The GLP-1s and the weight loss drugs. In fact, the call to action is that, you know, especially in older American older patients, is losing muscle with weight loss is not a good thing. In fact, you're gonna learn today that there's more to muscle than just function. It's also a metabolic tissue, and if you can restore that, or more importantly, preserve muscle, then you have a real opportunity to make a difference in the weight loss journey. So the big issue now is that the GLP-1s and the other agents that are coming through actually cause about 15%-20% weight loss, but that weight loss, about 20%-50% of that weight loss is muscle.
And so the way I like to think of it is that if you lose, and humor me for a moment, if you lose 50% of your total weight is muscle, then if you lose two pounds, one pound is muscle, one pound is fat. So the exchange rate is for every pound of muscle you lose, every pound of fat you lose, you have to give up a pound of muscle. The problem with that is that you have a lot more fat than you have muscle. And so this, if you look at this scan, this is an MRI, you'll see on the top of the MRI, this is what a cross-section across the thigh looks like, and that's muscle, bone, and that little white ring is fat. That's good, that's good muscle reserve.
But in an older patient, of which 42% of older patients over the age of 60 could benefit from a weight loss drug, and in that population, about a third of patients have so much muscle loss because of aging, natural loss of aging. They look more like that second scan, and what you see there is a little bit of muscle, a lot of fat, and the circumference of the leg looks fine, but when you look inside the leg, there's very little muscle. That's a patient that's in danger of a physical function, never mind not being able to lose weight, and that muscle is not gonna let you lose 50% of that muscle. You'll die. So there is a natural push me, pull you that's gonna take place as you start losing muscle.
In fact, this is starting to show up. Wegovy had its label updated, and it was updated because they saw in the SELECT trial, that important trial that showed a 20% reduction in cardiovascular deaths, but also from a safety standpoint, what they were able to show was there was a fourfold increase in falls and fractures of the hip based on because of falls in older patients over the age of 75, which are fourfold, and if you're a woman, then it was fivefold increase. So this is not happening because you had a traumatic fracture. This is happening because you had a fall. You fall because you lost your balance, and when you have muscle weakness because of loss of muscle, what you notice first is your gait and your balance changes, and that's why you fall.
We're seeing evidence. It is relevant. It is absolutely relevant that you're losing muscle. In fact, muscle also plays a role. Forget about function. We always think about function. It also plays a role metabolically. Now, what does that mean? Well, we're experiencing it. We're seeing now the two important points that are happening that's getting interfering with the weight loss journey. The first thing is called the, now they're calling it the Ozempic plateau. What that means is the patient is losing weight, and all of a sudden, they stop losing weight. So the way the GLP-1s work is they stop your, they suppress your appetite, but then what happens is, all of a sudden, you start eating again, and that's the only way to explain that you stop losing weight.
And that's probably going to be related to muscle, which I'll show you in a moment. Second thing that happens is when you want to stop the weight loss drug, because you've depleted muscle, you have this overeating that takes place once you stop the drug, that preferentially puts fat on and not muscle. And that ends up putting you in a worse position. In fact, the data is here. This is from the Wegovy approval. There are four studies here. Look at the one to the far. In your case, it will be the lower right. In the lower right, you'll see that in all these curves, you'll see that you lose most of your weight in the first 16 weeks, and then all of a sudden, it plateaus.
It means the next 50% takes about a year to lose. And then you'll see in the lower right, if you stop the medication, you get your weight back. This is a problem. Patients are so concerned that they got to their ideal weight, and now they can't stay there, and they stop the medicine. They get this rebound. So muscle is playing a role here because it turns out you can lose all the fat. That's fine. You've seen bodybuilders taking anabolic agents, and they get real chiseled, but you can't do that in muscle. You do that with muscle, you'll die. So what's happening in that plateau is the depleted muscle is telling the body to eat, and you have a pharmacologic drug that's telling the body not to eat, and you get a push me, pull you.
And that push me, pull you, you have to address the muscle. So the agent that we have is called enobosarm. It's a novel oral selective androgen receptor modulator. It works through the androgen receptor, and we have data from clinical trials and preclinical studies over the last decade that supports a once-a-day dosing. It works through the androgen receptor. We all know that testosterone works. The problem with testosterone is you can't give it to women because they get facial hair, and if you give it to men at inappropriate doses, you end up with testosterone turning to estrogen, you end up with gynecomastia and blood clots and that kind of stuff. So if you had a neutral, I call it, neutral anabolic agent, it can be given to men and women, and it builds muscle.
And not only builds muscle and improves function, but it also stimulates separately, because there's androgen receptors on the fat cells. It separately stimulates lipolysis, breakdown of fat, fat burning, and stops fat from building up, and then furthermore, it builds and heals bone. So this is an agent that is perfectly designed to be a companion product with the weight loss drugs, where you're, you know, you're seeing the muscle loss because it's non-selective. It's non-selective because you're, the GLP-1, the weight loss drug, is suppressing appetite. So your body naturally is gonna lose fat and muscle. It's not selective, and it's the muscle that we're trying to avoid. This is just a busy slide showing we've done five studies, over a 1,000 patients, in this space.
The studies all show an increase in muscle or maintaining muscle, depending on the patient population. It also shows that you're able to increase function or strength. The one I like is the second study, because this was done by Merck. Merck had a relationship with enobosarm at one point, a few years ago, and this was going after frailty, so this is muscle wasting with age. So they took women, gave them three mg of enobosarm for three months versus placebo. No change in diet, no change in exercise. Three months later, if you were on enobosarm, you had an increase in lean body mass of 1.5 kg. That's like a 50 oz steak at Smith & Wollensky. They grew that in three months, and they were able to leg press an additional 22 pounds.
It works, and it is a performance drug. The issue is, when you start looking at obese patients, what happens in an obese patient with an anabolic agent is different than what happens in a thin patient. With a thin patient, you maintain and build muscle, you have an increase in weight. In an obese patient, the opposite happens. What happens is, because of the fat-burning potential, when you have fat, you lose weight. This is showing you, in one of our studies, post hoc, we call it Study 504, which is a Phase 3 study, we looked at the subpopulation of patients that had a BMI greater than 30, and what you can see in your far left is lean mass in the placebo group went down, and we just held on to muscle.
This is at 84 days. We're not trying to make bodybuilders, we're trying to maintain muscle. Second thing that happened is they lost fat, and at day 84, they lost about 5.71%, 7% fat, and if you go to day 147, that actually translated to weight loss. These patients actually lost weight of almost -4.51%, at 21 weeks. If you give enobosarm by itself, and again, our strategy is to give enobosarm in combination with a weight loss drug, but if you give enobosarm by itself, in obese patients, it has the ability to decrease weight.
Now, these are two very interesting curves, because this is kind of telling you what happens when you give a semaglutide in combination with a androgen, a testosterone product. To the left shows you what it looks like with the semaglutide. What you see is, this is a weight loss over 4.25 years. This is straight out of the SELECT trial, and what you see is, around week 39, you're about minus 10% weight loss, and by the time you get to 4.25 years, you're, you've lost minus 10% weight loss. You have about a 4-year plateau. You hit a rock, you hit a wall. So the only way this can happen is you lose weight, but you're eating... and excuse me, your appetite's been decreased because of the drug, but you're eating because of the muscle loss.
If you looked at the far right, and people just don't realize this, this is an eight-year study looking at testosterone. This is in males. Can't get testosterone in females, but we use the same androgen receptor with a neutral anabolic agent. And what you see is, these patients do not have suppression of appetite, but yet they lose weight. In fact, they go, by the time they get to minus 10%, they keep going. The plateau is gone. So an anabolic agent, you can see weight loss over time, and you keep your muscle, and if you add the two drugs together, what would that look like? What would that look like? And so the clinical trial that we're doing is a Phase 2 called the QUALITY Trial.
It's a Phase 2 double-blind, placebo-controlled, randomized dose-finding trial of enobosarm, and the goal is to prevent muscle loss, increase fat loss, because the drug can do both, in patients receiving a GLP-1 receptor agonist for weight loss. I'm happy to report enrollment is complete, and the sample size is 165 patients in three arms. These patients are older patients, which means it could be informative, meaning that they have lower muscle reserve, over the age of sixties. I mentioned obese, and they're taking the GLP-1 for the first time. The one we picked is Wegovy, and they get randomized to three arms, and that is GLP-1 by itself, GLP-1 with enobosarm three mgs, and a GLP-1 with enobosarm six mg, and the primary endpoint is lean body mass at 16 weeks, using a DEXA scan.
This is high precision. You can measure this, and the reason we're going up on enobosarm is not to try to, quote, "build more muscle," because the goal is to preserve muscle, but it turns out that if enobosarm can burn fat, can we burn more fat and hold on to muscle? And what we do know is 16 weeks is plenty of time, because it turns out that 50% of the weight loss that occurs in patients with semaglutide happens in the first 16 weeks, and they lose about 40% of that body weight is in muscle.
And if you look at bariatric surgery, which is a good surrogate to understanding what's happening with the GLP-1 receptor agonist, about 55% of the muscle loss that's gonna occur happens in the first three months. So that means that window is a good window to look at whether or not an anabolic agent like enobosarm will work. Now, we're taking it one step further. Everything is focused on induction. How fast can you lose weight in the shortest period of time, and take no prisoners, take muscle, take fat? Well, the world's gonna change. People are not gonna accept that. But the problem they're having now with these new induction medicines is that they wanna stop the medicine. What happens when you stop the medicine?
You get the rebound weight gain that's mostly fat. So this extension study that we're doing is stopping the GLP-1 and keeping enobosarm. So the goal is to blunt that rebound. And so where we are now is a study, the study is fully enrolled, and we expect to have data in January of 2025. And then the second part, which is what happens when you stop the GLP-1, we'll have data in April of 2025. Now, people have come back and said, "You know what? Veru is gonna..." If you look at the research analyst reports, "Veru is gonna hit on lean body mass, 'cause this drug, that's what it does." Our concern is, are they gonna hit on physical function? Well, let's think about that for a moment.
So first of all, physical function is what the FDA wants, and physical function is, call it a next step after strength. So in other words, the first thing that happens is you build lean mass. That lean mass consists of muscle, so you build muscle. That muscle should increase strength, and that strength should translate to physical function and quality of life, and testosterone, again, we're using that same receptor, the androgen receptor. What do we see? We see an increase in lean mass and muscle mass. We see an increase in quadriceps muscles. Quadriceps are your upper legs. Your upper legs are weight-bearing muscle, so you're walking all the time and exercising, and if you have an anabolic agent, that's what you're gonna see. You're gonna see your legs get bigger and stronger, and that's what you see.
You see increase in chest and leg press strength. Leg press correlates with stair climb test. FDA likes the stair climb test, which I'm gonna tell you more about. Stair Climb Test is a function test. Patients have to get in and out of a chair, in and out of the tub, up stairs. They like it. It depends on leg strength, and it depends on leg function, and it turns out that testosterone, if you have strength in the legs, you have the, it correlates with improvement in stair climb, so physical function is all related, again, to lean mass, muscle mass, leg mass, leg strength, and then physical function. How about enobosarm? Well, we've shown with our multiple studies, you know, at least six studies, showing that we improve lean mass and muscle mass. We increase muscle strength.
Remember I told you about the woman that the postmenopausal woman had an increase of leg press of 22 pounds in three months doing nothing but taking the drug. We use physical function. The physical function endpoint we used was stair climb. Now, to pause for a moment, the FDA told us not to use grip strength, not to use leg press, not to use chest press, okay? So it's a functional endpoint. It's critical. So if a study is not measuring a functional endpoint the FDA wants, then it's not a functional endpoint. That's why I dotted that. So physical function and quality of life are endpoints the FDA views as regulatory endpoints. What has enobosarm shown?
We increase lean body mass, we increase muscle mass, we increase quadriceps muscle volume, we increase leg press strength, we increase physical function in stair climb test, unloaded, meaning the patient doesn't have a backpack on. They just walk up. So we know that from our three mg data. How about the six mg data? That's the unknown in the study, but the three mg dose, you know, it looks pretty good. So this is what we're doing. Now, the question becomes, okay, let's now ask the question. All right, I get it, but how about in the patient population that we're talking about, the patients with obesity, what do we know about these patients, okay, and muscle? Well, the first thing we know, if you look at the semaglutide treatment, they are actively losing muscle.
40% of the weight loss consists of lean body mass, which is muscle, by 68 weeks, and 49% of the total weight loss at 68 weeks occurs by 16 weeks. And if you go to bariatric surgery, which is patients that have surgery to stop their appetite, 55% of that muscle loss that will occur over that 12 months happens in that first 12 weeks. So we know we got the right window. Now, this is new data. This was just recently published by Abhikashi Savidjua, and this is showing that extreme weight loss by bariatric surgery. Remember, GLP-1s and weight loss drugs are so new, but the bariatric surgery has been around for a little bit.
So they actually did a meta-analysis, looking at 24 studies, consisting of 666 subjects and at three to 12 months after bariatric surgery. And yes, they showed significant decrease in absolute lower limb strength, and they also showed that the more weight you lost, the more weak you became. That's an important point, 'cause to date, you've been hearing in the press: Is it important? Is it clinically relevant? I just told you about fractures. It's clinically relevant. But now I'm showing you data that just came out this month from a meta-analysis done independently, telling you, yes, lower limb. Now, why lower limb? It's all about gravity muscles, anti-gravity muscles, being able to go up steps. Those muscles are what you need the most and are the most important for activities of daily living.
In our previous studies, enobosarm three milligrams increased lean body mass, quadriceps muscle volume, leg strength, press strength, as well as improved physical function by unloaded stair climb test, okay, between 12 and 21 weeks, and this study is 16 weeks. Now, to increase the sensitivity, I'm gonna show you what that means. We're gonna put a backpack on these patients. So what do you mean? Well, people saying, "Well, if you lose 10% of your body weight, you're gonna feel like you can get around better." Well, that's not the question. The question is, what's their strength? If you lose muscle, do you lose strength? So this is a stair climb, and the analysis is a power analysis.
This is an eight-step stair climb, and what you do is you put a computer pad that measures time at the base and at the top, and then you measure how the rise of the... which is your distance. And now you can see that, okay, you're pulling your body weight up those stairs for that distance, and you can calculate, based on how fast you go up, power... and it's gonna be in watts. And just an interesting anecdote, you know, one horsepower, humans do about a 1/10 of that. So 10 horses give you one, 10 humans give you one horsepower. And so what we're doing is we're saying, "Okay, come in." They do this stair climb, and we put a backpack on them with 10% of their body weight.
So if they're 300 pounds, they get a 30-pound backpack. Then they come back sixteen weeks later, they're losing all this muscle, and we're gonna stress them. We're gonna put that same backpack back on them, and so in some ways, we're kind of replacing the weight they lost. Now go up those stairs, okay? And now see what happens when you give enobosarm. So this is gonna be one of the first times that someone's gonna be looking in the right patient population, over the age of 60, in patients that will tell you whether or not they're weak because they have reduction in muscle reserve, and show that we hit a function endpoint. Now, the reason that's important is because the FDA has told us, for the endpoint, for our primary endpoint in Phase 3, they want an all-comer study.
The reason for that, they said, "Look, we'll let you get away with going after older patients, but, you know, muscle preservation is important for younger patients, too, for two reasons. One is they need function, and two, you know, if you're successful in the older patients, then we won't have the safety database we need for the younger patients." It makes sense. However, you know, for other companies, they've been saying, if you have an incremental weight loss of 5%, then you're good to go, okay? However, if you don't hit that 5%, then for these other companies that are not measuring function, like myostatin inhibitors are known to have a difficult time measuring function, then you're kind of in trouble.
'Cause you've shown that you put muscle back on cosmetically, and you're not even measuring function, and the weight loss that happens in the weight loss drug by itself, versus the weight loss drug plus your combination, you're in trouble. So in our situation, if we hit. The FDA is not committing to 5% weight loss. They're saying, "You have. If you have a greater weight loss, and you have function, that's a win. That's a win." That's why we're spending a lot of time with function. Now, the other pushback we got is a little bit about safety, because SARMs have gotten kind of a bad rap. Now, that's not fair, because we're the, you know, we're a SARM that's been around now for 15 years, 27 clinical trials, over 2,000 patients. So we have data.
We're not the ones that have data and ended up efficacy or safety falling out. A SARM has to be empirically tested, because you just don't know what the off-target effects are gonna be. We've been through that, and so if you look here, what you'll see essentially is we're not much different than placebo, and this is 500 patients in placebo, 500 patients in enobosarm at 3 milligrams. If you look at additional adverse events of special interest, again, you'll see we don't have the GI toxicity, so you're gonna give it with a GLP-1 drug. The GLP-1 drugs have a lot of GI toxicity. You don't wanna add to that. We also don't see. You know, people say, "Well, testosterone causes blood clots." We didn't see that.
ALT changes and drug-induced liver injury, we don't see that. ALT is elevated in this subset of 3.7% versus 1.4%, mostly Grade 1, a couple Grade 2, never saw a bili go up. So we have data showing you about safety. The other safety issue that people brought up is, how about the lipids? Okay, what do we see in lipids, right? We see a decrease in HDL, but we don't see a change in LDL, IDL, VLDL, trigs, so all the pro-atherogenic stuff stays the same. The anti-atherogenic stuff, HDL, and you've already heard that HDL's kinda got a bad rap because it's not about numbers. So that's important.
What's important is that you would expect, if you did, if you looked longer, and this is what you see with the testosterone data, you see with time, this is testosterone, HDL goes up, in spite of the fact it starts going, i t started out with a lower number, and then you'll see that LDL, triglycerides, all go down with time. But that's not what's important. What's important is the cardiovascular outcomes. Okay, well, we're very fortunate that testosterone has recently completed a two-year cardiovascular outcome study in 2023, in 5,000 patients. I know it's small, but, you know, you're welcome to look on our website, and we'll give you the reference. But if you take high-risk men on testosterone, follow for 33 months, there is no signal. There is no cardiovascular signal.
This has put to bed the testosterone, unfortunately, lingering issues of, you know, are you, can you get in trouble with anabolic agents? So that's, that's a check mark, say, "No, that's not, that's, that's not going on." So in summary, enobosarm is a non-steroidal, selective androgen receptor modulator. We have a lot of data showing that we can avoid muscle loss, improve physical function, directly burn fat. What I didn't tell you, because of that, you see a decrease in glucose, and it lowers insulin and reduces insulin resistance, builds bone, large safety database, and we're not converted to estrogen or dihydrotestosterone, which women can take it without masculinization. We have not seen drug-induced liver injury, and we don't have the GI side effects.
Now, other people are working on other things, but most of them seem to be in the category of myostatin inhibitors. Myostatin inhibitors are delivered by IV or SubQ. As I mentioned, the biggest issue is function, and so I think, you know, if you're gonna give a muscle preservation drug, I think you need to be prepared to show function, and if you have a category of drugs that have never shown function consistently, it makes the SARMs look so much better because we have shown, and testosterone has shown, physical function consistently. This market's not going away. Obesity is growing. What makes this very interesting for us is that all of these agents that suppress appetite, the body doesn't know.
When you suppress appetite, the same thing's gonna happen: you're gonna lose non-selectively muscle and fat, m uscle and fat. So every one of these agents that are being put out there, we're gonna need a drug that preserves muscle, and the more dramatic and drastic the weight loss is in that short period of time, you're gonna need a muscle-preserving drug. And that muscle depletion is setting off that rebound weight gain that happens when you stop the drug, then having an agent like enobosarm for maintenance could be very interesting. Our company currently has $29 million in cash, and our expectation is that, you know, we expect to see data for the Phase 2 quality study that had just been through. We'll see the data in January of 2024.
Because we know that that's gonna happen, then 12 weeks later, and a couple of weeks to scrub the data, we'll get the extension study. Again, the extension study is what happens when you stop a GLP-1, can we blunt that rebound weight gain so people can have a tool to use to stay at their ideal weight, and we'll have that data, and so I'm pretty excited about the opportunity. In summary, what I shared with you was that we're head of the pack now. All I know from the talking to people outside is that Lilly is not presenting data for Versanis Bio anytime soon.
Versanis Bio has a myostatin inhibitor that's being used in combination with semaglutide and for forty-eight weeks with a weight loss endpoint. So, you know, all the others are Phase 2 and kind of emerging, and it's all in that same category of myostatin inhibitors. But as a selective androgen receptor modulator, we're using the androgen receptor, we're gonna have data in January of 2025 . Look forward to going to the FDA at that point to design our Phase 3 program, and I'm proud of my team because, you know, November of last year is when we made the decision to do the hard pivot with all of this data that we had behind muscle and fat, and we'll have the answer in January.
So I appreciate your attention, and, if anybody has any questions, I think we have about a-