Efficiency. Both of these indications have the potential for near-term commercial launches, and we're well-capitalized to bring us through these milestones. I'll talk in a little bit more detail about what these rare diseases are, but galactosemia and SORD deficiency are both rare diseases that involve sugar metabolism. In the US, it is November 28th, which is just a few weeks away, and we're simultaneously under review in Europe, and we're expecting a CHMP opinion in the first quarter of 2025. The second rare disease called SORD deficiency, which we'll also talk about in more detail, is a rare neuromuscular disease. We met this past summer with the FDA and aligned on a submission under accelerated approval for SORD deficiency, which we're planning to submit in the first quarter of 2025. Aldose reductase is a target enzyme that govorestat inhibits. It's the first enzyme in the polyol pathway of alternative glucose metabolism. And this is an enzyme that isn't normally used to metabolize sugars like glucose and galactose, but when sugars build up at high levels, this enzyme becomes active and starts converting that sugar to a sugar alcohol, which is toxic to many cells, especially neurons. So we've developed govorestat for treatment of these two CNS rare diseases simultaneously. Galactosemia, which is a rare progressive metabolic disease, is affecting about 3,300 patients in the U.S. and a little over 4,000 in Europe, so it's a combined population of about 7,000 patients. And SORD deficiency, which is a rare neuromuscular disease, an axonal neuropathy, that affects between 3,500 and 5,000 patients in the U.S. and a little bit more in Europe. Originally, the estimates for SORD deficiency were 3,500, but we're understanding now that the disease is a little bit more prevalent than scientists originally thought. For both of these indications, we have orphan designation, we have pediatric rare disease designation on galactosemia, and again, they're in the very late stages of regulatory review and submission soon for SORD deficiency. I think it's important to note with govorestat that this is an oral small molecule. So as a small molecule, it's relatively easy and cost-effective to manufacture. We have a long IP runway. We have composition of matter through 2037, not factoring in extensions. We've built very strong KOL relationships and patient advocacy relationships over our years of development, and there's a strong commitment on both sides to both evaluate the potential of this drug and to ensure that it gets to patients quickly. What's nice about these two different rare diseases is that even though they're treated by different specialists, galactosemia is treated by metabolic geneticists or medical geneticists, and SORD deficiency is treated by neuromuscular specialists who tend to be neurologists by training. These two specialist groups are almost always at the same centers of excellence, so we can really leverage our relationships, our development, our sales forces as we move forward to target both indications, so going into a little bit more detail on galactosemia, it's a progressive metabolic disease where patients are unable to metabolize the sugar galactose, and galactose is a sugar that's found in foods, but it's also synthesized endogenously by our bodies. Because galactose is found in foods, there is mandatory newborn screening for galactosemia in the U.S. and in most E.U. countries. It's a blood spot test that's done on infants within a few days of life, and it's important to identify infants with galactosemia because they need to go on a galactose-restricted diet in order to survive, and unfortunately, prior to newborn screening, which became mandatory in 2005, many of these infants did die within a week or so of birth, so there's newborn screening. The population is 100% identified. Every parent that has a child with galactosemia knows that their child has this disease, and they start a galactose-restricted diet within a few days of birth. For infants, that's a soy-based formula, and they go on to maintain a galactose-restricted diet for the rest of their lives, and that keeps them alive. However, their body is also synthesizing galactose endogenously, and no amount of dietary restriction can stop that from happening. It's because of the endogenous production of galactose that they develop a toxic metabolite of galactose called galactitol, and this causes neurological complications that progressively worsen over time with age. These include behavior and psychiatric abnormalities, cognitive issues, low IQ, problems with memory and processing. It affects activities of daily living. As these children grow and become adults, they're unable to live independently. They can't care for themselves. It affects adaptive skills and also fine motor skills, and patients with galactosemia develop progressive tremor. It also results in seizures. All of this creates a very substantial burden on patients and families caring for those with galactosemia. It's a terrible disease, and there are no treatments currently approved for galactosemia, so govorestat is potentially the first treatment available for these patients. What's interesting about galactosemia is that it's not actually the galactose itself that's harmful to these patients. It's a metabolite of galactose called galactitol that's converted by the enzyme aldose reductase. That's why targeting aldose reductase with an inhibitor like govorestat to stop production of this toxic metabolite galactitol is an approach that can prevent the long-term complications in these patients. By blocking aldose reductase activity with govorestat, we instead shunt galactose through a non-toxic pathway. A different enzyme called galactose dehydrogenase instead metabolizes galactose into a benign product called galactonate, which is then removed from the body as glucose and CO2. In our clinical studies in both children and adults, we've shown that govorestat treatment quickly and effectively reduces galactitol levels in the blood. In adults with galactosemia, we also went on to show that galactitol reduction in the blood reflected galactitol reduction in the brain. In pediatric patients with galactosemia, we showed that galactitol reduction resulted in a positive effect on the symptoms that caused the neurological complications, things like behavior, cognition, adaptive skills, and tremor. govorestat has been safe and well tolerated. We have more than three years of continuous use in patients with galactosemia. Since galactosemia is a progressive disease, you can see that on the measures that affect these patients on behavior, daily living skills, adaptive skills, cognition, and tremor, the placebo-treated group in our pediatric study declined over the 18 months of the trial. This speaks to how quickly this disease moves, how urgent it is to treat these patients. Over just 18 months, you could actually see clinically relevant worsening of disease in the placebo group. In the govorestat-treated group, you saw either stabilization of disease, as we're showing here on Behavioral Symptoms Index and withdrawal, or you saw an actual improvement versus their baseline, as we saw in things like social skills and cognition. So govorestat is either stabilizing the disease or improving it in some cases, while in the absence of treatment in the placebo group, these patients declined. We have a very substantial safety profile of govorestat, both in healthy volunteers and classic galactosemia patients, and we'll talk in a few minutes about the SORD deficiency program, which is producing even more safety exposure data. But govorestat has been very safe and well tolerated. It's an oral once-daily suspension, so it's a liquid suspension that's easily taken by both children and adults. The burden of taking the drug is very low. It's easy to be adherent and persistent on treatment, and the safety profile was extremely well tolerated. You can see here that many of the patients that were on active treatment in the clinical trial have continued on in the expanded access program or compassionate use program and now have been on govorestat for more than three years. The patients who were on placebo in our clinical trials crossed over to open-label extension of govorestat and have now been on treatment for about 18 months, and I'm sure everyone has noted our PDUFA date is right around the corner, so we have been preparing for commercial launch. We've taken steps that I think are appropriate, building a right-sized and experienced commercial team every step along the way. We've been driving disease awareness and education both amongst the physician community and the patient and caregiver community. We've been very engaged with physicians and payers. And again, as mentioned, this is all of the commercial infrastructure that we've built for galactosemia, can also be leveraged for SORD deficiency. We've also built extensive patient support and access services for the galactosemia community, which again will also be meaningful for the SORD community when we get there. We built disease state education programs that were highly engaging for both physicians and patients. This program was originally called Galactosemia Together, which we strived to educate both patients and physicians on the mechanism of the disease, the burden of the disease, the urgency to treat, and of course, where appropriate, the mechanism of govorestat treatment. We've expanded this with Applied Connect, which is our patient access and services program. And I think these programs have suited us well. Our market research has shown that 89% of parents and caregivers would request govorestat once approved, and 80% of physicians are aware of govorestat, mostly medical geneticists, but high awareness also among general HCPs. When we asked those prescribers whether they would prescribe govorestat, 56% said that they anticipate prescribing govorestat in the first year and 90, sorry, in the first six months and 90% within the first year. 83% of payers recognize the high unmet medical need of govorestat, which is important with a rare disease and achieving favorable pricing. Moving over to SORD deficiency, this is a rare neuromuscular disease that presents as an axonal neuropathy. SORD deficiency is actually a subtype of Charcot-Marie-Tooth disease or CMT, and it's caused by genetic mutations in the enzyme sorbitol dehydrogenase, which is the enzyme that actually follows aldose reductase in the polyol pathway. I'll show you that mechanism in a minute. This is a relatively newly identified rare disease. Prior to 2020, these patients were symptomatically diagnosed as having CMT or Charcot-Marie-Tooth disease of unknown genetic cause, and it was a whole genome sequencing effort in 2020 that identified the sorbitol dehydrogenase enzyme and mutations in this gene as the cause of CMT in about 10% of CMT patients, so these patients have now been recategorized as instead of having CMT of unknown genetic cause, they have SORD deficiency, and the disease typically presents clinically in the teenage years. The average age of onset is 17. These patients generally present with lower limb deficiencies. They're tripping and falling. They're having difficulty running, keeping up with their peers. They're probably having difficulty going up and down the stairs and with balance. Many of these patients have foot drop, which is very easily recognizable by physicians. It does, over time, lead to decreased mobility and lower limb function. Eventually, these patients will end up in a wheelchair. In some cases, it does also develop into upper limb symptoms, and patients also report increased fatigue and pain. Originally, there was a generalized prevalence of 3,500 patients in the U.S. with SORD deficiency, but new mutations have been identified in the last few years, and scientists have now expanded that prevalence to about 5,000. And with all new rare diseases, we expect that may continue to increase in prevalence over time as more mutations and prevalence are measured. So aldose reductase, as discussed a few minutes ago, is the first enzyme in the polyol pathway of alternative sugar metabolism. Normally, in the case of glucose, aldose reductase converts glucose to sorbitol, and then the enzyme sorbitol dehydrogenase converts sorbitol to fructose, and it enters another metabolic pathway. In healthy people, only about 1% of our glucose is metabolized through this pathway, so it's a very low level that's going through the polyol pathway and ever entering aldose reductase or seeing sorbitol dehydrogenase. However, patients with SORD deficiency are missing the SORD enzyme and so even though it's only about 1% of your glucose that's going through this pathway, it gets metabolized by aldose reductase from glucose to sorbitol, and then it has nowhere to go and sorbitol builds up inside the cells. It causes metabolic derangement, mitochondrial dysfunction, energy depletion, and this eventually results in deterioration of the motor neuron and results in the difficulty walking and the symptoms that we see these patients presenting with. By blocking aldose reductase activity, we can stop that production of glucose to sorbitol so that even though these patients are missing sorbitol dehydrogenase, there's less sorbitol being produced, and the deficiency in that enzyme has less of a consequence, so we've studied govorestat in a few clinical trials now in patients with sorbitol dehydrogenase deficiency, first focusing on reduction of sorbitol levels in their blood. As we saw in galactosemia, govorestat produces a rapid and sustained reduction here in sorbitol. You see reductions within the first day of treatment, and they're maintained throughout the treatment duration. We initially started in a pilot study, and then we transitioned into a phase three study called INSPIRE. And this study was set up to look at sorbitol reduction, but also clinical outcomes, things like 10-meter walk-run test, four-stair climb, six-minute walk, and the patient-reported outcome measure that's relevant in CMT patients, which is called the CMT Health Index. And our goal here was not only to show sorbitol reduction in a double-blind placebo-controlled trial, but to show that that sorbitol reduction correlated with positive changes on the clinical outcome measures. And so at a 12-month interim assessment in this trial, we did demonstrate that we were highly statistically significant on sorbitol reduction and also showed a statistically significant correlation of sorbitol level and changes in sorbitol with changes in clinical outcome measures. It was on this basis that we met with the FDA this past summer to talk about a potential submission under accelerated approval, and the FDA agreed that this could be the case for us, and we have been preparing our NDA submission. We plan to submit for SORD deficiency under accelerated approval in the first quarter of 2025. This study has now been converted to open-label extension from double-blind, so there's no longer a placebo group here. Everybody has been transitioned over to govorestat treatment, and we're continuing to collect long-term safety data. Again, in patients with SORD deficiency, govorestat was safe and well tolerated, and we haven't seen anything here in any of these patient populations: healthy volunteers, classic galactosemia, or SORD deficiency that's concerning. In both galactosemia and SORD deficiency, we've been very fortunate to have very strong and involved patient advocacy groups. In galactosemia, there's one advocacy group. It's called the Galactosemia Foundation. It's a parents-led organization, and they've been very engaged with us all along the way from development through regulatory review. And the same is the case with SORD deficiency. So the patient advocacy groups involved in SORD deficiency are the CMTA and the HNF, also mirroring the organizations in Europe. And they've been our partners in doing disease state awareness, making sure that all patients who might have previously received a diagnosis of CMT of unknown genetic cause get correctly diagnosed as having SORD deficiency. So to sum up, govorestat is in late-stage review and development for two rare diseases: galactosemia and SORD deficiency. These are both rare diseases with high urgent unmet medical need. They're devastating progressive diseases with no treatments approved, so there's an opportunity for govorestat to really be life-changing for these patients and to offer the first potential opportunity for treatment for both of these diseases. For galactosemia, we're under review at the FDA with a PDUFA date of November 28th this month, and our MAA is under review in Europe, again expecting a CHMP decision in the first quarter of 2025. With SORD deficiency, we are planning to submit our NDA in the first quarter of 2025, so we have the potential to have two launches in very close proximity to one another, and we've spent a lot of this year preparing for that. So I think we're very well prepared. We're in a good place to successfully launch in both of these indications, and we're excited about the evolution of the company at this important time as we go from clinical stage to potentially commercial stage. Thank you, everyone, for your attention. I'm sorry that we can't do a Q&A at this presentation, but thank you.