Personalized Peptides for Cancer patients provide new hope with targeted therapeutics

Let's get real. Let's get loud. on America Talk Radio. This is the McCullough Report and Courageous Discourse Substack. I'm Dr.

Peter McCullough, president of the McCullough Foundation, and it's my great pleasure to welcome to the show Dr. John Catanzaro. And man, he has a background and he's got some red-hot ideas. And, you know, we've been looking for people in the biotech space to help us navigate through this really difficult time where 75% of Americans took a COVID-19 vaccine. Of those, 94% took a messenger RNA vaccine.

So for the first time, they took some foreign RNA in their body. John, welcome to the show. Thank you so much for joining.

And then I retired in 2017 and started Neo7 Bioscience, a biotech company that specifically focuses in on personalized precision therapeutic development. And I am the co-founder and the CEO of this company. It's privately held. And so I just wanted people to know that this is what our company does.

And basically, it. through the whole process, my work in molecular genetics, as well as proteomics, and working with, you know, peptide engineering had allowed me to integrate that into practice with with patients. for that, you know, almost 25 years, as I mentioned. And so we were able to collect a lot of data. through those years.

We made a lot of headway with many patients with resistant cancers and resistant illnesses. And we were able to make a significant mark in life extension, quality of life and and helping people to recover from pretty devastating illnesses using these type of personalizations. So with that, in our expansion into Neo7 Bioscience, because we've actually had opportunity to look at a lot of patient data, we have come across many type of resistant illnesses, including cancer, that have a strong association with the mRNA spike protein and and also segments of mRNA influencing ribosomal shifting and and pretty much corrupting transcription translation type activity, which cause causes more aberrant type molecular signals. So we get to see these aberrant molecular signals very plainly in the molecular data of the patients. So now we've been able, we've been able to compare some significant data data sets of patients that have these resistant illnesses, including cancer and chronic inflammatory disease, and people that have been vaccinated with the COVID mRNA.

And we find that correlation very high. I mean, a very, a very prominent part is when we see RNA transcription amplification. So we get to see some things like the WNT pathways, the notch pathways, people, you know, don't, maybe may not understand everything about what these pathways do, but they're cell proliferating pathways. They actually cause cell cellular dysregulation, which allow for a higher probability of excess mutations to occur. And we also see the DNA mismatch, repair proteins affected quite significantly.

And we also have been looking really in detail with immune, immune regulatory proteins that are skewed in most patient data sets. So we get to see immune regulation, fault, you know, faulting a lot of aberrant signals with these proteins in association with, you know, with that mRNA splice type segment of the RNA.

You know, peptides are building blocks of proteins. Basically, they're formed by an assembly of amino acids, and those amino acids build a protein, right? And our bodies actually have a significant number of functional proteins that keep proper function of the body, proper feedback of the body. So peptides are very important elements in protein building. And they are the result of the things we're talking about, genetic signaling, DNA movement into messenger RNA, you know, all this stuff that I was mentioning about, some frame shifting and stuff like that.

All of this, all of these elements are important in being able to code for those peptides to build in a strong structural protein. And what we see when these proteins are affected in a negative and adverse way, these proteins wind up having points of shifting to where we can see that the protein structure on simulation is not as tightly bound as it should be. So we get to see a lot of different molecular implications when a protein.

And we're seeing a lot more development to where there's more hallmarks involved. But like, for instance, a good example of a hallmark is dysregulated immune function, or tumor promoting, or cell proliferation, or DNA instability. There's a lot of different hallmark expressions. And these proteins are drivers for very dysfunctional activity in the landscape of the cancer. And so what we could see is the degree by which these proteins influence and how they then affect their sister targets down the line.

So in other words, you can have a top level signal target that can influence string sister relationship proteins that are also drivers in the cancer evolution as well. So what we do is we find the peptides that are direct influences that either will mitigate, potentiate, or regulate those proteins appropriately, and allow for signal changes in expression to assist with the ability to eradicate the cancer.

unnecessary? I mean, if one was to take them out with a monoclonal antibody, would that be a?

And I give you an example of that. When we had a patient whose mother passed away from breast cancer and she was BRCA2 positive, then the sister was also BRCA2 positive, but the other sister was BRCA2 negative. It was just a patient that we analyzed, and what we found was she had a expressed protein and the proteomics portion excreted in her urine, and the BRCA2 was positive in her urine. So she did not have a mutation in her main genomic dataset, but she had the disease-related protein being expressed in her urine, which is a very hot biomarker, right? So a lot of the times what, you know, you wind up detecting these things by looking at the genomics, by looking at the transcriptomics, by looking at the proteomics, and by looking at the patient's own HLA immunophenotype.

And when we actually see what their susceptibility and compatibility is, these are important drivers in being able to identify how to get more intelligent into that disease space, to influence it, to allow for eradication of that particular cancer or those cells or that particular tumor,

Excellent. We have high definition,

We can actually capture 6,000 plus proteins in the urine. Not all of those proteins are based on normal functional rhythms, but they're actually based on disease expressions, right? So we know which ones, in our confidence mapping, are specific to a disease type, not just cancer, but we also see it in autoimmune disease too. And so it's pretty amazing to see it. The technology that we use is an exosomal technology in our proteomics, so it's a direct, it actually uses direct and indirect, and it also uses exosomal extraction methods to be able to have a more high definition on the proteins that are captured.

And so we're pretty excited about our technology that way, because we can get proteins that no other institution can measure. And what type of detail can you get on these?

So we're using a very.

And this patient had three booster shots of the COVID vaccine. And so we actually just created an intranasal design for this patient that he will be starting pretty soon. But the thing about this is that when you know what the signal targets are and what's like, for instance, on his profile, he had some very definite vascular endothelial dysfunction. So that means that the capabilities of the vascular remodeling couldn't happen. And there was a lot of pro-inflammatory activity directly seen on his molecular expressions.

So when we actually looked at his data sets, we developed a mitigation regulation strategy and then enhancement strategies to allow for better vascular integrity, which we believe would have a very good potential, because he's got no other options. He's inoperable, he's a ticking time bomb, and nothing else to do. So we also coupled that with exosomes, which would allow for the delivery to the targets that we want to see. So we're pretty excited about this. But this is just an example of working with vaccine-related pro-inflammatory destructive proteins.

You know, as well as I do, the protein effect by this frameshifting, this ribosomal frameshifting and the open reading frame dysfunction that we see. And then this reincorporation of mRNA back into DNA by what we call a splice DNA movement from the retrotransposon action and using reverse transcriptase. So we actually see these type of activities by these transcription genes are definitely positive. So the data does not lie. Let's just say that the data is very, very pointed about showing us these discrepancies.

It actually has a direct cell lysing effect on the cancer cells without any toxic effects for surrounding cells. So that's a pretty well-known anti-cancer peptide. But now, when we talk about molecular personalizations, it's N of one. So that means that, you know, you could have two people that have the same exact cancer, but, and they may have the same two similar targets, but their peptide sequences to the target are dynamically different. So that means they'll have a different expression, and it's not just to elicit T cell responses.

So a lot of the time, the literature that's out there is kind of misleading because it's giving you kind of like a condition like, oh, we're just using them as fashionable neo-antigens and potentiating activity against the cancer cells direct on discrepant cell expressions, like the tumor-associated antigens. But the thing is, is that they're more than that. These personalized peptides are actually signal propagators. So they work through a self-assembly activity. Once they're in the body and they're properly scaffold, they'll get into the interior of the cell and begin to change programming, not like mRNA, because the peptides will work from a standpoint of facilitating a natural movement into a better relationship in the cell machinery, whereas mRNA has very fast decay rate and a very unpredictable rogue effect.

So you won't have that with a well-assembled,

And then we also pegylate. So in other words, pegylation allows just small fractionated peg that allows the protein to move to the target freely without it being hit by.

You're going to have very low risk of off-target reactions. You're going to have an immunogenic potentiation specifically to activate the immune system in a favorable fashion rather than an unfavorable fashion. And you're going to have more of a likelihood to overcome what you're seeing in the resistance of the disease itself, because you're allowing for.

So, in those cases, it's a very good therapeutic accent, right? Now, some patients that are hypersensitive, they might need some, you know, antihistamines, they might need a little bit of, you know, steroids to kind of just calm the system down a little bit, but very...

Now, in cases of like, for instance, an answer with tumor tissue, we also do tumor tissue, but a lot of the times the tumor tissue is inaccessible, hard to get, very difficult. A lot of times. institutions don't want to turn loose of it for various reasons that I won't get into here, but the thing is, is that we don't stop at that because we don't need.

The product mainly that Neosemin Bioscience is developing is investigational, experimental, right? So, it's all operating under an IRB. You know, it's not under a clinical trial, so we don't have any NIH studies on it. It's all IRB practice already to select. There's a lot of physicians that are Neosemin participating physicians, and they, you know, they're working with us to administer this to their patients, and so that's how we operate, you know, at this point.

Now, in the future, we're hoping to maybe get a little bit more research out there and establish it, you know, more in the research environment, more publications, but we've been real stealthy about how we do it because we've been helping a lot of people over the last four years. Now, is the company involved in these.

and or is the company working with what's considered naturopathic centers that, you know, are much different? More integrative?

In fact, I examined her and I depressed the tongue and the cancer just flipped up into view. It was just astonishing to see it face to face, and she's made up her mind. She says it's inoperable. I'm not going to go through chemotherapy and radiation, and, John, I have to tell you as a doctor, a non-cancer doctor, I always ask myself, is the appearance of the patient and their current illness, is it due to the cancer or is it due to the chemotherapy, radiation, and other things that have happened? I mean, the question does come up, particularly for advanced cancers where the survival rate is low.

What does a patient look at if they go to a holistic or integrative center? I know you work with these centers, but what's your vantage point? What's the approach when a?

And when we're working with these doctors, we're adding a level of sophistication as a hub strategy. So, what we say is that, you know, you're not going to be flying blind here. You're going to know exactly what you're doing with regards to the molecular influences of this disease. You're going to be able to intelligently hit those targets by using the personalized engineering. And you can couple any therapeutic with it.

So, like even if a patient decided to do radio, you know, targeted radiation or, you know, the proton therapy or something like that, you know, it works really well together in being able to facilitate the anti-cancer activity. But it also assists in being able to help the tissue to recover better. So, it helps with more rejuvenation of the tissue. And a lot of the times, you know, you are so correct with regards to when you're seeing the cancer itself. A lot of times, we do one step up that you see in the environment, where they're going from chemo to chemo to chemo.

They go to a stronger chemo. And what happens is it might work for three months and it creates a stronger resistant pattern, as you probably observed yourself. And then the cancer rages terribly, right? And I've seen that all my years of practice too. It's a terrible thing to watch.

But it's a very real thing that happens. So, the resistance is a reality with some of these conventional therapeutics.

It's not something, you know, when we're talking about sophisticated end-of-one personalizations, I mean, it's a lot cheaper than using traditional immunotherapy or conventional immunotherapy or some of these chemo strategies, you know, but it is more of a high-priced item going into it. And the thing about it is that patients actually are paying out of pocket, right? So, it's not covered by insurances. Though there are some patients that actually will submit itemized bills from their physicians to insurances, and some of them get up to maybe 35 to 50% coverage on it. But, you know, I can't speak that that's the norm.

It happens. It all depends on the insurance.

Yes. And then you would guide them from there in terms of samples, how it happens, the assessment, and then working with the doctor on the delivery. A typical course of peptide therapy for cancer, what are we looking at in terms of IV infusions, you know? How many, and at?

There are four courses in a year, and a course of treatment lasts anywhere between 21 to 30 days. So, these peptides are being administered over a 21 to 30-day period, right? And then there's usually a break of about four to six weeks, sometimes eight weeks in between, depends upon where the cancer is in its staging. If it's a pretty aggressive cancer, then there's no breaks in between. And it could be used with any conventional therapeutic modality.

It's not affected negatively by chemotherapeutics. So, we see very good complementary effects and much better effects than you see with people who are receiving chemotherapy, right, for them to be protected against the chemo effects. But as a.

Because there's some patients that have more robust responses than others, right? And it's all patient by patient. So, you can't, you know, you can't really, just, you know, standardize just the same thing for every one. One patient might respond where you have to adjust the dosing down a little bit and spread it out, maybe by 24 to 72 hours. But, you know, doctors know, our doctors know when to do that.

But for the most part, it's a 21 to 30-day regime, four times a year. And if you were to talk to a patient,

So, they don't just have the direct immune defense effect. They also have the immune editing effect. So, you get those two things working together. And, you know, in a system, especially when it's personalized to the patient's targets, then you're getting these actions to work on these different targets that are involved in that cancer expression. So, that's where, a lot of the times, you know, you're going to have a better opportunity to overcome severe resistance and migration by allowing, you know, these peptides to work on the different expressed targets, because there's more than one target involved in the cancer.

So, it's like, it's going to take a while for a new paradigm shift to happen in the research design, so to speak, right? But what I do see is I see a lot more intelligent aspect in being able to know, you know, how to hit targets more intelligently, right? And you know as well as I do is that in the conventional space, it's always about one signal target, like we see in these weight loss drugs, for instance, I get GLP, GIP, everybody is excited about this, and what you wind up doing is you wind up burning out those targets with chronic focus and you find that they don't work anymore, these drugs, the way they're supposed to, because of the fact that you're burning these targets out and it's like spinning your tires in place, basically.

But I do see that changing where the molecular expression that is more unique to the patient. instead of a stratified design, you got more of a precision personalized design happening. Whether or not it's going to make a shift totally to end of one, I can't see that happening like within the next 20 years, I really can't. It's a lot of complicated twists and turns. I could be wrong about that, but we are trying our best to participate in leading the way, in using, you know, a combination of human intelligence and artificial AI intelligence, and being in a responsible way to be able to use the best of the tools you can to get to that space of better precision.

and that's what we do is we're focusing in on better precision.

And we're learning so much about the fact that probably each person's cancer, just like each person, is unique, their cancer is unique. We're going to take a break for our sponsor and then we're going to be back and we're going to cover these messenger RNA, COVID-19 vaccines. I know John has a lot to talk about, a lot to say about them. So let's get real. Let's get loud on America Out Loud Talk Radio.

This is the McCullough Report and I'm Dr. Peter McCullough.

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Where are we with industry catching up to with the potential harms and diseases that messenger RNA vaccines can cause?

You have to look at all of these things together in correlated values, so that you can see what's amplified, what is underexpressed, how the environment is really responding to whatever mechanism of assault there might be, right? You know as well as I do, Peter, because I've been reading a lot of your papers. Thank you so much for your contributions, because it's amazing. It really helps to set a lot of clarity out there. One of the first papers that actually came out, which was the mRNA vaccine, the BNT162b2, right?

That first paper that came out when everybody was saying, well, no, I mean, it's never going to get back into the DNA. The DNA is not going to be corrupt. You know what? That's totally false, because the mRNA...

And that center part, the region that they could reliably know was going to be a good reporter region, that 444 base pair. I thought the paper showed, I think convincingly, it did get into human DNA. Now, are you telling me, as an expert, that you think that's legit?

And, you know, particularly, you know, in relation to accelerated cancers that are associated with, you can see tumor promoters and tumor suppressors totally out of whack where they actually switch roles. I mean, when you start switching roles, it's not just about the cancer evolution that's causing the switch in the role. When you have a destructive protein type of transcript message that's coming out there with rogue effects, then you wind up getting very poor expressed activity of these tumor proteins, tumor suppressor, tumor promoters that actually hurt. And a lot of the times we're seeing relationships with, you know, the mRNA getting back into, get into bad messaging, back into splice, splice variant type activity that happens with DNA. So, there's no doubt in my mind, we're seeing, we're actually seeing mRNA being reintegrated into DNA.

And then, as you know, this propagates over, you know, the cell progeny. So, with each cell progeny that happens, you know, you have, you're having these billions of copies that are happening, you know, with new cellular, with new cellular colonies forming. Well, now let me ask you, John, do you?

So, you actually wind up seeing a very loose, complex formation in molecular simulations to where the complexes are not tightly knit together. They become fractured and unbound. And when you're talking about anything in the complex of a mitochondria, you know, creating that type of a signaling flaw, you're talking about the electronic transport chain being affected, you're talking about bad packing of proteins being affected all the way around, the mitochondria dysfunction happens, the mitophagy happens with an accelerated rate, and then, you know, and then the cells begin to die very quickly, right?

There's thousands of mitochondria in the same cell. So, you know, it's not just like one or two. So, you have a lot of mitochondrial interface, and if you have a very strong, bad signaling complex, you're going to have mitochondrial overheating and destruction happening pretty rapidly. And a lot of the times. what you're seeing with mRNA splice segments affecting this is that it creates that accelerated aberrant.

Well, with an injection, people have tried, to, you know, get their heads around this. Does every cell encounter the messenger RNA? Is every cell, or is it going to be a mosaic, just some?

eradication of the virus with actual recovery and regenerative activity of damaged tissue. So, what you wind up seeing is that, like you're saying, it could be a mosaic, depending upon the susceptibility of the individual, okay? If they have a very strong susceptibility to, they're going to have a lot more destructive influence in their body. So, it could actually hit their kidneys, it can hit their, you know, their heart muscle, it can hit their brain tissue, and what you've actually seen, some significant.

correlative activity with various type of fibrous activity that's occurred.

So, what we could see is that you can correlate this with various type of, you know, like if a person is more susceptible to a specific viral strain than a, you know, some other person that has a very strong resistance against it. You know, certain HLA patterns demonstrate good resistance or the contrary, they can be highly susceptible.

It's showing dysfunctional proteins on the surface. So, in that way, you know, it may not necessarily be direct, but it would be indirect, depending upon the, you know, the cell cycling, because, as you know, the mRNA will definitely get back to more, like I was saying earlier, it hits the WNT notch system sideways. It's not the only system, but it also hits the DNA mismatch repair system, and then we start seeing some.

So, there is hope.

Catanzano, CEO and founder of Neo7 Bioscience, we're talking personalized proteomic in vitro diagnostics, coming up with a plan, cancer, vaccine, injury, and then administration of peptides that are therapeutic, that are disease mitigating, potentially curative. John, thank you so much for joining us on the show. Thank you, Peter. It's been an honor to.