Good morning, and welcome to Evelo's conference call to discuss the interim clinical data from its Phase Ib trial of EDP1815. [Operator Instructions]. Please be advised that this call is being recorded at the company's request. At this time, I'd like to turn the call over to Jessica Cotrone of Evelo. Please proceed..

Thank you, Operator. This morning, we issued a press release that outlines the topics we plan to discuss today. This release is available at www.evelobio.com under the Investors tab.

Today on our call, Simba Gill, Chief Executive Officer; Duncan McHale, Chief Medical Officer; and Mark Bodmer, President of R&D and Chief Scientific Officer, will review the positive interim clinical data for EDP1815 and discuss its significance for our strategy and future development plans.

Before we begin, I would like to remind everyone that statements made during this conference call that do not relate to matters of historical facts, including statements about our objectives and anticipated clinical milestones for 2019 and 2020, the impact of any of our monoclonal microbials and the timing and results of any clinical studies should be considered forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements are intended to be subject to the safe harbor protection provided by the reform act. Actual results could differ materially from those indicated by the forward-looking statements due to the impact of many factors.

Participants are directed to the risk factors set forth in Evelo's quarterly report on Form 10-Q for the quarter ended June 30, 2019, and the company's other filings with the Securities and Exchange Commission. Any forward-looking statements made today speak only to Evelo's operations as of today.

Evelo disclaims any duty to provide updates to its forward-looking statements even if subsequent events cause the company's view to change. It is now my pleasure to pass the call over to Simba..

Thank you, Jessica. Good morning, everyone, and thank you for joining us. Today is another exciting and important day for Evelo. For the second time, we are reporting positive interim clinical data. Our preclinical and clinical data support the validation of our platform.

Our clinical data provides evidence regarding our ability to harness the power of the small intestinal axis to treat systemic inflammatory disease. We believe we are the first company to have demonstrated this. The implications are enormous. We are developing medicines with the potential to be effective, safe, convenient and affordable.

We believe our platform opens up the potential for broad global treatment of patients with all stages of disease, helping millions of people. Slide 3 summarizes the key highlights from today's announcement of interim clinical data in EDP1815 in mild to moderate psoriasis in the high dose cohort. A few things to note.

Firstly, EDP1815 continues to be well tolerated. We continue to see safety and tolerability as an important area of competitive advantage for the treatment of inflammatory disease. The mean reduction in lesion severity score after 28 days of dosing in the high dose cohort is consistent with data we reported in August with the low dose cohort.

At day 42, two weeks post the completion of dosing, individuals treated with the high dose showed continued reductions from baseline in both LSS and in PASI, which may be indicative of a sustained clinical effect and dose response.

These clinical efficacy results, taken together with EDP1815 safety results, potentially represent an unparalleled oral therapy for mild to moderate psoriasis patients. We look forward to advancing EDP1815 into Phase II early next year. Before turning the call over to Duncan to review the data, I'd like to outline the opportunity ahead of us at Evelo.

Slide 4 shows that chronic inflammation is the central driver of some of the most burdensome diseases. As you know, many important and common chronic diseases, including the arthritities, neurodegenerative diseases, ATPs and metabolic syndrome conditions are linked to chronic inflammation.

Worldwide, 1 in 7 people suffer from a chronic inflammatory disease, and it is estimated that 1 in 3 die due to chronic inflammatory disease-related conditions. Targeting the small intestinal axis with Evelo's platform, we believe we have the potential to treat millions of people.

We chose psoriasis as one of our first inflammatory disease targets as it allows for rapid and informative clinical trial readouts, which have broad relevance in inflammation as well as allowing for potential rapid approval in psoriasis patients with mild to moderate disease for whom there is significant unmet need.

Moving on to the unmet need in psoriasis. On Slide 5, you can see that a significant number of mild to moderate patients are not treated today. Primary reasons physicians do not initiate or maintain treatment are concerns about long-term safety or tolerability and also, to some degree, the efficacy of currently available therapies.

Slide 6 shows the results of a study conducted over nearly 10 years by the National Psoriasis Foundation, surveying approximately 5,000 patients with psoriasis. Of these, about 40% of patients with mild disease and over 50% of patients with moderate disease reported being dissatisfied with their treatment options.

There is clearly a need in several million patients for an effective, safe and affordable oral therapy. Evelo's platform allows us to develop medicines with this unparalleled profile. Let me now turn the call over to Duncan, who will review the new data for EDP1815..

Thank you, Simba, and good morning, everyone. I'm pleased to be able to share with you today positive interim clinical data observed at the high dose of EDP1815. I'd like to begin by reminding everyone on the design of the trial, which is presented on Slide 7. The high dose cohort enrolled 18 individuals with mild to moderate psoriasis.

They were randomized in a 2:1 ratio to receive 2.76 grams of EDP1815 orally or placebo once a day for 28 days. Subjects were followed for 42 days in total due to the 2-week follow-up post completion of dosing. The primary endpoint of the trial is safety and tolerability.

And as Simba mentioned, EDP1815 continues to be well tolerated in this cohort with no overall difference reported from placebo. The study is also investigating a number of secondary and exploratory endpoints to evaluate potential pharmacodynamic responses. Slide 8 describes the endpoints that we're reporting today.

We're focusing today on the clinical scores, including both the lesion severity score and the PASI scores from both the low and high dose cohorts. The data from these endpoints provide insight into the pharmacodynamic effects and potential clinical benefit of EDP1815. So moving to Slide 9.

I'd like to remind you about the lesion severity score and how it relates to PASI. We have initially focused on the lesion severity score, which is a sensitive clinical measure of disease change in psoriasis.

The lesion severity score is generally considered a more sensitive measure for patients with mild to moderate disease for which individual lesions may be quite severe but the overall affected body surface area is small. It is also more sensitive when the dosing period is short as it can detect smaller changes from baseline.

The lesion severity score is a fundamental component of the PASI scoring system and measures the underlying changes in lesion severity from a single psoriatic lesion across the dosing period. The lesion severity score measures redness, thickness and scaling on a 12-point scale for the same individual lesion.

The PASI scoring system measures the same underlying changes in the psoriasis skin lesions as the lesion severity score but captures those changes across all skin lesions and weights the score by body surface area affected for each region of the body.

Now the lesion severity score and PASI scores are strongly correlated and would be anticipated to move in tandem, as is evidenced by the data we will present today. So moving to Slide 10, we can see the lesion severity score data from the high dose cohort.

The graph plots the change in lesion severity score observed over the 28-day dosing period and the subsequent 2-week follow-up at day 42. As specified in the analysis plan, we have pulled the placebo arms from both the low and high dose cohort.

This allows a correction for the asymmetric 2:1 randomization and improves the robustness of the placebo data. We saw a main lesion severity score reduction from baseline of 15% in the individuals taking the high dose of EDP1815 at day 28.

We were further encouraged to see that two weeks post completion of dosing at day 42, the main lesional score reduction continued down to 24%, suggesting a sustained clinical effect. Slide 11 shows that the observed lesion severity score changes were consistent between the high and low dose cohorts over the 28-day dosing period.

Day 42, however, you can see the low dose cohort returns almost to baseline, while the reduction continues in the high dose cohort, which suggests a possible dose response. Now Slide 12 shows the individual changes from baseline in the lesion severity score at day 42 for each of the individuals in the cohort.

On the bottom, we have a numeric score, and this is the baseline lesion severity score for the lesion that was trapped. Now there are a few things to note about this score. There's no baseline difference between the individuals who are dosed with placebo or those dosed with EDP1815.

And although the individuals were classified as having mild disease in terms of their body surface area, the actual lesions that were tracked had quite active disease. And in most of these individuals, the scores are between 8 and 10 out of 12. And 9 out of the 12 individuals receiving EDP1815 showed a reduction in their lesion severity score.

And in 7 of these 9, the reduction was 25% or greater. The maximum observed reduction in the EDP1815 dose group was 80%. We believe the magnitude of this effect at 42 days is remarkable given both the short duration period and the fact that these measurements were taken two weeks after individual's discontinued therapy.

Slides 13 and 14 show the analysis of the PASI data over the same dosing period. Slide 13 shows the population PASI results. The mean reduction in PASI score in the high dose is 16% at 28 days, and the reduction continues to improve over the next two weeks despite stopping dosing, and the reduction at day 42 was 21%.

The observed effects on the PASI score were very consistent with the trends observed in lesion severity score. Again, it is very encouraging that we get this level of response after 4 weeks of treatment. Slide 14 shows the individual changes from baseline in PASI at day 42 for each of the individuals in the high dose cohort.

On the bottom, we have the baseline PASI score, which ranges from as low as 1.2 to 18, reflecting the mild level of disease as measured by PASI that was present in these individuals. PASI reductions of up to 61% were observed in the EDP1815-treated individuals. So on Slide 15, I'd like to summarize the data that we've presented today.

This interim data strongly supports the potential of EDP1815 as a new therapy for patients with mild to moderate psoriasis. EDP1815 continues to be very well tolerated.

At two weeks post dosing, the mean reduction in lesion severity score was 24%, and the mean reduction in PASI score was 21% with maximal observed reductions of 80% and 61%, respectively. EDP1815 is showing the results we had hoped for as we look to develop an effective, safe, convenient and affordable medicine for psoriasis.

The data from the high and low dose cohorts provide a clear rationale for us to advance into Phase II. Slide 16 shows our current plan for Phase 2. This study will be a placebo-controlled trial in individuals with mild to moderate psoriasis and will evaluate clinical benefit, dose and formulation.

Primary endpoint will be a change in PASI score at week 16, which is a slight change from our previous guidance following key opinion leader feedback. In addition to psoriasis, we remain focused on evaluating EDP1815 in clinical trials in other inflammatory diseases as part of our core portfolio strategy.

We anticipate initiating these trials following the interim data from the Phase II study. Preclinical data supports the investigation of EDP1815 in diseases such as psoriatic arthritis, axial spondyloarthritis arthritis, rheumatoid arthritis, atopic dermatitis and asthma.

Taken together, there are millions of patients that could potentially benefit from monoclonal microbials. Let me now turn the call over to Mark to discuss how we consider these data in the context of our broader platform..

Thanks, Duncan. The small intestinal axis fundamentally changes our understanding of how our bodies are regulated. We evolved from small intestine over hundreds of millions of years, and this evolutionary process has laid down physiological pathways from the intestines to the immune, nervous and metabolic systems of the whole body.

Our physiology is controlled by what happens in our small intestine in ways that we have not previously imagined. It turns out that we can create monoclonal microbials whose action on cells within the small intestine has effects throughout the body with a drug not needing to distribute around the body.

These two insights, the small intestinal axis and its drug-ability are the foundation for Evelo's platform. We are harnessing central biology that has not been targeted by drugs before. It's a rare conjunction of profound new biology and drug development with the potential to have even greater impact than antibodies and cytokines.

We've shown over the last 3 years of preclinical studies the remarkable pharmacology of oral therapies that act in the small intestine with systemic effects without systemic exposure to the drug.

Today's interim clinical results demonstrate the effect of the small intestinal axis on inflammation in humans and our ability to make medicines which harness this effect. Our continuing research shows that we may be able to extend this new principle beyond inflammation to neurology and metabolism.

We have a candidate product for neuroinflammation, which clears inflammatory cells from the central nervous system in preclinical models through its action in the small intestine. We have also begun to screen microbials for metabolic diseases, and we've demonstrated effects on systemic metabolic parameters and weight in preclinical metabolism models.

In all of these models, we see a consistent ability of agents acting only in the small intestine have effects at least comparable to standard of care. We now have the first clinical evidence that this is true for inflammation, which also underpins the potential translation of our preclinical evidence for neuroinflammation and metabolism.

As well as expanding the disease scope, we continue to discover improved ways to engage the small intestinal axis with our potential drugs.

We are learning how to deliver the drugs in the right part of the small intestine for optimal therapeutic effects, and we have preclinical candidate drugs comprising sub-factions of microbes with potencies 2 to 3 orders of magnitude greater than whole microbes by weight of drug. There's one final point I'd like to emphasize.

Our drug candidates are modulators of cells in the small intestine. The key to their effects is the network connecting the small intestine to the rest of the body. Our medicines have no impact on the microbiome, either in animals or in humans. They are not intended to, and they cannot. They are effective when nonviable.

Our approach is much more than a hypothesis. It's evolutionarily, anatomically and pharmacologically demonstrable, and it has enormous therapeutic potential scope, which we've only just begun to discover. Simba, back to you..

Thank you, Mark. Mark has highlighted the exceptional work of our scientists here at Evelo to create a platform that has breadth of applicability across inflammatory, neuroinflammatory, metabolic diseases, cancers and beyond.

We are developing medicines with a potentially unparalleled integrated profile of efficacy, safety, convenience and affordability. Slide 19 shows the unmet need among patients with mild to moderate inflammatory conditions, including psoriasis.

With EDP1815, we aim to create a new market as a midline therapy and defer the use of injectable biologics and other specialty drugs, which can be burdensome to administer and/or may not fit the risk-benefit profile for individuals living with more moderate forms of disease.

Over time, we expect to expand into frontline treatment, early intervention and to offer EDP1815 as a foundational therapy for millions of people around the world. To that end, we are preparing for our Phase II trial and plan to initiate the study in early 2020 with 16-week interim data expected in late 2020.

In parallel, we continue to advance our broader pipeline. Again, I want to emphasize the breadth of applicability of our platform and the breadth of the pipeline we are developing, several potential product candidates, product forms and formulations for the treatment of a broad range of inflammatory diseases and cancers.

As we reported in our earnings release this morning and as you can see on Slide 20, we expect a catalyst-rich 2020 with expected data from each of our clinical stage programs, including data with our new formulations of EDP1815 and EDP1066 in atopic dermatitis in the second quarter and first quarter, respectively.

We have reported a progress update on EDP1503 in microsatellite stable colorectal carcinoma this morning and continue to expect to report further data from this study in the first half of 2020. I'd like to conclude with Slide 21.

We are excited by the interim clinical data for EDP1815 announced today which, consistent with data from a low dose cohort, represent striking effects on both lesional severity score and PASI. We also observed a potential dose response and sustained effect at the high dose.

These interim results support the validation of our platform and the potential of our approach to deliver an unparalleled profile of effective, safe, convenient and affordable medicines that can benefit millions of people. In closing, I'd like to thank our remarkable team at Evelo for their passion and dedication to our science and our vision.

I'd also like to thank the patients and physicians who are participating in our studies. Your trust and support in Evelo are critical for allowing us to advance our vision. We'd now like to open the call to take any questions you may have..

[Operator Instructions]. Our first question comes from Connor Meehan with Morgan Stanley..

This is Vikram on for Matthew's team. So two quick questions from our side.

First, how does the data that you reported today frame your expectations for the next-generation formulation data from which is expected starting next year? And then secondly, would you ever consider an active comparator study EDP1815 versus therapies that are early on the market?.

Thanks, Vikram. Let me take the first question, and then I'll let Duncan take the second. So in terms of new formulations, just to remind everybody, we reported a short while ago that in preclinical data, we have a novel formulation that shows up to 30-fold improvement in activity.

What we are now planning on doing is going forward in Phase II studies with 1815, comparing efficacy of 1815 with the novel formulation with the efficacy that Duncan summarized earlier with our existing formulation. So that will be the first part of our Phase II study.

Obviously, given the positive data that we've seen with the existing formulation and the fact that in preclinical data, again, we had a 30-fold improvement in activity, we're optimistic about what we will see in the Phase II as we compare the different formulations.

So on the second question, Duncan, would you like to answer that?.

Yes. The question about the active comparator, as is usually the case in early development, we're focusing very much on demonstrating the clear clinical benefit of EDP1815. As we move through development, we will bring in active comparators at the appropriate time point..

Our next question comes from Chris Shibutani with Cowen..

Great. We appreciate this update. Can you just remind us what kind of expectation we should have? You described the new formulation as having a 30-fold improvement in activity, and it seems certainly from the data that you've updated us with that we're seeing some evidence, as you described, of dose response and sustained effect.

So when we think about anticipating what the data may look like for the new formulation, can you maybe quantify to some extent, if in ranges at all possible, where do you think that incremental benefit may be? What is your hypothesis? Should we see greater depth of responses? Should we see quicker onset? And then as a follow-up to that question on the timing.

It's -- your time points at which you're measuring your endpoints for the various studies has been moving around.

Can you help us understand the rationale for the most recent update, in particular, why you're choosing to measure PASI? Where you are now? Which contrasts from your August analyst meeting?.

Thanks, Chris. I'll let Mark answer the first question and then Duncan the second..

So Chris, it's Mark. So two parts to the preclinical formulation story. One is that the reformulation gives us greater depth of efficacy at lower doses. So as Simba said, with the underpin of the effect that we're seeing in the current formulation, one thing this will do is to move us down the dose response curve.

And the other thing it has the potential to do is to improve the depth and duration of responses. Just to be specific about our understanding of the biology of this, what we find now very clearly in preclinical models is the higher up the small intestine, particularly in the duodenum, we can release a bolus of the drug, the more potent the effect is.

This has been our hypothesis for some time about how this would work, and it's very clear that that's the case.

So the fact that the current formulation is effective with its release profile compared to the new formulation, which will give us the release high up in the duodenum, if we continue to get translation from animal models preclinically to the clinic as we've seen it before, sets an expectation or an aspiration that we will see these effects on dose response and depth of efficacy as we take the new formulation into clinical trials..

Thanks, Mark. Yes. Just before handing over to you, Duncan, just to be clear, Chris, on your question, I just wanted to emphasize that the current formulation as we just described is driving very positive clinical data. So we're very pleased with that formulation.

And the new formulation basically represent something, but it's unexpectedly positive, but we're feeling very good about the current formulation. So I just want to be clear.

Duncan?.

With regard to endpoints, we haven't changed the primary endpoint at all for the Phase II study. This is always going to be PASI. The reason to do the lesional severity score in the 1b study, as we said previously, is just the sensitivity given the short dosing period..

Right. No. I realize that the endpoints have not changed. I meant the time point at which we measure them, I think, has been modified, and you described it as being based upon KOL feedback.

But could you help us understand what's driving that decision?.

Sure. So yes, the original 12-week interim endpoint based on key opinion leader feedback and precedents with other anti-inflammatory agents. The 16-week time point is probably a better time point to fully understand the clinical benefit of EDP1815.

And by taking individuals out to 16 weeks before the interim, there's little additional benefit of going out to 24 weeks. So we'll use 16 weeks as our primary endpoint. This is -- key opinion leader opinions were in line with ours there. And in addition, going out to 24 weeks with placebo was felt to be a challenge from a recruitment perspective.

So primarily, it's because 16 weeks is a much clearer time point to understand the full clinical benefit of EDP1815 rather than 1two weeks..

And is that 16 weeks at all vetted against any discussions with regulators?.

16 weeks is a well-accepted endpoint. We're obviously in the process of discussing with regulators right now, but that's not been an issue at all because it's well accepted with precedented molecules..

Our next question comes from Na Sun with BMO Capital..

Congratulations on the data. Just two questions from me. Learning from the psoriasis data update, how does that inform you for atopic dermatitis? Are we also going to be getting -- should we also anticipate reporting of a component of EASI or atopic dermatitis? There's also a lesion severity score included within EASI.

And then the second one is we have seen a signal for a longer duration of benefit post dosing at a higher dose.

Does this open up the possibility of extending the final treatment protocol from daily oral to maybe, say, like once weekly?.

Thanks. So a number of questions. Let me frame your first question, and I'm going to let Mark expand on that, and then I'll let Duncan answer the 2 clinical-related questions.

So in terms of how does this data with 1815 in psoriasis inform on what we're doing in atopic dermatitis, the highest level point which I'd like Mark to expand on is that what we've now shown in 2 independent clinical studies is positive data not just for psoriasis but actually for the central notion of the small intestinal axis and our ability to create a new class of medicines that act on the small intestinal axis.

So the first thing is that, a few years ago when we started the company, was an idea. Most people did not accept the hypothesis. There was lots of confusion with what I would call classical microbiome eco bioptic approaches, which is not what we are.

But what we've now done is very importantly shown that the principal work is not just preclinically but clinically, in 2 independent studies. So the most important part of the validation is around that central thrust of the small intestinal axis, which has application and relevance across all inflammatory diseases.

So we've shown, again I'm emphasizing this because it is a core point, that we can deliver single strains of microbes in relevant formulations to drive systemic therapeutic effects. That is the highest level and most important point.

In terms of the relevant biology, linking psoriasis to atopic dermatitis and additional points, I'll hand over that set of questions to Mark. And then Duncan can answer your clinical points..

So given the reach from the small intestine to other parts of the body, the skin here, there are a couple of points on the biology that we understand preclinically about this that we expect to translate.

The first is just simply, we've looked at relevant models of both Th17 biology in support of psoriasis studies and Th2 biology in support of atopic dermatitis and a range of other atopic march diseases, and we get effects on -- in both types of models, which is indicating that we're getting a broad inflammation resolution across multiple pathways.

Another comment to make is that although psoriasis and atopic dermatitis are described as distinct, one being Th17, the other being Th2, in reality, these dermatological conditions exist on a spectrum.

And actually, we think it's one of the strengths of this approach that we're not pathway limited, that we're getting coordinated resolution in multiple inflammatory pathways. So there are 2 parts in the answer to your question. One is we have direct preclinical evidence.

But secondly, we expect both for the reasons that Simba said and also for the reasons of the spread biological boundaries between these diseases that the psoriasis data have some predictive value for the atopic dermatitis clinical studies to be determined by the outcomes of the studies that we're doing at the moment..

Thanks, Mark. So Duncan, two questions on clinical. What are we going to measure in atopic dermatitis, relevance of lesional scores and EASI measures, and then would we move to once-a-week dosing were the two questions..

Yes. With regard to the clinical endpoints, we will -- we're measuring EASI score, at an IGA. They're well precedented. The kinetics of response to atopic dermatitis is quicker than psoriasis. So we expect to see responses within these clinical scores across the 28-day period. So those are going to be the key endpoints for us.

With regards to the dosing period, I think what is probably more important rather than thinking about an unusual dosing period is once a week. The intent here is that EDP1815 or another monoclonal microbial that works in atopic dermatitis or psoriasis will be dosed daily. However, what it looked like we've got is a forgiving therapy.

So that means that individuals can forget the odd dose, and that will not aggregate the clinical response. So from a patient perspective, that's a really important aspect. It makes it very patient friendly. So rather than thinking about once a day, this -- once a week, this will be a daily therapy, but it will be a forgiving therapy.

So for those of us who forget the odd dose, it will not get rid of the clinical effect..

[Operator Instructions]. Our next question comes from Chris Howerton with Jefferies..

Great. Again, congratulations on the data. I think a lot of them have been asked at this point.

But maybe on the psoriasis data, did you notice any body region effects, like was there certain areas that seemed to be affected more or less than others? And in addition to that, maybe you could help us understand how the focal lesion for the LSS score was initially determined? And then I also have one other question..

So actually straightforward. So as a nonclinical CEO, I will answer just because they're straightforward questions. So we did not see any particular body area specificity or anything along those lines. We're not reporting on any more detail right now -- but the answer, no.

And then the primary lesion was chosen by the principal investigator at the time of enrollment in the study. And in general, they picked the most severe lesion as a general principle..

Okay. Okay. Great. And then I think, obviously, you had a lot of discussion with respect to the new formulation and thinking about that.

And I guess my two questions with respect to that would be how are you thinking about translation of dosing from the current formulation to the new formulation, particularly, I think, in Cohort A of your planned psoriasis Phase IIa trial? And then the follow-up to that would be, is there any significant difference in terms of cost of goods you would expect between the two formulations or differences in processes that would make one or the other more or less amenable to CMC under GMP conditions?.

Yes. Let me take it in reverse. I'll take the first, and then I'll let Duncan answer the question in terms of dosing translatability.

So again, just going up a level on your question, Chris, related to cost of goods, appreciate it actually because one very important point we've always emphasized is that our goal is to develop effective, safe, oral, convenient and affordable medicines.

We're able to make that last claim somewhat unusually for a biotech company for a number of reasons. One is linked to cost of goods. So we're already at a stage where we can extrapolate to likely cost of goods at scale within the range of small molecules.

Very unusual for a biotech platform that is this potentially transformative if we compare ourselves, for example, to cell therapies, cell and gene therapies at the other end of the spectrum. So our cost of goods, whatever the formulation is, will be very low.

The new formulation certainly offers the potential because we have something, as I said, that's 30-fold more potent in preclinical studies to drive equivalent effect with up to 30-fold less active ingredient, which would have knock-on consequences of cost of goods and drive it even lower.

But we're not overly concerned about our cost of goods at this stage. It may help us in terms of formulations and so on in terms of driving patient compliance with less and less tablets, for example. But we're not worried about cost of goods.

It would be an advantage, having said that, Duncan, do you want to address dosing translatability?.

In terms of the dosing translatability for the Phase II study, we used the same total cell count for each formulation. So the total cell count is the same, and we use the 2 different formulations, and we'll use the proposed that many used -- the high dose, dose that we've used in EDP1815-101..

Okay. Okay. Great. And maybe if you don't mind, Simba, maybe I just misheard, but I felt like you said that you provided an update on 1503 today. Did I hear you wrong? I just wanted to double-check that..

There is an update in the press release. So just a quick summary of that. Essentially, what we've reported today is that we have completed enrollment of the cohort of patients with microsatellite stable colorectal carcinoma. A reminder that those are late-stage patients who have failed all previous therapies.

And a reminder that late-stage metastatic renal cell carcinoma is -- I'm sorry, colorectal is otherwise not immunologically responsive, and there are no effective treatments unfortunately today. We have not seen any clinical responses that are evident. We did see several patients in the cohort who have experienced extended stable disease.

And we've also observed cellular infiltration biomarkers, which we've taken from biopsies in the relevant patients after monotherapy with EDP1503, which are consistent with the preclinical observations we saw with EDP1503. A reminder that it's a combination study.

There's a monotherapy running window of two weeks from time of diagnosis, and then the patients go on for full combination study. So when we look in that monotherapy window, we biopsy a time of diagnosis, biopsy again after the monotherapy run in, and we can look at relevant data there.

So we continue to monitor patients in this cohort, and you can expect further updates as we go forward.

The other update we made was that given newly approved treatments for triple-negative breast cancer, what you'd be familiar with, we're anticipating that the majority of triple-negative breast cancer patients that we recruit, as we go forward, will have relapsed following prior PD-1, PD-L1 therapy.

So similar type of dynamic to the PD-1 relapsed cohort that we're already recruiting as well. So those were the updates. We remain on track for further release of data in the first half of 2020, Chris..

[Operator Instructions]. I'm showing no further questions in queue at this time. Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect..

Thank you very much, everyone..

Thank you..