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Talking Biotech is a weekly podcast that uncovers the stories, ideas and research of people at the frontier of biology and engineering.
Each episode explores how science and technology will transform agriculture, protect the environment, and feed 10 billion people by 2050.
Interviews are led by Dr. Kevin Folta, a professor of molecular biology and genomics.
Kevin Folta (00:00)
Hi everybody, and welcome to this week's Talking Biotech podcast. Now we've come a long way with cancer chemotherapy, from basic compounds that simply disrupted the way cells divide,
to more intricate mechanisms that integrate with the signaling mechanisms within cells that control cell cycle, that control angiogenesis, that control other aspects of metastasis. So there's a lot of interesting ways that science has come up to control the growth and spread of cancer. However, there are still some that are highly refractive to even the best therapies.
And as immunotherapies begin to take hold, we see a spectrum of different immunotherapies that are taking center stage as ways of combating the most insidious cancers. We're speaking with Dr. Alex Schneider. He's the founder and CEO of CureLab. Welcome to the podcast, Dr. Schneider.
Alexander Shneider (00:57)
Hi, and may I you personal favor? Could you please call me just Alex? If you are angry at me, or if you think I'm making wrong statements, then call me Dr. Schneider. But if we talk science and not something below that level, then call me just Alex.
Kevin Folta (00:59)
Absolutely.
yeah.
Okay. Well,
I, and I'm always Kevin. mean, I, even in my classes, I, I, I stay away from the title because I feel it creates distance. even though it gives you credibility, it's a, there's a distance that's there. And, I'm an approachable nerd who loves to talk.
Alexander Shneider (01:28)
Sometimes
those who try to be credible end up to be incredible.
Kevin Folta (01:37)
That's right. Now I find a lot of people who heavily use their titles in social media are the ones that you should ignore. So anyway, so.
Alexander Shneider (01:47)
For that matter, do you know what was title of Albert Einstein? You don't care because you just need to know what his main achievement was and then titles are irrelevant. Kevin, may I start in the most scientific and for a Lehman guy almost an impolite way to engage into a conversation, start with a partial decision.
Kevin Folta (02:13)
Absolutely.
Alexander Shneider (02:15)
agreement with what you just said in the statement. Let's look at hindsight. In 1950s, 1960s, 1970s, we already knew how to measure quantitatively, how rapidly cells divide. So,
Kevin Folta (02:18)
Okay, excellent.
Alexander Shneider (02:35)
When I say our, I mean humanity in general, because you and I, maybe we were not born at that time. But our society, frame of thinking, was based on the tools available to us. And the tools were pretty rudimentary. For example, to measure how cells.
how quickly cells divide. Thus, an idea was cancer cells must divide quicker and normal cells divide slower.
But today is 2026. In 2026, we already know that we were wrong. Why? Because majority of effects are chemotherapy, radiation therapy. All of them are, almost all of them, most of them.
predominantly are immune therapies,
drugs which were selected based on their ability to inhibit cell division. In reality, either they stimulate immune presentation during cell death or they're turning off switches of immunity. So this brings us
to a question which for funding agencies and for proper academia is almost a hit below the belt. How many good drugs did we throw away? Was it that we threw away the best drug candidates because we were selecting them under the wrong
Kevin Folta (04:15)
I see.
So I guess the question is, you know, back then drugs like culture, culture scene would inhibit spin cell division, for instance, and that those were considered chemotherapeutic agents because they thought they would control cell division. But yet what you're describing is that you're sure you're arresting cell division, but you're not producing the immune components that activate.
targeting of the cells which are apparently expressing proteins.
Alexander Shneider (04:45)
Yeah, oh, there are multiple ways. Let me give you a couple of examples. For example, immune cells do not randomly attack cells in the body. They need specific targets, specific markers to be presented at cell surface.
So it's called immune presentation. For example, I see here something.
What should not be here? Let's go and kill this cell because either the cell is infected with the virus. And now I see there is something presented to me. What should not be there? Maybe it is from a viral genome. The same with cancer.
Maybe this is cancer mutated too. Let's go and kill this cell. So what we could not measure back in those days because techniques were not here. What we couldn't measure was this.
releases.
Or number two, for example, if you look at the history of immunology, first, let's say, late 19th century, big part of the 20th century, what did we study? How to activate an immunity. If you look at the end of the 20th century, beginning of the 21st century, it lists as much.
is not how to turn immunity on.
Otherwise, every time you cut your finger when you were five, still would be burning wound today. So what does tumor do? Tumor hijacks good
necessary mechanisms.
and misappropriates. It's like a society, it has a societal analogy. Certain insidious organizations hijack instruments which society created for very kind, very generous purposes and misappropriate them for insidious goals.
And for example, T-Rack cells. It's T cells, immune cells, which are turning off some attacking immune cells. By Rack regulatory. Okay?
And what turns out that some drugs which were selected based on their ability to inhibit cell division in reality, at least as much of their effect was or is because they down regulate these T-Rex cells. So I think...
instead of only looking forward and thinking what new can we do, what new can we develop, we also should look back and ask ourselves what have we done wrong? Should we kind of revitalize certain drugs which were rejected?
unfairly based on our wrong mechanistic ideas.
These two guys, Kevin and Alex, didn't learn this, this and this. They were wrong on this, they were wrong on this, they were wrong on this.
Kevin Folta (08:09)
I fully expect that. think they're gonna...
Alexander Shneider (08:10)
Of course, that is why.
Because we have a conversation in a particular point in time. We always have to be intellectually humbled. Because tomorrow...
all our mechanistic ideas will be viewed partially wrong. Why do I think this way? Because looking back, we always say that their ideas are partially wrong. That is why every time we discuss drugs, we should calibre the priorities. What is the statement?
For example, empirically observed effect in mice, in rats, and God forbid, in humans. Because after all, we have so much success in mice and rats, and so little success in humans. So this is, what is this? This is the goal.
all these mechanistic ideas, they're just one of the instruments, not even the instrument, just an instrument. And when you come to your university for your faculty meeting and you repeat what I just say, they would consider you to be the worst.
person on the floor who should be expelled because this goes against the dogma. So Kevin, if you repeat it, blame it on me.
Kevin Folta (09:45)
No, but see, I kind of feel the same way. I think we add that for me, my entire career is built, the best discoveries are built on inadequate hypotheses. So in other words, I come up with an idea that we're going to test and it turns out that we under thought, you know, the data don't support the hypothesis, which really says that we have under thought the problem and we find additional data that tell a much better story than we originally planned.
So I'm a big fan of intellectual humility and kind of coming to the table and saying, I really don't know anything, but I'm a pretty good experimentalist. And so I'm good at seeking the interesting solutions to weird problems. know, so it's a really nice philosophical way to start the whole podcast. But, you know, let's let's segue over to to CureLab in that.
I really think this is an interesting therapeutic way of solving a problem that I really would like to dig into. And can we start out by talking a little bit about the diseases targeted? I know that that some of women's cancers have really high mortality rates. So triple negative breast cancer, platinum resistant ovarian cancers. Why are these so difficult to treat?
Alexander Shneider (11:00)
Okay, first of all, let's go disease by disease.
For
Platinum resistant to barren cancer. Okay. First of all, let's explain to our listeners. What does it mean?
Every eightieth woman will be diagnosed with a veteran cancer.
for certain ethnic groups, numbers.
And when a woman is diagnosed with ovarian cancer, first line of treatment is platinum drugs.
Many of them will respond to these treatments, although some would not. But unfortunately, sooner or later, virtually every woman, every patient will stop responding to platinum drugs, like cisplatin, for example. Some patients will not respond after the first round of treatment.
Some would be responsive maybe for five or six, maybe even more, but sooner or later, absolute plus majority of women will stop responding. Now, there is a marker, molecular marker, called CA120.
If a patient demonstrates elevated level of this marker, the prognosis is much worse. For example, 50 % of these women will die within 12 months. Roughly 90 % of these women will die within 24 months.
I would say 95 % of these women will die within 36 months, although there will always be some individuals who live much longer.
There are very few treatment options for these patients. Poxlydexel, Dexil, Gencitabin. And what, for example, our latest paper is about, that we took two groups of patients and one received Gencitabin, classic chemotherapy. ⁓
another or received gencitabine combined with our drug.
called Elanogen, and it doubled the duration of life of the patients. It's called overall survival. But this data is a huge understatement. Why?
because for some non-scientific reasons, we had to stop giving all patients a lineogen on a particular moment. It was July 2022. By that time, some patients received it for a very short period of time, let's say 0.7 months.
Some patients received it for a pretty prolonged period of time, let's say 30 months. So, circumstance created an opportunity for us to make an experimental mathematical analysis which we did not plan to conduct. We could analyze would it be a correlation for how long
you treat a person with this drug? Duration, how much did you, for how long did you receive it before it was stopped, and how long would you leave after? And it turned out that for first 12 months of product administering, there is very strong correlation, then it starts to kind of...
slowing down, slowing down, plateauing, but still was statistically significant by 18th to 24th months. So first, we know that in the future we will give our product for 24 months no reason to give it for longer. But second, we know that if you look only at those women
who received our product for 18 months or longer, we would expect a much greater response than what was published in our paper when we combined everybody together, those who received it for a very short period of time and those who received it
Kevin Folta (15:21)
Yeah, let me jump the gun a little bit there because what I'd like to kind of set up is these kinds of cancers are particularly refractive to the traditional therapies, right? And so when you're talking about gemcitabine or other ones, why does gencitabine fail in these particular cancers?
Alexander Shneider (15:24)
Absolutely.
Did it fail or did it perform to the level we want it to be? And it comes not only to junk sit-up but for other treatments.
Kevin Folta (15:50)
Yeah, so.
Sure. Yeah, that's a classic hallmark of cancer cells. find drug between drug pumps and other issues. They find ways to evade.
Alexander Shneider (15:58)
Yes.
⁓ Let me give you
a couple of examples. couple of examples. First of all, usually when we do something in life, we always do something envisioning desired results. And we often achieve those results. But what we usually do not take into account that
moving toward the desired results. We also activate processes which we didn't intend to. For example, you want to make your wife happy bringing home a big bouquet of flowers.
and right from the rainy street you run into your house and give her the flowers. Yes.
The problem is when you entered the apartment from the rainy street you didn't take off your shoes because your hands were busy with the flowers and you left dirty steps on the carpet and it was an undesired result which you didn't take into account. The same is on the molecular level. For example, ginsetabine and other drugs.
You give it so it would take care of cancer cells. But they activate chronic inflammation through activation of certain trigger of chronic inflammation called NFKB, an entire cascade of events. But then chronic inflammation deactivates those drugs. Thus, you...
initiate a negative feedback loop. Thus, even if the drug is perfect, it's not perfect because it's self-limiting.
serendipitously, we discover.
that our product, Elinogen, blocks chronic inflammation. Aha! Now, when we give it together with gencitabine or other drugs, many other drugs, we...
reduce, at least reduce, if not prevent, ability of a tumor to inactivate this drug.
And then, and it's not that we were giving women gencitabine and when they progressed on gencitabine, we didn't give follow-up treatments, for example, Paclitexal. What we did, that doctors were doing absolutely the same thing as they would be doing otherwise, but they were continuing giving Elenogen until July.
20, 22. So there were two groups, Those who were receiving standard of care, those who were receiving standard of care plus our product. But any story like this.
I'm incorrect even if I'm correct. Why? Because it is always a small piece of a big puzzle. Talking of drugs while they stop being active.
How else does Elanogen work? Because, you know, we all try to be a little bit
too comfortable, a little bit primitive in the way we think.
One drug, one mechanism. What is the mechanism of this drug? Hey, how about if it is not the mechanism? What if it is a mechanism? Because like a human, we have more than one behavioral manifestation or behavioral trait, the same are molecules. everything should start, like education, scientific education should start from liberating.
our mind from simplistic cliches. The mechanism of a drug. For example, laneogen, I already know four mechanisms, but maybe all of them will turn out to be minor, not incorrect, not incorrect, but minor next to what will be discovered by your graduate student 20 years from now.
Kevin Folta (20:13)
Yeah, I totally understand where you're coming from here. So we're speaking with Dr. Alex Snyder. He is the CEO and founder of CureLab and we're talking about ways to modify cancer chemotherapies to deal with more refractive cancers such as ovarian cancers. So this is the Talking Biotech podcast and we'll be back in just a moment.
And now we're back on the talking biotech podcast. We're speaking with Dr. Alex Schneider. He's the CEO and founder of cure lab. And we're talking about the drug, Elanogen.
and how it works. I that's the reason I wanted to have him on was because this is a really novel approach that I really think is super cool. So we talked about ⁓ ovarian cancer that are platinum drug resistant. These are treated with something called gemcitabine, but they develop a tolerance to gemcitabine, a couple of negative feedback mechanisms that are
causing the cells to become, they're inducing a state of inflammation which changes the cells' susceptibility to gemcitabine. Now you, as you mentioned, you add a lanogen and now all this, now you have something that is more susceptible to the treatment. So tell me about a lanogen. What kind of molecule is it? And this is the fun part.
What kind of molecule is it? And how did you come about this approach?
Alexander Shneider (21:41)
Okay, so the answer will consist of two parts. First, what was without me, before me, and...
utilized in my work and what I brought.
First of all, let's start with the word plasmid. Imagine a circle made of a DNA.
Circular DNA is called plasmid. But this circular DNA may be considered as an envelope. And is in any envelope you can put love letter or hate letter or business letter or stupid letter. You can put different genes into this circular DNA.
And then in our case, the most simple or the most straightforward, maybe even the most primitive case, you just have ordinary syringe and you inject what looks like water, or looks like saline, a solution of these plasmids, intramuscularly. There are multiple different ways.
to administer plasmids but just injecting intramuscularly.
Majority of these circular DNA molecules will be coupled by a relatively thin layer of cells around the point of injection. And a gene, which is inserted there, will start working, start producing a protein, which is encoded by this gene.
Still, some minor fraction of this plasmid
would go to limph notes.
and start working their producing.
and coded by the gene. Importantly, that these plasmids never integrate into our chromosomes. So from a safety standpoint, it is a very safe approach.
Okay, then I ask myself a question. What would be an ideal vaccine based on plasmids?
First, it has to train immunity to attack a particular target inside cancer cells which are selective, which differentiate cancer cells from...
I selected a gene called P62 because in cancer cells and cancer cells only, this gene is overproduced. And if you train immunity to attack cells where P62 is overly abundant, then by definition you are training immunity to attack cancer cells only. However,
There is a night's sweat of every vaccinologist and a dead end of many multiple most targeted therapies. Because cancer cells may stop producing a particular target. It could be a vaccine target. It could be a target for targeted chemotherapy. And then...
let's say out of million cells you find five cells or 15 cells which stop producing this target then sooner or later they will repopulate the tumor, regrow the tumor and it will be completely resistant to your previous treatment. So I had to select such a target.
which cancer cells cannot stop producing. With B62, cancer cells are biochemically addicted to them. They cannot.
stop overproducing p62 and if they do they would become extremely vulnerable to chemotherapy, radiation therapy and all other therapies. Thus it is selective and cancer cells cannot omit it and this was my original hypothesis and it was not wrong it was right but today in the hindsight I know that I was more lucky.
smart because then we had serendipitous discoveries, discovery mechanisms which I could not envision at the beginning.
Kevin Folta (25:45)
When you talk about the plasmid therapy, and I think this is really cool. the target is P62, which which which transform cells depend on in order to continue to maintain different aspects of metabolism and other things. So your target is P62. Is the plasmid that's injected a supercoiled plasmid that has any kind of nuclear localization domains? Or is it just that when you inject a certain amount of plasmid,
Alexander Shneider (25:46)
Bye.
Kevin Folta (26:11)
some finite amount actually gets into the nucleus of cells and is expressed.
Alexander Shneider (26:16)
So this is an entire era.
and there are multiple plasmid-based, mostly vaccines, mostly preventive anti-infective vaccines, which are developed. For example, in India, they have selected plasmid-based product for anti-COVID vaccine. But, and my original idea was to use a plasmid within COVID-P62 to induce
or selective immune response as a therapeutic, not preventive, but therapeutic anti-cancer vaccine. Then, today I even almost hesitant to use the word vaccine because it is both vaccine and a drug. Because later, serendipitously, without me expecting it, we discovered...
that it reduces systemically chronic inflammation. And if Pandora box could be used in a positive sense, not as a negative sense, it opened a positive Pandora box of further discoveries we're enjoying right now.
Kevin Folta (27:33)
No, I understand. is a bit interesting to me because I just think as a molecular biologist that if you're putting plasmid in, now does it doesn't have to go in in a nanoparticle or anything, it transverses membranes somehow. There's DNA uptake mechanism or.
Alexander Shneider (27:50)
It does go to nucleus and is getting genes there, getting expressed. I mean, listen, it's a huge field. And...
There are companies and labs which are developing particles to ⁓ shift the gears and make it even more efficient and deliver not intermasculally but for example through certain devices, through a skin. But you know with these P62 encoding plasmid with the laneogen
Because one of my crafts is evolution of technical systems and evolution of science. And when I lead my own team, I always try to lead it.
in accordance, in coordination with laws of technical system evolution and scientific system evolution. I know that certain things have to be done right here, right now as a first priority. And certain things should be left for later, because if you prove, demonstrate efficiency, for example, for...
particular disease, then a big pharmaceutical company which has many people on staff and knows the same tricks as you know, they will further optimize it. Small biotech company. If you start with optimization,
Board of Directors better get rid of the CEO and Chief Scientific Officers because these guys are just glorified lab techs. What you should do, you should do what brings the highest scientific yield could not be just achieved by random shuffling of all possible optimizations.
and leave big teams to do margin optimizations later.
Kevin Folta (29:49)
So, but to continue along that line, when you use a plasmid approach, why not just make a monoclonal antibody against P62 and use that as a therapeutic?
Alexander Shneider (30:03)
⁓
The simple reason wouldn't No. Or would work only to locate it.
Kevin Folta (30:05)
Wouldn't work, okay.
Alexander Shneider (30:11)
First of all, there are two types of immunity. B-cell immunity, which works through antibodies and monoclonal antibodies, they mimic this B-cell immunity branch. But for cancers and for viral infections, it's more of a T-cell immunity, basically proteins. Let's say you have million copies of a particular...
thousands of copies of a particular protein in a cell. Cell grabs a small sample size.
chops them into peptides, assembles them through a very specific mechanism with so-called MHC1.
or MHC1 complex and exposes it on its surface. Our lymph, our immune system knows everything what should be there. And they scan those cells and they say, aha, I know this peptide exposed in MHC1. This is my peptide, don't touch it. But if they see a peptide in...
MHC1 representation, which doesn't look familiar to an immune system. It says, you know what, this is a danger, maybe a virus, maybe a tumor, and then they kill the cell. Realistically, they don't kill the cell, they make the cell to commit suicide. But anyways, so monoclonal antibody does not work.
when we give a lineogen. Some of this plasmid is gobbled by certain cells which could either promote anti-inflammation or promote inflammation.
And when we're young and healthy, these cells promote anti-inflammation. When we're old and it is time for us to leave space for the next generation, they start promoting inflammation. Elenogen gets to these cells, reprograms them, and now these cells, instead of secreting...
for the inflammatory cytokines, they started secreting anti-inflammatory cytokines. More than that, they start secreting certain things, and by the way, I don't know yet what those things are, which could be sensed by remote cells, which never saw the plasmid, but they sense what is secreted, and they are getting reprogrammed.
and now they're secreting anti-inflammatory secretone. Then more cells do it. For example, I'm telling you a word, anti-inflammation. You come to two people who never saw me.
and you tell them anti-inflammation, anti-inflammation. Each of them comes to two people, so now it will be already four people. Anti-inflammation, anti-... They never saw me, but now they repeat it. So this is a self-amplifying cascade. And...
I can tell you about anti-tumor mechanisms which Elenigen induced and antibody would not induce it. But when I was starting this journey years ago, I would be uncertain.
Kevin Folta (33:33)
I
Alexander Shneider (33:42)
How much of a difference would we see between a plasmid and let's say for example monoclonal antibody? I would only say B cell response versus B cell and T cell response. Now I know that both of them may be just a tip of the iceberg and anti-inflammatory.
effect is contributing more and in a more unusual way than immune response itself.
Kevin Folta (34:13)
So, so, we've, we've, so we've spoken a lot about Elanogen, which is this plasmid that's injectable, which trains the immune system on P 62 changes, uh, inflammation cascade, uh, and affects cancer cells.
Alexander Shneider (34:13)
Okay.
Kevin Folta (34:28)
What have the clinical results been like so far with Elanogen in conjunction with traditional chemotherapies?
Alexander Shneider (34:35)
During phase one clinical study, we started with dose escalation. We had three groups. One received one milligram per injection. Another received two and a half milligram per injection. And the third received five milligram per injection. And then we added, I think, 12 more people.
to extend this phase one clinical study and we used different types of cancer. Because for the phase one study your most focus is safety and it is highly safe, very safe product, no significant side effects.
Then, although we used different types of cancers, not statistically significantly, but on the level of common sense, we thought that, for example, ovarian cancer and the deadliest form of breast cancer, which is called triple negative breast cancer, why is it called?
negative because patients don't have three things estrogen receptor progesterone receptor and her two they're kind of we had few patients but responses were pretty appealing so we said okay let's focus on platinum resistant of our in cancer because this is the deadliest form we only go
to those types of cancer where options are limited and life expectancy of patients are very short and time before disease progression is called progression free survival is very short. And by the way, here I have to say that everybody's talking overall survival, so for how long?
and progression through survival. To me personally, the third parameter is at least as important, if not more important, quality of life. And although it was not officially
part of the clinical trials, first and second phase, which we've done at SUS. Here, we are planning to start US clinical trials as soon as possible, and then monitoring and properly reporting, not just anecdotal self-reports, but systemically reporting improvement in quality of life or dynamics.
life will be very intrinsic part of our studies. So as I told you already, we had great clinical success and no side effects. But we also published papers in animals, different animal models for non-counsel's diseases.
in cancer in addition to a varian and breast cancer, we will go to other cancers. For example, the most logical to start with cancers where gencitamine is part of the treatment. For example, pancreatic cancer, lung cancer, but also melanoma.
metastatic, hormone-resistant, or prostate cancer. But also we will go eventually to non-cancerous diseases associated with chronic inflammation. For example, we published a paper which contains videos available on the internet how limping dogs with chronic pain
Aging dogs with osteoarthritis they were limping stop limping After we gave eight injections of our product because chronic pain comes from chronic
And we planned psoriasis, we published multiple papers on osteoporosis, because with osteoporosis, when you're young and sporty, your mesenchymal stem cells in the bones develop, differentiate into bone cells called osteoplasts. But when you're a woman,
after 60 or a man after 80, the mesenchymal stem cells will differentiate into fat cells called adipocytes. And giving our product in rodents, mice, rats, reversed this process. now, now the same mesenchymal stem cells give...
osteoblasts again instead of adipocytes. So we're planning to go to multiple diseases.
And if we reignite mesenchymal stem cells, reduce chronic inflammation, increase anti-inflammation, reignite stem cells,
But everything has to be done sequentially. First, we have great results with one of the deadliest forms of female cancers, which is platinum-resistant variant cancer. And then we will do...
the deadliest form of breast cancer, which is triple negative breast cancer, then we will do other cancers, then we will do other non-cancerous diseases based on the same mechanism.
Kevin Folta (39:52)
Well, and if everything goes perfectly well, about when might you anticipate these kinds of therapies being available?
Alexander Shneider (39:59)
First of all, I don't have crystal ball especially in our uncertain time for example the day before yesterday we received score I think 20 for our phase 2 SBIR grant application for ovarian cancer
National Cancer Institute. This is an excellent score. But they don't have money. Everything is on hold. And if you think I know the answer, if we would receive this money ever at all, you would be joking. So as...
Isaac Newton once said, can calculate motion of heavenly bodies, but I cannot predict insanity of the masses. On top of my science, on top of our excellent, brilliant, devoted scientific team of CureLab, there are...
investors, are governments, there are so many factors which I have no control over that I can pledge my dedication but I cannot pledge any particular tongue in the most
Kevin Folta (41:19)
Yeah, I totally understand that. I certainly appreciate that. And as a guy who gets great scores on grant proposals, but no money, I totally get it. But if people wanted to learn more about CureLab and Elanogen's progress, where would they look online?
Alexander Shneider (41:33)
Actually, they can go to our website where we mirror for free all our papers Which are on the PubMed and go through our website to PubMed or directly to PubMed and read those papers also
if they are part of any university or any podcast or organized group of scientific enthusiasts, either me or my brilliant co-workers, we do take invitations to speak, especially if it is patient advocacy group.
or science, especially for young people because our future belongs to our children and in the era of scientific misrepresentation somebody has to communicate a humble way to look at science. So there are many ways, there are many ways.
Kevin Folta (42:30)
Probably the best place to start would be at ⁓ cure lab oncology dot com. Right. That's the website for the.
Alexander Shneider (42:37)
It's you said it. didn't come here for
any promotion. I didn't come here for any advertising. So it's you who said it. And by the way, we also have a sister company, curlebveterinary.com, where biology is the same, but it's for dogs. saved 11, out of 11 dogs, we saved 10 out of 11 with breast cancer.
Kevin Folta (42:49)
Absolutely.
Yes.
Alexander Shneider (43:05)
with limping dogs and many things else. So biology is the same. Business science is different. But there are more ways than one to learn good science if you are interested to learn.
Kevin Folta (43:18)
Yeah. And that's a great place to stop. So Dr. Alex Schneider, thank you very much for joining me today.
Alexander Shneider (43:24)
Kevin, thank you so much and it was a pleasure and honor to be on your podcast.
Kevin Folta (43:31)
Well, yeah, thank you. And for listeners, you know, it really is kind of fun to think about how a little circle of DNA can elicit all of these immunological responses that can have important roles in combating cancer and other inflammatory based diseases. In this case of the P62 protein. But you can apply this to many different proteins and maybe the plasmid will be another tool in the toolbox like mRNA based therapies and other others.
that may define the future of cancer therapies. This is a Talking Biotech podcast and we'll talk to you again next week.