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Good day and welcome that the Aeglea BioTherapeutics Fourth Quarter and Full Year 2016 Earnings Call. Today’s call is being recorded. And at this time, I would like to turn the conference over to Paul Arndt, Managing Director of LifeSci Advisors. Please go ahead.

Thank you, Matt and good afternoon everyone and thank you for joining us for the Aeglea fourth quarter and fiscal year 2016 financial results conference call. During the course of today’s call we may make a number of forward-looking statements including comments on our business strategy, strength and priorities, the timing, plan and success of our clinical trials and related data, the safety therapeutic benefits and economic valuable of our product candidates, the advancement of our technologies and the proprietary product candidates, regulatory pathways for our development programs, the success of our collaborations, the competitive landscape for our product candidates, the potential for our Arginase I deficiency to be added to the neonatal Recommended Uniform Screening Panel, trends with respect to our revenues, expenses and cash flows, our ability to fund our research and development programs and our ability to manage our cost, uses of cash and other matters. These forward-looking statements are based on assumptions that are subject to risks and uncertainties that could cause our actual results to differ significantly from those suggested by these statements. Given these risks and uncertainties, you should not place undue reliance on these forward-looking statements. Please refer to our Form 10-K filed with the Securities and Exchange Commission on March 23, 2017 for some of the important risk factors that could cause actual results to differ materially from expectations including any forward-looking statements that made on this call. Except as required by law, we disclaim any obligation to publicly update or revise any forward-looking statements to account for or reflect events or circumstances that occur after this call. I’ll hand the call over to Dr. David Lowe, Chief Executive Officer of Aeglea.

Good afternoon. Thank you for joining us today. With me here today is our Chief Financial Officer, Mr. Charles York. This is our first clinical update conference call, since our IPO last April, a lot has happened since Aeglea became a public company and we had a productive 2016. We made progress in the clinic with three Phase I trials for our lead candidate AEB1102 in Arginase I deficiency, hematological malignancies and in solid tumors. I want to thank our shareholders for your support, and I believe we are well positioned to advance our clinical programs and built shareholder value in 2017. Aeglea is a leader in creating and developing novel engineered human enzymes, that are designed to degrade or deplete specific amino acids in patients’ blood. Our product candidates address two extremes of amino acid metabolism, as enzyme replacement therapy in rare genetic disease and targeting tumor metabolism for cancer treatment. In rare diseases we are working to treat patients with toxic levels of amino acids resulting from a growth in metabolic pathway, lowering these levels back down to the normal range. In cancer, work supporting [ph] a dependence of certain tumors on specific amino acids for survival, which potentially allows us to starve the tumor, while avoiding damage to healthy tissues. There is a lot known about amino acid metabolism and the disease pathways, we’re targeting across our pipeline of enzyme based therapeutics. However amino acids have generally been elusive, as drug targets due to the lack of direct product candidates from the human genome. We believe our engineered human enzymes represent a unique and important opportunity in drug development, working at the intersection of enzyme engineering and clinical need. We focus our research and development to identify product candidates that address unmet medical needs in diseases that are impacted by abnormal amino acid metabolism. We believe our approach has an attractive risk profile due to the well-known biology of the amino acid targets and a blood based mechanism of action for our enzyme based drugs. We believe these factors increased the probability of successful drug development in these patient populations that lack adequate treatment options. The lead product candidate to emerge from our efforts is AEB1102 or pegzilarginase, which we’re developing as enzyme replacement therapy to treat the rare genetic disease, Arginase I deficiency in cancer, two critical areas of patient needs. Mechanistically, AEB1102 is optimized human Arginase I, an enzyme that degrades or depletes the amino acid arginine in patient’s blood. In the case of rare genetic disease, we are looking to utilize AEB1102 as enzyme replacement therapy for patients with Arginase I deficiency and ultra-orphan disorder of the urea cycle. In these patients there is too much arginine in their blood. What is an otherwise normal molecule becomes toxic resulting in a seriously debilitating, progressive and ultimately life threatening disease with neurological and neurocognitive symptoms. In these patients we want to deplete arginine down to the normal healthy blood concentration. We are essentially replacing the function of a missing or dysfunctional enzyme. We believe this approach will benefit patients based on published case reports on the clinical benefit of lowering blood arginine. For example, from liver transplant or red blood cell infusion, the two major sources of Arginase in our body. Our second program for AEB1102 focuses on cancer. We’re exploiting a metabolic dependence on arginine for cancer cell growth, starving the tumor cells of a key amino acid. Our work to-date is focused on targeting tumors that depend on arginine for survival and where we have a potential biomarker or a companion diagnostic that allows us to identify tumors that may respond to arginine starvation. We've completed preclinical studies to focus future solid tumor expansion arms on cancers that are arginine dependent such melanoma and small cell lung cancer. And in hematology we’ve focused the Phase I trial on acute myeloid leukemia or AML and myelodispostic syndrome or MDS based on our biomarker studies, indications where we believe we have a likelihood of showing clinical benefit. As we progress further down the cancer path we are encouraged by a preclinical data we've recently presented that builds on the story of engineered human enzymes as the potential therapeutic options for patients. I'd like to highlight two key findings from this research. First, we presented preclinical data at the Society for Immunotherapy of Cancer Conference in November 2016 showing that contrary expectation arginine depletion with AEB1102 is not immunosuppressive when used in combination with immune checkpoint inhibitors targeting the PD-1 or CTLA4 pathways. Rather our data showed that single agent activity of AEB1102 and immune checkpoint inhibitors was additives or synergistic when these drugs were dosed in combination in models with established tumors. We believe this unanticipated result represent an important therapeutic opportunity at the intersection of tumor metabolism and immune-oncology and highlights that there are still many unknown surrounding this important area of tumor biology. As we complete the Phase 1 dose escalation in patients with advanced solid tumors and plan for expansion arms. We're exploring opportunities for combination trials with approved immune-oncology therapeutics or other existing or emerging standards of care. Additionally, we presented preclinical data at the Keystone Tumor Metabolism Conference in March of this year that demonstrated AEB1102 does not affect the development of immune memory where a combination therapy with AEB1102 and anti-PDL-1 resulted in tumor cures and immunization against subsequent tumor challenge. We're excited about what we believe to be a great opportunity ahead of us both in rare genetic disease in cancer where we see the potential for our platform of engineered human enzymes toward this clear unmet medical need. At this point, I'll review the clinical status of AEB1102 in each of these three therapeutic areas that we're now pursuing. In Arginase I deficiency we're pleased to present top-line data today at the American College of Medical Genetics and Genomics Annual Clinical Genetics Meeting, which describe the Phase 1 results from two adult patients. Now let me remind you Arginase I deficiency is a seriously debilitating progressive and ultimately life threatening disease where there is no -- where there is currently no approved therapy to treat the root cause of the disease. We are encouraged by the results reporting that AEB1102 is well tolerated and effective at reducing plasma arginine levels in both patients. Intravenous administration of AEB1102 lowered plasma arginine to normal levels in these patients at low doses and in a dose proportional manner. Most importantly, the data further demonstrated that when we capture dosing at 168 hours plasma arginine levels remains suppressed by 25% and 49% of pre-dose levels in these two patients, suggesting that a once a week dosing regimen could be achievable. From a safety perspective we were very pleased that there were no serious adverse events reported for either patients; no clinically notable trends in vital signs, no clinically significant abnormal laboratory results and no clinically significant ECG findings. To provide some further understanding about the trial results, let's look at the two patients in more detail. These two female siblings were in their mid-20s with moderate to severe neurocognitive and neurological deficits on diet therapy and nitrogen scavengers. This is important because as we've discussed in the past, diet and nitrogen scavengers have not stopped the disease progression primarily we believe due to the inability to effectively control arginine levels. In this trial we saw some evidence of the lack of benefit of current treatment options where the two siblings both clearly exhibited pre-dose arginine levels well above the upper range of normal and clinical presentation of disease. This further adds to our belief that the reduction of blood arginine to the normal range is the most appropriate path for effective treatment of these patients. And potentially provides a way of halting the course of the disease. We are quite encouraged by this first evidence of positive pharmaceutical dynamic results from our potential enzyme replacement therapy. This proof of mechanism together with the encouraging safety profile provides meaningful proof of concept to continue with our development program. With these results we believe the use of blood arginine is a primary endpoint in clinical trials linking to clinical stabilization and or clinical benefit puts us on a path to a once weekly IV drug. Now let’s discuss an update on the status of our Phase I/II clinical trial for treatment of these patients with Arginase I deficiency. As you know, following completion of dosing of the first two patients in our Phase I clinical trial, we submitted a protocol amendment in November 2016 to broaden the scope of our Phase I trial into a Phase I/II trial. The amended protocol include dosing of pediatric patients ages 2 and older and weakly repeat dosing in the Phase II portion with the intent to assess the safety, tolerability, pharmacokinetics, pharmacodynamics, and clinical response of AEB1102 in patients with this inborn air metabolism. In the first quarter of 2017, we received IRB approval for this Phase I/II protocol at multiple clinical sites. In March 2017, we received an information request from the FDA, which included comments and recommendations on the protocol amendment and a request for supporting document based on their review of our completed toxicology study, our dose escalation plan and supporting information for the inclusion of pediatric patients. As recommended by the FDA, we replied with supporting information and requested a follow-up meeting. At this time we believe our Phase I/II protocol, provides an appropriate tap to evaluate the safety and tolerability of AEB1102 in pediatric patients and pending FDA feedback we plan to initiate dosing in pediatric patients in the middle of 2017. In the meantime, we intend to continue enrolment of adult patients and plan to dose additional adult patients in the middle of 2017. Top-line data from this trial is accepted in the first half of 2018. Now on to cancer, the other extreme of arginine metabolism. Our Phase I dose escalation trial with AEB1102 in patients for the advanced solid tumors is ongoing. This trial’s key objectives are safety and measuring blood arginine levels following dosing with AEB1102. We are currently enrolling cohort 8 at a dose of 0.4 milligrams per kilogram and have seen compelling proof of mechanism of lowering blood arginine in a dose proportional manner. We expect to complete and announce results of this Phase I study in the fourth quarter of 2017 or the first quarter of 2018. As you know this timing is somewhat variable depending on reaching the maximum tolerated does or MTD. When the MTD is reached, we plan to initiate single agent expansion arms in specific solid tumor types and potentially in combination with existing or emerging standards of care as discussed earlier. In July 2016, we initiated a Phase I clinical trial in patients with the hematological malignancies AML and MDS in the United States and Canada. And so far the first three cohorts of this trial have shown as we might expect based on our advanced solid tumor trial proof of mechanism with dose proportional lowering of blood arginine. This Phase 1 multi-center single arm open label dose escalation trial is designed to assess the safety and tolerability of AEB1102 as a single agent and determine the recommended Phase II dose. We are currently enrolling cohort 3 at a dose of 0.48 milligrams per kilograms and expect to complete enrolment and announce phase on the results in the fourth quarter of 2017 or the first quarter of 2018. Much like the solid tumor trial this is also a dose escalation and the final timing is dependent upon reaching the MTD at which point we will initiated an expansion arm for AML and MDF patients. At this time, I would like to turn it over to our Chief Financial Officer, Charles York to review our financials.

Thanks, David. Given the alignment in timing of our data presentation at ACMG on Arginase I deficiency and their annual report we thought we would take this opportunity to build upon the clinical update that David just shared. And provide an update on our financials as well, including an understanding of our cash runway. In the fourth quarter of 2016, our net loss was $5.5 million or $0.41 per share compared to a net loss of $4 million or $6.36 per share for the fourth quarter of 2015, which was prior to our IPO. For the full years ended December 31, 2016 and 2015, our net losses were $21.7 million and $11.3 million respectively. Revenues in the fourth quarter of 2016 were $1.2 million versus $1.6 million in the fourth quarter of 2015. For the full year 2016, we recorded revenues of $4.6 million compared to $6.1 million in 2015. All revenues were the result of our $19.8 million grant from the Cancer Prevention and Research Institute of Texas, or CPRIT and those funds are being used to support the development of AEB1102 in cancer. The decline in revenue for the fourth quarter and full year 2016 was primarily due to the timing of qualifying expenditures associated with the clinical trials of AEB1102. Our fourth quarter 2016 R&D expense was $4.7 million versus $4.0 million in the fourth quarter of 2015. For the full year 2016, R&D expenses totaled $18.1 million versus $11.5 million in 2015. The increases were primarily due to expanded preclinical and clinical activity for AEB1102 including the treatment of two patients with Arginase I deficiency in our Phase I study. The continuation of our Phase I trial in patients with advanced solid tumors and the launch of our Phase I clinical trial of AEB1102 in patients with the hematological malignancies AML and MDS. Fourth quarter 2016 G&A expense was $2 million versus $1.6 million in the fourth quarter of 2015. For the full year 2016, G&A expense totaled $8.4 million compared to $5.9 million for 2015. The increases in G&A expense were primarily due to additional legal, insurance and personnel cost associated with being a public company. We used approximately $6.1 million in cash to support our operations for the fourth quarter of 2016 and ended 2016 with the cash balance of $63.5 million, which we believe is sufficient to fund our operations through the first quarter of 2019. And in addition to the funds received from CPRIT in 2016, we anticipate that we will receive an additional $10.2 million in grant funds from CPRIT in 2017 and 2018. And we expect our cash burn will increase this year to a range of $7 million to $9 million per quarter as we continue and expand our clinical testing of our lead product candidate AEB1102. With that let me turn it back over to David for closing remarks.

Thanks, Charles. In 2016, Aeglea made significant strides in advancing our lead program AEB1102 in multiple indications. In 2017, we look forward to our presentation on newborn screening for Arginase I deficiency tomorrow at ACMG and to receiving FDA feedback on our protocol amendment for the Phase I/II trial in patients with Arginase I deficiency. In the meantime we are working diligently to establish site readiness at our clinical trial sites with IRB approvals with the expectation to enroll both pediatric and adult patients in the middle of 2017. We anticipate reporting an update on this program and at an appropriate time in an academic peer reviewed form later this year. In cancer we are continuing to enroll our Phase I clinical trial in patients with advance solid tumors and we expect to complete and subsequently report results of this study late this year or in the first quarter of 2018. We also anticipate completing enrollment in our ongoing Phase I, AML/MDS trial and reporting those results in the fourth quarter of 2017 or early in 2018. Finally, I am pleased that we continue to expand our AEB1102 program as we present additional preclinical data on AEB1102 at the upcoming AACR Meeting next month, which will believe builds on the emerging story of the intersection of immune-oncology and tumor metabolism. In closing, I would like to add my welcome to Dr. Suzanne Bruhn who joined our Board of Directors last month Suzanne is a talented executive with substantial experience in the development of treatments for rare genetic diseases in cancer. We greatly appreciate her advice and counsel and look forward to her contributions to our company's future success. That concludes our prepared remarks. Now I'd like to open the call to your questions?

Thank you. [Operator Instructions] At this time we will take our first question, this will be Chad Messer with Needham and Company.

Great, thanks for taking my question and good afternoon. Just in Arginase I deficiency that 40 micro molar threshold, can you talk a little bit about what the line of evidence sort to justifying that? Is that something we're really confident is the right level of target for ultimate clinical benefit or is that something you'll have to continue to look at as you go to phase I/II?

Hi Chad, thanks for your question. That's actually a topic of conversation that we have on a regular basis and touches on a variety of topics. For our clinical trial that range was one that was provided to us by the FDA based on data from Framingham. But if you look at the testing and the newborn screening among the states, the normal range varies from lab-to-lab. So I think there is some more work that needs to be done to perhaps standardize the range that's being used. But for now 42 as the sort of lower limit normally is what we used. Other testing labs we know use 20 to 120, in the literature you'll even find 1 to 40 as a range for example. So I think where we stand with our standardization and we're comfortable with the range that we're in and we'll continue to work on sort of further harmonization.

Great, thanks. And then maybe just one on the financials, it seems you have extended out a little bit your expected cash runway great. Just wondered if there is any particular changes in assumptions that are driving that or if it's just a recalculation as time goes on?

Hi Chad, thanks for the question. From our perspective it's really just making sure that we have appropriate runway to ensure the clinical activities that we need to get done and making sure we meet milestones. I don't perceive any change in ultimate direction of 1102 as a result of increasing our timeline, just a true understanding of where we want to be in the future.

All right, great. Thanks for taking my questions.

At this time we'll move to Jim Birchenough with Wells Fargo Securities.

Hi, thanks for taking my call. This is Yanan in for Jim. So could you talk a little more about the FDA information request regarding the amendment of the protocol? Any additional color there?

Hi Yen and thanks for your question. Sure I'd be happy to address that. So the FDA requested additional information about the description of the toxicology studies and wanted to understand further background on the safety of AEB1102. And we provided them with that information and are awaiting any additional feedback from them.

Got it, thank you. And also a question regarding the lower the threshold. So, I am wondering, is there any safety concerns for reaching a level below the lower limit of normal 40 micro molar or some other threshold in the literature. Is there any particular concern in being below that threshold for an extended amount of time?

Well that’s a question that I think is best answered when by looking at the data from the cancer trials where we have treated now dosed over 40 patients. And we know from that work that patients can tolerate levels of arginine below the limit of detection, which is 1 micro molar for extended periods of time and by that I mean several days. So -- and that’s consistent with work in the literature using other approaches for arginine depletion as well. So I think we do have a -- I think a very good window as we think about the dynamic range of arginine that we can work with and the therapeutic index.

Got it, that’s very helpful. And also can you talk about the variability of baseline arginine levels in the general patient population and whether that is remains conducive to selecting one dose for all patients?

Well for Arginase I deficiency, we know from the literature that the blood levels of arginine can vary quite a bit from several times the upper limit of normal, which could be several hundred micro molar up to 1,000 micro molar. So our clinical trial design takes that into account with the Phase I portion as a single ascending dose study to in an intra-patient manner really determine the most effective or what is the effective dose to bring the arginine down to the lower range. And so we are studying at a very low dose, 0.015 milligrams per kilogram and then gradually increasing and you see the dose effect for that in the two patients that we presented today and how there was a different dose that proportionally brought the arginine down into the normal range for the two patients given how they -- even though they were sisters their arginine levels were quite different. And so they are sister with the higher blood arginine that require the next higher dose to bring her arginine level down to the normal range compared to the other sister. So I think we are looking at really understanding the dose proportionality on an individual patient basis that will allow us to understand the dosing for any given individual.

Would that be the strategy going into commercially or do you have to eventually select one dose or it could be a patient dependent dosing?

I think that really remains to be determined from our clinical experience with these patients and how would lowering of blood arginine maps to the trends in stabilization or trends in improvement and clinical signs and symptoms.

Got it. And last question, in a future clinical study plan is there a plan to look at whether diet restrictions and nitrogen scavengers could be removed as part of the benefit for AEB1102?

I think that’s definitely those are both topics of conversation that we have internally and I think are best considered in the context as an extension arm where patients are on therapy after the Phase II. But that the design and scope of those trials remains to be determined as we continue with our development program.

Got it, thank you so much for the answers.

Thanks for your questions.

[Operator Instruction] We will now move to Jeff Hung with UBS.

Thanks for taking the questions. How generalizable are ACMG Phase I data given that both patients were female siblings.

Hi Jeff, thanks for the question. At this point there is no reason for us to expect that there is any sort of dimorphism in the penetration of Arginase deficiency between the sexes.

Okay. And then the plasma arginine level at pre-dose [indiscernible] for each subsequent dosing seems to define so the plasma arginine level do not appear to return to baseline. How confident are you on the differential effect dosing every two week of that trail versus the increased dose?

Well this is a dataset that then goes into our modeling for the subsequent study the Phase II with the repeat dosing every week. And we need to really learn from that dose escalation experience on what the dose for the repeat dosing will be as there might be expected to be say accumulation of the pharmacodynamic effect overtime that will remain to be determent with our trial.

Okay. And then the last question around that 40 micro molar level, I guess the patients stopped after a different number of dose. So then in the commercial setting would you expect patients require regular monitoring of plasma arginine levels to determine if they need to hold off on treatment and so the levels returns above that 40 micro molar?

That all remains to be determined as we continue with our development program.

Okay, thank you.

Thanks for your questions Jeff.

At this time we will hear a question from Ian Somaiya with BMO Capital.

Thank you and congratulations David and Charles on the encouraging results. I had a couple of questions, I mean one maybe just housekeeping. The plan for the study was to enroll up to 10 patients obviously and evaluate up to 7 doses. Do you feel comfortable in the sort of where you're ending up from a dose standpoint I guess you've already made a decision on the dose schedule?

Hi Ian thanks for the question. We're comfortable with the doses that we've achieved for these two patients, and the design of the Phase 1 as a single ascending dose study effectively dose titration on a per patient basis I think really provides us with confidence going forward into the Phase II portion for each patient and the dose that they will receive. Does that help?

It does. And just from the FDA standpoint, are the questions related to evaluating 1102 in younger patients. So are we just looking at what I guess different level of safety a bit of caution on the safety side or are there uniqueness in terms of the analysis that they have asked of you. Just good to know what the line of thinking as a line of questioning coming from the FDA?

So the FDA is really interested in understanding in more detail the risk benefit of dosing children. So we’ve provided them with the appropriate background information on the prevalent population and the severity of the disease.

Okay. And just given the at least the safety data from these two patients as well as the data you've generated in the cancer setting and as you mentioned the higher doses. Do you feel like there is potential for delay from the timeline that you've laid out?

I have no way of predicting of how the FDA is going to respond Ian, but we are confident in our approach and in fact we have IRB approval for the protocol at a couple of sites. So I think that by independent review at least the risk benefit has been evaluated. And so we're looking forward to moving ahead with the trial as we get the FDA feedback.

Okay. And I know you mentioned that the goal of the next round of studies, set of studies would be to link blood arginine to clinical benefit? And just given the variability in the presentation of the disease just curious what endpoints you would look at when we think about sort of the younger patient versus the two older patients that you have data from in the part 1?

Thanks for the question Ian that’s really an important topic that we spent quite a bit of time studying and coming to a conclusion on. The trial design is available on clinicaltrials.gov for those of you that are interested. We are really focusing on really three domains principally a neurological and neurocognitive together with biochemical endpoints for example such as live function and so forth. For the neurological we are looking at seizures for example, abnormal muscular tone spasticity as measured by specific spasticity scales in addition to walk test for example. And then also evaluating neurocognitive function with a variety of tools that test executive function and other elements. And clearly these have to be tailored in an age appropriate manner to the patients in question. And whether for example is speech function appropriate to measure in a 2 year old as oppose to 12 year old for example. So there is some neurons there as well, but I think with the range of endpoints that we have as we line those up against our natural history study. I think we’ll be in a good position to understand. We hope the clinical impact of Arginase in lowering arginine in these patients.

Okay. And if you just allow me, I have two more questions. Just given the safety profile that we have observed to-date, just curious how much efficacy data the FDA want to see in the pediatric population to consider approval? And from an endpoint standpoint what matters most to them, have you gotten any feedback in that regard?

We have not.

Okay.

But our operating assumption is that normalization of blood arginine would be the primary end point and we need to link that to trends in stabilization or trends in improvement in clinical signs and symptoms. And as you look at sort of a basis symptom complex of the seizures, spasticity and neurocognitive decline, you see any one of those or a combination of two of those symptoms in children emerge and then before they are 10 years old you will see all three. And so you could imagine how a child that’s having seizures if we can show that we’ve obviated or reduced the frequency of those seizures for example or hyperammonemia crisis might be really meaningful clinically and linking that back to control of arginine.

Right. And the last question related to the guidance. As you think about your plans to potentially evaluate 1102 in combination with potentially check point inhibitors, different IO drugs, the guidance implies that you’re likely going to do some sort of an agreement data sharing agreement get access to the commercial drug the IO drug. Is that am I reading into it correctly and would just give us a sense for timing of that study and if there is likely to be a partnership what the timing of that could be?

Thanks for that question, on the cancer program in. We certainly have a strong aspiration that we would enter into some sort of an agreement with the company that has an approved IO therapy and we’re working to go down that path. At this point I can’t make any prediction on the timing there, but my aspiration is that when we complete the dose escalation in patients with late stage solid tumors that we are in a position to progress down that path.

Okay, thank you very much and congratulations again.

Thank you, Ian.

We will take the final question from Jerry Isaacson with LifeSci.

Hi, good afternoon guys. Thanks for doing the call today and thanks for taking my question. Unfortunately, it looks like the other analyst covered most of my questions pretty thoroughly, but I do have a couple of things. First of all, Charles, I just want to confirm that you said that this was a call that was coincident with results and you don’t plan to doing quarterly call going forward?

Hey, Jerry. Yes, that is correct our anticipation here going forward was to do these around clinical updates not necessarily around our timing of earnings. So this one just happen to work out well and that would be a good time to reset everyone for the status of where the company currently is.

Got it, thanks. And then just one other thing, David, I wanted to talk a little bit about the poster that you’ll be presenting tomorrow and I am sure you can get into the exact details and maybe you could talk about strategies and kind of problems opportunities you see with this postnatal testing?

Thanks, Jerry for that question. Happy to discuss the abstract has been presented and what we know what I can tell you is that unlike many rare genetic diseases, our arginine has been recommended on the secondary panel for newborn screening. And because it’s in immuno acid and readily detected it is actually part of the primary panel in over 30 states. However, due to the variation in metabolism of newborns the raw data or the raw level of arginine varies quite a bit. And so the data really isn’t used and how it is handled from state-to-state various considerably. So we looked at every state including the District of Columbia and what their standard and practices here and it’s different in every state. And so what we did is we took the lead from a publication that came out several years ago in California, New York where we were able to access the legacy testing data. We were able to show that instead of using raw arginine levels you actually use a ratio of arginine to another immuno acid that you rapidly or dramatically improve the sensitivity and specificity of the test. So I think we’re really in good shape to -- as we look to taking our product candidate potentially to approval to really line that up with having effective newborn screening in place by that time.

Yes, that actually what I was thinking as I imagine the availability of therapeutic to treat the disease would certainly encourage people to do more thorough screening?

Agree.

Okay, good enough. Thanks guys, I appreciate it.

That's all the time we’ve budgeted for today’s call. I’ll now hand the call back over to David Lowe for final comment.