In this session, Reason, co-founder and CEO of Repair Biotechnologies, offered a sneak peek into their product and technology – a Cholesterol Degrading Platform – enabled by genetically modified macrophages able to consume and degrade cholesterol plaques in arteries. Apart from showing promising results in mice, he also explained the mechanism of action based on which this approach works and compared them to other solutions to atherosclerosis, the #1 killer in the world, that are on the market or are in the process of development. Lastly he also offered some details about the opportunity to invest in their company.

Link for contact:, email: [email protected]


Presentation: Reason

  • I’ll go over the basics of atherosclerosis and then show why what we’re doing is novel and a big departure from the past approaches and very likely to work and solve the problem.
  • Contrary to the picture, plaque doesn’t just narrow the arteries, it also weakens them. So the two possible results are that either the plaque breaks and flows somewhere and blocks something, or the artery just ruptures. Either of those are horrible things and the least you get is a severe embolism somewhere in your body, which kills – a lot of people, in fact it is the primary cause of death in our species and many other mammalian species.
  • Atherosclerosis are both the #1 and #2 causes of death based on the World Health Organization. Some people debate whether it is 27% or 40% depending on the groupings, but anyway it’s a huge problem, at least a quarter of people die because of this.
  • What is the cause of atherosclerosis? It’s not really cholesterol, it’s macrophages. Your macrophages cells in tissue are in part derived in part from the monocytes that float in your bloodstream looking for problems. And when they find the problem – that the wall of your blood vessel is unhappy for some reason, they dive in and try to fix things. And the thing that they try to fix is that you have a bunch of gunk sitting in your blood vessel wall that needs to be ingested and thrown back into the bloodstream, so it can go back to the liver. Unfortunately as you grow older, macrophages become increasingly incapable of dealing with this problem. And what you get is visualized on the right – macrophages to become foam cells, because they are completely overwhelmed by cholesterol, because they stopped being able to process it properly. From there it just gets worse and worse and more pathological, you get into the plaque situation. But the root issue is the macrophages – when you’re young, you are just fine, and blood vessels are not covered in plaque.
  • So why are macrophages not able to do their job later in life? We need to understand cholesterol transport first. Cholesterol isn’t created or destroyed in the cells, it’s rather ingested and excreted, but cells don’t break down or get rid of the cholesterol they don’t want locally, they hand it off to other cells and parts of the system when they no longer need it. Cholesterol is created in the liver, gets stuck on the LDL particles and goes into the bloodstream, gets stuck in a blood vessel wall, macrophages eat it and then throw it back into the bloodstream to attach to the HDL particles that flow back into the liver. LDL and HDL particles do pretty much the same when you’re young and old, it’s the macrophages that stop doing their job.
  • So why exactly do they stop doing their job? Due to a variety of issues listed in the slide – namely systemic inflammation, systemic oxidative stress, and too much cholesterol, although the last is probably not the worst of those three.
  • What all this leads to is a feedback loop. Your plaque is a macrophage graveyard, and the signaling of that draws in even more macrophages trying to fix the problem. That is the underlying problem that causes atherosclerosis.
  • As you are aware, there’s an entire research community and pharmaceutical industry focused on purely lowering LDL cholesterol – taking that part of cholesterol transport from the liver to the rest of your body and tuning it down. This probably helps a little, since you’re reducing oxidized LDL, you end up with less altered cholesterol in the plaques, so you’re giving macrophages a little bit more breathing room. But it doesn’t work enough, even if you reduce LDL to 10-20% of what is normal in humans, you won’t get rid of the plaques, you won’t reverse it.
  • Even after decades of focus on lowering LDL, atherosclerosis still kills that 27% of everyone. And the drugs that we use still achieve only 10-20% mortality reduction, while the number being heavily debated as it is likely too high, many trials have shown no improvement.
  • Furthermore, whatever you do with blood cholesterol, if you already have lipid-laden soft plaque, there just aren’t any good options – getting rid of it is not on the table.
  • So we need a better way forward – yet all the companies are still focusing on lowering LDL cholesterol – some of those latest therapies from companies going public are trying to charge $500,000 per year for that.
  • What are the alternatives? Let’s start with those that don’t work. I mentioned that systemic inflammation is one of the problems leading to atherosclerosis. But if you reduce inflammation systemically, studies suggest you get about the same benefit as you would get from lowering LDL cholesterol. Which doesn’t mean that somebody cannot come up with a way that could do this in a better and more targeted way, but the tools available for systemic inflammation are really blunt right now.
  • The second alternative sounds much better, if your ceiling is mice. Reverse cholesterol transport is the pathway when macrophage sucks up cholesterol and hands it off back to the bloodstream. There are a number of genes involved in this – macrophages use ABCA1 to hand off cholesterol to the HDL particle initially and then ABCG1 helps add more cholesterol to the particle. Then the particle heads to the liver and is excreted and ejected from the body. Anything you do in mice to make one or more parts of this system work better, it all works great – up to 50% reversal of plaque lipid content in some cases. But every time it was tried in humans, it failed – there’s a whole list of clinical trials over the last 20 years that tried and failed. That tells us that we don’t understand something very important about the way in which cholesterol transport is rate-limited in its different steps in humans vs in mice.
  • So our approach is to make macrophages resilient to the environment in old tissues.
  • There have been a number of people trying this, some of it hasn’t made it very far, some of it is interesting, and sometimes there is overlap between those two. There is a recent paper with a hypothesis of effect they showed is that if you target lysosomes in macrophages with antioxidants, it prevents the oxidized LDL particles from messing things up, and therefore more macrophages are doing their job – reversing the plaque by 50% in a mouse model. It’s entirely possible their hypothesis is wrong and delivering antioxidants is improving something else in the picture, but it’s certainly something self-experimenters should pay attention to because these antioxidants are easily available.
  • Secondly there is the Underdog Pharmaceuticals approach – sequestration of 7-ketocholesterol, which is a highly toxic altered cholesterol, thought to play a big role in atherosclerosis. Unfortunately, the only way to really see whether it works is to test it in humans, because mice just don’t have enough 7-ketocholesterol to make a difference here. So we’ll see how they do, I hope it works.
  • Lastly there is our approach – genetically engineering macrophages to give the ability to degrade excess cholesterol, whether or not it is altered. The company is named Repair, since I believe that if you’re going to address aging and you can’t point to something you are actually repairing – a form of damage or dysfunction, where you can clearly say that you are fixing this – then you might not be doing the right thing.
  • We’re currently working with an investment bank on a capital raise for our clinical round, so that requires me to show this slide.
  • In summary, what we’re doing is taking a stepwise approach of allowing macrophages to degrade cholesterol and stepwise approaching the various atherosclerotic conditions in order of number of patients. So starting with an orphan condition – homozygous familial hypercholesterolemia, then you go into larger patient groups as you gain experience doing this. Unlike most therapies, we can actually apply ourselves to any form of atherosclerosis, whether or not it is genetic, we don’t care how you got plaques, we just break them down.
  • We’ve demonstrated our AAV delivery of our cholesterol degrading protein – has a very large effect of 40% in a month, which is very big in the scheme of things and compared to other approaches. Our goal is to produce a universal macrophage cell therapy
  • As I said, atherosclerosis is basically the encounter of an aged macrophage with cholesterol at which you get a lot of cells eath and cholesterol-based plaque. If you overwhelm existing systems of normal macrophages with excess cholesterol, they can’t do anything with it and basically become foam cells – they don’t have an inherent way to deal with that level of cholesterol.
  • So with that picture in mind, the whole spectrum of LDL lowering cholesterol drugs really only lowers the input to the problem. And they can’t lower it infinitely, because the macrophage is in the plaque, not in the bloodstream, and the plaque is packed full of cholesterol and toxic horrible nastiness, so you’re not really getting a lot of boost from lowering the input from bloodstream – the problem is the plaque that’s sitting there. You can’t reverse it by doing this LDL lowering approach, you still have macrophages exposed to excess cholesterol becoming horrible foam cells already.
  • And the horrible foam cells leading to your plaque gives you this point that has to be made to a lot of people unfortunately. Your risk of death is not due to LDL cholesterol, it’s due how much plaque you have. It’s exactly how much plaque you have and how much high risk plaque – the soft plaque. That determines your mortality. LDL cholesterol, while widely accepted as a surrogate marker, is just irrelevant, it’s not the cause of your death. That’s why different people can have different levels of cholesterol in their bloodstream and have quite divergent mortality rates.
  • And the fact that it is the plague is why we have this list of drugs, starting with the ultracheap statins and heading up to the ultra expensive ANGPTL3 inhibitors, which frankly are probably not much better than the PCSK9 inhibitors. Because lowering cholesterol can do at most 20% mortality reduction, no matter which way you do it and how much you pay.
  • The point of the exercise is to figure out what we should do differently – and that is making macrophages invulnerable to the plaque-based environment as best as we can. Our idea of best we can is to give a macrophage the capability to break down cholesterol safely locally. I should say that this is not a trivial thing to do, because a cell is basically an enormous lump of cholesterol – our body uses cholesterols everywhere in the cell membrane. The reason why we never evolved to break down cholesterol when it’s harming us is because our cells have cholesterol everywhere. So you couldn’t evolve something that just chews cholesterol whenever it sees it. And that’s why delivering things like cyclodextrins, as Underdog Pharmaceuticals is not quite simple either, because the first thing that will happen if you dump a bunch of cyclodextrins into somebody is that their blood turns to mush, because it will consume all your blood cells by hooking all the cholesterol out of cell walls. Underdog has a way around that, but they need to be very careful with that.
  • So the objective is a safe way of breaking down cholesterol, but only the excess cholesterol, which is what we achieve by putting in these specific mechanisms into these cells we’re working with.
  • We can demonstrate that by putting these mechanisms into any old cell, and the output is exactly the same – we get a catabolite that is safe and more soluble, and leaves the cell into the bloodstream where it gets rid off. It’s a technology that can be used pretty much anywhere.
  • What this means is that we can take macrophages and give them the ability to express our CDP+ proteins, and then if you dump cholesterol on them, the unmodified ones become very unhappy – the green is a foam cell behavior where they ingest cholesterol inside them and becoming pathogenic and inflamed. in the right image, showing the modified macrophages, you see very little of that behavior – they just eat the cholesterol and get rid of it. On the left you see incomptent macrophages in the plaque, on the right competent ones able to break it down – that’s what you want in your plaque.
  • Our proof of concept with AAV, we delivered a very high dose of AAV into atherosclerotic mice, and you can see the difference. Red in the cross-sections of the aortic route is lipid-laden plaque, and we’ve got something like 50% reduction in the plaque in a month following a single treatment – this is a very powerful effect.
  • So going forward, we take the iPSCs from mice or humans (from our partners offering well characterized human lines), the lines are then disrupted in certain ways to make them universal (you get rid of the surface markers that make them recognizable – very important technology that gets you off the shelf line of universal cells, you can look at Sana delivering universal iPSCs to primates and showing no meaningful immune reaction). We then differentiate macrophages that express CDP+ ourselves from these universal cells, and this is the way we produce a cost effective cell therapy. We’re already injecting mice with these cells over the last month and we should have some data within a year.
  • And then what we do with this is a stepwise approach through the orphan indication with very few patients and a much easier FDA process, then to the indication with more patients, and then to high risk subpopulations of atherosclerosis. People who have had scans with a lot of high-risk plaques. Ultimately we think you can take the lion’s share of death – 27% by atherosclerotic diseases – and use technology such as ours to completely remove that cause of death from humanity. How long is it going to take? Who knows, but the first most high-risk population is where we start.
  • So our pipeline looks much like this, as I just told you. The market sizes are increasingly enormous, with $22B for atherosclerosis subpopulations probably being an underestimate.
  • Here’s who we are.
  • We have a great scientific advisory board.
  • We’re raising aggressively right now, working with an investment bank to get $20 round together and fund our path to IND. As this is going on, we are very happy to raise from angels via SAFE note to extend our runway.
  • If you want to look for a comparison to us in a way, it’s Verve Therapeutics – they are only dealing with familial hypercholesterolemia, and are only lowering LDL cholesterol, and yet have a valuation of $3B. We think we are a lot better than they are.
  • Thank you!


There are also downsides to statins, so even if it results in slight reduction in atherosclerosis, it’s not a 10% reduction in overall mortality or quality of life, right?

  • Yes, the side effects of high dose statins are really bad for a large number of patients, and even for moderate dosage you have a percentage of the population who just can’t use statins, because it’s just not good for them.


Do you have an opinion on cyclodextrin (paper) in comparison with your approach?

  • Normal cyclodextrins bind cholesterol and are indiscriminate, which is why their dose limiting toxicity is initially that you lose hair cells in your ear, because for whatever reason they’re very sensitive to having the cholesterol hooked out of their membranes. The next thing that happens if you keep increasing the dose is that your blood turns to mush. So nobody really looked much at what happens after that point. The Underdog team has I believe engineered their cyclodextrin to preferentially bind only 7-ketocholesterol, which should greatly reduce its toxicity and allow them to dose at levels where you can get a significant amount of 7-ketocholesterol, at which point it is a great test of how important 7-ketocholesterol is to atherosclerosis.


Are there risks of applying this to everyone? Other than regulatory reasons, is there some reason to not just give this to everyone over the age of 40?

  • It’s a cost question actually, if you look at the cost of cell therapy once you crushed it down using a universal cell line, you’re looking at under $10,000 I would imagine. And the first generation stem cell therapies, those things are in the range of 1-10 thousands dollars if you get a good provider. And the first thing that any VC will tell you is that you’re crazy if you think you’re gonna treat a hundred thousand people with something that costs $10,000 – they don’t wanna hear that. So you really need to take that kind of therapy and apply it to the highest risk patient groups first. That needs to be your plan. And then later on, in the science world of the 2030s once we’ve had 20 years of cell therapy that everybody wants to use, maybe we can crush it down to the point at which you can treat everybody, I would certainly hope so.


Where do you come down on the role of coronary artery calcium and the possibility of regressing it?

  • I think that’s, funnily, a totally separate topic. There was a really good paper recently that reviewed the biomarker relevance of coronary artery calcification (CAC) testing vs should we be looking at plaque – and they found a great correlation. But these are really two separate processes, obviously there is some interaction between the underlying processes causing them. If one believes that calcification is an inflammation related topic, certainly there’s good evidence for senescent cells to be important in calcification, but it’s a thing that happens in parallel with whatever else is going on with the formation of atherosclerotic plaque – they are two separate things that end up making each other worse in the sense of likeliness of catastrophic outcome as a result of either of these. They need to be dealt with in quite separate ways, because they’re very separate problems unless you’re looking at the real root root causes – inflammation. If there was a way to stop all older people from having rising oxidative stress, rising inflammation, maybe you’ll have a whole lot less of both, but for entirely different reasons.


I thought that calcium is like the end phase – that there is a whole cascade process from a wounded artery, to macrophages, to plaque, and then calcification is the end state. Am I wrong about that?

  • That happens in plaque, but plaques are hugely inflammatory. So whatever calcification processes exist, you get more of them in that vicinity. But you also get calcification without plaque. If you are over age 50 and go get a scan of your lower body, you’re probably going to see calcification in your legs.


You’re mostly talking about coronary artery disease, or are you talking about circulatory disease in general? Is your product and company focused towards coronary artery disease or generally circulatory disease?

  • In general – how much calcification is going on in your arteries. And our approach is able to do both – we’re introducing macrophages, and they go everywhere. So you obviously measure the outcome in coronary arteries because that’s where you can measure the outcome, but you expect atherosclerosis to have a meaningful effect in terms of slow vessels as well. And it’s even harder to tell what’s going on over there, so we expect our macrophages to be heading there to do their job as well.


Is it something where you need to have the therapy regularly to remove the plaques or once the cells are introduced they just live inside for the rest of your life and continue cleaning up your plaques? If you do have to keep doing it, and they do live inside of you for longer, are there any risks since you have something that is genetically modified and conserved over a very long term?

  • Macrophages have a lifespan of a few months, so if you put monocytes into the bloodstream and they go to plaques, you’re looking at a treatment that’s going to last for a few months. The question of how often you would have to do it is more of a biodistribution, dose response type of evaluation, that we don’t really have yet. What we would like to have the outcome be is that you take this therapy at most once every few years when scans show you are in need of it. We don’t intend to replace the presence of LDL lowering drugs for those people who can take them, that would certainly be a hard job given their entrenchment, but there’s an awful lot – the remaining 80% – of excess mortality due to cardiovascular disease that is there to be dealt with. And that’s what we will do.


How did you start the company? How did you get the idea, meet the people?

  • You can blame Aubrey de Grey for that. He introduced us to Richard Honkanen, knowing I’ve been very interested in this part of the field for a while and it kind of went from there – it was obviously too great not to do. Richard originally did the work at university and is still partly there. It’s actually not his wheelhouse, he’s interested in molecular biology of certain aspects of cell behavior and that led him to the discovery that this could be used to cure atherosclerosis. Hence why he came to present it at Undoing Aging and from there it was sort of inevitable that I would end up talking to him. We said to the university to give us a great deal and we’ll prove whether it works in mice.


What are the long-term goals for the company?

  • I have a million things I would like to do – I would love to take this company public on the strength of this program and from there become an umbrella company that does many other things. Whether or not that is the fate or Repair, who knows, but I would very much like to pick up our program on the thymus again and do many other things once we’ve proven we can do this and have access to public funds in the public markets, there are a lot of other things we can take up and move along.


Would you maintain that talking of an M1/M2 dichotomy is useful?

  • Macrophages like all cells are state machines and they live in a state space, so when people say that macrophages are M1 or M2, where M1 is inflammatory and horrible and useful for pathogens, and M2 is inflammatory and reparative in the sense that it participates in tissue maintenance more, this is obviously slicing your very complicated state space into a buckets and fitting everything into one of two buckets. It’s not a switch, it’s about where it is in a complicated space of tendencies – about expressing some things more than other things. But I think it’s useful, because you can clearly take a bunch of macrophages and stick them a flow cytometer and stain for various surface markers and you will get quite clear distributions that are sort of M1-ish and M2-ish and of course maybe like 10% being off doing something weird like M0. I think it’s useful in the sense that there are ways to push macrophages in one way or another, and you’re really dealing with aggregates. If you look only at an individual cell, that was probably not a research you should have undertaken. You should be thinking more about the aggregates of macrophages and what the aggregate behavior is, and that’s the best you can do, so it is a useful model.


It just so happens that macrophages are from the same lineage – cells in the bone – that through polarization states regulate the deposition of calcium. Is there any evidence that it is the same mechanism by which calcium is being deposited in the arterial plaques?

  • I don’t recall, I thought that was more of a smooth muscle problem – convincing smooth muscle cells to start behaving like bone cells through inflammatory signaling. At least that’s my recollection of the literature I’ve read on that topic.


Do we know what the precise mechanism is by which oxidized ldl causes macrophages to die? This is related to cholesterol crystals.

  • That’s a good question, if you go read the average review paper on cholesterol, it will not offer an opinion on that. I think it’s very much up for grabs. That antioxidant paper that I mentioned in which they target antioxidants to lysosome and see effects, they obviously took a bunch of cells in a dish and shove oxidized LDL particles into them and show that they go into the lysosome and the cells become dysfunctional. So something with lysosome being overwhelmed, which is well known to be a problem in aging in general and long lived cells, whether some version of that is happening in macrophages, who knows. Our take is that it may not be as important as the fact that you have these oxidized ldl particles being taken up through scavenger receptors by macrophages, so it’s not necessarily the LDL, it’s the oxidized LDL particles themselves, it may just be the matter that then you are just dragging in more cholesterol than you can handle.


That scavenger receptor you mentioned is the same gene in bone that regulates calcium deposition – that’s something I’ve been trying to figure out for a while now.

  • Evolution loves reuse.


I thought that at least for coronary heart disease, HDL to total cholesterol, HDL to LDL and HDL to triglycerides is a much better predictor of disease than just LDL levels. Now oxidized LDL levels are another thing, that’s obviously a good predictor. Do you care about that?

  • Not really, I think, like the evidence suggests, that doing things with HDL doesn’t work in humans. It doesn’t help the problem. We should distinguish what happens over your lifetime in response to your ratio of LDL and HDL. Because obviously over lifetime your balance of cholesterol transport in the body changes, and in theory more HDL is going to be good, and in practice HDL is good. But that is not the same as what you can do for therapy, where you’re operating in a very short timeframe. In that case I think the clinical trials over the last 20 years have really shut the door on just putting more HDL in humans, because it doesn’t work. In terms of lowering LDL cholesterol – great – you get the aforementioned at best 20% mortality reduction, and that’s not the solution to the problem either. Once you have plaques, they will kill you, they will continue growing no matter what you do to HDL and LDL.


I was a little unclear on your position on systemic inflammation. Sometimes it seemed like you were saying it’s the thing that is driving the trouble, on the other hand there was a slide saying that reducing inflammation has failed?

  • It’s both. Again, distinguishing the “over time” versus “how do you fix the problem” – two separate considerations. Over time, it’s clearly a contribution, because you’re going to die sooner of atherosclerosis – over years and decades. If you’re trying to fix the problem and reverse plaques, reducing inflammation just doesn’t seem to help that much, because the problem is the plaque is sitting there being inflamed, full of garbage, and toxic, and macrophages just can’t deal with it.


I see, so there’s a lot of things people can do with lifestyle interventions and drugs to stop or slow the progress of the disease, but in terms of reversing the disease with a short term intervention, that’s what you’re looking at and that’s a whole other issue, right?

  • Yes, and in my opinion the whole community diving in on these human mutants who have low cardiovascular disease – that’s just never going to work, it’s a huge red herring and a waste of time. The only thing we’re get out of that is more LDL lowering drugs that have the distinguishing feature of being vastly more expensive than previous LDL lowering drugs. Those two things are actually a virtue in some circles because it’s easier to make profits off that.


Why not shut down the mechanism driving macrophage invasion of cardiovascular tissue?

  • If you do that, you’re never going to get rid of those plaques. Nobody else is going to deal with them. In theory we could get every cell the ability to degrade cholesterol and shut down the macrophage invasion, but why do that if you’re already making the macrophages good.


Isn’t that also a problem in the sense that some of these processes that turn into chronic disease progression are actually useful in a healthy person in acute causes like infection or injury and so you don’t want to shut them off?

  • Yes, exactly – which is another reason to favor the sort of thing we are doing, because it’s an enhancement which does not otherwise change how things work, other than just letting them work.


Would it be possible, in theory, to apply a permanent gene therapy that makes macrophages do this stuff permanently?

  • In principle I think so, with the caveat that gene therapies are really hard to target properly. Not just from the point of view of how you are connecting it to only express in the cells you want it to be expressed in, but also how you get it to where those cells are. Macrophages are everywhere. You really want to get the macrophages that are in plaque, which means you have to target blood vessel walls, but then you also have the other 50% of macrophages that are sitting in your spleen that you probably want to get. You could take the approach of targeting hematopoietic stem cells, and in the case that nobody would ever want to do, you could do a hematopoietic stem cell transplant, such that you get genetically engineered immune cells and in those immune cells only macrophages express the genes of interest, but of course nobody’s ever going to go for that – the FDA would laugh at you if you try to propose treating atherosclerosis in this day and age by getting people hematopoietic stem cell transplant. So in principle yes, in practice probably not a viable approach.


We know that the oxidized LDL goes into the lysosome, but I’m wondering – does it go to the lysosome’s membrane?

  • That’s a good question, I am not really familiar with the precise details of that. I was reading up on that most recently in connection with that paper I mentioned, our take on that is likely more to do with the oxidized LDL being an additional source of cholesterol coming into the cell, over and above of what it would pick up normally, so you’re overwhelming the cells ability to deal with cholesterol that it’s intaking because the oxidized LDL is using a different set of receptors and gets taken up quite aggressively. This is probably a consequence of oxidized LDL actually binding to a receptor that “isn’t for that” – that has actually evolved for some other purpose. But we’ll see, it’s an interesting question, there’s definitely more work to be done on why oxidized LDL is bad.


I just looked at the photo of a lysosomal membrane and I’m seeing your scavenger receptor right in there, so I wonder if it’s not clogging the inside of lysosome as much as it’s clogging a receptor on the outside of lysosome.

  • That’s also possible, we know that lysosomes are important for autophagy and aspects of cell function.


What could this group collectively do to further you and your work. I know you’ve talked a little bit about Repair actively seeking investors, but could you be really precise? If anyone is super inspired by your work, what would they do to help you and your work flourish?

  • Aside from throwing us vast amounts of money, which would help, the most interesting things that you could do are in the realm of self-experimentation with respect to what one can do with atherosclerosis. There’s very little that one can do at the moment. But there are some interesting approaches one can take, such as trying to get some idea about nattokinase. That was the Chinese study that showed 36% reversal of lesions after nattokinase use for half a year. And then somebody else published a 3 year study in the US and said that it doesn’t happen at all. The US study used a ⅓ of the dose of the Chinese study. So at the end of the day you’re left throwing up your hands and saying somebody needs to do another study. Self-experimenters can do this stuff. It’s pretty simple. So along those lines, I think there’s a lot that can be done in order to help expand our knowledge about potential therapies that are not quite yet baked in terms of clinical trials and where we’re not going to see a lot more data anytime soon coming from the establishment.
  • For contacting me, [email protected], if you’re interested in investing or just have questions about what we’re doing, feel free to send me an email.


Seminar summary by Bolek Kerous.