Thanks, Nick. Good morning, everyone. Thanks for joining us today for Oppenheimer Rare and Orphan Disease Summit. My name is Justin Kim. I'm one of the research analysts at Oppenheimer, and it's my pleasure to welcome the Regulus team, CEO, Mr. Jay Hagan, to give a presentation on the company. Please take it away, Jay. Thanks, Justin, and thanks to the team at Oppenheimer for including us in today's Rare and Orphan Disease Summit. We're pleased to be providing an update on our ADPKD program. That'll be the main focus of the discussion here. I will be making forward-looking statements. Actual results may differ materially from those expressed or implied today. I encourage investors to read risk factors associated with our business in our SEC filings, including our most recent 10-Q. Bear with me one second here. I've got the Blocking my screen. In terms of recent highlights, we announced this morning in a press release, and we'll be sharing today an update from the first cohort of our phase Ib study of patients with ADPKD. We've been able to successfully demonstrate target engagement, so hitting miR-17 with a significant increase in key biomarkers in the first cohort of patients. The safety profile that we've seen to date is very encouraging with anticipated pharmacokinetic properties as well. We're completing our preparations for planned FDA engagement around the remaining partial clinical hold requirements sometime mid-year. Meanwhile, our next-generation ADPKD compound is advancing towards the clinic with an IND submission anticipated in early Q1 of next year. Importantly, we've recently completed robust non-GLP tox study at significantly higher exposure levels, indicating a differentiated product profile as designed. Late last year, we were able to successfully restructure our partnership agreement with Sanofi, as well as our debt agreement with Oxford, where we received $10 million from Sanofi for achievement of milestones and transfer of certain materials to them. With that, we were able to repay $10 million of principal to Oxford, and in exchange, received an extension of the interest-only period through 2021, resulting in a significant savings for us this calendar year. We have about $4.6 million remaining, which we'll begin to repay next year. With all that, we completed a nearly $20 million private financing with a top group of existing as well as new institutional investors. We entered into the first quarter, as we reported with our 10-Q, with $31.6 million in cash on the balance sheet, which was slightly ahead of the amount we ended the year with. We were able to utilize our ATM facility through the course of the first quarter judiciously to increase our balance sheet. We're burning about $2 million a month, with this cash, we have a significant runway through the first quarter of next year, during which we anticipate significant additional milestones, which we'll talk about at the end. Just a quick overview about Regulus. Regulus was founded as a joint venture between Ionis and Alnylam, where they combined their technology and intellectual property to design oligonucleotides to direct them against microRNA, which are upstream of where those two companies focus, which is on messenger RNA. MicroRNA are short non-coding RNA that bind to and control expression of messenger RNA. You'll hear a little bit about that when we walk through the mechanism with our lead program in ADPKD. We do have two programs in the clinic, Lademirsen or RG-012 in Alport syndrome, which is being managed by our partner, Sanofi, as well as RGLS4326 in autosomal dominant Polycystic Kidney Disease. We focus our pipeline on targets where novel biology and areas of unmet need provide a competitive advantage for us in terms of pursuing a microRNA target. Importantly, we've been able to further optimize that foundational technology to develop a proprietary targeting of oligos to the kidney with these anti-miRs, and we filed IP on that. As I walk through a bit about the preferential distribution that 4326 possesses, you'll understand better how we can utilize that for other genetic kidney diseases. Quick snapshot on our pipeline. The Lademirsen or RG-012 for the treatment of Alport syndrome is currently enrolling in a phase II randomized global program. We'll touch on that in just one second. RGLS4326 now is in the second cohort of the phase Ib study in patients with ADPKD. We do have a next-generation molecule, as I mentioned earlier, advancing towards the clinic with an IND anticipated in Q1, and then additional research programs in kidney disease behind that. Programs beyond just nephrology-focused in infectious disease, CNS, and cell-based therapies. Just to touch on the Sanofi partnership, this goes back to a partnership that the company struck prior to going public near its founding, focused on miR-21 and miR-221 in the areas of fibrosis and oncology, respectively. Lademirsen advanced to the clinic as a first indication where that molecule binds to miR-21 to try to reduce the fibrosis associated with the disease. Importantly, we've been able to complete a chronic dosing study with a handful of patients that rolled over into that open-label extension after a biomarker study. Excuse me, after a kidney biopsy study. We were able to show that treatment was well-tolerated. We dosed chronically for a year, every other week. No SAEs reported and had very promising trends in key disease biomarkers. Prior to that open-label extension, we were able to show with biopsies pre- and post-dose that we were able to achieve an exposure in the kidney that would be predictive of efficacy based on the animal models, as well as binding to the target miR-21. We recently received, as I mentioned earlier, a $10 million milestone. We're eligible to receive another $25 million milestone upon completion of phase II under certain circumstances. Now turning to our ADPKD program. This is an orphan disease, and it's due to a mutation in either the PKD1 or PKD2 genes. It's a haploinsufficiency, though, where you have one functioning allele. These mutations lead to a proliferation of fluid-filled cysts in the kidneys, ultimately leading to end-stage renal disease. About 85% of the diagnosed patient population have a mutation in the PKD1 gene, with the remaining 15% having a mutation in the PKD2 gene. The PKD1 mutant form tends to be a more progressive disease or aggressive disease. There are about 160,000 diagnosed in the U.S. with an ICD-9 or 10 code, of which three-quarters have not yet progressed to dialysis. As you can see, they have a very significant health burden, with those that do progress to dialysis as understood its impact on quality of life, and about 50% of patients ultimately require dialysis by the age of 60. There are estimated to be a significantly higher number of people with the disease based on demographic trends. However, it's believed to be underdiagnosed because there hasn't been anything available to treat the disease until the recent approval of tolvaptan from Otsuka a couple of years ago. A little bit more about the disease. It is the fourth leading cause of kidney failure in the U.S., and you have bilateral, meaning both kidneys get enlarged with these fluid-filled cysts. As you can see in the picture on the left, it grows quite large, up to 35 lbs. A healthy kidney should be about the size of a clenched fist. This, you can see, this is at the time of explant, grows as large as an American football. There are other extrarenal manifestations predominantly in the liver and as well as seminal vesicles and pancreas, but the primary organ of toxicity is in the kidney. There are other complications as well, hypertension and cardiovascular complications that go along with declining renal function. You can see on the right-hand chart, though, this cystic expansion doesn't lead to end-stage renal disease until later years in life, where it ultimately squeezes out normal kidney function. In terms of the competition, tolvaptan or Jynarque works through vasopressin. It was approved in April 2018 for the indication. It does have a boxed warning due to potential for drug-induced liver injury and thus requires a significant REMS program with restricted distribution where you need to have a clean liver function test before each new prescription is filled. Nevertheless, it has done quite well thus far, about $700 million in the U.S. last year and estimated to grow from there this year. In terms of what's in the development pipeline, there's bardoxolone, works through Nrf2 and currently enrolling a phase III program in ADPKD, and then venglustat from Sanofi, a molecule that's being repurposed from an earlier indication, currently in a phase II/III study working through the sphingolipid pathway. Finally behind that is a compound called lixivaptan, which works through the same mechanism as tolvaptan and will be anticipated to have a similar side effect profile due to its mechanism, where patients on therapy need to drink significant amounts of fluid due to thirst that's derived from taking the treatment and polyuria associated with that. I do want to mention venglustat as an example of where the FDA has provided now an opportunity for an accelerated pathway towards approval, that's been recently reaffirmed from the division where approval on an interim milestone of a reduction in total kidney volume compared to placebo is sufficient for an accelerated approval so long as a sponsor has enrolled a phase III cohort that would go towards a GFR endpoint. Offering an opportunity for more accelerated approval and consistent with the division's efforts to drive innovation in kidney disease. The preliminary product profile for our compounds here is that we're designed to bind miR-17, we'll talk about why that's important. It has been demonstrated to be overexpressed in both animal models of the disease as well in human ADPKD cyst cells. The consequence of that, it regulates PKD1 and PKD2 expression. We would anticipate that if successful, that we would be able to modify the disease by slowing the progression of cystic expansion, and we'll share some slides on that in terms of what we would have shown in animal models. That ultimately will result in a clinically significant reduction in height-adjusted total kidney volume compared to untreated controls and ultimately lead to a reduction in the decline in GFR associated with the disease. Obviously, an acceptable safety and tolerability profile would be required, and this would be a subcutaneous injection dosed every other week or potentially monthly based on the half-life in the kidney. How does our compounds work? In a normal kidney, in the cartoon at the top, you can see miR-17 has both direct microRNA targets, or excuse me, messenger targets, specifically PKD1 and PKD2, which encode for Polycystin-1 and Polycystin-2, leading to normal functional levels. With excess miR-17, you inhibit PKD1 and PKD2 expression, leading to reduced levels of Polycystin, that's been correlated with disease severity and cystic expansion. Our objective here with the bottom cartoon is to bind that excess miR-17, effectively enabling expression of the PKD1 healthy allele, leading to increased levels of Polycystin, ultimately reduce that cystic expansion. Now just a bit in terms of more of evidence of miR-17's role. On the left-hand side here, you can see that in animal models of the disease, the red being the PKD1 knockout and the blue being the PKD2 knockout, you have increased levels of miR-17, about 50%-70% higher levels of miR-17 than control animals. The right-hand side with in situ hybridization probes, you can see in the ADPKD kidney, higher levels of miR-17 compared to normal healthy kidneys. Why that matters here is you can see on the top two panels that, highlighted in the white window, you can see that this is the specific binding site on the three prime untranslated region of the PKD1 gene and on the right, the PKD2 gene. That sequence that you see there, GCACUUUA, is what miR-17 recognizes and binds to. When it binds to that, it keeps it from being able to be expressed, inhibiting it. On the bottom two panels, you can see here we can mimic the disease state by increasing levels of miR-17 with a mimic and show a repression of PKD1 and PKD2 expression. Now, if you mutate that binding site, it has no impact. Evidence here of miR-17's role in excuse me, decreasing PKD1 and PKD2 expression. One other point in terms of the top two panels, as is known about microRNA, they're highly conserved across species, lending credence to the notion of their importance in disease, from the human at the top all the way down through dogs, cats, bats, and so forth. That also is helpful in the context of designing molecules for preclinical validation. Just one quick slide in terms of what we're aiming to do here. This is a PKD2 knockout mouse, so not the same as the human condition. These have both alleles knocked out. You can see with treatment with RGLS4326, in terms of the picture there of the kidney, that the kidney doesn't get anywhere near as large, and that's quantified in the bottom left panel, where kidney weight to body weight or normalized kidney weight is reduced compared to untreated controls. The amount of proliferation of cysts quantified on the middle lower panel. That's associated with an increased expression of PKD1 and PKD2, the way the molecule is designed to act. We've been able to show in human ADPKD cyst cells, so these are cells that are taken at the time of explant when somebody goes in for a kidney transplant due to the disease, we're able to harvest cyst cells, grow them up in a 3D Matrigel culture. We've been able to show in those systems, it's been published, that we can reduce cyst count and total cyst volume. Here we also show that we can increase levels of Polycystin- 1 and two in vitro, the gene products of PKD1 and PKD2, or the protein products of those genes. A bit more about why it matters. On the left-hand side here, you can see in samples of ADPKD patients versus healthy volunteers, you can detect a clear difference in levels of Polycystin- 1 on the left panel and Polycystin- 2. This is in using the assay that we've developed in collaboration with the team at University of Kansas and Dr. Chris Ward lab, where we're able to isolate exosomes excreted in the urine that are packaged with Polycystin and measure differences between healthy volunteers versus disease patients. You can see they're about around 100% or so higher than in disease. On the right panel here, we can also correlate disease severity on the horizontal axis here. You can see height-adjusted total kidney volume correlates with levels of Polycystin. The lower the level, the higher the disease state. Now just jumping to a bit of genetic validation here. This is a bit more of analogous to the human condition. This is what's called a Pkd1flox/RC or hypomorph, where one allele is knocked out, the other's a hypomorph to make protein. You can see these are animal experiments that take quite a bit of time here. These animals live median survival about 200 days. These were published back in 2017 by our collaborator, Dr. Vishal Patel at UT Southwestern. You can see on that background, if you knock out miR-17, that you have quite a significant impact on mortality as the Kaplan-Meier in panel B. If you look at the serial MRIs, you can see the kidneys don't get anywhere near as large, and you're able to preserve kidney function as measured by creatinine and reduce proliferation. Clear genetic validation of the role of miR-17 in the disease. We've been able to recapitulate this with treatment of RGLS4326 in the same animal model, which will be hopefully published sometime soon. As I mentioned earlier, we've been able to identify a specific chemistry motif, if you will, or design, what we call our ShortMer technology, where we have preferential uptake in the kidney. These are naked oligonucleotides. They're not conjugated with anything in an aqueous solution. What we found is that when we get down below a certain length of oligonucleotide, that we have preferential distribution to the kidney. Normally with a longer oligonucleotide, you typically would get about 50/50 exposure in the kidney versus the liver, and here you can see we can direct the vast majority of the molecule to the kidney. On the right-hand side, you can see when we co-administer an antibody to the PS, that is the chemical modifications on the oligonucleotide or an antibody that you can see lining up all in the various collecting ducts and cyst cells. This is a technology now that we want to employ with other kidney-directed therapeutics, and it is unique to our oligonucleotides because we are not recruiting any RNase H-type activity with an antisense or SI approach where you simply cannot get a ShortMer to do that type of activity. A little bit on PK/PD. Here you can see with a single dose of a molecule quantified here on the left-hand side. You can see with the red line, it is rapidly cleared from plasma. We get about 70%-80% of the compound excreted in the full form, unmetabolized in the urine within 48 hours. You can see rapid plasma clearance, half-life of about six hours, I believe, in this model system. You get about tenfold higher exposure at a minimum, tenfold higher exposure and Cmax exposure in the kidney versus the liver with 1/2 -life of about two weeks in the kidney. In the right-hand side, you can see a very nice correlation between activity, the pharmacokinetics, and then the pharmacodynamic, as measured by miR-17 displacement, which lags about seven days from the dose. This is consistent with our other work where we see peak target engagement about seven days after dose target engagement, meaning binding to miR-17. That's relevant because when we get to the data that I'll share in a minute on the highest observed levels of Polycystin being 28 days after the last dose, it'll become clear our emerging understanding of the relationship with PK and PD as measured by Polycystin levels in the urine. Just a bit of a comparison here. This is an orthogonal model. Pcy model is a slower growth model here, and you can see with weekly dosing we're able to have a statistically significant impact on both kidney weight to body weight as well as cystic index. You can see we've also dosed quite low here, down to 1 mg /kg weekly in this model. We compare that with tolvaptan, the published dose levels that have been utilized to show efficacy of tolvaptan in an animal model. This is the only one where we've been able to see activity with tolvaptan. You can see we have an impact on cystic index where they don't. Now with these data, we are planning a combination study because that's an obvious question of how you might be incorporated into standard of care. Given that we have a different mechanism, we would hope that we can find a way to be used in combination with tolvaptan for those patients who are already on tolvaptan. In that same model, that pcy model, just another study we've done here where we've done serial MRI. You can see the pictures on the lower D panel here over time. We were able to then quantify the size of those kidneys on the right-hand panel E, where when you look at the green best fit line, you can see that we have basically arrested the cystic expansion compared to untreated. Whoops, sorry. I got auto lights. Where we've been able to arrest that cystic expansion here that you see in the disease models. Just a quick update on where we are with the MOA study. We've completed the SAD/MAD study, and we announced that earlier in healthy volunteers. The SAD up to 6 mg/kg, the MAD up to 1 mg/kg every other week times four. Well tolerated with no SAEs and dose proportional PK. The phase Ib is underway. We're currently recruiting a second cohort. We'll talk a little bit about the results from the first cohort in just a second. The first cohort was dosed at 1 mg/kg. The second cohort, we're coming down to 0.3 mg/kg. A little unconventional. The reason why we're doing this, though, is really to try to define a dose response curve. We'll talk about our expectations with respect to exposure in the kidney at different doses in just a minute based on our extensive PK work we've done with the molecule. We're obviously measuring safety and tolerability and pharmacokinetics in this renally compromised patient population, as well as employing that biomarker assay to measure target engagement and changes in Polycystin levels in patients. We're utilizing 13 sites across the U.S.. What we've been able to demonstrate here with this cartoon in this first cohort, that four doses dosed every other week at 1 mg /kg, that we achieve sufficient exposure in the kidney, which inhibits the miR-17 function, this excess miR-17, which then leads to a de-repression of the PKD1 and PKD2 genes, and ultimately leads to an increase in functional Polycystin, which then is packaged in these urinary exosome-like vesicles, which are excreted in the urine, which we're able to collect and then measure changes. What I want to make sure I emphasize here, there are a number of kinetic steps here that are different than what you might see with an ASO or siRNA approach, where somebody takes a tissue sample and measures changes in genes. Here this is downstream of that, protein changes, and then collecting that in urine upon excretion. There's more time involved here than, say, what you would expect with a siRNA or ASO approach where you take a tissue. What's beneficial about it is it's a non-invasive technique here that we can utilize here as we move forward in clinical development. These are the data, previously we described as greater than 50 and greater than 20. We wanted to share an update with investors at this important conference today. You can see here at the end of study at day 71, mean change in baseline in Polycystin- 1 and Polycystin- 2, you maybe can't tell, but it's 58% and 38%, respectively. Now with that ninth patient at day 71, it's actually moved the change in Polycystin- 2 to a statistically significant result of 0.026. PC1 moved quite a bit more. We believe that potentially the genetic mutational status may be driving this difference between the two, and we're working actively with our external thought leaders in the space to further understand the balance of Polycystin- 1 and Polycystin- 2 levels. As I mentioned in my introductory remarks, 85% of patients with the disease have a mutation in their PKD1 gene versus 15%, potentially leading to why we're seeing a higher change in Polycystin- 1 versus Polycystin- 2. Finally, these do form functional heterodimers at certain ratios that line cilia involved in flux. Additional data from this, as we mentioned earlier, treatment with RGLS4326 was well-tolerated by all nine patients with no SAEs. The reported AEs that we did have were mild to generally transient nature, just grade one AEs. The overall PK profile was similar to what we've seen in the prior healthy volunteer study. As expected, the half-life was a bit longer, about nine hours in plasma versus six hours in healthy volunteers, but with that type of half-life and dosing every other week, we see no accumulation in plasma. Cmax was a bit higher, likely due to slower excretion in a renally compromised patient population, about 3 mcg/ml versus 2 mcg in healthies. At higher plasma exposure, we would anticipate them to lead to higher because it's around in the plasma a bit longer, that you're going to see a higher exposure in the target organ, the kidney here. We're in the process of modeling that, but nothing concerning from a PK profile standpoint. Now what I mentioned earlier, in terms of where we expect to see a minimally efficacious dose, on the left-hand panel, we've taken all of our animal studies at different doses and measured the kidney exposure with those different doses. With that, where do we start to see a plateauing of efficacy, which is when we hit 90% inhibition of miR-17. This is using a proprietary assay that we developed called the polysome shift assay, so where we displace miR-17 from the polysome, and you can see that occurs in exposure of 11 mcg/g. With all this extensive PK work we've done to build the model to address the remaining clinical hold requirements, we can also utilize that data to understand what type of kidney exposure we'll see at different dose levels. At 1 mg/kg with either one dose or four doses on the far right-hand panel, you can see the predicted kidney exposure over time, and the one on the right is after the fourth dose, as evidenced by the days we show at the bottom. This is seven days post-dose, recall that that's when we reached the maximum miR-17 inhibition. You can see we've drawn a horizontal line at an exposure level of 11 mcg/g. The blue line is what we would predict at 0.3 mg / kg, and you can see we would exceed 11 mcg/g after the first or fourth dose. The red line is at 0.1 mg / kg. Importantly, the purple line is what we would model as we required to just exceed 11 mcg/g, and that's estimated to be somewhere between 0.05 and 0.17 mg/ kg. The reason why we provide a range there is because there's allometric scaling one utilizes to try to understand what's the anticipated exposure in a mouse versus a human, and these are taking the range of allometric scaling, one being no scaling and the other being the most conservative scaling assumptions between the two. We look forward to getting the results from our second cohort here, sometime mid-year Q3 timing, to see what kind of results in changes in Polycystin levels we see. Finally, as we disclosed earlier, we've been also working as everybody in the drug development field, and particularly in small molecule drug development, the team in the research lab is always looking to improve product profile and develop next-generation molecules. Our goal here was to optimize a new compound with a differentiated profile. We undertook a focused SAR campaign to engineer out a putative off-target activity believed to underlie the dose-limiting tox that was seen in the chronic tox studies at the top dose. At the same time, maintain all the beneficial attributes of RGLS4326, specifically the preferential kidney exposure as well as PK inhibition of miR-17 as well as duration of action, in vitro and in vivo efficacy models, favorable from physicochemical properties as well as good safety profile. This next-generation molecule has completed all of these studies above in terms of demonstration of in vitro, in vivo efficacy, inhibition of miR-17, preferential kidney exposure. As I introduced this, has completed a very robust non-GLP tox studies at significantly higher dose levels than where the dose-limiting toxicities was seen with 4326. IND enabling activities are underway with a regulatory submission in Q1 of 2022 for this compound. I do want to emphasize that we have completed chronic tox studies with RGLS 4326 with acceptable NOAELs to permit dosing of those durations. It's really a theoretical risk of longer-term dosing that remains a concern for which we need to build a model to predict exposure of extended duration and determine appropriate safety margins to any dose or dose frequency that we would like to advance further in the clinic with RGLS4326. Overall summary, FDA lifted the partial clinical hold when we completed the chronic tox studies and as I said, had acceptable NOAELs, and safety margins of those to permit initiation of the phase I study. The NOAELs were with the mid dose in both mice and non-human primates, which were at significant margins to the dose levels we're testing in humans right now. The healthy portion of the SAD/MAD was completed. When we received the requirements for the partial clinical hold, they included the need to build a model because available non-clinical PK data we had at the time of the hold was really inadequate to be able to assess exposure of extended duration to simulate what would happen if we dosed for a much longer time than in a chronic tox studies. We've completed those additional non-clinical PK studies, which form the basis of this model, and now we're working to input the final bit of data from the first cohort to predict exposure in humans of extended duration and discuss those with FDA. As I mentioned in my earlier remarks, we've seen significant increases in excreted PC1 and PC2, validating target engagement of miR-17 as designed. RGLS4326 has been granted orphan drug designation last year in July, and our next-generation molecule is moving towards the clinic with an IND anticipated in Q1. In terms of upcoming catalysts, we plan to engage FDA for feedback on the model, as well as where they are comfortable from a dosing standpoint to move forward, and that is all focused on safety. We anticipate top-line data from remaining RGLS4326 phase Ib cohorts. Cohort two, we anticipate in Q3 of this year. Based on where we are in enrollment right now, we are more than halfway through enrolling that first cohort. We will not initiate the third cohort. It's an adaptive design, as I mentioned in my earlier remarks, where we want to see the results from the second cohort and what kind of change in biomarkers before we choose the dose level for the final cohort. If we see continued significant trends in Polycystin- 1 and two, we'll go down to 0.1 mg/ kg. If we see it drop off, we'll come back up to 0.5 mg/ kg so that we can establish a three-point dose response curve in terms of changes in biomarkers. Potential resolution of the remaining partial clinical hold would come in the second half of the year after our meeting with FDA. We're on track with our next-generation molecule filing. We could be in the process of potentially initiating a phase II study for RGLS4326 in ADPKD patients, pending resolution of the remaining hold requirements here. That phase II could start sometime next year. Our near-term focus is really aimed at driving forward with this ADPKD program. The team and our Chief Scientific Officer, Dr. Denis Drygin, do continue to work in other interesting areas of targeting microRNA, but predominant focus of our resources and effort right now is advancing this program given our excitement around the target miR-17 and the extensive validation of its role in the disease. With that, we're happy to take any questions. Great. Thanks so much, Jay, for that really comprehensive update. Maybe just to begin, as you think about sort of second-generation compounds and sort of the full speed ahead sort of work being done on RGLS4326, do you envision that the sort of potential to demonstrate the translation of PC1, PC2 activity into sort of clinically relevant endpoints, could facilitate sort of a glide path for the Gen 2 program that sort of G en 2, if it did sort of a successful phase I, could become pivotal, that you could sort of leapfrog there, with the work being done for RGLS4326 potentially along the way? That's a great question, and that's exactly what our thinking is. If I was to share with you the structure, we're in the process of filing patents on the next gen. It's remarkable what very subtle changes in these molecules can have an effect. We started employing panel screens in all of our drug discovery efforts now to understand structure and activity. Particularly, we know on target it's designed in terms of a Watson-Crick base pairing to hit a specific target. We understand that. These do behave more like small molecules than I think was originally appreciated and the benefit of panels, which have been widely used in all small molecule drug development, helps you design molecules and identify potential off-target effects. With just a very small tweak, we've been able to engineer out the putative off-target effect. As we predicted with all of our in vivo and in vitro work, it looks a lot like RGLS4326 save for this one little bit. Yeah, we have a lot of optionality with this next gen. We're asked a lot about that, and particularly even in our partnering discussions with potential partners is how do we think about positioning the two. Either life cycle, we remain committed with RGLS4326 and believe that it can have acceptable safety margins. We look forward to engaging FDA on that. If our assumptions around dose and exposure are correct that I walked through earlier, and a dose of as low as 0.1 mg/ kg can be effective, we have very significant safety margins there and throughout the doses we're testing. Nevertheless, having a cleaner product profile, as our commercial colleagues would always say, is going to be more beneficial. There's a number of ways to think about it, either from a life cycle standpoint or, I think is what you were alluding to, de-risking the biology here and then having the ability to rapidly advance the next gen in favor of 4326. We have those options available to us and obviously it will be pending regulatory interactions and additional work we have to do here. I think what I want to make sure I emphasize is our enthusiasm for this target, miR-17, and its role in the disease. Our unique capability of targeting the kidney with our technology base and preferential uptake in the kidney with our ShortMer technology. Understood. Great. It's an exciting time for the company and really appreciate it. Wish we could continue further, unfortunately, we're out of time. Thanks again, Jay, and thanks everyone for tuning in. Terrific. Thank you. Take care. Thanks everyone.