For everyone. If you wanted to meet with [Joram] when we finish the session, right out this door to the left, the second door is where track one, one-on-one Q&A. If you want to go for any of the speakers, ask more questions in detail. Same goes for Jonathan Javitt, I will be announcing here on stage next. Right after, go meet with him, Q&A, all that good stuff. If you wrap early or one of you speaking, you wrap up early, you want to take questions here from stage, that is perfectly fine. Encouraged, actually. Get some interaction going. With that, I would like to introduce from GeNeuro, Jonathan Javitt, CEO. GeNeuro is a clinical-stage biotech targeting diseases linked to ancient viral DNA in the human genome, including MS and ALS. So big round of applause for Jonathan. There we go. All right. This is going to be a little less passionate, a little more low-key than the last two talks, mostly because I have never done this talk before. Most of you know me as founder and CEO of NRx Pharmaceuticals. GeNeuro is our newest subsidiary, and the ink is barely dry on the acquisition documents. So you guys are the first people getting a glimpse of this. Three weeks from now, I have got to be able to in front of 1,000 people at the Biotech in Europe Forum in Basel, so I really count on your coaching. By the time we get to the JP Morgan conference, this is going to be a powerhouse presentation. I do not mind talking about it in a low-key way, because we are talking about drugs that can literally change the face of humanity, only one of which is a treatment for ALS that could potentially be approved by 2029. If you are wondering how all of this happened, EUR 180 million of R&D was done over in Europe, mostly funded by the European Investment Fund. Management made some decisions that turned out not to be the best ones. It wound up in a Swiss bankruptcy, and we bought it. Now we are unpacking that trunk. Just to give you a sense of this is moving forward, just yesterday, we got notice of approval of a Europe-wide patent for using the technology I am about to share with you for diagnosing ALS. Probably a lot of people in the room have heard of the word retrovirus in various contexts. But is there anybody in the room who does not work for GeNeuro who has ever heard of an endogenous retrovirus? Yeah, nobody. I had never heard of them either. Obviously, we are doing testing the waters. Moody Capital is going to be putting up a Reg CF raise for us, so this is a testing the waters presentation, and obviously what I am telling you about are forward-looking statements. So I had never heard of an endogenous retrovirus before I came across this technology. Actually the way it happened was David de Rothschild, during his last three months as Chairman of the bank in Paris, introduced me to Professor Marion Leboyer, who is the leading psychiatrist in France. Marion started telling me about work that she had done identifying retroviruses as a cause of schizophrenia. I said, "Well, what are retroviruses?" My question for you is, what if the very worst diseases in humanity are caused by ancient viruses that already live in our DNA? Diseases that cause cancer, neurological disorders, autoimmune disorders, chronic inflammation. In terms of the low-hanging fruit, we are talking about ALS, multiple sclerosis, schizophrenia. We have a path to the cure. When I got my biochemistry degree at Princeton in 1978, Arnie Levine taught me that 8% of the human genome was junk DNA. Arnie at the time was a brand-new professor of biochemistry who was teaching molecular biology. If anybody in the room knows molecular bio, Watson and Crick, "Molecular Biology of the Gene" was in its second edition that year. If you get a molecular biology degree today, you learn that 8% of the human genome composed of retroviruses that live in what is called the dark genome. That is a part of the human genome that under ordinary circumstances is not in the reading frame. Those genes, those bits of DNA are not translated to RNA. They are not formed into proteins. They just sit there dormant, except when they do. Arnie went on to be the founding chairman of molecular biology at Princeton. He went on from that to be the president of The Rockefeller University. Today, he leads the biology program at the Princeton Institute for Advanced Study, which was the institute that Albert Einstein founded. He is the chair of our scientific advisory board. It has been fun to come full circle. What we are learning is that although these retroviruses were critical at times in our evolution, critical in evolving from primates to humans, when they misbehave, when they start to replicate themselves later in life, all hell breaks loose. The important thing to understand here is nobody can catch a HERV infection. The genetic coding is already in the DNA of every person in this room, of every human being who has ever walked the planet. It is not that these viruses can suddenly emerge and start infecting other people. It has been millions of years since they had the ability to actually become infectious particles. Instead, the envelope proteins from these viruses and some other viral proteins have retained the ability to be translated, and at least in two cases, retrovirus W and retrovirus K, those envelope proteins are highly inflammatory. In fact, the way people got onto this is Hervé Perron, who now serves as our Chief Scientist and was the chief scientist of the company that went into liquidation, originally discovered what was called MSRV, multiple sclerosis retrovirus, and found these particles in the blood, in the CSF of the majority of people with multiple sclerosis. Then he and Marion Leboyer discovered that 50% of people coming into French and German psychiatric hospitals have the envelope protein for retrovirus W floating around their plasma and in their CSF. Why did this happen? Why have these particles, why have these viruses been conserved within humanity? It turns out that these are some of the elements that enabled us to evolve from squirrel and cynomolgus monkeys into chimpanzees, gorillas, and later Homo sapiens. They play a critical role in the development of the human placenta, and in the development of a placenta that's capable of supporting the growth of a human brain. Without these retroviruses, there would not be humans. There's a reason they've been conserved, but now we're learning that they cause some of the worst diseases that affect man. They have a dark side to them. In the case of ALS, it turns out that the vast majority of people with ALS have HERV-K, Human Endogenous Retrovirus K envelope protein, floating around their cerebrospinal fluid. People with MS have HERV-W Human Endogenous Retrovirus envelope protein floating around their blood and CSF. I've already told you the story with psychosis, and much more recently, we're starting to find out that people with glioblastoma have HERV-K activated in that tumor. Let's just talk about this one case of ALS, recognizing that within this technology portfolio, ALS is just one small piece. You're talking about a disease that causes progressive motor neuron degeneration, paralysis, respiratory failure. 6,000 people get ALS every year, and they're dead within three to five years. Our partner in this is Dr. Avindra Nath, we call him Avi, who is the Clinical Director of the National Institute of Neurological Disorders and Stroke of the NIH, and he's the co-inventor on the patent that we share with the U.S. government on this. Avi will tell you that half the patients he treats at the NIH Clinical Center with ALS ask for euthanasia, because you're talking about a disease where you spend the end of your life, if you die of natural causes, completely locked in. You can think perfectly, you just can't move anything. What's the evidence that retrovirus K envelope protein, and remember, a virus is a little bit of DNA with a protein wrapped around it. If you didn't have the protein, the DNA would get chewed up in the blood in milliseconds. The envelope protein is what keeps a virus intact. What's the evidence that the HERV-K envelope protein causes ALS, and that an anti-HERV-K envelope antibody might prevent neurodegeneration? Well, first of all, this HERV-K envelope protein is found in the CSF of more than 75%, the cerebrospinal fluid of more than 75% of people with ALS, and it's not found in the CSF of people who don't have ALS. It causes neurotoxicity if you inject it into mice or into human neuronal cell culture. In fact, if you take the CSF from a patient with ALS and just put the cerebrospinal fluid into a mouse or into human neuronal cell culture, you will cause motor neuron degeneration. You'll cause the same disease that's seen in people with ALS. At a nonclinical level, we've demonstrated that you can block that effect in mice and in human cell culture with a monoclonal antibody that mops up retrovirus K. I've been in the monoclonal antibody world before. I was one of the people who was on the teams that developed the first drugs for macular degeneration. In that case, you're talking about a disease that used to blind everybody who got it. A disease where vascular endothelial growth factor causes abnormal blood vessels to grow in the retina. Well, nobody has figured out how to keep VEGF from forming, but if you mop up the VEGF, either with an aptamer, which was the Eyetech Pharmaceuticals drug, or with a monoclonal antibody, which was Lucentis, you prevent the biological effects of VEGF. Well, the same thing is true here. If you make a monoclonal antibody against HERV-K envelope protein, at least in mice and human cell culture, you can block the neurodegenerative effects. There are three ways to counter a neurotoxic protein. You can use CRISPR and try to slice out the DNA. That would be pretty hard to do here because you actually have many copies of these genes in your genome. A CRISPR solution would be a long way from now, and we do not actually know that it would be benign to slice these genes out of the genome. You can do antisense RNA to try to silence expression. That is sort of over the horizon, and one day we will figure out how to do that. Or you can do what we know how to do right now, because seven out of 10 blockbuster drugs today are monoclonal antibodies. You can make a monoclonal antibody against these neurotoxic proteins, and that is exactly what was done by GeNeuro, and that is exactly the technology we own. In fact, just three weeks ago, Mike Taylor and I were over in Vienna. We kicked off manufacture of the ALS drug with a company called Polymun, which is a family-owned business that just does a sort of impeccable job of making these biologic compounds. They made the first 5 million doses of the BioNTech COVID vaccine. We now have this drug in production, and we are expecting to have human-grade drug in our hands ready to go into the clinic in July of 2027 with NIH as our partner. We are doing a small raise to get some of this underway. We have already been qualified for the first round of the Congressionally Directed Medical Research Programs, so we made it through the tough part of the funnel, and our final bid is due on September 30th. There has been $80 million already written into the 2027 defense bill to support a clinical trial in ALS. Now, it does not have our name on it, so if there is somebody else who is ready to do a clinical trial and a disease-modifying drug of ALS, we will have to compete with them for that money. But there is an awfully good chance that we are the only clinic-ready compound right now for this disease. As I said to you, there has been EUR 150 million already invested in getting the technology to the point where it is, but because the asset was washed through bankruptcy, none of that money is on our cap table. We have a completely clean cap table. I put this in because FDA has just published a really impressive case study. There is a very small subset of people with ALS who have what is called a SOD1 gene mutation. SOD is superoxide dismutase, and if you have that mutation, this drug, QALSODY, is effective. You can see how powerful an effect they saw in the clinic, and they got an FDA approval. The reason I am telling you about this is FDA approved this drug based on a biomarker. They did not require this drug company to get to the point of showing longer survival. They didn't require them to get to the point of showing a meaningful clinical effect. All they required to get this drug into patients was showing a decrease in neurofilament light chains, which are the chemical elements that are let loose into the blood when a motor neuron cell dies. So it's a laboratory measure of motor neuron cell death, and FDA put this study on its website to talk about how it's ready to do accelerated biomarker-based approval for diseases like ALS. That's why we think we have a $25 million path to a humanity-changing drug by 2029. The antibody is completely characterized. As we speak, the master cell lines are being grown up in Vienna. They're going to go into the bioreactor and start producing antibody in the January timeframe. We're going to have them in our hands, and we've already done, or the prior company already did five clinical trials with the anti-HERV-W antibody. They showed a decrease in neurodegeneration in patients with multiple sclerosis. More than 400 people have had the HERV-W antibody with no safety issues. They were forced to do six months of a full monkey study. So there's already a tremendous amount of background information to take to the FDA and explain to the FDA why we shouldn't have to kill a lot of primates in order to get this drug into the clinic. It just happens that the head of the Congressional ALS Caucus is also currently the Chair of Defense Appropriations in the U.S. House of Representatives. So, there's two sort of military connections. One of them is that people who are combat veterans have 2x-3x the risk of ALS as ordinary people walking around. That's also true of pro athletes who've played football and soccer and other contact sports. So there's a reason for the military to be funding this, and there's deep will within the current Congress to get something to the clinic for people who have this horrible disease. We've put together a leadership team that's done this before. Mike Taylor is a reformed bond trader. He's doing this as part of his penance. Rick Panicucci, 25 years at Novartis, and then he built the WuXi AppTec manufacturing footprint, has four NDAs to his name over the last four years. Phil Lavin, our statistician, has his name on more drug and device approvals than any statistician in human history. As I mentioned to you, Arnie Levine, the chair of our scientific advisory board, was my molecular biology teacher in 1977 and is one of the most published molecular biologists in the world today. Avi Nath, who is Co-chair of the scientific advisory board, is the head of ALS at the NIH, and we own these patents in partnership with the U.S. government. We control them under contract. The government gets a 3% royalty if this drug ever gets approved. Marion Leboyer is the Professor of Psychiatry at Inserm, which is France's largest research university, and she discovered the HERV-W schizophrenia linkage, so she's Co-chair for that. Wayne Pines, who's done one successful thing after another, former associate commissioner of FDA, has joined our board. Keep looking for new talent because we're bringing it. As I said, we're partnered with the NIH, with the Congressionally Directed Medical Research Program, with Target ALS 501(c)(3). We're working with the Paris Brain Institute, the University of Basel. If you'd like to be part of bringing forward a drug that has the potential to change humanity, but also has the potential to fail, please see us. Moody Capital is putting up a Reg CF, so we're going to bring in the first $5 million on a crowdfunding basis. This is a testing the water conversation for that. If you go on the GeNeuro.us webpage, you'll see seven patent families with multiple approvals in multiple jurisdictions. I think we're up to 25 patents around the world, and by the time this gets to the clinic, you'll see 100 approved patents because we have yet to have a patent rejected. I'm at time. I'm happy to take questions in the breakout room. Thank you for being at the inaugural talk for this really exciting opportunity.