open.

Thanks for taking the question. Again, on 002, can you indicate when we might be able to get a first look at the effect on right-sided heart pressure in PVR specifically? Is that being measured in Phase 1b or is that going to have to wait for Phase 2? And Bryan, I might have missed it in your prepared remarks, but how should we think about operating expenses going forward?

Yes. So pulmonary vascular resistance [indiscernible] the data comes from right heart catheterization and is really the primary endpoint of our Phase 2 trial. So that's, again, the 24-week endpoint for Phase 2. And so that will be – naturally that will be robustly characterized. And so that's when you should plan to see that. From the Phase 1b, that is more around, again, clinical biomarkers, disease activity and potential echocardiographic imaging, but not really hemodynamic data. And then go ahead, Bryan, on operating expenses.

Yes. So, Josh, I said in my remarks that all the capital available to Gossamer takes us into the second half of 2023. I'm cautious to give greater guidance than that just because as we are kicking off these two important Phase 2 trials against the backdrop of the pandemic, it's still too early for us to make predictions on enrollment timelines and thus costs. But we do feel very good based upon the totality of the book of work, shall we say, that we're doing at Gossamer that the capital we have takes us well into the back half of 2023.

Okay. Thank you.

Your next question comes from the line of Carter Gould. Your line is now open.

Great. Thanks. Good afternoon. Thanks for taking the questions. I guess first, maybe to come back to 002. I know you guys have been engaging with a lot of KOLs and I’m just trying to understand the landscape. I appreciate you guys bringing up the imatinib experience in Phase 2. But I guess when you think about sort of the hurdle for clinical meaningfulness, either in terms of PVR, six-minute walk distance, how do you think about that in this population kind of – what's the, I guess for lack of a better term sort of floor, and what you need to see? And then maybe on 1275, the poster talked sort of delineated sort of 50% to 75% reduction on MDSCs. Can you maybe just help put that in context? And if there's a target or there's some sort of hurdle you guys are looking to reach and just kind of help think about some of that biomarker data? Thank you.

Sure. Yes, I think it really gets – your first question really gets to the unmet need of what we're trying to achieve here. So, just as a reminder, everyone knows there are these three classes of vasodilator therapies that have been improved in PAH and that are predominantly used in functional class II, III and IV. And most patients are started off in a combination regimen usually with some type of PDE-5, ERA type of combination. When processes like those are added, obviously, and depending on how severe the patient is could be added on even earlier in the disease state. And then there really are no other approved treatment options beyond those two classes of vasodilator therapies. So for those patients who have a continued symptomatology, continued deterioration in their functional status, and real impairment on the hemodynamics leading to right heart failure, and morbidity and mortality with the high rate of mortality, and there's a 50% to 75% mortality rate for patients who are functional class III and IV who are controlled or continuing to progress, which is – really rivals any oncology indication. These patients have no available therapies. So we're really looking to add on to these classes of [indiscernible] and see if we can just really show any functional improvement, as measured by six-minute walk distance, which is obviously very clinically important because we need to see that functional improvement. And the objective parameter of looking at human dynamic improvement is obviously very important and critical, especially at this stage of development for us to get the type of information. That's why we put this as our primary endpoint for the Phase 2 trial. But we will also be measuring our impact on functional improvement as well. So that's really what we're looking. We…

Yes, absolutely. So that is a question for all therapies that people have grappled with. What is enough? And basically, what I think most people including us have landed is it has to be going down in the right direction and it has to be beyond just significant, so very significant. So it's not just [indiscernible] observation. But to Sheila's point, I think that other folks and us including have really zeroed in here. Do we have then proteomics biomarkers that go with it? You see some significant change in cytokines, in chemokines, which we do, and that is really that you want in fact in the biology. And then as Sheila mentioned, at the end of the day the tumor is all about the T cells, specifically the CD8. And are you seeing an increase in CD8 into much infiltration? And we are. So I think it is the totality of the data rather than a specific number. That number just has to be consistent enough for us to know that it's not just a fluke. And that's I think what everybody else is doing with these MDSC modulating therapies.

Yes. And I noticed that it's getting back to the clinical data as well, so this has been very reassuring to us that we're seeing these biomarker changes. Again, looking at the periphery, looking at the cells themselves, looking at the proteins, looking at the gene expressions for myeloid derived genes as well as inflammatory genes if you look at interferon type responses, and then the tumors themselves. And a few things we've been able to get biopsies, which has been a really great effort from our team. I want to thank our team because it's not been easy during the COVID pandemic to actually get a biopsy. So I think that's been incredibly productive and fruitful for us to be able to see – we are seeing this influx of cells and see a positive T cells, which are again really critical for the mechanism and validation of that biologic activity. And then we see the clinical activity. Just to remind everyone, you guys know this, but these are very sick patients. Most patients who are coming in all have at least two lines of therapy, many of them have five or greater prior lines of therapy across very difficult to treat tumor types that have not shown good responses either – mostly secondary resistance to checkpoint inhibitors and also primary to the checkpoint inhibitors as we've seen with patients who've been treated with CPI that has about a two-month duration of response prior and then lost that. And then we're seeing responses with combination. So I think that – in terms of stable disease, I should say. I think that is really encouraging. Just to have again five of the seven prolonged stable disease at the 800 milligram or greater, including again a confirmed PR at this point, given just the Phase 1 experience we're in, we find really encouraging. And that's in about 16 evaluable patients. So if you're seeing, 5 out of 16, that's really I think encouraging information for us.

Your next question comes from the line of Emma Nealon. Your line is now open.

Hi. Thanks for taking the question. So turning to GB004, you see – given some of the physician feedback from the recent Phase 1 data, can you just speak to why the early profile is so potentially exciting to physicians in this mild to moderate setting? And where it could fit into the evolving commercial landscape? And then just in terms of potential future combination work, are there any specific mechanisms that you think would be logical?

Yes. I think it's just – the excitement really is such a differentiated mechanism. So as I've mentioned on the call, it's really not that typical immunosuppressant and there are a number of effective therapies, of course most of them are biologics but also some orals that are entering into the marketplace. We have the JAKs that are approved. I think the SOP [ph] receptor modular that’s analog has very exciting Phase 3 data. And I think others will potentially be entering this space, but those are really focused on targeting the immune system. This type of therapy is actually a therapy that clinicians have been looking for, both in terms of the differentiated mechanisms focused on epithelial barrier function and repair and the integrity of the mucosal lining and being able to heal that the mucosa in the gut for these IBD patients that have had a disrupted epithelial lining, which leads to further inflammation and continued kind of disease symptomatology and severity. So I think that's really very exciting from – again, a differentiated mechanism that could be used alone, especially in earlier stages of disease, as well as in combination from other immunosuppressants and hopefully in a safe and synergistic manner, as well as the ability then to take that and to target an earlier population in terms of really that more moderate disease, especially 5-ASA and steroid failure patients who have not progressed on to moderate or severe disease at this point, because right now is a pretty big leap of faith for patients to have to go from their 5-ASA and steroids and maybe some other generic immunosuppressant therapies that are commonly used to a biologic or to a really potent immunosuppressant oral that has the risk of infections, the risk of malignancies, and other monitoring that may be required. So it's a really big jump and leap of faith. And really patients and clinicians would prefer to have another therapy that could be in the gap to be able to use, such as GB004. So I think it's really again that pre-biologic, that pre-moderate to severe positioning, as well as a differentiated mechanism that is resonating so powerfully. And they're so excited about this type of approach, which makes really tremendous sense when you look at the biology of the disease area. And so I think that's really what we're focused on addressing with our trial design, with the SHIFT-UC study to really capitalize on what we understand about the mechanism and who are the best patients to benefit. And I want to have Luisa add her thoughts on this as well, because we've been doing a lot of work on the mechanism. And then we could talk about the other combination approaches too.

Yes. So we do – we have really spent some time because, as Sheila mentioned, this is really – the mechanism of action is self complementary to the immunomodulators that are on their standard of care. So we have gathered a lot of data both on translational endpoints with organoids and cocultures as well as the in-vivo models, including patient samples. And really we are seeing that synergy, not just complementary, but also synergy in a lot of – quite a few endpoints when you combine with specific therapies out there, including the JAK inhibitors as well as anti-TNF. So more to come and we will absolutely share the data. But I think not surprisingly, we are seeing very good synergy between these two approaches.

Great. Thank you very much.

Your next question comes from the line of David Hoang. Your line is now open.

Hi, guys. Good afternoon. Thanks for fitting me in. So I just had two questions; one on PAH and then one for ulcerative colitis. So for PAH, I note that Acceleron with sotatercept, they have a supportive Phase 2 trial that's looking at cardiopulmonary exercise testing and really looking at peak oxygen consumption. Is that something that you would ever be interested in pursuing for 002? And do you think having that info would be informative or additive to the drug’s profile?

Yes. That's a very – obviously very interesting study and we applaud them for taking those types of measurements. We have discussed this extensively with our investigators as well. We have not built in that type of detailed and rigorous in terms of intensive, I should say, assessments into some of our trials in our Phase 2 study specifically. I think we're focused on we think the most relevant endpoints at this stage of development in terms of looking at the pulmonary vascular resistance and the measurement on the hemodynamic parameters, as well as right heart function. And that's, again, through again the right heart path data that we’ll be getting in lung echocardiogram imaging to really assess ejection fraction. So I think those are some of the areas that we – I think we think that were the most relevant for where we are. The other biomarkers that we're assessing, again, around proBNP levels is the marker of right heart screen and would be also very important to BMPR2 to really think about the mechanism in greater depth, I think is important. But those are things that we are looking at potentially doing over time and in supportive studies. We are looking at some other imaging modalities that I think will be very exciting to potentially try to get at what's happening in the vascular structure and really in the vessels themselves in the lung. And so those are things that we look forward to discussing, again, at our webinar in December. And I think those are some other novel techniques of imaging that we'll be employing in our program, which we have decided are probably the best at this time.

Got it. Great. And then just on ulcerative colitis, I know that some of the S1P receptor modulators are interested in moving earlier into the treatment paradigm. And so, for example, I've seen that Etrasimod has a Phase 2 trial in moderate patients. I think they're going from Mayo score 4 to 6, endoscopic score of at least 1. Is that a patient population that overlaps with who you're enrolling in your Phase 2, or will you guys be different or maybe even earlier in the treatment paradigm?

I will say that there would be an overlapping disease population if you look at the totality of the Mayo scores and the endoscopic scores. I think the question will just be what is the profile for Etrasimod long term? And we obviously know the profile for ozanimod. We know ozanimod very well having developed the drug. So, I think that we know the safety and other liabilities around monitoring for that therapy. And while we think it's a great therapy, I think if there will be maybe potential challenges in their uptake, given some of those safety liabilities that have that drug, then the treating clinicians will have to deal with. With S1P, I think the question is, over time will the liabilities be for any S1P modulator completing their large development programs that we have to see that and then how can they move up into the treatment algorithm? So, I think that will be a question in terms of how it’s positioned and how it will be used by the clinical community and how it will be received by patients. There is something around just significant lymphocyte reductions, which can be scary to clinicians, especially because they have had to deal with PML risk with Tysabri. Obviously, they've gotten a lot more comfortable with that within TVO with abituzumab looking at all alpha-4-beta-7 targeting therapies. Having said that, it's always a risk in terms of thinking about potential infection risk, when you have really reduced the number of circulating peripheral lymphocytes. So, I think those things are real and will always have to be managed by clinicians and always thought about for patients. So the question is, how will that profile impair the ability to be treated to be really used in that mild to moderate population…

Got it. Thanks for the insights and taking my questions.

Your next question comes from the line of Patrick Trucchio. Your line is now open.

Thanks. Good afternoon. Just a few follow-ups on GB004. We've seen the shift in recent years in terms of regulatory guidance and endpoints for IBD with the preference for the measuring of mucosal healing that’s confirmed by histologic analysis and the validated PRO measures. So with SHIFT-UC enrolling, I'm wondering how we should view the endpoints in IBD. And we see particularly – and with this mild to more moderate patient population, do you believe the endpoints regulatory bar is still shifting or is it fairly stable as we look ahead to an eventual update in the SHIFT-UC study? And then I have two follow ups?

Yes, great question. For ulcerative colitis, I would say there's been, of course, a lot of regulatory dialogue on the proper endpoints. But it does seem to be able then, for example, Crohn's disease which I think is still an evolving area and has additional challenges. I think the importance of clinical remission is so very relevant. So that is looking at really the Mayo score primarily, looking at, again, not only signs and symptoms, primarily still frequency and rectal bleeding, but looking at the endoscopic improvement and looking at endoscopic remission to really be able to be counted as that clinical remitter. And so I think there's a lot of confidence in that endpoint. I think the higher bar is mucosal healing. And it really gets to – as our medical evac [ph] like to say and has spoken to many of you on the phone here, the tissue is the issue. So we do say that a lot at Gossamer. And we believe that greatly because it is very true, that if you can show that histologic remission on top of the clinical remission and really get to mucosal healing, that's just such a meaningful endpoint. So if you can show resolution of inflammation, and again as we define histologic remission, it's very, very detailed. You have to have, again, really absence of neutrophils and other inflammatory cell types and multiple layers of the colonic tissue. And so to be able to get to that high hurdle, mucosal healing endpoint is, again, I think is definitely a higher bar. And it's something that we'll be measuring very closely. It's where we saw really the best data coming out of our Phase 1b. And so we're going to measure that in our Phase 2 trial. But I do think the approvable endpoint of the clinical remission is I feel very solid. And so I don't think that's going to shift dramatically during our development program. I could be wrong. But I think having clinical remission as your primary endpoint and then looking at histologic remission as a very important secondary endpoint, and then mucosal healing as well as important secondary endpoints to characterize your efficacy, and getting at that the ability to have sustained long-term remission will be very important to the regulators, it will also be very important to treating clinicians and to patients.

Got it. And then just regarding potential movement to Crohn's disease, would the plan be to wait for the outcome from SHIFT-UC before moving ahead in Crohn's disease, or what would determine if 004 moves ahead in Crohn's?

That's currently the thinking that we have planned for Crohn's disease and believe – based on rationale, the scientific rationale that it will work in Crohn's disease. But I think right now our lead indication is ulcerative colitis. And based on the data we see there and as we get more experience, we'll be moving Crohn's forward.

That’s helpful. Thank you very much.

Thanks, Patrick.

[Operator Instructions]. There are no further questions at this time. You may continue.

Thank you so much for taking the time and asking us all these great questions around our portfolio. We’re pleased to be able to speak to you all again and looking forward to hopefully seeing you at the webinar in December and more discussions to come. So thank you again. Goodbye.

Ladies and gentlemen, this does conclude today's conference call. Thank you for participating. You may now disconnect.