Good morning, everyone, and welcome to the Tonix session. It's our pleasure to have CEO Seth Lederman with us today to discuss recently approved Tonmya for fibromyalgia and also the increasingly diverse pipeline in CNS and immunology. Let me step aside and let Seth give the full presentation, and we'll leave a little time for Q&A afterwards. Thanks.
Thank you for that introduction. Thanks for inviting us to the conference, and thanks everyone for coming. I'm Seth Lederman, CEO of Tonix. We trade on the NASDAQ as TNXP. This is our standard safe harbor statement. We'll be making forward-looking statements. It's a very exciting time for Tonix. We are between FDA approval and launch. We had approval on August 15, and we've announced that the product will launch commercially in the United States before the end of November, so only about two weeks left. We work in a number of different areas, as Annabel mentioned: CNS, immunology, infectious disease, rare disease. We are relatively unique in that we are a truly fully integrated company where we've taken Tonmya all the way from concept to FDA approval, and now we're launching it together with some products we already market.
We just put out our Q earlier this week, and we had $190 million at the end of September, no debt, simple cap table, simple balance sheet, and we guided that we have cash runway into the first quarter of 2027, and that's fully funding our launch. We have a number of partnerships with leading institutions, both major universities and the United States government that I'll mention during the talk. Tonmya, here's our new label, our logo. As I said, before the end of November, we will be launching it commercially in the United States. The active ingredient is cyclobenzaprine, and it is a sublingual tablet, meaning an under-the-tongue tablet. The tablets are 2.8 mg, and for adults, it's two tablets every night for long-term or chronic dosing for the treatment of fibromyalgia.
This is the first product approved for the treatment of fibromyalgia in more than 15 years. I've been working in the fibromyalgia area generally for about 30 years. Before going into biotech, I was a professor at Columbia University Medical School, including, among other things, in the Division of Rheumatology, which is the subspecialty of medicine that takes care of fibromyalgia patients. Our product, Tonmya, is first in class, and it is a first-line medicine. It is unique, highly proprietary technology in its formulation in terms of efficacy, delivery, and absorption. The market is big. There are 10 million American adults who suffer from fibromyalgia, and it's a big unmet need because the existing products don't satisfy the patients out there. The current treatments, there are three FDA-approved products.
They have a high rate of patient and prescriber dissatisfaction, and that contributes to, among other things, a high amount of off-label opiates. Tonmya has a distinct profile, efficacy, and tolerability that I'll discuss in a minute. It's a very unique commercialization opportunity because we're launching into a space where we have a 100% share of voice and no counter-promotion, and our patent exclusivity on issued patents is 2034. Fibromyalgia is a big unmet need. It is a chronic pain disorder. It's a chronic pain disorder that originates in the brain, in the central nervous system, and it originates because of amplified pain signaling in the brain and also probably some kind of a defect in being able to filter out pain signals. Chronic pain and acute pain have not really that much to do with each other.
Chronic pain is usually defined by different syndromes, and fibromyalgia is considered the prototype of a new kind of pain called nociplastic pain. Fibromyalgia symptoms are chronic widespread pain, non-restorative sleep, and fatigue. Chronic widespread pain, I think, is self-explanatory. It's pain all over the body. Non-restorative sleep is a particular type of sleep problem where people go to sleep, but they wake up feeling unrefreshed. They don't get the benefit of sleep. Fatigue is generally a low energy. These three things together are kind of the triad of fibromyalgia symptoms. Fibromyalgia drugs are currently approved just on the basis of decreasing pain. There's a lot of dissatisfaction in the fibromyalgia market, both among doctors and also patients. As I show here, a high proportion of patients fail first-line medicine. One of the big problems is tolerability. Consequently, there's high patient churn.
We think that there are always patients looking for new products, and they're switching. They're taking more than one product, and almost 80% are on multiple medicines at the same time. A lot of that polypharmacy relates to patients playing essentially kind of whack-a-mole with these different symptoms. It's not uncommon for patients to have one thing for the pain, one for the sleep, and one for fatigue. This is a survey that we commissioned by a third party looking at patient claim database about what are the prescriptions that fibromyalgia patients get within 18 months of diagnosis. At the top of each one of these bars, it says whether they're on label or off label. The bottom is the name of the medicine, and then they're kind of color-coded about which kind of class of medicine.
The first point to make is that the FDA-approved products are not taken very much. Most commonly prescribed FDA-approved product, duloxetine, is in about 23% of patients. If you look for the other approved products, you have to go to pregabalin, which is only used in about 14% of patients, and then a tiny slice, about 1%, take milnacipran. Of those, the only one that's still on patent is milnacipran, and that's marketed as Savella. The most commonly used, the most frequently prescribed drug is gabapentin, which is actually off label. It's similar mechanistically to pregabalin, which is on label. The really alarming thing is the red bars in the middle. Basically, more than half the prescriptions that are written for fibromyalgia patients are opiates: hydrocodone, oxycodone, and tramadol.
This is pretty alarming because actually the best medicine and the scientific guidance is that opiates should not be used in fibromyalgia. Not only are they not effective, but for many, there's a lot of evidence for many patients, they actually worsen the problem. They increase pain sensitivity in fibromyalgia. Fibromyalgia, like several other chronic pain conditions, are really at the heart of the opioid crisis, I think much more so than acute pain conditions. Coming into this, we have a new product. As I said, there are 10 million people affected, and it's predominantly women who are affected by fibromyalgia. No one understands the sex distribution, but it's real. Of the 10 million, only about 3 million are diagnosed and treated. That would be, call it the low-hanging fruit for a product launch. We're looking forward after launch to growing our market.
Here's our product. We announced the WAC recently, and the WAC for adults, which is two tablets a day, is one price, and we have actually proportional pricing so that for geriatric patients and patients with mild hepatic impairment who only take one tablet a night, the price is half. We have put together a very experienced sales team, and we're that have launched similar products, and we're about to hit the ground running. We already have unbranded promotion going on, and we've been reaching out already to prescribers, alerting them to the idea that Tonmya will be available soon. We're doing the launch by targeting fibromyalgia prescribers, and we're highlighting the amount of fibromyalgia prescriptions that they write more than the specialties that these prescribers are from.
Tonmya is already added to our existing contracts with wholesalers and specialty pharmacies, and we intend to have at launch robust patient access and support services. Generally speaking, there are 25,000 healthcare providers who prescribe about 70% of the fibromyalgia prescriptions. We are going to interact with these prescribers in a number of different ways that I think generally are called omnichannel. We expect that our field force of 90 reps will have personal promotion with about 70% of these 25,000 prescribers. In terms of access, we have a lot going on in terms of payer education engagement, digital pharmacy, and traditional pharmacy savings programs. All of these will be available at launch. Now I'm going to take you through some of the technology of Tonmya. Remember, it is a sublingual tablet. It goes under the tongue, rapidly disintegrates, rapidly dissolves, and enters the bloodstream quickly.
The rapid absorption is part of what we think makes this effective. One of the most important things we think is that it bypasses first-pass hepatic metabolism. When cyclobenzaprine is metabolized by the liver, it's demethylated into norcyclobenzaprine, and we believe that norcyclobenzaprine interferes with the therapeutic effect of cyclobenzaprine. That's why we think that this is a fundamental change from oral cyclobenzaprine, which is approved as a muscle relaxant, which is a completely unrelated condition. Our drug is a chronic bedtime medicine that targets non-restorative sleep. These figures are from the package insert, trial one and trial two. These are called continuous responder analyses. You can see the darker line is the response lines for the drug, and the lighter lines are the response lines for placebo.
Going from left to right, the vertical line is the 30% responder line. That is what people in the field, rheumatologists, key opinion leaders generally regard as clinically significant or clinically meaningful. I think you can see that in both studies, there was, in the first study, 47% responders on drug and 35% on placebo. In the second study, 46% versus 27%. In both cases, these had p-values that were less than 0.05. The effect in two studies showed an increase in the 30% responders, meaning that they had a 30% reduction in daily pain at the end of the study. One of the differentiators, we believe, in the marketplace of Tonmya is its tolerability. The most frequent side effects related to administration site reactions are so-called oral adverse events.
That is not surprising because this is a rapidly dissolving tablet that breaks apart under the tongue. Only in one case in each of the two registration studies did anyone withdraw because of this. In fact, they were, for the most part, self-limited and mild. I think more importantly, we did not see significant weight gain or blood pressure changes. There were no reports of cognitive dysfunction or sexual dysfunction, and there was no evidence of abuse potential. The label does caution about pregnancy testing in women of reproductive potential and advises against using it in the first trimester. In 2023, we bought two marketed products. They are both treatments for acute headache. These are great products, but we really acquired them so that we would have the commercial foundation to have an effective launch of Tonmya. I think they have really delivered on that promise.
But they are interesting medicines in and of themselves. Tosymra is an intranasal spray, and it has the Intravel technology. It's the same technology used in, for example, Nephri, which is an epinephrine spray. And there's also a related benzodiazepine spray. Zembrace is an autoinjector that we think is elegant and easy to use. We've been marketing these now for two years, and that has really given us a strong foundation to launch Tonmya. Now let me turn to our pipeline. We have a number of programs in or headed to clinic. The bulk of our pipeline are actually line extensions for the Tonmya product. In their experimental uses, it doesn't use the Tonmya name. It's called TNX-102 SL. One study is ongoing. It's a study of acute stress disorder.
One study is slated to start in next summer, which is for the treatment of major depressive disorder. In immunology, we have an anti-CD40 ligand that's been through phase one and is headed for phase two. In infectious disease, we have a phase two ready preventative for Lyme, and finally, for potential treatment of Prader-Willi, we have an intranasal oxytocin. 102SL for acute stress disorder. This study is a physician-initiated study at the University of North Carolina, and it's actually enrolling people immediately after automobile accidents. This is a model that the United States Department of Defense thinks is relevant to combat trauma and military-related events. This study is funded by the United States Department of Defense. The main endpoints are these early conditions called acute stress reaction, acute stress disorder.
Ultimately, the idea is that this may be a preventative for post-traumatic stress disorder, which is a chronic psychiatric condition. The number of automobile accidents in the United States is quite high, so it could be a very interesting market if two weeks of TNX-102 SL decreases symptoms in this acute stress reaction, acute stress disorder. The next one that we've recently announced is we have a cleared IND, and we have submitted, we filed the IND. It has not yet cleared, excuse me, for major depressive disorder, but we've announced a successful phase one pre-IND meeting. This study will start next summer in major depressive disorder. We think it's a differentiated treatment, and this is based on some data that we got in the second pivotal study for fibromyalgia, which showed an improvement in the Beck Depression Inventory in fibromyalgia patients.
This will test whether major depressive disorder without fibromyalgia acts like depression in fibromyalgia. Anti-CD40 ligand, it's a very active area in big pharma, mid-stage pharma. CD40 ligand was one of the first targets for immunology inflammation. The first generation of drugs was associated with blood clots. A lot of science was done and traced the problem to the FC portion of these antibodies. There was a second generation, a number of different molecules, and the second generation, and ours is an example of one of a few drugs that would be called third generation. What we've done is we've made very specific mutations in the FC region of the antibody. After pretty extensive monkey and animal testing, we conclude that we have addressed the risk of thrombosis problem. Our ultimate goal for this is to treat autoimmune disease.
Sjogren's and lupus are important targets for some of the other companies that are in the space, and ultimately, they will be our targets. In the meantime, we're targeting allograft rejection. Allograft rejection is a very appealing market, very appealing first indication, because the transplant surgeons are very excited to study this, and it is a very compelling proof of concept. If you have activity in preventing allografts, you're very likely to have strong activity in treating autoimmune disease. We recently announced a partnership with Mass General Hospital where we'll be starting a phase II study in allograft kidney transplant recipients. That will start in the first half of next year, pending FDA clearance of the IND.
We've already completed and mostly reported the phase one study, which shows that we have monthly dosing and we have what we think is best-in-class activity based on pharmacodynamics. The newest addition to our portfolio is TNX-4800, which we licensed this summer from the University of Massachusetts. We licensed worldwide exclusive rights. This is an antibody that targets the OspA protein on Borrelia burgdorferi, which is the causative agent of Lyme disease. This is actually the same molecular target as the vaccines in development. The vaccines in development require three challenges to make an active immune response against OspA. We see that as a limitation. First of all, you don't get protection until you've had the full course of immunizations. The second thing is there's a spectrum of how people react to active vaccination.
Not everyone makes a good response to OspA. We were very excited to be able to partner with the University of Massachusetts Chan Medical School on this because this, with a single dose, provides pretty much immediate protection. It is also a long-acting antibody. The concept is that someone can be dosed, they can be treated with this preventative in the spring, and it will provide protection throughout the summer. Basically, roughly speaking, from March to November. Since we are providing this as passive immunity, everyone who receives it will get the same kind of strong protection. It is also a very unique kind of preventative because this is something that actually blocks the infection of Borrelia. It is very unusual. The site of action of this antibody is in the mid-gut of the tick.
When the tick swallows the blood, when they bite a human, they're sticking there, the blood gets into the stomach, they also ingest this antibody, and it kills the bacteria in the belly of the tick. We already have completed a phase one study, so this is phase two ready. There is also compelling animal data showing that this can block infection even with in experimental challenge models. Final program I'm going to talk about is treatment for Prader-Willi syndrome. Prader-Willi is a rare disease. It starts early in life where the kids have failure to thrive, but later it results in essentially hyperphagia, which is an eating disorder of eating too much. It's a strong compulsion to overeat. The hyperphagia can be the primary endpoint of studies to get approval for the treatment of Prader-Willi.
Shown here in this cartoon is oxytocin, which is the active agent of our drug with magnesium in the middle, and then the oxytocin receptor. I think you can see that the magnesium is not just a passive participant in the interaction of oxytocin and magnesium. It is right in the middle. Our product has a unique formulation where it combines magnesium and oxytocin. In animal studies, what we have shown is that by having the magnesium there, we inhibit what is called high-dose suppression, and we get rid of what is called the inverted- U. We plan to start a Prader-Willi study, a potential pivotal Prader-Willi study in the second half of next year. One of the reasons we are so excited about this is there is a very compelling animal model for Prader-Willi called the MAGL2 knockout mouse. Oxytocin has profound beneficial effects in the MAGL2 knockout mouse.
I don't know of other treatments in development or even approved for Prader-Willi that have shown these kinds of effects in the MAGL2 knockout mouse. Let me just touch on our milestones. You can see we've been very busy. Just in 2025, we announced top-line results for our anti-CD40 ligand antibody. Very satisfied with these results. Monthly dosing, best-in-class activity in terms of the pharmacodynamics. Next, we initiated enrollment in the line extension study of TNX-102 SL in acute stress disorder, acute stress reaction. In August, we got FDA approval for Tonmya for the treatment of fibromyalgia. We got it on time. As I said, very pleased with this because we've taken this product literally from concept through development and now to approval. We just submitted the IND for the study next year for treating major depressive disorder.
This month, so imminently, we will commercially launch Tonmya using our existing sales force that's already been recruited, trained, and are ready to go. In the first half of next year, in collaboration with Harvard Medical School and Mass General Hospital, we expect to start dosing the phase two kidney transplant study with anti-CD40 ligand. Mid-2026, we'll initiate the major depressive disorder line extension study for 102 SL. In the second half of next year, initiate the trial for Prader-Willi. We are strategically positioned for the future. We expect to deliver a best-in-class launch. We're advancing some promising mid-stage pipeline programs. We expect, from where we are positioned right now, to drive sustainable growth and value for our stakeholders. Thank you very much, and I'd be happy to take questions.
I have a quick question on some of the line extensions. I guess it kind of makes sense that MDD would be related to fibromyalgia. How is the acute stress disorder related? Because it's an acute versus a chronic condition. Can you give us a little bit of information about [audio distortion]
Yes. Great question. Thank you. I'll just quickly repeat it because I don't know if your mic was on.
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The thing was it seemed like, while we have a strong rationale for developing depression based on data from our fibromyalgia development, what's the basis for developing the product for acute stress disorder? Along the way in our development of 102 SL, we actually have done three large, actually registration quality studies for post-traumatic stress disorder. Each of the three studies missed on the primary endpoint. Nonetheless, we developed a very extensive database of information related to the product in this vulnerable population. I think that we and other groups working in PTSD are very frustrated with the new primary endpoint called CAPS-5, Clinician-Administered PTSD Scale Number 5. The existing drugs for PTSD, there are two SSRIs that are approved, were approved based on the CAPS-3 or the CAPS-4. I think there's widespread frustration in the field about the CAPS-5.
There was just an adcom for a different product where the company made a very compelling argument that they might get approval even for missing the CAPS-5 because the way the questions were reworded has not worked out. The new scoring system and things like that, it is something where it has been very frustrating. We had very compelling data, in our opinion, using measures like PGIC, Patient Global Impression of Change. We think that the data that we got from the studies shows a compelling benefit versus a very acceptable risk. In the end of the day, we think we could have a very successful product for PTSD. It was because of all of this data that we have done, the two biggest studies in military PTSD that I think have ever been done, highest quality data, and based on PGIC anyway, a strong signal.
That's really what got the interest of the UNC investigators and the Department of Defense to study this for acute stress disorder and acute stress reaction, which I said are thought to be prodromes for chronic PTSD. The overall paradigm is what we're doing is targeting non-restorative sleep. Sleep problems in PTSD are a big issue. Also, it's believed that in the prodrome for acute stress reaction, acute stress disorder, poor sleep quality correlates closely with increased risk of PTSD. I think there's a strong mechanistic rationale and a lot of phase two/three data.
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This study is two weeks of treatment. Yes.
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Okay. Number 50.
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Okay. Thank you very much.
Thank you very much.
Okay. Thanks for.