Trades on the Nasdaq under the symbol CLNN. It's a late clinical stage biopharmaceutical company focused on improving mitochondrial health and protecting neuronal function to treat neurodegenerative diseases. Happy to welcome President and CEO Rob Etherington and CFO Morgan Brown. Welcome to the conference, gentlemen. Happy to have you today. Thank you. It's a pleasure to be back and good to see your listeners as well. All right, the floor is yours. Call me when you're ready for questions. Thank you. Some of you may be familiar with this deck, but I'll jump through it nonetheless and look forward to doing so. Clene is a pretty interesting company. You've seen a number of these forward-looking statements previously. I'll be making some forward-looking statements today as we plan and prepare for what we hope will come to pass in the coming months, and we are working accordingly to do that. That is indeed pioneering catalytic nanotherapeutic suspensions as a drug for the possible treatment of multiple sclerosis eventually, and amyotrophic lateral sclerosis potentially more on the soon side. What we're doing is targeting the improvement of the mitochondrial function, which you and I depend upon to power and to energize everything that gives you and I life. Indeed, impaired mitochondrial function and compromised metabolism of energy within the cell is what we need to presume occurs for your and my central nervous system to take care of everything that we rely upon for our daily housekeeping. It was mentioned in the introduction that we're a late-stage clinical. Just to be clear, we've completed five phase II proof-of-concept studies, including two in ALS. Because of the gravity of ALS, its devastation, the extraordinary compromise that this disease gives patients, it has been a long road to drug development. There are very few treatments. In fact, most of the world has one. Some countries have two. Some countries have at most three to treat this disease. Clene has been working for some time with a growing body of clinical evidence on this path. We also have a second program in MS, and we mentioned earlier that we are discussing that with the FDA right now to come to the next stage, phase III. I'll explain that a little bit in a moment. Now, what CNM-Au8 does is, excuse me, CNM-Au8 is basically oral administered. If you were blindfolded and didn't have any idea what you were taking between a glass of water at room temperature and our acid, you would not be able to tell the difference. As I mentioned already, we target energy metabolism. There's a penetration in the blood-brain barrier. That is a critical thing to occur. The volume that you see here is 60 mL. That's about a quarter cup. If you're using an American measuring system, 60 mL is a modest amount, about a couple ounces. What we're doing is driving, as I said earlier, energy into the mitochondria by raising NAD, by raising ATP, by reducing an output of this energetic system called reactive oxygen species. That taken together is enabling the energy that you and I require to keep us moving, talking, thinking, breathing, and effectively the way we move and walk and talk and eat and chew and breathe, as I often say it. One of the reasons why we're even able to be in front of the agency right now with this possible regulatory path is because of the extraordinary safety that we've seen with this asset. We have now over nearly a thousand, in fact, just over a thousand participant years of exposure to CNM-Au8. We have individuals that have been on our asset in our various studies up to five and a half years now, and we have still not a single related serious adverse event that has been attributed to CNM-Au8 across these clinical programs. That isn't to say we don't have any side effects. We have occasionally nausea, some headache, but on balance, we have no adverse effects across our program, and the asset is considered extraordinarily safe. Knock on our collective wood here, we're super grateful about that. If the patient can drink a glass of water or can take such water in their feeding tube, they can take our asset. Critically, our asset is not metabolized, which also means that our asset can be taken on top of whatever standard of care drugs the participant or the patient is already using. We ask the physician to bring the participants in our clinical studies to us or into our compassionate use on whatever therapies they best be on, and our drug is placed on top of those other assets. RESCUE and HEALEY, as I mentioned earlier with the brief slide, are our two phase II proof-of-concept studies. They both missed their primary endpoint. I want to be clear about that. They missed their primary endpoint. RESCUE was a nine-month study. HEALEY was a six-month. The amount of data that we've been otherwise able to see is very interesting because in both cases, we achieved clinical worsening. In both cases, we achieved a survival benefit, HEALEY in the pre-specified secondary endpoint phase. In both, and rather in the case of the HEALEY study, we also achieved a benefit during the pre-specified six-month period of a biomarker change in neurofilament. I'll talk about that a little bit further coming up. Now, as to our safety data, excuse me, survival data, the secondary endpoint in HEALEY was looking at time to death or permanently assisted ventilation. That is somebody who requires a mechanical ventilator to breathe for them at least 22 hours or more a day. 22 of 24 hours where I need to be on a mechanical ventilator is obviously a pretty onerous situation for their diagnosis. ALS clinical studies are assessed, as I say, either by time to death or whether I need that 22 hours of breathing assistance. We saw during the double-blind period a p=0.04 on that program. We saw also in the exploratory of HEALEY, as you see here on the right, a 74% improvement in clinical worsening with the p=0.03. Just to be clear about what clinical worsening is, that is whether or not a person dies, an obvious devastating and tragic example of clinical worsening, but also whether or not they need a tracheostomy because they can't breathe on their own, full-time BiPAP, CPAP because they can't breathe on their own, or a gastrostomy tube because they can't eat food or water on their own. We saw a 74% risk reduction improvement, and on RESCUE alone, 71%. I mentioned earlier the neurofilament biomarker. Many of you, I hope, are unfamiliar with neurofilament. I say I hope because if you're familiar, that means, well, that means that you're familiar with how devastating a destroyed or diminished neuron is because as the disease ALS or other neurodegenerative diseases attack the neuron, it leaves behind a cytoskeletal protein remainder in the bloodstream, and I can measure it in either the serum or the plasma or in the CSF of the spine. Measuring that, if I've got a sky-high neurofilament or a rising neurofilament, that's indicative of neuron death. We've now been looking at neurofilament, we and many others, as a clinical endpoint for a biomarker understanding of what's happening with the disease. Clene has the blessing, good fortune, the achievement to have a six-month benefit in the HEALEY study during the double-blind period and was pre-specified with plasma in Clene's case and serum in the Harvard HEALEY's case. Both of them were statistically significant, p=0.04 in the case of plasma. The interesting thing about the slide you're looking at on the right is the longer one is on the drug and also critically, those placebo individuals where you see the neurofilament is rising. At the end of the double-blind period, we have an opportunity to offer active drug to everybody who was on placebo. The vast majority, more than 90%, chose to go on active drug. We find that those individuals, once they get to steady state, also start to drop their neurofilament. You see an equivalent slope. That doesn't mean that all is good because the placebo folks, having lost that six months, there still becomes a better benefit in neurofilament as we continue to follow these patients over time. We took this data to the agency who asked us to understand and to look at whether high neurofilament was tied to a lesser risk reduction of passing away, a better survival benefit, in other words. We did see indeed that the greatest benefit on CNM-Au8 were those individuals that had a high baseline neurofilament and then it started to drop. Those are the ones that had a higher likelihood of survival. You see here whether we're talking about those with the top tertile of neurofilament or the top median. In both cases, no matter how you kind of cut that data, you see an 83% and 84% risk reduction in survival, both of which were significant. You see on the bottom here in the yellow boxes, 0.3 and 0.1. The agency also wanted to understand to what degree is there a neurofilament drop versus placebo. That answer is about twice, the 57% in green versus the placebo individuals at the six-month period. Of those individuals that had a decline in neurofilament, were they tied to a survival benefit? That is, if I'm declining in neurofilament in any capacity from something to something bigger, in other words, any decline from something to something bigger, is that tied to a survival benefit? We see that indeed it is, that the long-term survival benefit with any neurofilament decline at the six-month period is a 91% risk reduction with a p-value of 0.01. This is very important data that we started to understand how it correlated. When we talked to the agency about this in November, they proposed that they wanted to have us look at additional data on neurofilament reduction. We're levering right now to increase the persuasiveness of our finding that you've seen here, the $45 million that we received over four years from the National Institutes of Health in an exhaustive expanded access program, a protocol which basically means individuals who can come into CNM-Au8 or take CNM-Au8 on active drug in a compassionate use program. In that respect, the reason why this is relevant is because we see a long-term benefit of survival as we're basically on the drug now for three years plus against survival natural history controls that are propensity matched and covariate adjusted. We also see a long-term survival benefit in our real-world experience where we've looked at compassionate use that Clene has paid for in the past, our so-called EAP02 and EAP01 programs where patients, when they wrapped up the HEALEY program, they could roll over to active drug or individuals that were too sick to come into our phase II proof-of-concept study, they could just run to compassionate use as well. Taken together between our two EAP that Clene pays for and the one the NIH pays for, we've seen nearly 500 individuals that have been able to take CNM-Au8 and we're seeing a survival benefit occur there. The NIH program was designed when it was funded by this great grant that we received last year to look at neurofilament up to every six weeks, from baseline to every six weeks. That data is maturing for all the subjects at six months and many of them at nine months over this coming quarter. We're going to be evaluating that and sending it back to the agency because if that is concordant to the HEALEY data set, if we see two similar arguments that are presenting that teach us that our drug is reducing neurofilaments, then there is a course that we are hoping for, planning for, working towards of filing a New Drug Application by the end of the year on a neurofilament biomarker path in heterogeneous, that is kind of all-comer ALS disease. Now, independent of that, we also have an interesting discussion going on with the agency as we speak, a meeting that's coming up that we've already sent a dossier in for, as we've mentioned publicly on June 30th, to discuss the possibility of survival as a surrogate for the possibility of an accelerated approval. Indeed, this data you're looking at now on the far left is the all-randomized full analysis set of regimen A in the HEALEY study versus regimen C. Now, let's just be clear about what's going on here. HEALEY e nrolled 480+ subjects and then they were randomized with the same inclusion, same exclusion, same protocol, same clinical trial sites into one of three arms. Clene was regimen C. Patients also could have been randomized, 160+ of them, into either our arm or regimen B or regimen A. Regimen A, unfortunately, had a full futility. The DSMB had to call the study because of futility of efficacy. Patients had been on drug for some time. They never had access to CNM-Au8. They went obviously to their own placebo. It was a fair database. We're super grateful to the regimen A sponsors for sharing some of this survival data with us, as we've talked about earlier. We've seen against that data, if one treats it as a concurrent control, given that they were randomized at the same time, same inclusion, same exclusion, same trial sites, same protocol, save for randomization, they would have been our patients that were in regimen A, that is, rather, excuse me, regimen C. We see an interesting survival benefit that was statistically significant in that case as well, 28% risk reduction. On the far right, if we lever the learning that we have for our RESTORE phase III study that we're planning now and just commencing in the coming months to be underway fully, we see that if you look at patients that have already an elevated neurofilament and already some functional compromise, as indicated by TRICALS risk, they even have a stronger benefit of survival with a stronger p-value. That's our ALS story. We'll be finding out when our neurofilament data arrives, as well as from the survival conversation with the FDA, if Clene c ould file a New Drug Application by the end of the year with a possible review of and a PDUFA date set for CNM-Au8 sometime in the first half of 2026. Independent of all of that, same drug, same dose, has completed a phase II study called VISIONARY in multiple sclerosis. As we announced on June 30th, again earlier this summer, we are having an end of phase II meeting with the FDA this quarter to discuss proceeding for our phase III program in MS. That study needs to be funded by possibly a partner or by other equity or by commercialization in another rare orphan disease like ALS. In other words, we have some work to do to still proceed this into a phase III program. We are very excited about what we see here because the primary endpoint was vision improvement. The secondary endpoint was a composite endpoint, including vision, including cognition, including fine motor. What we saw here is in the double-blind period, a p=0.56 and a p=0.2 in a half-enrolled study that was COVID impacted. We pre-specified a p-value of success below p=0.1, yet we almost missed a classic [p=0.05]. What's more interesting to us is that as we continue to follow these patients for two further years in the open label, their vision continued to improve, improve, improve, as you see by this on the left. For the placebo individuals who were moved off basically colored water and put on CNM-Au8, they started to have the same vision improvement. Equally relevant, their cognition improved as well. The patients on active continued to improve on active for the full three-year period. The placebo individuals, once they converted to active, also saw a commensurate improvement in cognition. Indeed, the single-digit modality score you see here, an improvement of beyond five, six, seven points is the equivalent of somebody who was earlier too ill to work now being able to go back to work. In all this data, by the way, the vision improvement, the cognition is nicely correlated. The same people who are having a vision improvement and a cognition improvement, we're seeing statistical concordance between them. In short, very interesting second half of the year for Clene. Active conversations going on with the FDA for which we are super grateful, both Division of Neurology I and Division of Neurology II, two different divisions all under neurology to discuss our MS and our ALS program. We'll be finding out from DN II, Division of Neurology II, whether or not we can proceed into phase III in 2026. In Division of Neurology I, whether or not our safety data and our efficacy on the secondary exploratory of the biomarker path is commensurate with the possibility of a conditional approval in an accelerated approval path in 2026. In that respect, we just announced at the end of the year a cash position that, I mean, at the end of, excuse me, last week, in fact, a cash position. I'll let Morgan speak to it. Yeah, thanks, Rob. I mean, tons of exciting stuff happening here at Clene and, you know, enabling that is the cash that we have. As Rob mentioned, we announced our June 30th cash position of $7.3 million. Just last week, we filed our 10-Q. Concordant with that, we also announced two subsequent event-type transactions that occurred post-June 30th. One being we have raised an incremental $1.9 million off our [APM]. The second being we've increased the debt facility size that we have, which happens to be a convertible debt structure, by another $1.5 million. When you think of sort of a pro forma cash balance, we have almost $11 million in pro forma cash, which we said in that earnings release is sufficient to get us into the first quarter of next year. Clearly, it gets us beyond all these different FDA interactions that Rob talked about. It gets us beyond the neurofilament light data readout. In fact, it even gets us beyond the NDA filing by the end of this year. Very blessed and thankful for those that continue to believe in Clene. That's evident over the course of the last three or four days. Our stock price has significantly appreciated from high threes to we're into low fives right now. Definitely appreciative of those investors that believe in our story and the opportunity that's ahead for Clene as we work through this FDA regulatory pathway. Anna, at this point, we're welcome to open it up to questions. Perfect. Thank you. Congrats on all that. Let's talk about maybe a good specific upcoming inflection point. What might that be for Clene? Rob, you want to take that or do you want me to? I think Rob, we lost Rob. I think it's all you, Morgan. Yes, I get to take that question. As Rob mentioned, lots of very interesting upcoming near-term inflection points, the most near-term of those being our FDA interaction this quarter. Sometime in the next month, we'll be meeting with the FDA to talk about our survival benefit. Rob talked about the analysis we performed comparing our regimen to regimen A, as well as all the other unique survival benefits that we've shown across all of our trials. We have that opportunity to have that conversation here in the next 30 or 40 days with the FDA. Shortly thereafter, as Rob mentioned, we'll be exploring that NfL data in our NIH-sponsored EAP trial. If that data is concordant with what we've seen in our HEALEY t rial, we plan to file that New Drug Application by the end of the year. Once again, in the next two to three months, we have lots of very interesting, exciting inflection points, Anna. If you can dive a little bit deeper, Frank, our viewer, wants to know what results and study completion data are we waiting for currently, if any? Yeah, so in terms of the NIH data, we and the FDA have agreed with a cutoff date at the end of August. That's what we're effectively waiting for. We've got another, what, 11 days in the month of August at which that data from that NIH-sponsored expanded access program will be cut off. All those blood samples that Rob mentioned will be shipped off to an outside lab called Quanterix to do that analysis. That takes that outside lab probably about a month to conduct all that neurofilament light analysis. That data will then be sent back to Clene and our statisticians, which will then take another, you know, probably 10- 20 days to do that final analysis according to the statistical analysis plan. Once again, waiting for August 31st to hit that cutoff date, and then the analysis will begin. Steve asks, have you seen any reversal after completion of a treatment? Yeah, when we talk about reversal, this is definitely a drug that's meant for chronic therapy. Once a patient goes on Au8, it's intended for that patient to remain on Au8 for the duration of their disease. I would say yes, as people have gone off treatment of Au8, at that point, any improvements they've shown or any survival benefits they've received would be negated by the fact they've gone off therapy. Leon asks for the Au8, what is the dosage and how often? You take it every morning in the clinical studies. People take it just as soon as they wake up, previous to bed, I'm sorry, previous to breakfast, rather, excuse me. It's 60 mL. That's a very modest amount. It's a couple ounces, 1/4 cup if you think about it like that. Perfect. A follow-up question, Madeline asks, have the only side effects you've seen to date been headaches and nausea? These are individuals with terribly distressing neurodegenerative diseases. We see other side effects as well that capture in our database. Whether or not those are attributed to drug is a different question entirely. Serious adverse events, we go back to the clinicians and we ask them, do you attribute this side effect to the drug or do you think it's the course of the disease? At the moment, we have no serious adverse events that have been attributed to disease. We see other side effects, I'm sure, but the primary ones that we have been following that folks comment about but are not showstoppers is occasional nausea, occasional headache. Ronald asks, because Recursion Pharmaceuticals and [Wool Company] are located in Salt Lake City, would you two ever work together to bring a successful drug to market? I know Chris Gibson quite well. Chris is a lovely CEO, wonderful guy. There are a number of going to market or already public companies in Salt Lake City, actually. It's a burgeoning biotech sector. We're thrilled by that, that kind of finally, Salt Lake City, that's been on the genetics map and on the device map, is now getting also on the biotherapeutic map. You know, what he does, Chris does, is very different than what we do. It would be, in some ways, you know, we already do collaborate, which is growing the sector. If there's ever the right opportunity, the answer is, in short, yes. Matt asks of the status of partner discussions for MS. We were quite active at the bio meetings. The bio meetings, if your listeners are unaware, happen every June, and there's a lot of speed dating, I'll call it, that occur there. Clene had more than four dozen meetings, in fact. As we've mentioned to previous forums, we have different partners now under diligence, under... in our data room, deciding what they are going to do next. I trade notes with them and/or answer questions almost on a daily basis. What does "good" look like in terms of FDA interactions? Robert asks, what is the status with the FDA? As we mentioned earlier, what "great" looks like is that our data is concordant on the neurofilament side, that the agency understands, respects, and concurs with the survival benefit that we're showing, and lets us file a New Drug Application that they'll take under review. We'll find out that, as we say, in the coming months. Perfect. Are you confident in being able to file an NDA by the end of the year? If the neurofilament data is concordant with what we'd already seen in HEALEY and/or if there's a survival benefit that the agency respects and agrees with, as I said a second ago, we're planning to file either on a neurofilament biomarker path and/or a survival path, both as surrogate endpoints for the possibility of accelerated approval, and by the end of the year is indeed the timing we hope for. Perfect. Thank you, Rob. Thank you, Morgan. Do you have any closing remarks for our viewers today? We all recognize that ALS is a remarkably devastating disease. For every family member out there and every individual with this disease and for every caregiver, our hearts go out to you. We are working night and day. We are so grateful for the support you've given us, even in participating, many of you, in our clinical studies. For the sake of new therapies, we are grateful you're giving us the opportunity to even consider the possibility of taking this asset into FDA regulatory discussions. Thank you so much. We appreciate also the investor support of ourselves in this same journey. Perfect. Thank you, gentlemen. We appreciate your time, and we look forward to seeing you again real soon. Thanks, Anna. Thank you. Thanks, bye. All right, we'll be right back, everyone. Stay with us.