So Greg, we're incredibly excited. Thank you so much for joining. I'm super excited for a progress update on what you've been up to in terms of thymus rejuvenation.
Okay, well, thank you. Thank you very much, Allison, it's great to see everybody, I see that among our audience members, we have at least one volunteer in the trim x trial. So if I lie to you, she will straighten me out on this. So I'm going to share my screen if if we can manage to do that I actually have a presentation to give to you this time. And let's see if we can manage to make this work. Okay, so Allison said that this doesn't really needed an introduction. But I'm going to give you an introduction anyway, just to make sure everybody sort of up to speed on this, we start off from the same basic point. And by the way, thank you, Alison, for your invitation. This is a special group. And it's always a pleasure to interact with this group. Okay, so you know, all of this, but this is different graphics than I usually show. So I'm going to show this to you anyway, just to make sure that there's no stragglers in the audience is not quite up to speed on this. So. So the the general idea that we started off with is that the thymus is very important, and it withers away with age. And so you can see in the diagram on the bottom, the pink area would be the functional thymic mass, and the white area would be fat. And by the time you get up to 70 years of age, there's very little left in the way of functional phytic mass. And that is diagrammed in terms of the app, how the, it affects the anatomy of the thymus on the on the bottom of that figure. The reason that this is important is that we die because of this. And I've shown figures before about how mortality rate goes up, his immune system function goes down, I'm not gonna even repeat those for you and what you all know about COVID, I don't have to go through that again, with you. So the idea is that we have to do something about this, so that we can prevent our T cell population from being depleted, and Laos stop by the slings and arrows of outrageous aging. So that's where we started. And as you all know, the finances in your chest cavity. And the beauty of this approach to aging is that it's doable. So thymic involution, which is what this process of deterioration of the thymus is, can be reversed in many different ways. And there's a list of, you know, some of the ways that exist out there on the on the left. But I've highlighted the first item here, growth hormone or Soma tropen, because it's my favorite way of regenerating the thymus. And it's my favorite way for all kinds of reasons. One of those reasons is that it has been proven effective in many different species. So in rats, Keith Kelly, in 1986, showed that you can regenerate the thymus, both structurally and functionally. And in rats, and later on, it was shown that you can regenerate the thymus of the dog using growth hormone. And there's even a cat study showing the giving IGF one cat, which is what is increased by growth hormone radically changes the structure of the cat five moves the cortex. It's all pale because the fleet of cells on the right, and the old cat kindness and the rejuvenated cat, thymus, everything comes back to normal. And then before we came along, was even a few studies on HIV victims, using CT to show an improvement in thymic structure. So that's one reason
the dogs have their own special growth hormone. That's a different sequence.
I believe that they do. I haven't investigated that specifically. But presumably they do. And that's that's actually a key question because I'm also working with different people on a dog aging intervention study. And one reason that I'm not really thinking about trying trim on dogs right now is that I don't know how to get dog growth hormone and any kind of serious way. But if anybody has an idea about that, that would be great. Having said that, there are a lot of studies in which is a human growth hormone has been given to animals and been shown to be biologically active, but I'm afraid that that may lead to some side effects and so I think is probably not the way to go. So this is one reason that I like growth hormone is that it seems to work across the board. But there are other reasons too, which some of you are familiar with. One of them courses has to do with Safety, you know, there's a long clinical experience giving growth hormone to growth hormone deficient adults since 1996. It's pretty safe, the side effects are known. And they're reversible and mild. And it has an addition to not having too many bad side effects. A lot of positive effects, including accelerated wound healing, helping with learning and memory, you know, promoting various good processes in your brain like making new synapses, new neurons, posing Alzheimer's disease, and then in the periphery growing cartilage, which might help to forestall arthritis, as we get older. And what we're illustrating in this figure is, it's the last couple of points, this profound effect of building up body, lean body mass and burning fat. So you can see what happens to us as controls, if we're not treated with growth hormone, lean body mass goes down, and the mass of your liver and your spleen and your kidney, in your in your muscle, it all goes down with with age, the only thing that goes up with is fat, which is just the thing that most of us are not that fond of having increased with age. But if you start growth hormone, and keep it going for a year, all of these trends tend to reverse. This is really a deep, deep biological, profound change. And as part of this if regrowing back, your liver, and you're growing back your muscle, and you're growing back your skin, it turns out, you're also going back to your thymus. And that's really the thing that people have overlooked, for the most part in the past is that key part, the thymus, which you need in order to stay alive. So there is a, you know, a particular side effect that I was concerned about, which is that growth hormone induces the production of insulin. And that is a pro aging factor. But I was able to show many years ago that that can be blocked by co administering the growth hormone, a DMCA. And the good thing about that is that the WGA, in and of itself has many different anti aging features. Every This is all cause mortality, etc, etc. It's also known as the neurosteroid. It's present in the brain, it probably helps protect against brain aging, like growth hormone does. And some people when they're taking the HTA, especially women tend to experience an improvement in mood and that sort of thing, perhaps related to its actions in the brain. But sometimes THC is not enough to counteract the veto genic effect of growth on this, this increase in insulin. And for that we add in Metformin, which has another number of advantages. You guys have heard Nir Barzilai speak about the virtues meant forum, and it's an insulin sensitizers. So it strikes at the heart of this problem. It also has a lot of other beneficial effects. So I think this is a winning combination. And all these interventions are obviously pretty powerful. In combination, the sum of the of the combination is, is more than the sum of its parts, basically, which helps to explain why we got some good results we got, I think, so we started the chrome trial with
Greg very quick, am I missing a question? Yeah, very quick one during the previous slide. Um, do you know that if you if one monitors with a continuous glucose monitor, which is easier than monitoring insulin? How does that affect this? Like, do you think that Metformin and thta are just so good that even if you don't have an insulin problem, it's a it's a win? Or do you think that this is really mostly because of the anti insulin genic features of those?
Yeah, I know that DJ has effects that are in addition to its anti insulin effects, Metformin may have as well. But obviously Metformin was developed to be, you know, an anti diabetic drug, and that's probably one of its major foe sigh of action. But I think that the HCA is its effect on insulin is only present if you're raising insulin with growth hormone, it seems to be particularly aimed at that that particular endpoint. There's one study that indicates that the HCA can lower insulin in ordinary people. But the vast majority of studies say that it cannot. So the only the only case in which I think is really reliable in reducing insulin is when insulin is raised by growth hormone. I think that that's not a coincidence. That's the reason that I propose the he in the first place is that when we're young, we have plenty of growth hormone, but we're not diabetics. And so I think the reason for that is that we also have plenty of thta. So by combining the two, you the HA naturally physiologically opposes the CBT genic effective growth hormone, whereas Metformin is just there is a general purpose, insulin sensitizer, that helps without having any built in physiology behind it. Okay,
let me let me ask you a slightly different way very quickly. Okay. Does growth hormone, increase insulin without increasing blood sugar? Ah,
well, it depends. It's a matter of degree. So the first thing that happens as the installing goes up. And if you keep increasing the dose of growth hormone too much, eventually, the increase in insulin is not enough to overcome the insulin resistance that's induced by the growth hormone. And then at that point, your your glucose can go up as well. So both of them will go up, but it's a matter of dose. Thank you. Okay. You're welcome. All right. So that's kind of the background. And because of all that background as well, now, we did the grim study, based at Stanford University was held from 2014 to 2015, or two cohorts. The first cohort was the larger one, which you see the center, second cohort, which is three guys, and you see them on the right there. And the aim was to regenerate the thymus using this novel combination of drugs called, you know, growth hormone, DHT, and Metformin. FDA consider that a new drug entities, we had to get an ind from the FDA to do this study, but we did that only had nine calls. In the end, we actually had a 10th guy who dropped out after about a month due to anxiety primarily. Yet, he never actually should have been in a trial, he had a high familial cancer, cancer risk. And he was worried about taking growth hormone, but he wanted to get his time as regenerated. So he entered the trial in the first place, but then got better of it after week after month and dropped out. So the treatment is you give this combinations cocktail four times a week for a year. And items are juggled and optimized for each individual, frequently throughout the course of that one year. And as you know, we published this in September of 2019. And it got a lot of attention. So the trial was pretty successful. Even though it was only intended to be a pilot study and a dose ranging study, it turns out all kinds of interesting things came out of this trial. And here are a few of them that related to safety and Immunology. The first thing was that we did regenerate the thymus, as you know, and we documented that by disappearance of thymic fat. But since the thymus is located under the breastbone, the sternum also has fat in the bone marrow of the sternum. So we looked at the regression of fat in the sternum as well. And we saw a regression of fat in the, in the bone marrow of the sternum as well, but it wasn't nearly as profound as what we saw in the thymus. Probably because we're not just burning fat, we're actually regenerating functional thymic tissue. And evidence for that is shown in the in the middle set of figures on the on the left, showing an increase in naive T cells, and recent time, Democrats. And then below that, in terms of safety, we saw several indications that cancer risk is actually going down. Even though when you're given growth factors like growth hormone, you're always worried about whether you might be promoting cancer, but we saw a reduction in PD one cells, which are cells that are basically in competent and they prevent your body from attacking cancer. Those declined with time. We also saw a decline in prostate specific antigen, which is a marker of cancer risk in the prostate. There's a spike in the Mental there, because some of our guys got a little out of control and
engaged in sexual activity before they got their blood drawn about six months into the trial. And so that screwed up the ass. But as soon as we corrected that behavior, by telling them not to do that right before getting their blood drawn, everything can walk right back down to normal. So that's kind of another aspect of the treatment, which is a good side effect, actually. And then there's something called the lymphocyte to monocyte ratio, which correlates with all kinds of cancers, and high ratio is good. And our ratios went up, at least based on the way that this ratio was measured at Stanford University with their sophisticated sight off measurement techniques. So we felt very reassured that cancer risk was not being exacerbated. And then in terms of other immune aspects, C reactive protein actually decreased in the in a trial, which is a sign that we're not increasing inflammation. Globally speaking, we're actually decreasing inflammation, that list is sensed by CRP. And then the last thing was insulin. So we gave Metformin and VHA to control insulin levels. And we were not completely successful with that. But we did suppress insulin fairly well. And most people in the trial had insulin levels below the median for the general population, even in the face of all this growth hormone that we're giving, except for one guy whose insulin went up at the very end of the trial and kind of screwed up our statistics. But generally speaking, it was it was satisfactory. And then unexpected results that you've probably heard of, there's one guy in the trial in particular, who had his hair start getting darker. In the course of the trial, his wife pointed it out to him. So we started paying attention to him. And we have several photographs of this change. A couple of other people in trial seem to have had the same effect, but we didn't have the chance to document them quite as well. A couple of things that we were not expecting is that the estimated glomerular filtration rate that the filtration rate of the kidneys, actually went up. Over time on that was statistically significant in different time points. And overall, it seemed like it might have even been continuing after the treatment ended. And then, the last thing here is that this increase in lymphocyte to monocyte ratio, which I mentioned to you before, has really driven mostly by a reduction in monocytes and monocytes actually destroy tissue and AD. And depleting tissue and ad is a great way to get yourself aged. So reducing these cells might be one reason that we saw some of these benefits which seem to go beyond just immune system aging, and makes you wonder if there was a global aging reversal. And as you all know, now, that's what we saw. So just to summarize this for you, we measure the epigenetic age based on four different epigenetic aging clocks, before treatment, and during the course of treatment. And we measured the change that took place is the difference in epigenetic age minus age during the the treatment, compared to the epigenetic age minus age before treatment. So the epigenetic age minus age before treatment will vary from every individual. But if we subtract that for each individual from what's going on in time, we isolate the effect of treatment, independent of somebody's background, as you can see, in every case,
they start DNA methylation aids, the fino age hanham, aging clock, and the grim age clock, epigenetic age went in reverse. And you could detect it at nine months into the trial. And you could also detect it at 12 months, even more so. And what you see in panel is an average of all of these results, which are measuring epigenetic age in different ways. And then as you know, probably, if you look at the difference in slopes from zero to nine months, versus nine to 12 months, and do a statistical test on the slope, you find that it's statistically significant, which means that the epigenetic aging reversal effect was accelerating over time. And you're going about four times faster in the last three months of the crowd, and you were in the first nine months. So it takes the body a while to respond and realize it's supposed to be younger than it is. But it was it was an interesting result. So the question that we're left with is result of all of this Is this real? Is this some kind of a fluke, as some kind of error on our part? Or is this actually a real phenomenon. So the rest of the talk will be pretty much devoted to looking at that question from several different angles. So you may have seen this figure before, I've shown this several times, I'm very impressed by this data. This is a compilation of results from five different individual experiments that were done and published separately. And this all sort of put together. So it's, it's been shown in the past that if you give a thymus transplant to an old animal, you can improve the crosstalk between brain cells through beta receptors found in the brain, because the beta receptor population plummets with aging and it restored by a thymus transplant, and you can lower plasma insulin levels. So the it seems like the dymo somehow helps insulin sensitivity as well. And in the liver as your as you get older, and you happen to be a rat or a mouse, you develop this condition of tetraploidy, a lot of liver cells have twice as much DNA as they're supposed to. And that's actually reversed by the thymus transplant. So we knew that thymus regeneration seems to have the ability to reverse non immunological aspects of aging. And that's kind of what we saw in trim. So that's consistent with, with our our study actually having a real effect. But it's not just the thymus because if we actually correlate epigenetic age reversal with reversal of thymic, involution, you find that there's, there's no statistically significant correlation. So we think that there's two independent effects that may be driving aging reversal. And in our, in our volunteers, we've mentioned that lowering the monocyte level may restore tissue and ad and if you restore tissue and ad in mice, you can reverse mitochondrial aging and other aspects of aging and, and postpone the onset of age related mortality. So that's another possible reason why our effects can be sort of considered to be plausible. And then, as I mentioned before, each one of these agents that we're using has been shown to oppose aging in various ways, probably, to a large extent, in complimentary ways. So combining them, it's many different anti aging pathways. In this this catabolic effect of aging has been opposed by the anabolic effects of both growth hormone ndhca. So it's kind of believable that that it might have some profound effect on aging. And I just point out in passing here that we're, we've all heard about heterochronic parabiosis. And there's debate about whether it's youth factors going from the young to the old animal, or old age factors just being diluted from the old animal, probably they're both true. But last time I spoke, I really can't play about this, I kind of convinced her that the evidence is supportive of the youth factor idea, you know, despite her arguments to the contrary. And I just have to point out that in youth, you have lots of growth hormone a da ga, so that might be part of the effect of this heterochronic parabiosis effect, benefiting the older a pair of bionic but here's some new evidence that you haven't seen before. So Steve Horvath decided to go back and retro retrospectively look at the trim data
using a different measure of aging. So we look at the fino age clock, epigenetic aging clock before. But that requires that you take DNA samples and that you measure methylation sites, and that you wait until the end of the trial. And so you don't get results during the trial itself. But there is a component to the female age clock, which relies only on testing things that are available and plasma or blood, some of the white cell populations or red cell populations in the blood. And so Steve went back and recalculated this plasma aspect of female age four guys in the trim trial, and found that on average, just as we found with the epigenetic clocks, time going back by two and a half years in the female age, plasma clock kind of went back by two and a half years as well. And these are just our best four examples probably from from that retrospective analysis, showing female age going backwards in time using this This fifth way of estimating biological age. So that kind of gives us more even more confidence of what we saw based on the original. for aging clocks, we now have a fifth agent clock that we can add to that. And it has the advantage of being able to be something we can check on in real time, we don't have to wait until the end of the trial to get some idea what may be going on. And we're actually doing that in tramex, as you'll see in a bit. And I just will say, parenthetically, on the left, what you see there is the female age, versus the actual age, the chronological age. And all the white gods are people who were in the trim trial in different stages of being in the trial. And the the line, the identity line is the heavy black line. And you can see everybody in the trial was pretty much younger, biologically than they were chronologically at the start of the trial. And yet, we can see this reversal of aging based on the female age clock in spite of that, which also agrees with what we saw with the epigenetic aging clocks. Okay, so I've given you a lot of hand waving about, gee, you know, we think that this is real, we think that all kinds of reasons to believe our results, but the only way to really know is to repeat the experiment. So that's, that's what we're talking about for the rest of his present famous presentation. And as the main point of this talk, since is the part you haven't heard about before, too much. So we have launched something called the trim x trial, x standing for extension of the original trim trial. We're repeating it, we're extending it a number of ways. It's on clinical trials.gov, if you want to read about it, and it includes both men and women now with an expanded age range from 40 to 80 years of age. So far, we have not enrolled anybody less than 50. But we have enrolled people right up to the age of 80. In fact, we've got one guy in who formerly qualified for the trial about one day before he turned 81. So he just managed to squeak in by the skin of his teeth. But we have been starting this and the trial is now headquarter, local to us for convenience. It's at the Lundqvist, one quist Institute. I'll tell you a little bit more about Lundqvist in a second. And you can see our first cohort of three people. And at the end of November of last year, standing there in front of our headquarters building, the banquet system with Bobby Brook, our CEO next to them. Okay, so I used to know about something called harbor UCLA. It was it's a big medical complex in Torrance, California. But it's part of this larger
medical and research complex of buildings and structures. And somewhere within that big general medical research complex, there's something called the Lundqvist Institute, which has several component buildings to it, which are sort of blown up and magnified on the on the right. So the upper right of that figure, there's a building called the medical research laboratory, also called the bio labs. This is where our corporate headquarters is located. And it's where we give seminars to cohorts that come in for the trial. We have two modes of signing up for the trial, you can either come in person, if you want to have some specialty tests done, or you can participate entirely by telemedicine if you wish, if you don't want to have these extra tests done. But we give informed consent, we give seminars, we can have medical exams done either in person or or by telemedicine at the at the bio labs. nearby the bio labs are three other buildings of interest. The first one, which is highlighted, you know, when the green box on the left side is building where we can get a dexa scanning for body composition, your lean body mass, before and after treatment. And also, this is where you go to get your blood drawn by the way everybody participating in the trial is set to get a COVID-19 test as well to make sure that you're not infectious before being on the premises of the of the camp campus. We also in addition to offering people these is body composition scanning refer them CT imaging of the thymus and arts, we can look at them as regeneration. And we've had a number of people take us up on this, including some of the women in the trial, because we have no data on thymus regeneration in women so far, actually, nobody does. So we're going to get the first evidence ever on that score. And we can also image coronary artery calcification, which correlates with with the risk of death and disability. And we don't know if that will be affected by our treatment, but it would be fantastic if it were affected by our treatment. And then the last building on is where you can get cardiopulmonary exercise testing done, and leg strength examination, they want to know if you get stronger as a result of being in the treatment, and whether your exercise capacity improves, because that's a measure of frailty, and frailty, of course, is not good for anything. Okay, so this kind of shows the course of the enrollment activity so far, we began on Thanksgiving week, in November of last year. And the total number of enrollees has been going up pretty steadily ever since we only have five women in the trial at the moment, you notice that there's a dip in the enrollment numbers around month three. That's because we had two people in the trial who were sex hormone enthusiasts and decided after passing their enrollment blood exam, that they wanted to tank their testosterone and estrogen levels up to above the normal range, like vastly above the normal range. And we pointed out to them that that will involute their thigh muscles and destroy the effect of the treatment. But they didn't want to hear that. So they eventually dropped out after about a month or so. But everybody else has stayed in the trial. And as you see, by the black lines, at the end of these curves, we're expecting right before the end of the six month, which is May, that we'll have another cohort of one added onto the list. So we're still continuing to enroll people. Our target for enrollment is on the order of 80 people, something like that. In trim, we had nine people, as you know, here, we're up to about 23. And so it's been an interesting challenge for me, because this is a very customized, hands on kind of treatment protocol. And so we've had to work out ways to handle that. So this schedule for the week, has been uniformities for almost everybody. And of course, there are exceptions sometimes as we go along. But
we start here with Monday. So we usually if we want to test how people in the trial are doing, we have their blood drawn on Monday, they don't get an injection that day, that they're going to inject it on Tuesday night. And by drawing on Monday, we have plenty of time for the results to come in soon enough for me to look at them over and contact the volunteer on Saturday on Sunday, and let them know how we want to change their doses for the next time that are full of the trial. So usually on Sunday is when the doses are updated and, and new doses are tried out, basically. But we had to do it this way. Because if we draw blood on Thursday or Friday, sometimes they do not get analyzed quickly because of the weekend. So we we measure some esoteric things that have to be shipped between different laboratories. And sometimes that creates problems. So by doing it this way, we can update everybody on the same schedule. So I only have to work on updating people basically, on Friday, Saturday and Sunday, and mostly on Saturday and Sunday. So they usually burns by entire weekend, every single week. So we'll see how much we can expand this population. But thanks to Bobby's brilliance, computing, we're able to download the blood chemistry results into a specialized Excel file that takes all the data puts it where we want it and then allows me to copy it into specialty files for each individual. So I can track how each individual is doing with respect to all kinds of different parameters and ratios of parameters and all kinds of things so that I can I don't have to manually transcribe the data like I had to before which is a huge help. And we're still working on algorithms to help me with the those updating process. But it turns out to be fiendishly complicated, and it's not going to be all that easy to reduce this to an algorithm. But we're starting to do that now. So that's how we're managing the practicalities of the trial. And just to tell you how things are going, in general, how the volunteers are reacting to the trial, some people have said that they can feel themselves getting younger. Some people have said that their massage therapist tell them that they are more ripped than they've ever been. People feel more energetic, I've actually experienced that myself, because I'm one of the guinea pigs in this trial myself, I finally enrolled myself in the in the trial. And so I can attest to this sort of thing. Some people have reported joint pains, but so far, nothing has gotten to the point of making anybody have to back off on their doses or, or drop out of the trial. Even though, you know, joint pains are known side effects of growth hormone administration is because it wants to grow you and that includes growing your bones. But of course, after puberty, you cannot grow your bond. So in the short run, you may have some arthritis type pain. But my my theory is that in the long run, you're actually better off because you're pretty strong restoring cartilage that we tend to lose the age. And if you have more cartilage, then in the long run, that should be beneficial for you. So nobody's dropped out to the side effects. We did have that those two dropouts for the reasons that I described, I have to tell you also, that sort of similar to the experience, we had to trim, the trim x volunteers are extremely smart. They're very health conscious, they flood me with information, mostly about themselves, a lot of them are bio hackers. And they have been tracking themselves for years and years. And they have reams of data. And some of them are some send us data that that are collecting parallel to the trial through other doctors and other lab
clinical chemistry labs. So we got plenty of data. In fact, some of the volunteers actually asking us to run more essays on, which is pretty cool, because it allows us to look at things that we otherwise wouldn't be able to look at. And, and that's actually been illuminating in many different ways and learning all kinds of new things about female sex hormones that I didn't know before, how they're processed, and all kinds of stuff. So it's a learning experience. We also have a lot of people in this trial that are not in such great health. We have people with Bell conditions, we have people with borderline kidney failure, you know, the not of not in kidney failure, because we don't allow that, but people are kind of on the edge. And so we have, you know, pretty old people and pretty skinny people and all kinds of people in here that we didn't have in trim. So we're learning all kinds of new stuff about how to handle these cases and how these cases respond. So it's, it's really a positive experience. And then I'm going to spend the rest of this presentation talking about preliminary results. Now, as I've shown you, we're only less than six months into this trial so far. And that's just for the first three people. And in the end the trial, most people are in it for less than that. And we have a year to go to finish the first cohort. And we'll have a year to go after we enroll in last cohort. So our final results are going to take years to come in. But we do have preliminary results, and some of them are interesting enough to share with you. And some of them are expected meaning that they're actually replicating what we saw in trim, which is the whole idea of trim x is to see if we can repeat some of the things that we saw before. But we've also seen some really interesting things my view that are unexpected and new. And so I'm going to I'm going to share those results with you. So one of the things that we were hoping to replicate is this effect on CRP c reactive protein. You know, people have worried that regenerating the thymus and restoring immune system function might be bad, because one of the things that happens with aging as you have inflammation, and that's an immune function. And so if you augment immune functions, you might increase inflammation, but in trim, we did not see that. We saw a decrease in C reactive protein. And I'm just going to be showing in these figures I'm taking three exemplars and plotting their results out. So the first three time points, generally speaking, are baseline data. So we have our pre screening data point and then And when they enroll during the enrollment week, we take two more baseline samples. So generally speaking, those three samples are in agreement with each other. So that forms sort of the baseline for everybody. And then once you get beyond the vertical dotted line, now you're into treatment time. And I'm not specifying exactly what the time points are here, just to keep things simple. But what you can see in this case is that for two males and one female and these particular examples, you can see that C reactive protein is holding up fairly constant between one and two, but before treatment, and then falling in each case after treatment. So that seems like preliminary evidence that we're actually reproducing this anti inflammatory effect of the treatment. Another preliminary result that is consistent with the dramatic result is improvements in kidney function is one of the more extraordinary results of trim is that normally, as we get older, our kidneys always get worse. But in trim, the kidneys seem to get better. And we're seeing that in in trim x as well. In this case, these are all males. But you can see that the trend is pretty distinctly upward. And pretty quickly for the most part in all three of these cases.
We also saw in trim an apparent improvement in prostate health, meaning a reduction in PSA level and an increase in the percent free PSA, we're seeing both effects in trimix. So that seems to be reproducing the trim results as well. And these are just three examples. One person who had a relatively high PSA actually above the normal range, but had prostate Titus and we knew it wasn't cancer, starting to reverse pretty significantly after a couple treatments, or a couple of you know, intervals of treatment. And the other people starting out with pretty low PSA is but still improving, which we also saw in trim we saw in trim that regardless of what your baseline PSA was, it always went down no matter what. So, so these are pretty encouraging signs that we're able to reproduce at least some of the aspects of the trim trial. Here's the beginning of some new things that we've seen. So these two people showed a reduction in their triglycerides. Normally, I think what the trend is going to turn out to be although we don't have all the data yet, so we can't speak to this definitively yet. But I think that what we're generally going to see for most people is that as you begin treatment, and you begin breaking down fat from your fat stores, your triglycerides, your blood triglyceride levels tend to come up. And then as you sort of take that to a point of completion or steady state, then it will come back down again. But in these two cases, the the triglyceride levels came down right away, and in one case, pretty profound. So you'd like your triglyceride levels to be lower rather than higher. And so this is an interesting new observation that may pertain to a subpopulation of people in the trial. Similarly, we like our lows to be low or LDL cholesterol has to be low. And we've we've seen that in some cases, that's the case. So what you're seeing on the bottom part of this figure is that we had sort of historical data for some of these people, we haven't done a lot of lipid analysis and the trial. So in some cases, the LDL level had been measured pretty far back in the past, we didn't have any enrollment, weak data points, we didn't have data points two and three. But we can compare at least the legacy values of HDL to, I mean, to LDL to what we had very quickly in the trial and, and saw that the, the levels had come down significantly. So we're seeing all kinds of things like this. And I don't have time to go through all of the data. But this is another encouraging sign that we may be improving cardiovascular health, at least in a subset of our of our population. So we've discovered some new things also, that seemed like they're, they're likely to have some generality to them. Again, these are just three examples. And this happens to be a man but we've seen trends like this and women as well. So blood urea nitrogen, so I've already showed you that kidney function seems to be improving in trim max just as a dead end trim, measured by the GFR. But we're finding this new effect independent of GFR. So even people whose GFR is have been fairly stable Not not improving, sometimes show a reduction in their blood urea nitrogen level. And I'm very intrigued by this because my interpretation of this is that this is a sign that you're taking nitrogen out of the blood and putting it into tissues, you're building up your lean body mass, blood urea nitrogen is a consequence of amino acid turnover and breakdown. It's a waste product of amino acid metabolism. And to pull it out of the bloodstream, independently of urinating it out, implies that it's going into new proteins, making new proteins in the body. So very early stuff here, but I think kind of provocative and we'll see how this goes over time. Here's another one that I was very interested in lung function. So
I personally seem to have some kind of issue with gas exchange in my lungs, I've been looked at. And so I'm kind of conscious of co2 levels. If your co2 levels go up to around 30, or 33, are beginning to get above the normal range, which means that you're starting to have impaired lung function. And this tends to get worse and worse as we get older and older. And so here's an example then four different cases, two of them females and, and two of the males, in which the co2 levels seem to be going down pretty quickly with respect to the onset of the treatment. And yes, the data bounced around a little bit, but you can see that the trends are pretty consistent. So it's possible that in addition to the other things that we observed in trim that we're actually observing here, and improvement of pulmonary function, improve lung function, gas exchange function, that would be a very exciting new development to add into the list of benefits of a trim treatment. And is very, very new. So we also had the opportunity to check on something else that's been, you know, in the back of my mind for a long time. And that is how long do the epigenetic aging reversal effects of trim lasts. So we saw in trim that six months after the end of treatment, in some of the epigenetic aging clocks, there's a little bit of backsliding back toward sort of catching up with your true chronological age. But in grim age, for example, there was no backsliding six months after the trial, you were just as young relative to your chronological age as you were at the end of the treatment. But we had an opportunity here because one of we actually have two of the guys who are in trim are now in trim x. And we have this data for one of them. Where I was able to sort of reconstruct what happened to him over the last six years. So he finished his treatment six years ago. And we, you know, Steve Horvath, went back and back calculated his fino age plasma level, which we're calling fino bio age on the right, or PBA. So, pardon me for the inconsistency and nomenclature here, but we're talking about the same thing. So looking at it, this particular volunteer, based on the fino bio age, or female plasma age, at the beginning of trim, he was 56 53.6 years of age, but his fino bio age is 55.2. So based on that clock was actually 1.6 years older, you know, biologically than he was chronologically at the beginning of that trial. Now, if you look at Steve's calculations, on the left, you see that he started, he went from that starting age of 55.2, based on fino bio age, down to a biological age of about 42 at the end, which is, again in epigenetic age of 13.2 years. So you know, we you know that in trim people reversed by on average about one and a half years, but some people did better. And this is an example of that sort of thing. So, because he's now the same guy, and he's now in the new trial, and we can still calculate his female bio age in the same way that we did before. We can now look and see where he started trim. And he started trim with a female bio age of 2.6 years younger than his chronological age. So if you if you take into account the fact that he should have been at least 1.6 years older than his chronological age, based on what we saw in trim, he's still 4.2 years better off now than he would have Then if he had not been in the trial at all, and this is six years after stopping treatment, so this is encouraging this, this implies that this may actually last for a while, of course, it's only fino bio age, it's not all of the epigenetic aging clock, not DNA methylation. You know, it's in so it's it's preliminary data, but it, it indicates that maybe not only, you know, can we reproduce an anti aging effect in trim x, because we're actually seeing Well, actually, I'm jumping the gun a little bit, you'll hear about that in the next slide. Suffice it to say, we can still detect the effect that we induced six years earlier in this one volunteer.
That's encouraging. So here's the second aging clock result, we have the show out of the chromax. And again, this is all based on fino plasma age. So what you're seeing plotted on the y direction is the difference between fetal plasma age and in chronological age, and same data representations you've been saying. So before treatment, you know, to the left of the vertical dashed line, you see pretty stable, or even increasing differences, which vary quite a bit from volunteer to volunteer. But as in trim, our people were pretty healthy. And most of them have biological ages, at least based on this measure that are younger than their chronological ages. But as we began treatment, we're seeing in these three cases, at least, that the female plasma age is beginning to regress almost immediately. And this is interesting, because this is spread out over both males and females, and over age ranges. So the older female is up at the top, she's near the upper limit of age, for people who are eligible to enter the criminal trial, she was going in the wrong direction, depending thing at the beginning, but then she just showed this nice, steady improvement over time in her fino plasma age afterwards, and then compare him her to the other female, who started off ahead of the game by about 11 years or so. But in spite of that great advantage going into the trial, she rapidly went down to about minus 15, from minus 11. So she picked up four years of fino plasma age in a very short amount of time. Now, what we're seeing more generally, is that people don't respond this fast, usually, but that these people are responding pretty quickly, I think that we're gonna see a different pattern and other people, which is going to be very interesting in and of itself. But the other day that we have is consistent with this data showing that it looks like even at trim x, at least, if you go on the basis of this one, sort of do it on the fly kind of clock, where we're able to see evidence of aging reversal once again. So that's the preliminary results that we have so far. So far, everything that we can measure seems to be going in the right direction. So we're encouraged as so. And in conclusion, you know, things are going pretty well. And it looks like we're reproducing the the trim trial results. But of course, it's going to take years before we can really prove it. This is all sort of very preliminary stuff. But it's I'd rather have preliminary results that look like this than that, though. So I'm really happy to share this with you and to share with you the news also that looks like even in ways that we didn't know before that we didn't see and trim itself. Maybe because we just didn't think about it at the time. The aging seems to be going in reverse in these new ways as well. So I hope that that was illuminating to some of you, and sorry if I went to too much of the background, but I wanted to bring everybody up to speed. So thanks a lot for your attention. And if there's any further questions, if there's any other questions that you have, I'd be happy to discuss it.
Thank you so much, Greg, you have no idea how many questions you have. We have a few down voted, and maybe a few people have to drop off anyways because we're at the hour but I wanted to check Would you be able to stay on a few more minutes? Sure. Sure. Yeah. Okay. Well, let's see how many we get through let us know in case you have to drop off and you will be very outspoken with that. We won't we won't stop. I will get started with the first question. I may stop sharing your slide just for now. So we can all see each other but we may get back to eventually okay, but Thank you. This was incredible. First question without any ado, Andy,
great talk, Greg. I'm just curious, with the cohort being biohackers Have you controlled at all for other things like taking nr rep my son are fascinating. are you tracking those to see if you get additive effects?
Yeah, we those are ongoing issues with a lot of people. We have some people taking mass quantities of nr and no man, people taking a lot of resveratrol. Actually, you guys may know this, but the evidence in favor of resveratrol has fallen apart recently. And so some people who are fairly enthusiastic about resveratrol, I've been sending out this video, just demolishing the idea that it actually helps with with, you know, sirtuin function in humans. So yeah, and then there's this constant tension between what we're trying to do and Cr. A lot of the people in our trial are pretty skinny, and they are really CR Divo, tasers, one car guru who signed up for this thing at the beginning, but then when I told her she has to, sort of back off on CRS, he decided not to, she just couldn't part with it. But other people are working with me on that, because CR is a catabolic state, right it. But by depriving yourself of energy, you start to tear down your own cellular protein stores and energy stores to you know, give yourself the energy that you need to stay alive. And that's good because it tears away old damaged molecules. But what we want to do is the opposite, we need to grow you we need to build you up, we need to increase your lean body mass, we need to give you new cells in your thymus. And that's all inhibited by calorie restriction. calorie restriction in humans is immunosuppressive. And so we can't really have too much of that. On the other hand, we don't want to deprive people of the benefits of it. So we're trying to find the way to sort of optimize the balance between those things. And I can't say that we've exactly found that yet. But we're working on it. I'm
going to suggest a cycling, photography and refeeding and a cycling of growth hormone and caloric restriction mimetics rather than simultaneously doing all of it.
Yeah, you really don't want to do it simultaneously. So I point out to the guys and gals in the trial, that, you know, calorie restriction is good, but thymus is good, too. So you know, you don't have to do one thing all the time, you know, you can go from one thing to the other, it's like the, the song, you know, to turn, turn, turn, there's this to everything, there's a season, you know, there's a time to build out, there's a time to break down, right, there's a time to be on growth home, there's a time to be on car. So I think that you have to use your time and trim. Or you know, if you're doing trim, to maximize your trim benefits. And if you take a holiday from CR for even a year, you're not going to age by more than a year anyway. But the fact is, you're actually going in reverse. So the thing about the trim protocol is it actually makes aging go in reverse calorie restriction does not make aging go and reverse how the restriction slows aging down. It does not reverse it. So you can be calorie restriction all day long, and you will live longer, but you will not stay young indefinitely. So what we want to do is to make sure that you get the benefits of trim, and then to the extent that you can but combine that with a little bit of car. It's a good thing, and we want to allow that to happen. But we're still working out the correct balance.
All right, well, we need to make such a song. Okay, see your next. Yeah,
great presentation. My question is about the your speculations as to altering the protocol to make the growth hormone growth hormone administration less frequent, possibly to remove some degree of growth hormone resistance that might be induced, but also to make it let's say, you know, medically or commercially more acceptable for people. And in terms of, you know, the combo therapy, do you think that that that your protocol of administering them all at the same time would be the way to do it? Or do you think that there may be some different kind of protocol where the growth hormone and the Metformin and the VHA might be administered on different protocols?
I'm not totally sure I understand. But yeah, so the the real question is that you give things like Metformin and vhda when You're not giving growth hormone. And I don't see any good reason not to for the most part, there are some hazards of both. Sometimes you can go wrong with Metformin, sometimes you can go wrong with the HCA. So you have to be a little bit smart about it. But those hazards are probably no different, whether you're taking growth hormone or not taking growth hormone. So in trim, we ask everybody to take all these things simultaneously four days a week, and not to take them on the other days just to keep things simple and to and to reduce costs. But the cost of these things is really minimal, so that the cost issue is very minimal, minimal. And so in trim x, some people are taking these things more frequently than four times a week, and some people are not. And we're beginning to reconstruct some information about which way most people should go and exactly how you adjudicate that. But we're still in the process of figuring all of that out. But your point is well taken that we're using Metformin, a tha for a specific reason, in our protocol, and that's to block the diabetes genic effects of growth hormone. But that makes perfect sense to take them at other times as well, because they have independent benefits. So we're going to have a lot more information about that. They actually have some preliminary data, which I find very interesting, which I'm not going to go into more detail about right now. But But yeah, there's there's something to be learned there. Definitely something to be learned there. That's a great question, Steve. Yes.
Thanks, Tom.
Yeah, this is an economics question, which is whether or not investors are willing to support more expensive, larger clinical trials for drugs that are off patent. And there's a number of economists like Susan athiya, at Stanford, who have written both about this problem, but also different approaches to solving that market failure.
So you'd like me to just comment on that? Yes. All right. So here's the ultimate comment on that, actually, there's two, two major ways of addressing that issue. One is to create new pharmaceuticals that they're not off patent. And two is to create work around so you don't need the high cost items. So that the economics of it work out much more easily. We're actually working on both of those are, we've we've worked if you know, a fair amount on finding alternatives to growth hormone, which is the expensive item in our cocktail. So far, I'm not satisfied with those results. So we're not really ready to go down that pathway yet, but we're continuing to investigate that we're probably going to be getting more information on that with some volunteers, later this year. But there's another there's another way, and that is to make the growth hormone ourselves. So you know, growth hormone may be off patent. But every time you make a new variation, you have to go through another approval process with the FDA. And growth hormone is not perfect. So there are certain features of growth hormone that could be improved, without actually changing the molecule itself. If you change the stabilizing solution that the growth hormone is in, you may be able to gain some market advantages and matters of convenience for the consumer, that would allow a new patent and would allow that proprietary aspect to be overcome. And turns out that I'm a crowd biologist and my day job, I preserve kidneys at cryogenic temperatures and things like that. And so I know something about how to stabilize proteins. And I've got some ideas and nobody's had before. And I think that we can come up with a version of growth hormone that we can make ourselves about five times less costly than was what is commercially available now, that will be superior to commercially available growth hormone. And we have some people that are interested in helping us do some pilot studies to prove out that concept, if we can do that, then we'll own that growth hormone version, we will not have a patent problem, we will have a massive selective advantage over any potential competitor in the sense that nobody will be able to offer the same price that we can offer to our own treatment clients. And so I think that that can lock the door to 10s of millions of people getting our treatment, because then it will be much, much much or more affordable. And all of the marketing issues will be overcome. So that's a major thrust of our interest going forward. Unfortunately, we have very little money in the bank right now. But we have enough that we we should be able to move forward on that fairly soon. And we have a couple people we're talking to about that. So the That's, I think what the ultimate solution is. And that's the future of our company, I think. And then if we can develop lower cost alternatives, we will do that too. There's a one wrinkle there one particularly interesting possibility there that no one else has been pursuing that we're going to hopefully get some data on in the next year or so. And if that happens to work, it'll be really, really interesting. And that's all I can tell you about it.
So are you actively looking for investments at the moment I actively taking on investors or funders?
Yeah, we're always looking for investors. But unfortunately, the investors are not always looking for us. So and it's, it's for just the reason that Tom brought up, you know, they, they say, Well, you know, growth hormone is out there, you don't own it, you know, etc, etc. And we have a patent application on our on our treatment, but people worry about bootlegging and things like that. So we're we're growing our company by organic growth, even though this is a trial, we're allowed to make a small amount of margin for each person in the trial, beyond the cost. So we have our administrative needs covered. And we're, you know, we're actually demonstrating that there's a market for this product, even despite the high cost. And nobody's sort of going into competition against this so far, so at least not that we've been told. And so I think that we have a way forward through organic growth. And that will eventually lead to these new products that we were just discussing. But if somebody wants to jump in at this strategic moment in time, I think it could be a super good investment. That's that's my opinion.
All right, duly noted. a referral. Next question.
Hello, Greg, thanks for the presentation. I have a question. We know that there are some soft tissue like, you know, nose and hair that continue to go off throughout life. And I was wondering if you think that as the effect on this as it would increase this both? Not at all, the growth of
the both of you're saying the growth of hair? Oh, no. Here,
the nose, for example, the nose, our heels, I think they're going, you know, and do you think it just goes be increased by firemen, injections?
So let me just make sure that I understand the question. I'll restate it. And then if I restate it wrong, you can correct me. Okay, Raphael. So Raphael is saying that there, there are things in the body that go go on growing throughout life. And one reason that we look older, is not necessarily because we're falling apart. But it's because things keep growing. So older people have big ears, and they have big noses, and they tend to have big chins. And it's because your nose never stops growing. And your ears never stopped growing. And so if you take growth from wonder, you're gonna actually look older, because you're looking more like, you know, a big nose big eared old person. And I think Time will tell on that. But we haven't really noticed anything like that. I will say one thing, and that is that, even though all of the evidence says that we're reversing aging, people are not really looking younger, facially so far. And we may change that. I don't know if you guys have seen these advertisements on television for this product called Cerro vide call. Kim Douglas comes on and says, Oh, I heard about this youth hormone and it even gets rid of wrinkles. But you know, we're just not seeing that. And actually, I think their product doesn't work. So I think that we're not quite at that point yet. But we may get there. If we continue to refine things, we actually have some interesting ideas in mind that maybe help helping us out in that regard. But all I can say is that we didn't notice anybody's noses or ears or nose hairs or ear hairs or things like that getting worse and trim. And so far, nobody's complained. Actually, there's one person in trim x, who I will not respond to by name here who is suffering from the opposite problem from excessive hair growth. There's actually a problem with hair loss, but I don't think that's necessarily related to the to the trim x treatment. I think that's an ongoing problem. So I don't know if that answered your question, but that's about as good as I can do on it. I think.
I just wanted to quickly jump in on that. Greg, our follow up question. Are you on that subject? Are you gathering like daily facial pictures? Because I'm usually interested in that for measuring aging, but yeah, based on what Raphael just said, it's like a double reason to want to collect Yeah,
yeah. So we have taken photographs of people at baseline and we took a lot of pictures of people's hair. It baseline also, because we don't want to miss out on a hair darkening effect this time like we like we did last time. So yeah, that is part of the case. Yeah. Thanks. Okay, no problem.
Next up we have kale. Kale. Hey, how are ya?
Hi. I'm not now that great talk. I am stoked. Yeah. Yeah. So exciting the trends of the into, you know, phase two here. I have a question. And that has a finance market implication. And that question is this. So you mentioned improvement in GFR and glomerular renal function? And that question is, is this what this protocol be compatible with somebody who's had a kidney transplant is therefore on immunosuppressants? Because if you could extend transplant life by a year, okay, by two years, you're going to be generating a short term immediate. Besides for the health benefit, financial benefit that's going to tie right into, it's gonna tie right into Medicare. Okay. Yeah, you got a potential financing opportunity here. So what's so what's the deal? What do you think?
That's a really smart question. So I like to sort of amplify that a little bit. So there's all kinds of ways in which these subjects may intersect, you know, the kidney transplant subject, and what we're doing. One thing is consider the cost of the trim, x treatment, and all the monitoring, it's pretty expensive. For a lot of people, it's 18,000 a year, but consider the cost of a kidney transplant. Yeah, you're talking, you know, more like half a million or something like that. And then consider the cost of dialysis every year, which is, you know, in excess of 18,000, for a lousy quality of life, which you're dead about five years later, on average. So yeah, if we could marry these things, the cost aspects of the trim x treatment, even with all the monitoring thrown in, which is a big part of the overall cost becomes negligible, you know, in the context of treating somebody with a kidney transplant. So that's one aspect of it. Another aspect of it is that growth hormone seems to benefit kidney function. So if you have a transplant, it's not quite up to speed, but we might be able to even compensate for that deficiency. And, and help you in that ways as well. Now, there's two then competing additional considerations that have to be factored in. One is that, as you know, the reason that we're giving the growth hormone in the beginning is to regenerate the thymus not to improve immune system function. As you pointed out, if you have a kidney transplant, you're on immunosuppression. And so there may be a bit of a tension between those two things. So that's the first, the first aspect is, is that by improving immune system function, you may accelerate transplant rejection, and that would be a problem. But the other consideration is, is this other lofty goal, which I've had in the mind in mind for the last 20 years or so, which we haven't had a chance to work on yet. But again, this is another thing that investors can help us with a lot. And that is that there's a way and Gail, you've heard this story, because Gail was sitting in the room when I first introduced this concept of the Crim treatment to the world at a at a meeting in the Bay Area, called the health extension salon, I believe. And I mentioned at the end of the talk, that there's something that I called thymic magic at the end of the talk. And, and the thymic magic aspect has to do with the fact that the thymus actually has two jobs, it manufactures cells to destroy enemies, and it also manufacture cells that did not do not destroy a friend, in other words, self. And it's that second aspect, this is really interesting, because if you have a thymus, which most of us don't, you know, to speak of after the age of 30 or so, but if you have a decent amount of thymus, you can actually re engineer the thymus to accept any graph itself and not rejected. And this has been shown in every animal model there is of transplant and it always works, including in large animals. And it seems like something that would be doable in humans are based on what we saw in trim in other words and trim We saw we were able to regenerate the thymus.
That means that there's some place to do this engineering work on. It involves a minor surgical procedure to introduce the right antigens into the thymus. But once you do that, just give it a few months, and your transplant rejection should be eliminated for life, you can then go off immunosuppression for the rest of your life, and keep that kidney as though it were from your identical twin, which means it will last for 25 years instead of for five or 10 years. But it actually gets better than that, because you can then apply the same technology to curing all autoimmune diseases for exactly the same reason. Because an autoimmune disease is when the body forgets that you are you and it starts attacking you. But you can reprogram the thymus to recognize that that thing that is being attacked is actually you and delete all of the cells that are engaging in the attack. This also has been proven to work in every animal model has been tried in, which are a large number of them. And nobody has tried this in humans, just as nobody's tried to transplant rejection in humans yet, either. So we succeed as a company, these are other multibillion dollar areas that we want to get into. And again, that would be a nice place for investors to jump in here, I actually run this company called 21st century medicine during the day, we have a pig colony in the building, so we can do pig experiments. And there's a lot of interesting immunological work done on pigs. So we could actually test this rejection issue in the pig bottle with relatively relatively little overhead because the colony already exists. And I run the lab, so I don't have to charge my other company that much money to do these studies. So you know, that's another potentially highly strategic way that actually having investment in the company could help us, which will take us another 20 years to raise the money at the rate we're, we're going out right now. But of course, I expect that to accelerate. But just for any investor types out there. These are not fantasies either. I mean, the the animal studies are unequivocal. They're numerous, both with respect to transplant rejection and autoimmunity. It's just that nobody is bothered to try this. And people for reasons that escaped me, just as nobody bothered to try to regenerate the thymus in humans, until we came along, except for a few brave doctors working on HIV patients, because their patients were dying in front of their faces. And even they have seemingly given up on that process. Because they're worried about their patients getting cancer, which they haven't gotten cancer, but they do. So even that has been sort of dying out. So somebody's got to do these things. And darn it, we're going to do it if nobody else does,
one way or the investment number for those individual procedures, just to we won't hold you to
Well, we're looking for at least a million, but of course, that's nothing. So you know, we could use five or 10. But, you know, that all depends on the investor and what they're interested in, and so on, so forth, and investment terms, which we think we can make favorable. So we would we would talk to anybody who's interested. Let's just put it that way.
Very nice. Okay. This is the information that I want to we have met with one more question. And then I want to have one more wrap up questions of how to perhaps help how this group could help you moving forward, but thank you.
Thank you. Hey, there, can you hear me okay? Yes, yep. Great. So, two questions. So hopefully, I can sneak that in and Allison's okay with that. The first is that we all want this to work. And I want to make sure that we're not engaging in like unconscious cherry picking or motivated results seeking. And so I'm, I'm curious how you, as you've approached this, have made sure that you're not like falling into your own unconscious bias that you want it to work?
Yeah, it's always a problem. It's always a question. But in the end of the day, you analyze the data, and the data are what the data are, and there's not a lot you can do about it. So I'm aware of that, you know, potential bias, I can't swear that they, you know, could not affect me, but I'm not aware of that being an issue right now. So that's about all I can say. I guess there's one thing that I should bring up here, because I never get a chance to mention this. And it kind of is up that tree, you might say so I've been very impressed with the lymphocytes and monocytes ratio result that we got in trim. And partly because of the story that it tells about the energy connection between what we're doing and aging. So if we if we increase the lymphocyte to monocyte ratio by reducing cd 38, positive monocytes. And we should increase tissue stores of na da, and we should really rejuvenate the body and get the results that we are seeing. And by the way, as far as the epigenetic aging reversal is concerned, Steve Horvath that all of those tests for us, I didn't touch any of that, and the fino plasma clock results that I showed you. It's all based on mathematical formulas that cannot be fudged. And that I do not do myself. So there's no bias in any of that, that Steve Horvath is about the most non biased person you'll ever run into. Thank you,
everyone. I will do the epigenetic clock analysis. I'm incorruptible, whatever comes out comes out, you know, that's true. And I, I'm kind of blinded, you know, so
yeah, yeah. He, he's very, he's very objective. Yeah, that's one thing we like about him, he has no susceptibility to bias. I think he just lets lets the the chips fall where they may. But but the complaint the story, you know, so I may be a little bit biased in this in this respect, so that I want this lymphocyte to monocyte ratio to mean something, right? Because the story makes so much sense, right. And we had highly statistically significant results, there's no doubt about it. But, um, there's this bizarre aspect of this thing, which I've never had really a chance to explain to anyone. So here are, here's true confession time, you do not see an increase in lymphocyte to monocyte ratio. If you measure it with ordinary techniques, you only see it if you measure it with these ultra sophisticated techniques that are used at Stanford osipov method. And I'm still hitting myself in the head trying to figure out how that how it's possible for there to be a discrepancy between these things. But I haven't quite figured it out yet. So I, you know, maybe I'm doing something wrong and analyzing the conventional blood data. So I continue to present that result, because I just don't think it can be wrong, because the statistics Don't lie. And the you know, and then on top of that, we have the connection to nit, but it could be wrong in some bizarre way. I don't know how I don't, I really cannot explain how it could possibly be wrong. But if you have a discrepancy like that, you need to check your premises. And so that that can be an example in which I want that to be true. So I've been presenting that without really being good enough about presenting that caveat. So now, I've come clean on that. But as far as everything else is concerned, I think I'm pretty much objective. And then I did show you results, preliminary results for chromax. That were favorable. I didn't show you any results that were unfavorable. There have been some results that are not as favorable. But we're so in the early end of the trial, I don't think they mean anything yet. And, and the and the results that I did show you are supported by other results that are less obvious. So I think that it's right. But again, as I told everybody, we're less than six months into this trial, we got another year and a half to go probably before we have all of the data in very limited number of people blah, blah, blah, we only have 1/4 of the population that we're shooting for 1/3 to 1/4. So it's all very early stuff, right? I just wanted to give you a flavor of what we're seeing what the trends look like, things that are exciting to me, and hopefully will all pan out. But I'm not I'm not seeing any red lights. I'm seeing things that look favorable, globally. So I think that much is objective.
Nice. So I'm curious if results are neutral to positive? Is there a structure that allows the trials to be self funding where essentially like anyone who wants to join the trial can pay for all infrastructure costs, and you deliver it at cost? Or is that something that the FDA things creates moral hazard and therefore it's not allowable?
No, there are provisions at the FDA for that kind of trials. Matter of fact, chromax is that kind of trial because we do investment money this time, so everybody in our trial is paying their own way. And that that one thing that that leads to is very committed volunteers, so you get very good behavior and you get very good communication from the volunteers. They want it to work out and they're extremely interested in results. So that's all good. And like I said, we're able to make a little bit of margin on each on each person. Since our bank reserves are increasing slowly, not a lot, but you know enough to keep us alive as a company and allowed us to pay the bills. And that's all allowed by the FDA. And as a matter of fact, the trial plan that we submitted to the FDA is on this basis and, and they approved it. So trim x is going forward under our original ind with the FDA. And it is also under approval of an IRB that is aware of that cost sharing aspect of the study. So yes, so we can expand that one beauty of this mechanism of funding is that since it's self paid, there's no limit on the number of people we can enroll in the study, we can make the study as large, as you know, is there is a demand for people to enter it up to some point. And at some point, it's going to have to be converted from a trial into something else. But we're not close to that point. At this point, I think so if the FDA knocks on our door, you know, a few years from now and says, Hey, you know, you've got 100,000 people that have had this treatment, they're all paying you, we think, you know, this is no longer a trial, you need to ask for approval, well, then we'll ask for approval at that point. But we'll have data for 100,000 people, so we'll should easily get the approval at that point. So there's a limit to it. But for the time being for the near future, this mechanism functions for us. Sounds great. Yeah. By the way, that that's one, that's just a very, very quickly, I know, time is going by, but that's another area for investors to participate, because we can convince people to pay for getting actually a treatment, but it's hard to pay for people to it's hard to get people to agree to pay for being controls and not getting the treatment. And so if we had some investment money coming in to cover the cost of controls, and we could run more controls. So we're looking at different kinds of control. endpoints try to find a way that makes it attractive for people to be controls. But if we had a little bit of investment to cover their costs, that would be even better. Alright.
Okay, so I just want to make sure that we finish with without letting you go without you telling us what this group of people listening could help. And we've already heard a little bit about investment. But let's say I'm guiding other people to this talk. And I'm saying, just if you look at one thing, then look at the last minute, then you know, I guess what would you say in terms of Do you need specific participants? Do you need specific types of investment if there was like, you know, one wrap up, and like a call to action that could help? I would really love if we could have that in concise way at the end, which would be now.
Thank you, Allison, I really appreciate that. And that is a that's a unique feature of these seminars that you put on, nobody does this, you always do this, you always ask the speakers how you can help. You know, that's fantastic and highly appreciated. And so I have, you know, two simple answers. And basically, the one the one answer is tell your friends and let them know that trim x is open for enrollment. Because the way that we keep things moving forward is by enrolling more people in the trial. It's our only source of income right now. But it's also our only source of knowledge. So anyone who is interested in the trial and can pony up is $18,000 price tag which is pretty steep. I agree I know we're working on it but anyone who's who's able to get to that sort of thing will be helping us and will be appreciated and then the other thing would be tell not just your friends but tell your investment friends also just in case they may want to take a shine to one of these other things that we talked about either the growth hormone or the immuno engineering aspects or anything else that
they may be interested in. And best way to conduct you would be to go on intervene immune website.
Yes. So my Yeah, www dot intervene, immune calm, it's hard to forget and fe at intervene, immune calm, also pretty hard to forget as long as you know my name.
All right. Well, Greg, I cannot thank you enough. This was really, really fantastic. And I can't tell you how excited people were to have you on and I'm hoping that we hear from you again, maybe a year or so for another update with much more exciting data. Much more funding and having brought the price down then Add to add to negligible bounce. So maybe all went through it at this point. So thank you so so so much. This was really really really valuable for all of us.
