Dr. William Chamberlin: EpiBro and Crohn’s Disease

Video Transcript

This is the talk that I’ve been waiting for 15 years to give. This is very near and dear to me. I have given my heart and soul for this, and the people who know me probably know it. So I’m not even going to pretend to be totally even on this. I am biased. I believe that this therapy that I’m going to be talking about is going to be smashingly successful for Crohn’s disease. And all I can do is share my thoughts with you, so take what I say in that vein. I haven’t proven this yet. I hope to. I think this will be fabulous therapy when combined with properly chosen antibiotics, perhaps along with the MAP vaccine that Amy’s going to talk about next. But this has not been proven. We’re not there yet. There is a way to go. We’ve got a number of hurdles to overcome, but this treatment has been in over 250 humans so far for other infectious diseases. It is safe. There have been no serious side effects. The only side effect seen was a little soreness at the injection site. I’m obviously very, very optimistic about it.

And so what is this new therapy? Well, first of all, what you’ve heard so far is that we believe that Crohn’s disease is associated with an innate immune deficiency. So a good therapy’s got to find a way to enhancing the immune system; enhancing the innate immune system. We’ve talked about the damaging inflammations that we see with Crohn’s disease. This therapy down regulates the inappropriate, damaging cytokines associated with inflammation within four days or five days when it’s been trialed.

And we’ve been talking about Crohn’s disease being a disease; an intracellular disease of macrophages. How does the immune system deal with intracellular, microbial infections? It does so through what we call the Th1 cell mediated immunity, where the immune system orients the immune network. Because it’s not one cell, it’s a whole network of interacting cells that augment each other through the release of cytokines, driving up intracellular killing mechanisms through autophagy, signaling to other cells through the proper display on the antigen presenting cells. It’s a very complicated, complex network that has evolved over millions and millions of years.

This treatment also orients itself towards a Th1 cell mediated immunity that we expect it to do. And so what is this treatment? It is a synthetic steroid. What’s a steroid? It’s a six carbon circle, six carbon circle, six carbon circle, and then a five carbon, and you hang off side chains. Now when you start talking about the permutations and combinations of those side chains, you’re talking about 100 million variations on that theme. And of course you can hang side chains off of side chains, and the potential is immense.

Now, if you’ve got a molecule, a signaling molecule like one of these steroids, then you’ve got to have receptors that can sense it. At least this is one of the concepts. Now, there are 46 steroid receptors in the human genome. OK, very important. We know about five or six, maybe seven, of the natural ligands for these receptors. And they’re  such molecules as androgens and estrogens. There’s one hydroxyl group; one oxygen and hydrogen that makes the difference between testosterone and estrogens. And you can see the downstream effects that it has, OK. These molecules were key to evolution. They’re key to embryology. They are key to the orchestration to the different complex metabolic pathways in our body, and clearly they’re key to the immune network.

We know that one of the steroids is cortisol, prednisone, that down regulates. A very strong anti-inflammatory and unfortunately it down regulates the immune system. This steroid enhances the immune system but has an anti-inflammatory effect on par with prednisone. Prednisone without the side effects, imagine that. Orienting the immune response towards the type of immunity that we’re looking for; a cell mediated immunity to deal with intracellular infections.

Obviously, it’s not proven to work in Crohn’s disease yet. We’re trying to get the support to run that. Now, so running though; it decreases inflammatory cytokines, it stimulates innate immunity and it stimulates the Th1 responses. It has been trialed in numerous different infections. There was a biotech company in San Diego that started it. The guy thought big, it was Hollis Eden Pharmaceuticals, and he was going to use this to treat the major epidemics of mankind in the developing world. OK – HIV/AIDS, tuberculosis and malaria so it was trialed in these. It showed activity against all of these diseases.

And I’ll tell you why the company went under, or why this wasn’t developed right now because you’ll be wondering. Despite the fact that this showed effect and they were really gearing up to go after tuberculosis, especially when you were getting multi-drug tuberculosis; with the best of intentions and the noblest of hearts, the politicians got involved and said, Aha. Look at the poor developing countries. Drugs are too expensive for them to afford. Therefore, the governing bodies adopted the policy of mandatory licensing which says that any company that developed a drug that was effective against these epidemics in the developing world, were mandated to share their knowledge with other drug companies so they could make the drug for cheaper.

Well, it cost 1 billion dollars to take a drug to market. And then, if then all of a sudden as a country says, well we’ve got the epidemic and you’re forced to give all your treatments away, well that’s just suicide. So the company dropped, just dropped the drug after spending a lot of money showing that it worked and they were on their way. I happen to think that that was one of the crimes against humanity. And it was, but it was done with the best of intentions and the W.H.O. signed off of it and you can just see how every politician and every well meaning person got behind it. But that’s just not the economics; if something doesn’t have economic viability it just doesn’t happen. And that’s really why drug research for the developing world has dried up. Hopefully they’re going to change that policy.

So what are the characteristics? It’s an intramuscular injection.  In the trials it was given every 6 weeks; one cc every six weeks and trialed. OK now here, this was in one of the AIDS trials, and they looked at these cytokines. You can look at TNF. This is four days later. It has almost normalized. Here’s a drug that’s cheap, without side effects, that enhances innate immunity, and your TNF levels are down to almost normal. But not just the TNF levels, it’s down with the other pro-inflammatory cytokines because it’s affecting higher level control mechanisms and not just molecularly, surgically removing a key cytokine. It’s sort of orchestrating the immune response.

I’ll point out Il6 is another key pro-inflammatory cytokine and then the Il1Beta. That is another biggie that gets released by the inflammasomes that are all part of the processes involved with autophagy. This is, the potential here is just exciting, and that’s all I’m going to say. I don’t want to overdo it.

So what do we know? We know that MAP is associated with Crohn’s disease. We know that more now that we did a day ago, thanks to Amy and John. We know that compromised innate immunity, and specifically impaired autophagy is involved in the Crohn’s disease. We know that robust autophagy is needed for control of pathogenic mycobacteria. And we know that this drug, which we’re calling EpiBro, enhances innate immunity. We have not tested it against autophagy yet, but logic suggests that EpiBro will be effective against intracellular mycobacterial infections.

So, once they saw, well they looked for an effect on AIDS patients, and saw a statistically significant improvement in getting opportunistic infections. Since these trials were done in South Africa, the AIDS defining opportunistic infection was tuberculosis. So they said, wow, there’s a real effect on TB, and so they went back and quickly looked at mice. And you can see what the effects are on acute tuberculosis in the mouse model. And then they did it in the chronic infected mouse with tuberculosis. And you can see it’s effective in there also.

So then this is the, this is what really gets me excited. What you’re seeing is this Dr. Stickney, who was running the trial, they call this the stair step to hell because each time you see the little stair step up, that’s another patient dying. And you can see that after HE2000’s been onboard, and these were with patients with CD4 counts of 49. These were the walking dead. That after this drug rebooted the immune system, the innate immune system, patients stopped getting tuberculosis. This drug was in patients for 400 days. That’s why I’m excited about it.

So in summary, and you can read this and we’ll get this up on the internet, but essentially it says, Crohn’s disease is associated with an immune deficiency. Immune deficiencies predispose to intracellular infections. MAP is one such infection. We need to treat it. Now how do we treat it? Well, we want to direct our treatment directly against the microbe itself with properly chosen antibiotics. We want to have a drug that stimulates the immune system, and there’s two ways that I know of doing that now. It’s with EpiBro and then it’s hopefully with Amy’s father’s vaccine, his therapeutic vaccine, which you’re going to hear about right now.

Now to put the plug in. Now I am on the advisory board for a company that is trying to move this drug forward. It is called Immunikas. You can find out information about it. I’ve got Dr. Biesecker there who’s affiliated with the company. We need support. We have zero money but we’ve got a lot of knowledge and we just have to do this. It has to be done. Are there any questions? Amy, you’re next.

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