Protagonist Therapeutics, Inc.

Good afternoon and welcome to Protagonist Therapeutics 4th and full year 2020 earnings conference call and audio webcast. At this time, all participants are in a listen-only mode. Please be advised that today's webcast is being recorded. If you require any further assistance, please press star zero. With that, I would like to hand the conference over to our first speaker, Don Calcolfin, Chief Financial Officer. Thank you and please go ahead.

Thank you for joining us today. As a reminder, certain matters discussed in today's conference call and are the answers we may be given to questions asked may include forward-looking statements that are subject to risks and uncertainties related to the future events and or financial performance of the company. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the risk factor sections of our annual report on Form 10-K for the year ended December 31, 2020, on file with the SEC. A question and answer session will follow the formal presentation. And just as a reminder, the call is being recorded. I now like to turn the call over to Dinesh Patel, President and CEO of Protagonist, to provide a company update.

Thank you,

Don.

Good afternoon, everyone, and thank you all for joining our conference call to discuss Protagonist Therapeutics, financial results and corporate highlights for the fourth quarter and full year 2020. Don and I are joined on today's call by Samuel Sacks, our Chief Medical Officer, David Blue, our Chief Scientific Officer, and Sunil Gupta, Chief Development Officer. 2020 was an exceptional and transformative year for Protagonist, during which we expanded our clinical pipeline, and we now have five different new clinical entities, or NCEs, that are being advanced in six different clinical studies, and all of these studies are expected to be completed over the next two years. As many of you know, each of our clinical assets has been developed through our proprietary technology platform, and currently we are developing novel therapeutic options across three distinct disease categories. One, various blood disorders influenced by excessive red blood cell production, that is, excessive erythrocytosis, or by excessive iron overload conditions. Two, inflammatory bowel disease, or IBD, such as Crohn's disease and ulcerative colitis. And three, various inflammatory and autoimmune diseases that have already been clinically validated by the Interleukin 23 or IO23 pathway. I would like to start today's call by reviewing Ruspatide, previously known as PTG300. As a reminder, Ruspatide is a peptide magnetic, often natural hormone hexidin, which is a key regulator of iron homeostasis, as it controls the absorption, storage, and distribution of iron in the body. Ruspatide was developed to have superior drug-like properties, including its potency, heart-life, solubility, stability, and ease of synthesis, in comparison to the natural hormone. Our most advanced clinical program with this candidate is in patients with polycythemia vera, also known as PV, a rare and progressive blood disorder affecting about 160,000 patients in the United States alone. In May of 2020, we presented a very small but robust data set for 7 patients from our ongoing Phase 2 PV trial, and that proved to be a turning point for protagonists. In December last year, in an oral presentation at the ASS conference, we shared the data for 18 patients from the same study, and were pleased to see the continuation of the robust clinical responses observed earlier in May. To quickly recap the data, Ruspatide appears to be safe, well tolerated, and very effective in managing hematocrit control below 45% across the 18 adult PV patients evaluated. This tight hematocrit control also led to a dramatic decrease in the need for therapeutic lobotomy, the most common treatment modality for this condition. Furthermore, we also observed a reversal of iron deficiency in these patients. Iron deficiency is a typical undesired outcome of therapeutic lobotomy in these patients. While lobotomy is the current mainstay of PV treatment, many patients are unable to maintain hematocrit levels below 45% as per the NCCN guidelines. And this is unfortunately true even for those patients receiving frequent lobotomies and receiving treatment with cytoreductive agents. So to develop a clear understanding of the current treatment regimen and evaluate its true effectiveness, last year we took a large scale retrospective analysis of real-world patient data of over 28,000 patients, and we also obtained hematocrit measurements from blood test results for a subgroup of over 4,000 patients. Our findings were an eye-opener, and it showed that hematocrit levels were poorly managed for a majority of patients. In fact, only 22% of the patients on current treatments had consistent adherence to NCCN guidelines of keeping hematocrit below 45%. This is concerning at many levels, including the fact that with high hematocrit levels, PV patients may be exposed to higher risk of life-threatening traumatic events. This analysis further confirms our belief that there is a large and glaring need for better treatment options for these PV patients. Based on our promising Phase II results, we believe that a natural hormone mimetic like Rasprotide can potentially provide PV patients with a safe, non-cytoreductive and effective therapy that improves upon the standard of care options not only for patients receiving frequent lobotomy, but also for patients who continue to receive lobotomies in combination with other pharmaceutical treatments. Our ongoing Phase II Rasprotide PV study is progressing on track. Recruitment has in fact recently accelerated, and we expect to complete the enrollment of 50 patients by mid-2021. With the compelling clinical trial data in hand, we are consulting with U.S. regulatory authorities in the first half of 2021 to discuss and finalize our registrational study plan. I would also add that Rasprotide has received FASTREC designation for PV from the U.S. FDA and ORFANREC designation from both the U.S. and European regulatory agencies. The advancement of Rasprotide to a pivotal trial in this indication will be a key turning point for protagonists in 2021. In the future, if approved, it's possible that Rasprotide could reshape the treatment paradigm in PV and become the main long-term non-cytoreductive therapy of choice for many patients living with this challenging condition. Now, Rasprotide's clinical momentum does not stop at PV. We are also evaluating this candidate for Hereditary Hemocrymoptosis, or HH, in an open-level Phase II -of-concept study. HH is a disease characterized by iron overload, where persistent iron overload can lead to heart and liver damage that could ultimately lead to more life-threatening situations. Today, HH impacts approximately 1 million patients in the U.S. and Canada, and phlebotomy is the only therapeutic option for these patients. There are no FDA-approved drugs for this indication. Efforts are also under way by us to better understand which subpopulations of these 1 million HH patients may derive maximum benefit from a drug like Rasprotide in comparison to phlebotomy. We are pleased with the progress of the current Phase II study, and we should be able to share preliminary results in the second half of the year. Based on these results, we will determine next steps and the path forward for Rasprotide in the indication of Hereditary Hemocrymoptosis. Beyond PV and HH, we are actively evaluating additional indications for Rasprotide and plan to select one new therapeutic program for Rasprotide in 2021. The core idea is to capitalize on the excellent clinical attributes of this natural hormone memetic and expand its utility to multiple diseases influenced by excessive iron accumulation or erythrocytosis in patients. Finally, we are also working on an oral HH in memetic which may ultimately bring more convenience and preferable options to patients with certain conditions. Now, I would like to turn the conversation towards Infamatory Bowel Disease or IBD program. First, let us talk about our fully-owned asset PN943 in the IBD space. PN943 is a -in-class, orally delivered, gut-restricted antagonist of α4β7's integrin, a validated biological target for IBD. We believe that gut-restricted α4β7 integrin blockade is unique and potentially groundbreaking in treating IBD as it allows us to achieve receptor target engagement directly and locally in the GITC compartment. More importantly, let me remind you that we have already established clinical proof of concept through a -2-A study in patients with moderate to severe ulcerative colitis with our first-generation drug, PPG100. PN943 is our second-generation drug that is at least three-fold more potent across all in vitro, in vivo, preclinical, and clinical measures of potency and efficacy that we have assembled to date. We continue to advance our 150-patient -2-IDEL study evaluating the safety, tolerability, and efficacy of PN943 in ulcerative colitis. While we stopped providing guidance in 2021 for this study because of -19-related impact on enrollment, we are very pleased with the current enrollment rates and are forecasting the completion of this global study in 2022. Finally, I'll discuss the ongoing strategic collaboration with Janssen Pharmaceuticals. The partnership was initiated three and a half years ago with a $50 million upfront, and now an additional $30 million has been earned so far from achievement of various milestones. It's a very rewarding deal structure with more milestones in the future and up to double-digit royalties and U.S. co-detailing rights. It's also a very productive collaboration with now a portfolio of three distinct candidates in different stages of clinical development. The Janssen protagonist partnership aims to discover and develop oral R23-receptive antagonists with application in various diseases that could be approached with the blockade of the R23 pathway. While the pathway is a validated therapeutic mechanism, orally delivered therapies for blocking this pathway have not yet been made available. Excuse me. With our collaboration with Janssen, we are working to change the treatment paradigm through differentiated assets that could facilitate transition from injectable to oral targeted therapy. In the past few months, we added two new entities, PN235 and PN232 to the clinical development program with Janssen in addition to the first collaboration asset, PTG200. A phase one trial of PN235 and a phase one trial of PN232 are expected to be completed in the second half of 2021. Additionally, for PTG200, enrolled and continuous for patients in a phase two proof of concept study for Crohn's disease. All three candidates were discovered through our technology platform, which further demonstrates our versatility in finding therapies where there are no adequate treatment options. The multiple products should provide numerous strategic and clinical development options to Janssen and protagonist. So in summary, we are incredibly excited with simultaneous progress in three specific categories. One, the Respiratory program for polycythidia vera and hereditary macromotosis. Two, advancement of the gut-restricted oral integrin blocker PN943 in emphyretic colitis. And three, progression of three different oral R23 receptor antagonists in clinical development in partnership with Janssen to treat various inflammatory and autoimmune diseases. With that, I would now like to turn the call over to Overseer

4 Don Kalkatham. Don? Thank you Dinesh. Once again, thank you all for joining us this afternoon. Today, we issued our earnings release for year end 2020 and are filing our 10K where you can find further details on our most recent financials. On the call today, I'd like to review some of the key financial highlights for 2020. Starting with our revenue, we reported license and collaboration revenue for the full year of 2020 of $28.6 million as compared to $0.2 million for the full year of 2019. As you may recall, last year the company's 2019 revenue was offset by a one-time cumulative adjustment related to the application of revenue recognition principles following the amendment of the Janssen Biotech Agreement in May of 2019. This had reduced the 2019 revenue recognition by $9.4 million. The 2020 revenue increase over prior year was also related to recognition of revenue from providing preclinical and clinical development activities under the Collaboration Agreement with Janssen for both new assets PN235 and PN232 as well as an update to the forecast of the remaining services to be delivered under the collaboration. License and collaboration revenue for the fourth quarter of 2020 was $5.7 million compared to $2.7 million for the same period of 2019. Moving on to our expenses, our research and development expenses were $74.5 million for the full year of 2020, up from $65 million for the full year of 2019. And our fourth quarter R&D expenses were $19.5 million for the quarter into 2020, up from $15.9 million for the fourth quarter of 2019. The increases in R&D expenses in 2020 were primarily due to the advancing of our clinical trials with our pipeline assets Ruspratide and PN943 as well as all three of the IL-23 receptor antagonist assets under the Janssen Biotech collaboration. Our general administration expenses for the full year of 2020 were $18.6 million, up from $15.7 million for the full year of 2019. And our G&A expenses were $5 million for the fourth quarter of 2020 compared to $4.1 million for the fourth quarter of 2019. The increases in our G&A expenses were primarily related to higher professional fees, insurance costs, and employee compensation related expenses in support of the growth of our operations. In summary, we reported a net loss of $66.2 million or a net loss of $1.92 per share for the year into 2020 compared to $77.2 million net loss or a net loss of $2.98 per share for the year into 2019. And for the fourth quarter of 2020, we reported a net loss of $18.9 million or a net loss of $0.48 per share compared to a net loss of $17.5 million or a net loss of $0.63 per share for the fourth quarter of 2019. Moving over to our cash position, protagonists aimed at 2020 with $307.8 million in cash, cash equivalents, and marketable securities. Also of note, through our successful capital raise activity during the year, including our two public offerings and our ATM program, we raised $255 million in 2020 for the company. We forecast the company's cash, cash equivalents, and marketable securities along with access to our debt facility will fund our plan operating and capital expenditures through mid-2024, allowing us to complete the current ongoing trials as well as fund our key clinical, regulatory, and operational activities through mid-2024. This concludes my summary of the fourth quarter and full year of 2020 financial overview. Now I'd like to turn the meeting back to Dinesh. Thank you, Don.

We are very pleased with our progress to date and we look forward to continue our strong momentum as we move to 2021. We thank our shareholders for their support and the confidence in our work. We thank the investigators who advance our clinical studies and the patients who participate in these studies. Finally, I want to personally thank the protagonist team. Amid the challenges that 2020 imposed on the world at large, our employees not only fit the course, but instead excelled in several functions. Their unwavering focus and dedication is what has made the progress possible that we are describing today. Collectively, as a team, we look forward to even more exciting progress in the months and years ahead. With that, I would now like to open the call to questions. Operator?

Thank you. At this time, if you would like to ask a question, press star 1 on your telephone. If you would like to withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Your first question comes from the line of Yasmin Rahimi with Piper Sendler.

Hi, team. This is Rachel on for Yasmin. Thanks very much for taking your question. So our first question is, can you help us understand how the regulatory pathway could differ between development in low risk versus high risk PV patients who fail on current treatment options? In other words, can you help us understand what part of the phase 3 design is set in stone and which factors remain to be assessed? Thank you.

So that's a very important question and distinction, and I would have our CMO Sam

take the call. Yeah, I would just say that we can't obviously at this point articulate definitive guidance on the FDA design, but I can tell you that our phase 2 study is open to patients whether they're on cytoreductive or not, and the common theme is patients who require too many phlebotomies. So while patients are divided into high ML risk categories, patients are divided into those who are receiving cytoreductive agents like hydroxyurea and ephiron and those that aren't. The commonality between all the patients is that they're receiving frequent phlebotomy. I'll also ask Neil Gupta if he wants to say anything else about the clinical design.

I think we've covered all the important aspects. I think there's nothing more

to add. I think the short answer is from the phase 2 study, it seems the drug is very effective in both populations. So obviously we want to have as broad a utility as possible. Our theme is basically this is a drug for choice where the current therapy is ineffective.

Thank you. That's very helpful. As a follow-up, based on your discussions with the FDA, do you believe that the FDA and the EMA view the regulatory pathway in TB through the same lens? Thank you.

Well, the unknowns are the unknowns, and I think we sound like a broken record, but I think it's still the most meaningful statement. The dialogue is ongoing, and when we have clarity, we'll share it with everybody, the

people who are involved in the dialogue. So I think that's a very important point. I think the FDA and the EMA are very important, and I think we're going to have to have a very good conversation about this. I think the FDA and the EMA are very important, and I think we're going to have to have a very good conversation about this.

Great. That's very helpful. And as our last question, can you tell us what other indications beyond TB and AGH for which the therapy would make mechanistic sense for? Thank you.

Yeah, we've been thinking about two general areas, not to get specific here, but just the kind of self-evident, if you think about it, based on the results with PV. One is diseases that are treated with phlebotomy, and the other is diseases that are one of the hallmarks of the disease is erythrocytosis. So obviously in PV, those patients have erythrocytosis of a particular type, and they need phlebotomy. So we're trying to think about both of those as avenues for further development and other indications, and there are multiple diseases in each of those categories. Yeah, so the

triangulation of phlebotomy as a therapy, iron overload, and ecstasy, erythrocytosis.

Great. Thanks very much for taking our questions.

Sure thing. Our next question comes from the line of Chris Howerton with Jeffreys.

Great. Thanks so much for taking our questions, and obviously congratulations on all the progress across the board. So maybe as a first question, just as a follow-up to some of that questioning with respect to PV and the regulatory path, if we could focus on the primary endpoint here, what are kind of the key features that you need to come to alignment on with the FDA with respect to the primary endpoint? Is it the specific endpoint that you want to go after? Is it the duration on therapy and follow-up? And I guess what is your initial view in terms of what are the kind of categories that one needs to satisfy to get a registrational study completed? Yeah, so I'll make a

general statement and then send in China, that the current data that we have from the ongoing phase two study leads us to believe in itself, evidence that we have amazing hematocrit control and joint to the hip, that observation is a drastic reduction in the phlebotomy requirement, and that has been sort of the cornerstone in this disease indication. So we are good with whatever the final outcome would be,

but then... Yeah, I mean, this is a chronic disease, and so we believe that we'll need data over a reasonable period of time, and as Dinesh said, the hallmark is keeping the hematocrit below 45. That's what's in every guideline, that's what is in every medical textbook, and so 24-7 keeping it before, keeping it under 45 over a significant period of time will be an important aspect of the primary endpoint. How it's defined, how it's analyzed, what else could be in there, we're not ready to say that, but again, from historical precedent and just from what we know about the disease, it's clear to us that the backbone of the primary endpoint will involve keeping the hematocrit below 45.

Okay, all right, that's very clear, thank you. And maybe as a second question, if we can maybe shift our focus to PN943 or the IBD, I think obviously there's been recent recognition and focus of early stage receptor occupancy data, and I think one of the questions that I've received numerous times from investors is, how does this local or gut-restricted activity and kind of how does that work? It seems like there's some confusion out there, so it might be helpful if you could compare and contrast local delivery in a gut-restricted manner versus systemic and kind of what you see in terms of the relevance of receptor occupancy data. Thank you. Thanks,

Chris, that's a very important question. It is also one of the most common questions that we are receiving in recent days, and I'll give some general answer to it, and then our CSO David Liu will chime in with some more details. The way we look at -beta-7 integrin is obviously it's a validated target, it's one of the most safe and IBD-specific targets as established by MTBO from Takeda. Now, there are two types of approaches over here. One is where the action is through systemic exposure, and over there we have the injectable antibody drugs and orally bioavailable small molecule drugs. The other approach which Protagonist has undertaken, and in fact Protagonist is the only company in the approach. So now the main action is not in the blood compartment, but rather tackling the target in the GI tissue compartment. So while we are the only presence over here, then the question is, is that a risky proposition? The answer, in our opinion, is no, because as you know, with our previous first-generation drug, the PTG-100, we already established clinical proof of concept in a phase 2a study in ulcerative, in moderate to severe disease ulcerative colitis patients, where we got clinical remission rates of 16%, similar to MTBO in a phase 2a study, and from the biopsy samples, colonic biopsy samples of these patients, we got 44% histologic remission. So yes, ours is a unique approach, but we already have the clinical proof of concept from the first-generation drug, and now we are moving forward with the second-generation drug 943, which is at least threefold more potent by all in vitro, in vivo, preclinical, and even phase 1 blood receptor occupancy measurements that we have conducted so far between these two drugs. The blood receptor occupancy component, this is where David, you may want to chime in and take over the conversation.

Yes, thank you Dinesh. So I think everything that Dinesh mentioned that has been observed for the benefit of our approach in the clinic was presaged by all of the work that we did preclinically. So looking at trafficking, looking at pharmacodynamic responses that were associated with the trafficking, with disease outcomes, as well as histological outcomes in preclinical models of colitis, and that was all basically predictive of what we eventually observed in the clinic. With regard to the pharmacodynamic responses, as shown predominantly by receptor occupancy in the blood, we believe that the surrogate of essentially what was initially high target engagement locally on the immune cells is residing in the gut. And as those cells are trafficking back out, they can't reenter because of the very tightly bound 943 to the surface of that cells on the integrin. In addition, we think the high local target engagement engenders a very nice effect on cells that are trying to proliferate and be activated from -beta-7 engagement as a co-stimulatory factor. And we've shown that from in vitro studies that we can certainly block that mechanism. So high local target engagement blocking both trafficking and local activation of the T cells.

And what I would add, Chris, is that for our gut-restricted approach, we have established based on our clinical POC data, the efficacious dose in the ulcerative colitis study, that translated to 74% blood receptor occupancy in phase 1 study in healthy humans. So that is our guideline for the gut-restricted integrin blocker approach. And in a phase 1 study of 943, we know that we can surpass that 74% number easily. So we can achieve a 3 times lower dose versus the previous drug. Now for the systemic drugs, you know, 100% RO, blood RO is a goalpost that we know, and we don't have to get into the details, but the minimum dose at which one can achieve 100% RO is significantly lower than the actual efficacious dose that has been used for the systemic drugs.

Right. Okay. Well, thank you very much for that color, and I appreciate the perspective.

And thanks. Your next question comes from the line of Joseph Schwartz with SVB Learing.

Hi. This is Kelly Gershkis on for Joe. Maybe one about indications outside of IBD for your oral IL-23 antagonists. How are you approaching or maybe thinking about the bioavailability differences that might be needed for more systemic indications versus those that are more gut-restricted? And are there any attributes of your new agents, PN235 or 232, that you designed in or selected for that might lend themselves to a more gut-restricted or more systemic profile? Thanks.

That's an excellent question, Kelly. Really appreciate it. And as you know, we are a peptide technology platform company, and we like to be the pioneers in the advancement of the field of peptidic science. So initially we went on the journey of discovering peptides that were as potent as antibodies. The next step was that making peptides that are orally stable and gut-restricted, and maybe the ultimate holy grail in the field of peptides would be where we could make peptides orally bioavailable. So for the IL-23 program in general, our future undertakings, we would not be shying away from targets or approaches that actually require some sort of systemic oral bioavailability. But that's how I would frame it.

Great. Excellent. And thanks for taking our questions.

Our next question comes from the line of Anupam Rama with JPMorgan.

Hey, guys. Thanks so much for taking the question. Just two quick ones for me. First is more of a clarification question on PTG300 Phase 2. At the conference and then in your press release today, you talked about updates at medical conferences in 2021. So is this an ETA and ASH strategy or an sort of ASH-only type of strategy post-enrollment completion mid-year? That's our first question. And second one is one of the questions we've been getting a little bit on PTG300 is in PB, based on the profile that's emerging post-ASH, where does this drug fit in the treatment paradigm based on your market research? Thanks so much.

Sure. Libby, I'm sure Sam will want to elaborate, but very quickly, No, we aren't going to just wait until the end of the year to present things at the ASH conference. There are significant conferences in mid-year and throughout the year. So it is our full intention to present updates at medical conferences throughout

the year. Yeah, remember the first part of the study is an open-label Phase 2 study. So since it's open-label, we have no problem with reporting on it and being transparent over time. The second part, which is randomized and blinded, that would require the last person completing the study before we could update that part of the study. With respect to where we see this being used, as we kind of said earlier, we're not trying to replace any particular therapy. We think that people who have too many phlebotomies have demonstrated two things. One is too much time spent above an adequate of 45, and we think that's a guideline for a reason medically in terms of preventing events. So we think that's not a good thing to be spending time above 45. And of course, the people who have many phlebotomies are the ones who have the highest degree of iron deficiency, because obviously the more phlebotomies you're doing, the more iron you're taking out of the body on a regular basis. And those are the patients where we would expect to see, if we see a symptom improvement, obviously that's where we'd expect to see it the most, is in the people who have the highest degree of iron deficiency. So again, it's not a strategy of saying don't use any particular other therapy. If you and your doctor decide any other therapy is useful and important for you, that's great. But what we see in the marketplace is with the existing therapeutics that are available, that there are many patients who are on other drugs and have too many phlebotomies, or on phlebotomy alone and have too many phlebotomies, and those are our patients.

Yeah, so apart from the way I would phrase it is that essentially this is a drug, this could be a drug of choice when the current therapy is ineffective. And our symphony data survey basically shows that majority of patients will fall in this category. And if you look at our current phase two study, the data we presented at Ash on 18 patients, it's like eight patients are on phlebotomy alone, then seven patients are on hydroxyuria, we also have three patients that are on interferon. And remember the qualification for getting into our study is in spite of those treatments, they require frequent phlebotomies, at least three or more phlebotomies in a six month period. So that translates to more than six phlebotomies annually. And it demonstrates two things. It's that the current treatments are ineffective, and too many phlebotomies are not a good thing for the patients ultimately. And that is where we would like to see the performance of

our drug. Yeah, we presented our symphony data at Ash. It's in a poster in Ash that was presented by one of the key opinion leaders. And the punch line is whether you use celloreductives or use phlebotomy alone, many patients are not receiving treatment according to the treatment guidelines.

Understood. Thanks so much for taking our questions.

Absolutely. Your next question comes from the line of Douglas So with HC Wainwright. And you're alive?

Hello? Hey, Doug. Thanks. I'm sorry, I was having a little trouble with my line. So just in terms of the new IL-23s that are nominated by Janssen for development, just curious at what point should we start to get a sense of what indications that you're thinking about? And obviously, you know, I would presume the horizons might be a little broader than just in IBD. Just given how, you know, as you alluded to earlier, right, it might not just be sort of got restricted. You know, obviously, STAWARA has pretty wide use.

Yeah, Doug, it's an excellent

question.

And as you can imagine, you know, over here, this is a partnership with Janssen. So we have to be mindful of the statements we make. But I would just like to phrase it this way. Our collaboration with Janssen is not on IBD. Our collaboration with Janssen is on IL-23 receptor antagonists. So wherever the IL-23 pathway, intervention of the IL-23 pathway leads to a medical utility in a particular disease indication, that is where we are theoretically going with the multiple optionalities. And so the idea is like, hey, let's add a few promising candidates in the development bucket. We have at least three as of now. And then the various strategic and clinical options will become more clear down the road as we get more data from the current Phase I and Phase II studies that we are conducting with these candidates.

Dinesh, you just sort of went right into it. I guess it sounds like what we learn from the Phase I in terms of bioavailability, PK profile, et cetera, will really sort of help determine which of those indications, especially outside of IBD, which the candidates might be best suited for.

Yes,

it would be

hard to disagree with your logic.

Okay. Okay, thank you so much.

Thanks, Ted. And with that, this concludes our Q&A section. And I would like to hand it over to Dinesh Patel for closing remarks.

Thank you again, everybody, for joining us this afternoon. And this formally concludes our fourth quarter 2020 and full year 2020 conference call on Webcast. Thank you.

This concludes today's conference call, and you may now disconnect.