Q2 2021 Synlogic Inc Earnings Call
[music].
Good morning, and welcome to city Logics second quarter 2021 conference call. At this time all participants are in a listen only mode later there'll be a question and.
Answer session at the end of this call.
Please be advised that this call is being recorded I would now like to turn the call over to Daniel Roseanne head of Finance and Investor Relations. Please proceed.
Thank you operator.
Good morning, and thanks for joining us on today's conference call. This morning, we issued a press release, which outlines our second quarter 2021 financial results and additional business updates. The release is available on the investors section of our web site Hudson logic, TX Dot com.
Joining me on this call our Doctor Ether, Brennan, President and Chief Executive Officer, and Dr. David Harbour, Chief Scientific Officer. Other members of the management team will also be available during the Q&A.
This morning, Eva will provide a review of second quarter highlights and recent progress Dave will share the latest advancements in applying our synthetic biotic platform casino Ketonuria and Eva will then return to provide an update on our metabolic portfolio, including enteric Hyperoxaluria.
Finally, I will summarize our financial results for the quarter.
Following our prepared remarks, we will open the call for your questions.
As we begin I'd like to remind everyone that comments today may include forward looking statements made under the private Securities Litigation Reform Act of 1995.
These forward looking statements are made as of the date hereof and are subject to numerous doctors assumptions risks and uncertainties, which change overtime.
Actual results could differ materially from those contained in any forward looking statement as a result of various factors, including those described under the heading forward looking statements infill logics press release from earlier today or under the heading risk factors into logic. Most recent form 10-K or in later filings with the SEC.
<unk> cautions you not to place undue reliance on any forward looking statements.
Now I'd like to turn the call over to you.
Thanks, Dan Good morning, everyone and thank you for joining us.
I'm proud to share with you today update our recent execution and progress across the portfolio as well as our financial results from the second quarter of 'twenty 'twenty one.
Before we dive in and as I'm sure you're already aware I wanted to first tank Dr. Richard Greece all of his contributions over the last few years, serving as Synaptics Chief Medical Officer.
We wish Richard the best in his new exactly.
As our programs continue to build momentum we remain in good hands with a highly experienced executive team.
I'm personally excited to tap into my CMO.
Nishu, it's very tricky CMO, who can lead our growing clinical development organization and Shepherd our programs as they transition into later phases of development.
Now back to the business.
We're executing on our plans to demonstrate the clinical potential of our synthetic biotic platform in 2021.
With Christmas mechanism established in our two lead metabolic programs.
Strengthened balance sheet and an exciting new partnership we are well positioned to deliver a proof of concept and multiple high value indications.
Like all companies have ongoing clinical studies, we continue to watch the impact of the Covid 19, pandemic and particularly the Delta Varian to carefully.
Especially on clinical sites in the south Eastern United States.
We're pleased that our team continues to execute with the singular goal of developing synthetic biotic medicines, which provide meaningful treatment for patients with serious diseases.
Let me turn to those programs now.
I'll begin with our PKU program.
We believe patients with PKU continue to need additional treatment option to manage this devastating disease.
And we believe that it is efficacious oral therapy, regardless of genotype remained one of the most attractive clinical profile.
This is why we keep executing on our plan to evaluate our lead PKU candidate Cindy 16, 18 into phase III clinical study we call Symphony.
We're thrilled to recently published a compelling proof of mechanism results for our phase one study of <unk> 16, 18 and nature metabolism.
The Symphony study is on track to deliver data later this year.
This quarter. We also took another important step forward by initiating the phase one study of Syn beat 19, Turkey for.
<unk> 1934, and involve strain of <unk> 16, 18, and in a moment, Dave will tell you more about the science behind our PKU program.
Let me tell you why we developed can be 1934.
Because we never stopped to asking the question how much more efficacy can we deliver for patients.
Synthetic biology tools are progressing rapidly and our team has access to the best of those two both internally and through our network of collaboration.
By deploying a new suite of directed evolution towards just couldn't be 16, 18, we were able to generate a candidate which may have even more fee consuming capacity and move rapidly into the clinic.
And then tech hype Rockstar urea, we also see a significant opportunity to make a meaningful difference in the lives of patients.
Cindy <unk> to our other lead metabolic program is designed to consume the toxic metabolites oxalate in the Gi tract in patients with enteric Hyperoxaluria, a leading cause of oxalate nephropathy and recurrent kidney stones for which there are no approved therapies.
As we previously communicated Timothy H H O. Two has demonstrated the ability to consume oxalate in the Gi tract with healthy volunteers exhibiting.
Exhibiting a robust and dose response of urinary oxalate reduction.
We are now evaluating the oxalate lowering potential of can be a T. So two and a phase one b study in patients with enteric Hyperoxaluria. Following we won Y gastric bypass surgery.
This study gives us an opportunity to demonstrate a highly clinically clinically attractive profile.
We are taking the learnings from our co lead metabolic programs and applying them to novel approaches to address other diseases enrich the Gi based approach may be relevant, including inherited and acquired metabolic disorders as well as autoimmune conditions.
We recently entered into a research collaboration agreement with Roche.
The discovery of a novel synthetic biotic medicine for the treatment of inflammatory bowel disease or IBD.
I B he remains an area of high unmet need and which new approaches are urgently needed.
We're delighted to be working with an organization with unparalleled depth and immunology and look forward to exploring the potential of synthetic biotic medicines in IBD.
Our team has done a tremendous job executing across multiple programs. During what continues to be trying times for all of us in 2021.
Zillions and teamwork has set the stage for multiple meaningful readouts in 'twenty 'twenty one.
Thanks to our careful capital stewardship, these milestones occur well within our cash window.
In summary, 2021 has been an incredibly exciting year for the company. We now have demonstrated proof of mechanism in humans from both our lead metabolic programs at PKU in enteric Hyperoxaluria.
A phase one study of our next generation strain in our PK portfolio and initiated an exciting new partnership in immuno modulation.
We have the opportunity to demonstrate proof of concept in a co lead programs and advanced our mission to bring the transformative power of synthetic biology to medicine.
Now, let me turn the call over to Dave to go deeper into our PKU program.
Dave.
Thank you Lisa.
It's my role today to share the exciting science, which underpins our PKU program and our next generation stream Cindy $19.34.
Before I do let me remind you the challenges faced by PKU patients and caregivers.
PKU is an inherited metabolic disease in which children are born without the ability to metabolize phenylalanine or feet.
Consuming even modest amounts of dietary fee causes irreversible neurocognitive deficits in patients with PKU.
Despite the availability of dietary management and approved treatments.
A large proportion of patient struggled to maintain blood fee levels and the target range required to avoid this irreversible damage.
It is clear to us that both current and emerging treatment options continue to leave too many patients behind.
And so we have set as our target product profile, a safe tolerable reversible and oral therapy, which would reduce plasma fee levels for PKU patients regardless of underlying genotype.
The scientific hypothesis behind our approach is quite simple.
It is well understood that reducing the dietary consumption of filling out.
It reduces plasma fee levels in patients with PKU.
Our team is built on that biology to introduce a synthetic biotic medicine into the Gi tract.
Which is specifically designed to consume fee.
And break it down to produce TCA and <unk>.
TCA or trans cinnamic acid is sentiment.
HCA has a further breakdown product of TCA.
Both are generally regarded as safe substances, which are harmlessly excrete it from the body.
These measurable biomarkers TCA and <unk> are key.
They allow us to determine the fee lowering potency of our strains in a consistent manner.
Across in vitro in vivo healthy volunteer and patient studies.
As you know our first generation PKU candidate.
<unk> 16 to 18.
As shown promising activity.
Dose dependent increases in TCA seen in healthy volunteers.
This indicates that the strain is consuming fee in the Gi tract at escalating levels correspond closely with how much shouldn't be 16.18, we're administering.
Based on this observation, we have moved <unk> into phase III clinical development.
However, our scientific team. It's in logic has continued to ask how much fee consuming activity coming engineer into a synthetic biotic medicine.
Especially a synthetic biology tools have advanced rapidly at the time since 2018 was engineered.
That curiosity led us to soon be 1934.
A strain that has been evolved from <unk> <unk> with the potential to provide increased fee lowering efficacy for patients living with PKU.
Preclinical in vivo and in vitro studies demonstrated a greater than two fold improvement in the ability of syn <unk> $19.34 to consume and breakdown fee compared to Cindy <unk>.
<unk> 1934 was developed using a directed evolution approach.
Using a biosensor engineered into a tool stream.
Which was designed to respond to TCA.
This allowed us to generate hundreds of variants of the fee consuming enzyme pal.
And to test their wholesale activity in a translational irrelevant environment.
After multiple rounds of selection, we chose the top candidate strains and confirmed their increased activity and stimulated Gi compartments in vitro and.
In in vivo in non human primates.
Which is the most predictive animal model for humans.
This approach resulted in a doubling of fee consumer activity between <unk> 1934, and <unk> 16.18.
Which we are now seeking to confirm in phase one.
This rapid progression of Cindy $19.34, which went from candidate selection to first in human dosing in less than eight months.
Demonstrates the speed and power of our synthetic biotic platform.
While we evaluate can be $19.34, we also continue to progress the symphony one phase II proof of concept study with utmost care and attention.
Our goals in this study are to demonstrate the potential of <unk> 16, 18 to lower blood fee in adult PKU patients.
And to validate our pharmacodynamic model to better understand the relationship between the strained Biomarkers we have spoken about.
And plasma fee lowering and a disease setting.
Yeah.
Patient consent, when you have no therapeutic options.
They're ineligible inappropriate for or unresponsive to existing therapies.
These are patients left behind by today has limited treatment options.
The study is powered to detect a 20% reduction in plasma fee.
PKU patients and investigators tell us at 20% fee reductions.
In an oral tolerable and reversible therapeutic.
It was effective for a coupon non responders would be a welcome treatment option.
In summary, the phase one multiple ascending dose study of <unk> 1934 will evaluate the safety tolerability and feed consumption activity of <unk> 1934 income.
Including a head to head comparison that should be 16.18 in healthy volunteers using biomarkers of feed consumption.
Based on the data from the head to head comparison as well as results of the ongoing phase II study of shouldn't be 16 to 18 patients with PKU.
So in logic plans to select one therapeutic stream for late stage development.
Data from both studies are expected by the end of 2021.
The willingness of advocates caregivers and patients to engage with us and other sponsors it's critical to advancing new treatment options for this devastating disease.
We want to thank them for their partnership.
Let me now turn the call over to Eva to share progress in enteric Hyperoxaluria.
Thank you, Dave and congratulations to your team and the tremendous progress in bringing potential new treatments to patients with PKU.
Now, let me turn to our co lead metabolic program can be a T cell to in enteric hyperoxaluria.
And Paris, Hypoxic area, which we just called Hawk is a devastating condition with no treatment option and rich dangerously high levels of urinary oxalate leads to progressive kidney damage.
Often occurs as a result of the primary insult to the bowels eating malabsorption, such as inflammatory bowel disease Sharp eyes syndrome are the result of surgical procedures.
Chas bariatric weight loss surgery.
If left untreated the day the high levels in Europe actually caused recurrent kidney stone formation, Napa <unk> and progressive damage, resulting in chronic kidney disease.
Vince oxalate its presence in many healthy foods enteric hyperoxaluria is almost impossible to control with dice alone that means the patients at risk for serious kidney complications.
For most patients enteric hyperoxaluria isn't just standalone problem, because the pathogenic absorption of boxes as a result of an underlying bowel disorder.
This means in clinical practice it is patients who already have the complexity of living with short bowel syndrome chronic pancreatitis.
D or who have undergone bariatric surgery, who now have to face the devastation challenge of the current in chronic kidney stones.
In this patient population the pain and disruption of recurrent kidney stones is a significant challenge in their overall care.
There are approximately 75000 to 90000 patients with enteric hyperoxaluria and recurrent chronic kidney stones are high risk of significant kidney damage in the United States.
They have no treatment options today, and we believe the synthetic biotic platform could provide a meaningful new approach.
Meeting the needs of this population that is to develop and be a SEC, so too and oral synthetic biotic medicine to metabolize the tactics substance oxalate in the Gi tract and converted into formation with just harvest the exclusive from the body.
As you May recall, we have demonstrated a peso to proof of mechanism and a dietary high crop for your study.
We have now moved to part D effects study in quick Cindy a J, so too will be evaluated for the potential to lower yearly athletes in enteric hyperoxaluria patients.
Let me walk you through both parts of this study.
The primary outcome of part a of the phase one study was safety and Tolerability, which would be used to select the dose for further study in patients with impaired hypoxic area in part B of the trial.
We completed dosing of five cohorts in part a of the study.
And the efficacy analysis the percent change from baseline urinary oxalate levels with 28, 6% compared to placebo at the 311 lifestyle dose a clinically meaningful level of oxalate degradation.
This dose is well tolerated and is being used in part b of the study.
Similar to our prior programs, we did not observe any systemic toxicity and there were no SAE or serious adverse events and he does.
Adverse events were generally mild to moderate tbi related and transient.
We found that a dose ramp significantly improve the tolerability profile.
N D H H O two as a non collyn I think non reproducing strain and hears from subject after cessation of dosing.
We were thrilled to see substantial Jeremy oxalate lowering across multiple dosing cohorts.
This consistent and dose responsive result is very encouraging.
And part B of the study patients with enteric Hyperoxaluria and yet post roux en Y gastric bypass surgery flip dangerously high levels of your already Oxleas would be assessed in a crossover design.
We have chosen a dose of 311 lifestyles for part B of the trial.
We believe it could provide a clinically meaningful reduction in urinary oxalate levels in this population.
In parallel we will also continue to evaluate it can be a case or two and additional cohorts of healthy volunteers as we explore further optimization of dose and dose frequency.
Overall, this study will inform and enormous amount as we've progressed in V. H S O to preclinical development.
We were better understand not only the activity it can be a phase two and dietary hawk for OXXO urea disease model, but also in patients with enteric hyperoxaluria itself.
As well as the degree of colonic activity and the potential for less frequent dosing.
Moving forward, we believe the regulatory and clinical path in this indication is relatively straightforward with significant precedence by sponsors and related diseases, such as primary hyperoxaluria for the importance of urinary oxalate is one critical endpoint.
Our initial efficacy assessments will evaluate clinically relevant reductions in urinary oxalate levels.
Feedback from our key investigators suggest greater than 20% lowering in patients would be clinically meaningful.
Lowering dangerously high levels of urinary oxalate is the only way to reduce the risk of disease progression and reduce or eliminate oxalate nephropathy were.
We're pleased that <unk> has demonstrated the potential to lower urinary oxalate levels in healthy volunteers with dietary hyperoxaluria.
We're looking forward to advancing the program rapidly into patients and providing additional data at later this year.
As we move forward with both of our lead metabolic programs in PKU in enteric Hyperoxaluria I'll come back to you with more information as the studies unfolds.
Now, let me hand, the call over to Dan to briefly run through our financial results.
Dan.
Thank you and good morning, everyone. This morning, we released our financial results for the second quarter.
32021, and I'd like to review the highlights of those results with you now.
Research and development expenses were $10.7 million for the three months ended June 32021, compared to $12.9 million for the corresponding period in 2020.
The R&D expense for the three months ended June 32021 consisted primarily of costs related to our collaboration with Ginkgo bio works. So the optimization of synthetic biotic medicines as well as clinical study activities associated with simply 16, 18 and shouldn't be it'll too.
Ongoing should be 18, 91 phase one study and the initiation of this should be 1934 phase one study.
General and administrative expenses were $4.1 million for the second quarter of 2021 compared to $3.5 million for the same periods in 2020.
For the second quarter of 2021, the company reported a consolidated net loss of $14.5 million or 28 cents per share compared to a net loss of $15.5 million or.
Or <unk> 44 per share for the corresponding period in 2020.
Revenue was $2 million for the second quarter of 2021 compared to <unk> 4 million for the same period in 2020 revenue was due to the recently initiated collaboration with Roche for the discovery of a novel synthetic biotic medicine for the treatment of IBD.
Now turning to the balance sheet.
So logic ended the second quarter of 2021 with $115.5 million in cash cash equivalents and short term investments.
Compared to $104 million as of.
To sum up to 31.2020.
Under our current operating plan, we expect our cash and cash equivalents will be sufficient to fund the company through the second half of 2023.
This will enable some logic to advance our clinical programs through important data readouts over the coming months.
Thank you for your attention and we look forward to keeping you updated on future calls.
Now I'll turn the call back over to your thoughts around that.
Thank you Dan our team has made tremendous progress across all of our programs both in and outside the clinic.
Executing effectively and with a sense of urgency we look forward to demonstrating proof of concept and our co lead programs in PKU in enteric Hyperoxaluria basically this year.
We will now open the call for questions.
Thank you to ask a question you'll need to press star one on your telephone.
I would draw your question press the pound key.
And our first question comes from Rob <unk> with H C. Wainwright Your line is open.
Hi, This is speaking on behalf from H C. Wainwright, thanks for taking my questions.
In terms of the Symphony one phase II trial for <unk> <unk>.
Phase one for 1934.
Can we expect a combined data release at the same time later this year.
With your announcement of your selection for one of the compounds or development.
Yeah. So thanks, so much for the question, it's very difficult for us to predict exactly when those.
Lead ads will come we know that they are both on track for the second half of this year and I think it really will depend on how exactly the timing falls, whether we can make a single announcement or would have to do two separate announcement. So I can't give you a straight answer to your question other than to let you know that they will fall within that.
The second half of this year is all continues to plan.
Okay. It makes sense, we would just curious and if 1934.
As indeed selected what kinds of bridging studies would need to be.
Done to move to a pivotal status.
And as the formulation of 19, four already optimized or not.
Yeah, So Andy.
I see about 1934, I think it's very similar to 16.18, you use the same enzyme pathways. It's just with an optimized version of the gene for power. So we were really able to leverage a lot of the work that we have done for <unk> and <unk> as we were developing 19, Turkey for you I think that's evidenced by how quickly new.
From clinical candidate to IMD to being in the clinic and we anticipate that it will continue to benefit from kind of having a deed and leave program. That's a very very similar and right now the phase one study is being done by a lot with our Lyle formulation of 19, Turkey for so we were able to go into the clinic with already.
Kind of how they can take conducting SEC to lilac.
We anticipate that it would move very very quickly thereafter in terms of what we would need to do before initiating the phase III study should we decide to ask rich to 19, Turkey for our we haven't provided a lot of guidance in terms of the specific steps suffice it to say that we think that it can move very very rapidly.
Because it's been able to take advantage of all of the learnings we've had with 16.18 and of course you know.
Any regulatory prime would be subject to agreement with the FDA and other regulators after that kind of all we can say at this time.
Okay. Thanks for the clarification and just finally regarding business development and the recent gastroenterology collaboration with Roche and this triggered any interest and momentum for.
Further partnership opportunities.
Yeah. So the Roche agreement as you know it was very exciting for US we're absolutely thrilled.
Exactly the kind of deal that we want to do in and inflammation in tech in immuno modulation generally as we've disclosed the Roche collaboration with the random single specific targets that had that that organization are interested in based on their research and in immunology.
Obviously, we will continue to advance our own programs that today's group are working on and continue.
Continue to have discussions with potential partners.
And around the same the same kind of <unk>.
<unk> broadly Dave anything you want to say it back to the immunology strategy, just more broadly to add to my comments there.
Yes, sure I mean, I think you've summarized it well I mean, I think we still believe there is a lot of biology, that's going to unlock them using using the platform. We have a number of internal programs that were that were working on at the preclinical stage and.
There'll be opportunities to explore additional either additional partnerships are to advance our own pipeline is as those mature so I think.
It's all pretty consistent with the strategy we've been following in the end.
We're excited about the Roche agreement in and that is a highlight of kind of that strategy going forward.
Alright, thanks, very much for taking my questions and congrats on the exciting developments in the pipeline.
Thank you.
Our next question comes from Joseph Schwartz with SBB Leerink. Your line is open.
Hi, I'm Jerry dialing in for Joe I. Thank you for taking our questions. My first question is on can be a eight O. Two I was wondering do you think it helps frame how we should be thinking about the phase one part b data in patients with <unk>, resulting from a ruling Hawaii gas.
Castro bypass surgery when it becomes available how representative is this group from other manifestations of E Hawk, such as inflammatory bowel disease. That's really ask me are there any biological considerations, we should be taking into consideration about the scrip or is this a fairly good representative of the overall E Hawk.
Operation.
Yeah. Thanks for that question, Terry and number one I'll say that our goal is to develop a product for patients with severe enteric hyperoxaluria, regardless of their underlying Gi disease or condition. So that's our target is that segment of patients with enteric hyperoxaluria recurrent stones that are we.
Really having a very high burden of disease for whom there is currently no treatment.
Based on the precedent and others, who have done work in this area. We don't believe SEC, there's going to be a difference based on the underlying at Gi in felt that that has occurred from reflected prior studies that have been done in this indication what we see is very similar and consistent treatment effect across all of the underlying.
<unk> kind of conditions, we made the decision to focus it on a kind of a relatively homogeneous group to get proof of concept and I think that was kind of say a development tactic doesn't necessarily indicate that we'll be pursuing a very narrow and group our narrow underlying gi.
As we move forward in development in fact, I think the next step in the development program would be for us to evaluate efficacy in in a much broader population, including patients with the disease and he just mentioned their jewelry like inflammatory bowel disease short bowel syndrome, chronic pancreatitis, I think theres a lot of diseases that.
Can result in a in enteric hyperoxaluria and we plan to pursue all of them.
Okay, great. Thank you that's Super helpful. And then my second question is kind of building on an earlier one so I'm wondering if you had any color on the order in which well in which we will see your Hawk program relative to your PKU program.
Yes. Unfortunately, we get asked that frequently and you don't have them.
Line of sight to be able to provide guidance around specific order them. Both are on track for at results in the second half of this year in terms of which way they will fall from a sequence perspective, we just don't know.
Okay, great. Thank you for taking our question.
Thanks Terry.
Thank you. Our next question comes from Mark Breidenbach with Oppenheimer. Your line is open.
Hey, good morning, and thanks for taking the questions.
Just looking at the Symphony protocol.
And remembering that you ramp up to dose level, but are about an order of magnitude higher than the previously established mcd for 2018.
I'm wondering if you can remind us what's giving you confidence that you can safely dose up to those levels and symphony.
And with respect to the upcoming 1934 data later this year would that be inclusive of both healthy volunteers and PKU patients or healthy volunteers. Thanks for taking my question.
Yeah, Yeah, great Mark. Thanks, So much for gives me the opportunity to clarify the first point.
I think youll remember that we did an early study with the liquid formulation of 16.18 are we studying small cohort of patients with PKU and the doses that were currently using in defense. We study our log higher than the doses that we previously used approximately.
With the liquid formulation in patients with PKU. So I think that's where the lag piece comes.
But they're not a lot higher than the maximum tolerated dose in fact, when we did the bridging study with the <unk> formulation in healthy volunteers. The maximum tolerated dose. There was 2012, so they're absolutely still within the tolerated dose range that we established in healthy volunteers with the Lyle formulation, there just a lot higher than the dose.
We used in the prior PKU at cohorts with with the liquid formulation. So.
That's just a clarification there in terms of the safety and the dose that we're using in symphony.
Terms of the second part of your question around 19, Turkey for no. The current study is designed to evaluate 19, Turkey for head to head with 16.18 in healthy volunteers and we'll look at the production of the strain specific biomarkers to make a determination around whether 19, Turkey for is actually more act.
As in humans compared to 16.18. It will not include any data in patients with PKU.
Super helpful. Thanks for taking my question.
You're welcome.
Thank you. Our next question comes from Ted <unk> with Piper Sandler Your line is open.
Great. Thanks, Good morning, everybody. Thanks for the update really.
We appreciate you guys linear sort of the.
Our core some for me in terms of what is sort of a win and I'm wondering you know what.
Next steps assuming positive data.
<unk>.
Yeah, So I think and put it in the second half of this year, we have data from symphony as well as from 1934 I think the first step is going to be in determining which strain of those two that we're going to take forward into the next phase of development.
And I think that the next step from there will be you know planning and getting regulatory alignment around our phase III plan.
With any program so starting that conversation with regulators in the regions globally that we would intend to commercialize the product and starting to plan for.
That kind of confirmatory phase of development as we move forward with the program and that's the kind of the the two step obviously a lot of work going into that second step preparing to move to phase III, if not for the faint apart, but in kind of the.
The logical flow would be making a decision on which strained and then starting to kind of lay out the phase III plan and getting engagement with the various stakeholders.
Does that make sense Ted.
Our next question comes from <unk> Mackay with Shannon Your line is open.
Hi, yes can tie from Chardan.
My question is for E H.
Recently, we saw another company who is developing.
Drugs for primary Hyperoxaluria sure Phil Russo result in the type two patients and you guys have done a great job in prior presentations in explaining the differences in pathology.
Metabolic pathways for IH versus ph, but I guess the takeaway from that field study in ph is.
Just a lack of understanding of what they thought the pathway. It was.
Prior to <unk>.
<unk> prior knowledge, so how confident are you.
Did you understand the pathway for EHR and just building on that prior question in a different patients with different underlying insult.
Yeah, Yeah, so I'm, assuming you're referring to sharing our results, which that's correct showed nice yet showed nice activity in the type one, but but not said Nokia expected activity in the tech Q3.
So number one thing I'll say is we don't believe that that has any bearing on our program.
Pink and the tight the primary is as you mentioned you know very different disease due to a genetic liver defect overproduction of oxalate a number of different mutations that result in that kind of opened over production there, but we think it's a very very different disease, a very different etiology very different underlying profit.
The geology.
But I will say about enteric Hyperoxaluria is you.
We have pretty good understanding back due to over absorption of off lease and we know that these patients have fat Mal absorption that results in a lot of free oxalate being available in the GI tract that then continues to be absorbed at a much higher rate than individuals who have a normal gi.
Pathophysiology that would be so across the oldest diseases you know what they all have in common pancreatitis IBD short bowel syndrome is that they have this maintain kind of underlying pathophysiology or having a lot of free fatty acids in the Gi tract lumen.
Based on our understanding of the pathophysiology of enteric Hyperoxaluria that appears to be the kind of unifying component of driving the elevated urinary oxalate levels.
And so I think that's you know that gives us confidence that you'll be able to kind of address the broader population regardless of underlying Gi himself, but obviously the proof of the pudding is going to be in the clinical study. Once we you know assuming that we get nice results and the impact if the current study our next step would be to broaden.
To include some of those other Gi diseases and to enter that from evaluate whether we get similar efficacy in that broader patient population, but as I said based on what we know today about the pathophysiology and the precedent from prior studies and the entire Kai proxy already population and we believe that there isn't it.
A substantial chance, we'll be able to address that broader group of patients.
Okay, Great and then just just.
In terms of the <unk>.
<unk> genius newness of the bypass patients.
Something specific about the population that makes them more consistent versus some of the others.
Within.
Disease States.
Yeah. So the bariatric patients have all had similar surgery right. So that's a.
A nice component in that field that'd be quite you know you try and early development, you're trying to do at a smaller study and get as much information that you can as you know limited treatment numbers said that the more homogeneous they are often that the tenure the signal is.
You go out into <unk>.
Different groups of patients E. R. You know for instance, you're going into IBD could come with those patients have active inflammation, making their gi tract.
Could there be other you know con meds that you worry about you know so there's different things that you need to take into consideration as you look across broader patient population. So it was really around you know keeping it homogeneous as well as being able to <unk>.
Executing a relatively straightforward study that that led to that decision, but I think the next chapters I've mentioned would be to broaden out and look at different a different patient types as we move forward in development.
Okay, well, thanks for the color on both those questions.
Okay sure.
Our next question comes from Tom Shrader with <unk>. Your line is open.
Hello, Good morning.
Dialing in for Tom.
Just one question regarding the PKU program, So I know youre power for a 20% reduction in reality, though.
Regarding like.
Like what does that mean for patient, there's a 20% reduction based on the low yields that a patient and Jeff. Thank.
Thank you.
Yeah. So thanks for the opportunity to clarify that our current study is being done in patients who have.
Blood female clothes that are greater than a $610 million. So their patients who are not on the controls I asked or maybe they are semi controls but.
Have elevated blood female both at baseline.
We believe in those patients being able to Ritchie and blood fee levels by 20% of meaningful it may bring some of them into the you know less than 600 range, but really importantly for US. We think that this is the gateway to moving into other patient segments, including patients who are maybe on diet, but not achieving their goal.
Or are patients who are on a very strict diet, but we'd really like to be able to eat additional protein.
That's particularly important consideration in the pediatric patients we consistently hear from parents that.
In the pediatric group managing protein intake such that kids are getting enough. So that they feel full their safety aces in their growing normally is a real challenge with them very very restricted diet that these kids have to be on and when we kind of extrapolate costs, 20% fee lowering in adults.
Whose uncontrolled could mean for pediatric patients in control, we estimate that that could mean being able to double the amount of natural protein that that kt is able to eat on a given day, which I think would be a huge a huge boost to that did that kid from both a clinical and quality of life perspective, So we really do see be nave.
To demonstrate 20% fee lowering in the current population is kind of a.
At.
Step two further evaluation across patients with different kind of pattern.
Different clinical scenarios and we'll continue to build that value story as we move forward in development and execute additional studies.
Thank you that's very helpful.
Thank you and there are no further questions in the queue I'd like to turn the call back to you for Brennan for closing remarks.
Great. Thank you operator, and thank you everyone for joining us today and very exciting Europe for us it's in logic and we look forward to keeping you up to date.
Thank you.
This concludes today's conference call. Thank you for participating you may now disconnect.
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