Welcome back, everyone. We have an update from Clene Inc., trades on the NASDAQ under the symbol CLNN. It is a late-stage biopharmaceutical company focused on improving mitochondrial health and protecting neuronal function to treat neurodegenerative diseases. Happy to welcome back President and CEO, Rob Etherington. Welcome back, Rob. Let us jump right in due to time. Now, congrats. There has been lots of positive news coming in lately from Clene, so give our viewership an update, including the ongoing discussions with the FDA, the status of the NDA filing, and some upcoming inflection points. Thanks for hosting again, Anna. It is a pleasure to see you. Literally, I guess it is now eight days ago, Clene announced the outcome of 90 days of work. Just to remind your viewers, we met with the agency in late March. The agency sent us in early May, and we announced this, I think it was May 3rd or May 4th, what the agency asked us to do, and I am actually holding these minutes from the FDA here in my hand. Just to give you some sense of that, and I think it is helpful to see a direct verbatim. The agency said, "The proposed data may be capable of supporting a submission and review of a New Drug Application under the Accelerated Approval pathway for the treatment of ALS, but we want you to give us a lot of neurofilament light data." They actually said, their exact words were, "We need you to demonstrate the evidence of effectiveness of CNM-Au8 on reducing neurofilament and show us that the magnitude of change in neurofilament is connected to clinical benefit." We have been working on exactly that for 90 days and announced last Monday, a week ago Monday that is, that we have seen a survival benefit that is specifically concentrated in participants with the neurofilament biomarker response. I am going to give some context to that in the next few minutes. Basically, if patients on our drug are declining or stabilized on their neurofilament, those are the ones that are expressly living significantly longer than a series of concurrently randomized controls from the HEALEY study. We also showed, and this is the first time Clene has showed this, and we have been asked for this for three years, that there is a functional benefit in patients that have a neurofilament decline or stabilize. For your viewers, that is either ALSFRS or SVC. SVC is slow vital capacity, my ability to breathe. My intake and outtake of breath is my slow vital capacity. What we saw is that the functional benefit, that is an ALSFRS change, that stands for ALS Functional Response Scale. It is this very important scale for people with ALS. The FDA has levered ALSFRS for three decades. In fact, that is exactly the primary endpoint in almost all the failed studies, including Clene's. What we found is that though we did not see it in the primary efficacy endpoint from HEALEY, we see from HEALEY that those individuals who have a neurofilament decline or stabilization are expressly the ones that are getting the benefit on function and stability. This is absolutely critical because let me go back to what the agency has asked us for. The agency said this. The agency noted that neurofilament could serve as a reasonably likely surrogate endpoint, but we need to provide information between the connection of this reported magnitude of neurofilament change and the clinical benefit. That is exactly what we spent 90 days, three months, the months of May, June, and July organizing. Now we are at the final throes of the final pieces of submission of what is called clinical study reports that all go into this very large package of New Drug Application to the agency, and we have stated we are going to send that at the top of the fourth quarter. Just to be clear what we have done, let us go through the data real quick and just highlight and contextualize this. When I say survival and function, I mean that patients who are randomized to CNM-Au8, they had a 74% lower risk of death after 12 months to these controls. That was a p-value of 0.1. I mean that survival that improved in those patients who declined or stabilized, and if we look over the full follow-up period, that is a p-value also of 0.3, and that full follow-up period is actually four years. When I talk about ALSFRS and SVC, that is also significant, a p-value of 0.3 for ALSFRS and 0.03 for SVC. We also were asked by the agency, they said this, and again, I will give some context. They said, "We agree that neurofilament is prognostic," which means higher neurofilament levels lead to more mortality, "but Clene needs to show both correlation and causation." Causation is a specific biostats approach. In the data that we have just shared, a lot of your viewers might not be so familiar with what the agency is actually asking for, but we have showed that if we look at survival benefit, it was actually concentrated in neurofilament responders, and this was able to be shown with a randomization-based causal analysis as well, exactly what the agency asked for. Taken together, this comprehensive package is now going to the agency. We have included our VISIONARY-MS data, but really the crux of the issue is going to be that we have a drug that is very safe. We now have 1,250 collective patient years. We have people on drug collectively now, or not collectively, but consistently for 6.8 years, still on drug. In ALS, that is remarkable. People that started our drug in 2019 that are still on drug today, and we know these names. They've been key advocates for us. The agency's asked for all this efficacy data connected to neurofilament benefit that they can tie the neurofilament drop to a clinical benefit. We think and are pretty confident about the package we're sending. The agency will then take all of this, review it, and then decide by possibly the end of the year, is our hope, if they're on time, for whether or not we have a PDUFA date, which is a timeline of review. That timeline of review would take Clene to the possibility of a commercialization decision by early summertime in 2027. We're pretty excited. It's been a bucket load of work. It's been a ton of effort to get to this point. It's taken us a bit longer than anticipated to checkmark through all the things the agency asked us to do in the May minutes, but we've now got to the end of that. We're now finalizing the pieces to submit to the agency in the coming period, and we're super excited to do so. Wonderful. Congratulations on that. A few questions for the time we have left. How consistent was the NfL response across HEALEY ALS, RESCUE-ALS, and the expanded access program? That's actually absolutely critical, is the expanded access that the National Institutes of Health sponsored was a 10% reduction there, as well as a 10% reduction in HEALEY. We remain one of the only, if not the only, programs to see a double-blind, statistically significant reduction in neurofilament in a phase II program. That was HEALEY. The same percentage reduction, roughly, was seen in the EAP population, which are much sicker. That's the same. The interesting thing about RESCUE, and we announced this actually in our press release a little bit ago, is we used RESCUE as, if you will, a second proof source to show that we saw the same benefit of reduction in RESCUE that we were seeing in HEALEY, and we did succeed that. We were quite thrilled by that outcome also. Is the strongest argument for CNM-Au8 the biomarker reduction itself, or the fact that biomarker changes appear to correlate with survival? It's the latter. The agency has in their statute that there needs to be a surrogate endpoint change, and we have that. They've been very clear, there needs to be connection of the neurofilament drop to clinical benefit. Let me just read again the agency's language to add context to your question. We need to see the evidence of effectiveness of CNM-Au8, its ability to change neurofilament, and to show that neurofilament change is, I'm quoting now, "reasonably likely to predict clinical benefit." That's exactly what we've done. We've looked at that drop, which is relevant. Again, as I say, we're the only phase II program to have seen such a drop, but we need to show very definitively, as we've announced in the press release a week ago, and as constituted a fair piece of what we've submitted to this agency, we will be submitting to this agency in the coming period, we need to show that it's clinically benefit connected. When I say clinically benefit connected, I mean what I said at the beginning, that a survival benefit is concentrated in patients that have a neurofilament drop, and a functional benefit, again, in functional ALS, ALSFRS, breathing function again, is concentrated in a patient with neurofilament biomarker response whilst on CNM-Au8. Wonderful. Thank you, Rob, for this update. It was brief, but it was impactful, and we appreciate you coming back on this conference. Thank you. It's a pleasure. All right, everyone, we'll be right back.