I, V, M. No idea why we do that every time. I think we should tell our listeners that simplified is the podcast which when you wonder lonely as a cloud that floats on high over Wales and Hills and all at once you see a crowd not golden defidels but for hosts of simplified so wow. If I need to address any words worthless.
But very nice. What Tony was referring to was that we seem to be using that as a sound check prompt every time so in today's episode we have somebody extremely special over here so welcome to the show. Good to have you back to your bedroom after the prolonged absence of no episodes but no jokes about one of the smartest people I know one of the funniest people I know at Tony this is not you. We have a guest who is my good friend Bertie.
Hi Bertie. It's fair to say that we use the phrase you know someone who wears many hats slightly but Bertie actually literally and figuratively wears many hats. Actually you know what yes I should have brought my hat along. One thing yeah one thing I have to say here that even Chuck says you're the smartest person you know or you're smarter than any of us.
It's not saying much so. I also go one thing just to mention that I'm getting a bit of FOMO because I'm the only guy without a Y in my name. Oh, very nice. Oh, I have.
Oh, very nice. Very interesting because the Y came into my name because a small mix of that my dad did. I was B.E.R.T. I actually for a long time and then my mum was a school teacher and then I had to bring one of the ICAC pamphlets which said okay fill up the name of your kid and I gave it to my dad.
My dad was a fan of the German football team who's coach was Bertie boats B.E.R.T. Y. And in some moment of momentary lapse of reasoning he put my name as B.E.R.T.Y. Although there are huge blacks with award everything B.E.R.T.I.
right in front of him and then I forgot about it. My dad forgot about it. Then standard marks, I see it says B.E.R.T.Y. and my mum looks at me and they look at that and they're like ah, this is school records and trophies and all that.
That and all is fine. Not of too much consequence in the larger picture. After this episode of the episode please tell us what the name should be on the simplified episode. That's the way it really matters.
B.E.R.T.Y. So was your mum a fan of B.E.T.Y. would have said? My grandmother.
Yes, she was. But interestingly B.E.R.T.I.E. on Google will get many B.E.E.T.Y. only two.
One of them has been. So my dad upped my SEO. So far divisionary. Not a phrase I expected you to.
I mean I expected to say many things today but my dad upped my SEO was not wonderful. But when you search for Bertie actually I'm sure Google says they do me nationally but. Now it does. Who is this?
I remember seeing him a couple of I mean seeing. Our gentleman lady who was the Australian Open. Oh actually OAS is a layer. Oh she's played cricket as well.
The women's BBL and also a second start. So I'm a B.E.T.T. Sorry buddy. So Bertie there are many topics that we could discuss.
I mean I did. I'm afraid you start. We actually didn't tell the listeners what all Bertie does. I think it's the answer to the discussion.
I was about to get. So I mean there are lots of topics that we could talk to Bertie about. And I have done Zoom sessions many times on various aspects of rock music and things like that. So Bertie is okay here's what I know and I haven't read your CD and things like that.
You are a quizr. You are a quiz master. So that's one. You have not heard of many quiz books.
Yeah. And the article on Sunday on the Hindu what makes this day important in history and all that. So that's one that's a quizzing site of you. Yeah.
And also a questions on there. Yeah. That is that's the article. Oh that's the article.
That's the quizzing site of Bertie 30% taken care of over there. And then there is a musical site of Bertie. He is a found of musical knowledge and he is a big music fan. His house in mother is basically like one vinyl warehouse along with all sorts of instruments ranging from a sitar all the way to a seven-spring guitar.
Well string but yes. I was hatching on to that. Oh yeah. Oh yeah.
Oh yeah. Oh yeah. So that's a musical site of you. By the way Bertie can have a five hour long discussion on any artist ranging from I am assuming King Floyd to Harry Prasad Sora's.
Oh absolutely. There you go. See there you go. So let's start with our one.
And then there is the stuff that you do that and then and then of course you're a huge F1 fan which to me is the only fault that you have but let us not argue about that because. No we can have one episode on that. So it's actually one of the very very rapping for actually I will join you. So yes.
So then of course there is a book itself that you do which is what you will talk about for the rest of the episode you are assigned this at the end of the day but have a disdoubt on anything like as a spy chart missed anything and please don't say some obscure thing like you have a toothpaste expert or something like that. So like it says something that you actually like. I'm a good teacher for the apartment kids so I take guitar glasses. In the process I've become a very interesting midway point between all the parents and the kids so I get all the glasses from the parents I get all the glasses from the kids.
In the entire apartment complex guess who knows all the tea. Wow. This is very very niche spaces that you work in butty and I still think that you would have been a great lobbyist. There's this old archilex one cartoon I remember now.
This politician is coming to a bunch of small school kids and asking what do you want to be when you grow up. It's something teacher painter I want to be a middleman. I want to be a funny at that point. Anyway so let us actually go on to let's go on to what do you have one you have a very interesting like sort of like set of interests and things that you do and stuff and we'll get to how you balance all that later but tell us about the work you do and what is it's very interesting.
Like the first time I heard about this and keep in mind and also you must keep in mind that my friends circle most of us make PPD so we're living right. So to see somebody who actually does things that actually like makes a difference in the world is kind of rare so please tell us what is it that you do and how you got into it. Before I do that I had to say you guys do make a lot of difference. Especially your PPD's have any difference because if at any point of time if your PPD has led to something happening at let's say and it's seven that's made a lot of difference.
No, no, no, don't do that. No, no, no, don't do that. This is what I'm going. So I'm a molecular biologist right.
So I work with DNA and RNA. It's not a thing you can do as a group. It's like I sit in the microscope or sit with the bi-safety level container or something or I have an intern or a colleague that's about it. And it's long hours of a lot of statistics and all that stuff.
The only thing that gives me a lot of comfort is the music that I use. Do I have a foot of a head force? Right. So if anything that you do has led to me finding a new musician or to a technology that I use.
Wow. Hey, you made a difference to my world. So thank you guys. Wow.
Wow. But adding to your list of the AI, it's a motivational speaker. I think. The ability to find some good in every car.
Every car. You should actually become national leader or something. Why are you disparaging him now? I mean, there's a very mean thing to say.
Right. But do you say you have like four or five headphones? I was just thinking how many headphones would Ravanan need to listen to? Oh, good point.
Okay. He has like 10 pairs of heads. 10 heads. But all 10 brains also have their own listening.
Wow. So like 5.1 he can have 10.1 input. 10.5. He can't process like different.
He's like, he's a different brain. Right. So the brain by itself processes as one. But so if he listens to the same song with 10 heads, it's basically a concert.
The only thing we can do is I would love to do an experiment is that have him the same song, but each was slightly different in tempo. Okay. One point to be able to have 110. And then we got at what?
BPM is legs watching dance. Oh. Okay. Basically two legs.
Yeah. Exactly. Listen, listen, listen, dance to the 120 people track is on the left forehead or the 110 people on the right. Or it's like an average of all the BPMs.
I feel with all due respect to your scientific knowledge. But I feel that if I'm not going to show up in the world, I don't think making the map dance would be the best of priorities. Right away. I get a sponsor.
Headphones on. Guys. I mean, let's process this. Okay.
Let us go on. It's been about 20 minutes. We've been talking about everything except what you do. I know you're very modest, but please spend the best time in this telling us what you actually do, how you got into it.
And all that. I know it's a fascinating story. I am a molecular geneticist. So I play around with really small things like DNA and RNA.
So basically everything in our life, everything that we turn out to be everything that is pretty much written in our DNA. Right. So we know because of great work as one of the greatest people said standing on the shoulder of giants, not all of this is, but I said Newton is that mental Darwin and all these people said that there is a genetic reason as to why the human civilization has developed because of what we learned and what we invite from the people before us. And that's the information that written in DNA and RNA.
So the thing is when information travels from one, let's say code to another as it is, as it moves along, if it will establish in a proper manner, then everything is good. Right. And that is a proper genetic heritage. Sometimes that's one mistake.
That's a mutation. That's what we call it. Okay. This one letter in code, like for example, the 26 alphabets that they had numbers are infinite and so you're writing code in the computer.
The number of chances that could go wrong are much, but in DNA, there's only four, A, D, G and C. And it's only multiple combinations of this which make up everything that we are. But even in that, sometimes the tiny tiny mutation where a T becomes a G or an A becomes a C or something of that sort. What that leads to is a complete breakdown of machinery in which a protein is formed.
Now protein is basically a thing that carries out all the functions. If the DNA and RNA are the ones that have the information, the protein is basically the machinery that does everything else. So what I do or what I used to do before my current job was to study this process as to how the DNA becomes a protein. What is the process that goes through it is that's what's called molecular biology studying the molecules at that level.
What happened in 2015 was I was working on stem cells and when a friend of mine called me and said, listen, there's this project going on. It's through that diseases and he had to go to Australia in two months and said I needed someone to take care of themselves right now. Please I know you can do it well. I'll give you a nice place to work with and I will allow you to wear headphones at work with you.
This is true. Okay, he's Dr. Arun Shastri. He said okay I know about working on this right now, you're working in a government institution.
They won't allow you to wear headphones. They won't allow you to wear T-shirts. Okay, in my lab, you join. You can wear whatever you want to talk about your books.
But all right, I didn't ask about the money. I didn't ask about the money. I didn't ask about the money. I didn't ask about the money.
That's a lesson here for all HR managers. I know the person, know the employees. That's how I got it. And what I got in at that time was to do with rare disease called dushion muscle.
The organization that I'm part of is called that, which sounds pretty nice. The full form is distrophy annihilation research. One of the very few organizations that has the word annihilation in it, which is not a death metal band. It's definitely a band.
So the distrophy is the disease that's caused by mutation which leads to the protein brain. In this case, it's broken. So all of you muscular gentlemen and also the wonderful people are listening. If you feel your muscles over here, they are like, you feel some resistance.
That's because of the distrofen protein doing its job. In these kids, what happens is the distrofen protein is not able to be that very strong protein. It starts becoming like jelly and eventually loses its shape. And what that leads to is your muscles and your body slowly losing their ability to handle stress.
Now for a child, when a child is like three or four, that's not a big problem. You just get up slower. You don't get tired and stuff like that. But at age of eight or nine, it becomes a little more obvious.
You're not able to walk and all these start using crushes. And by the age of 12, you're calf muscles and if I'm supposed to be your weight and you start to use a wheelchair. But the age of 19 or 20, two very important parts of your body, their muscles start going on. It's your heart and that's when it gets fatal.
So at the age of 24, 25, eight of the heart of the lung, one of them gives up first. So it's a fatal disease. And that is the course of Dushan Musculidistrophy, which is all because of one tiny mutation in a billion code sequence. Right?
Now, till 2008, 2009, there was no way to counter this. If you have a child who has BMB, the doctor will say, sorry, ma'am, sorry, sir, your son is going to die. By the way, it's in the ex chromosome. So that means only boys suffer from it.
Girls don't know it because it's an ex chromosome. Boys have an ex and a Y. So if something wrong, they're ex chromosome, they don't have a backup. So they suffer from it.
Girls have two ex chromosomes. So something's wrong here. The other one makes up for it. So these boys, when they're born, they have trouble.
You ask the doctor and if you're the therapist, you'll be like, give massage, take care of him. But sorry, it's fatal. We can't do anything. But 2009, two researchers, one in Australia and one in the Netherlands discovered some technology called exon skipping.
This is an interesting bit. Now in DNA, even if you go further into it into chromosomes and nucleus and all the way in, there are small things called exons and introns. So your cell, the genetic information is written as exons and introns. Now, when a missionary reads this, it produces a distrofic.
Just imagine that it's like one of those satellite things which sit on a track, reads, track, and end of it, reading information on the track, it produces a protein. Now to stop it from doing all the time, which is what cancer is, the body has a built-in mechanism where it has introns between the exons. So it lands on the track, reads, that's an impron. Okay, fine.
So that means this is not supposed to be the thing goes off. Whenever a body needs a protein to be produced, it takes away the introns, puts all the exons together, and it reads, and then you have a protein. Now for distrofic protein, you have a track that is 79 exons long. It's very interestingly the longest in the body.
For everything you have, there are a number of like 13 or 14 or 20 exons. For distrofic, which is a very important protein, you have 79. Now what happens is in the 79 different exons, somewhere one gets disfigured or gets cut out or even duplicated, the missionary comes and gets stuck. And so it's not able to produce the distrofic.
But these two people discovered was, aha, so imagine this is a track. It's a jigsaw puzzle of 79 individual pieces. It's a linear jigsaw puzzle, right? And your missionary that reads, it gets stuck here.
These guys realize, what if I take out this traffic jam, whatever, I take it out. Okay. And then attach these two and make a shorter version of it. So what happens is now, instead of 79, it's only 77 exons long, but it is completed puzzle.
Right. So the whole thing reads and produces a less quantity or a less stable form of stuff, but at least something. Now earlier, these kids were getting nothing. Now, there is something.
So what we are doing is we are not stopping. The disease, we are not curing the disease, but we are slowing down the process of the disease. So what happens is these kids who would have passed away at age of 21 or 22 now live a longer life, probably up to 30 or 32, they're beginning the more quality of life and extending the life to, for example, to a longer period where we know we might find something else in the future, which will be abused with them. So that's what we do.
And here's the interesting part. Every single kid has a different mutation because everybody is different. It's different. So we make personalized customized medicine.
Every single medicine is for a kid, which obviously are because then that's the thing. People are like, listen, you say you're the only one. Like right now, you're the only one doing it. We're the only ones who have the clinical trials going on.
So people are like, why aren't farmers doing it? Why aren't companies doing it? Why are they this idiot and bang would have to do it? The reason is, customer is extremely expensive.
You make, for example, let's say I have to make something for Chuck. Okay, let's say Chuck says I want to go on Afro. Right? And I make a genetic medicine to make that happen.
But the thing is, I spend millions of dollars in this time, especially for Chuck because he works only on Chuck. I can't say like anybody else. And I'm not going to sell it for $2 million because he's not going to give me $2 million. Right?
So there's no money in this at all making personalized medicine. So big companies don't do it because there's no money in it. And that's why we had to step in and do this and where we make personalized medicine for every single kid. And that is how we as a company, the store family services, brought in personalized medicine to India.
In 2019, we became the first in the country to clinical trials on one kid. Wow. So I used to call that a lot of things. So it's different for each kid.
No, the data is the same. The mutation is different. Now there are 79, right? So each, so each exon has these ADG, ADG, whatever.
For some kid, the leading becoming a for some kid, a G become a C for some kids. What happens is, for example, the kid that we were in 2019, the kid we have later trial is between 50 and 51. That was an issue. So the mission used to get stuck exactly at 50 didn't go forward.
So what we did was we took out 50 and 51 and 49 and 52, we joined together. Okay. So that it reads like now there's another kid, which we are hundreds of kids. But for example, we have another kid patient number two, who's 48 is malfunctioning.
So we have to take a 47 and 48 because 48 and what's on the place where the meat is malfunctioning. So then 46 drive it all the way up to 48 put it together and then continue it. Yeah. So that's what we do.
Wow. I mean, I don't know what to follow that up. So I'm going to leave this to nothing who looks equally flabbergasted. I mean, I'll do what I do.
What's my, like I don't do everything in this. Okay. So my job is the in molecular biologist is to make sure that every kid we do the experiment or not expect the therapy on, it doesn't backfire. Okay.
Now here's the thing. Right. We're not going to and we can't use a mosquito because it's unethical. It's illegal.
So we can't do that. We are making a present for them. But how do we make sure that it's the right medicine and it's not doing something weird. That's why in vitro, while this company, I've been intro is Latin for inside glass in vivo is inside a body in vitro is glass.
So what I do is I take a small sample of skin from these kids, grow it in a petritish and then convince the skin cells by using magic enzymes that they are muscles and the skin cell include your muscles. We can do it. We can do it. And the skin cells become muscles and now you're muscles.
Now that means I can work on them as muscles. So now I have a whole petritish of cells which are muscles. Although they started off as skin cells transitioning. So the muscles cells then we can put the small drugs in and then we can see it.
Okay. This is the amount of thing it works for this kid. This is what happens for now. And then we do a test and finally we're like, okay, guess what?
It works on the muscles of this kid. That means when escalated to a big amount, it would work on the kid as well. So that's where my specialty likes to make sure that in vitro it works well. This convincing skin that their muscles is basically similar to what Donnie does with CSK.
So you can do it. You can do it. I don't know how to follow up questions. Yeah.
No, so many fascinating. We get the meta question. Okay. So a specific suppose we can just go on discussing specifics all day and not because this is something which has really evolved very rapidly in the last few years.
Absolutely. You literally wouldn't have, you know, you're inventing techniques all the time. I'm sure there are some techniques you have developed which probably either don't exist anywhere else or if they do, they've been parallely discovered. We have two patent printings right now, printing patents.
And then we have written a couple of papers. Yes. The meta question is how can, so I know he's no more. I know one child who had muscular dystrophy.
I don't know if it was the same thing who passed away in I think 2007 at the age of 20 or 21. And it was heartbreaking. So I know the family was so, you know, it's sad. I mean, it's something even out from looking from outside.
I wasn't very close to them. I knew them. And it was terrible. They must be many such diseases, which of course were hopeless in the past.
But now these techniques make it possible to either improve the quality of life or just give them all to get out. How can we have many, many more? Yours is probably the only institute in India. So you can handle maybe a couple of hundred children.
How do you, how if you are to handle maybe a hundred thousand children, you need many, many more facilities. How do you think that would happen? If that would happen. Okay.
Thank you. So that's why it brings us to monogenic disorders. So the reason that we are able to do this because DMD is a mono genic disorder. A mono genic is a single mutation which causes a problem.
If that's long as it's a single mutation, right now we can deal with it. Clearly just we could deal with other things, but there are too many hypotheticals. So one of the genetic disorders, any mono genic disorder we can deal with. That's a thing.
Now, as for number of children, here's the thing. Thanks to the government of Karnataka, we were able to also start actually start up. How do you say start a startup? Start a startup.
Start a startup. A separate entity called hundred therapeutics, which allowed us to open up our technology for commercial use. That's also ours. It's on the side and it's go run by the government of Karnataka.
So the obvious is that I work with, oh, by the way, I forgot to mention this, that was started by parents and is run by parents, 10 parents, kids who have this disease. So these parents, technically when they discovered that the kids had to disappear, they met around the world and said, can anybody do something? They would just like, no, we have to take our pockets first. If you're on the US, US kids get it.
If you're the US kids, US kids. So they came back to India and said, listen, people all over the world are doing something. We do something. So they came together and started this organization.
So I don't belong to a private, it's a nonprofit organization, but it's not run by a company. It's run by 10 parents. So they fund the entire system. I can't believe I'm using this.
It's bootstrapped by the parents. Yeah, the first 6.8 crores came from parents selling their houses, selling off the jewelry, running math, doing all the kind of stuff to bootstrap the first foundation. After that, I came in, I started writing grants and got the government and now we have three X that are more than thanks to the grants, but it was started by parents. Today, my CEO is a DMD and pretty much 60% of the people who decide what to do.
They're all parents of children from DMD. Yeah. Now that is skin in the game. Yeah, exactly.
So in 2018, we became SIRO, which is scientific and industry research organization by the government of India, the Department of India, which says we're the only according to the knowledge of our knowledge, which is a vast number of knowledge, are the only parent or organization in the country to have that tag. You know, by a car and big companies, but we're the only parent or organization to have. It's a different definition of parent and company. Yeah, it's a big thing.
So, Shana, so the thing is we can work with any monitoring disorder. Okay. Now the thing is, right now we can deal with up to 300 kids, right? Like we have the capacity.
So the thing is this, the part where you have to customize the way that the molecule acts, that is in step four of five. Up to step four, you can actually produce things on a large scale, right? All the consumables, you think it's produced. That's where you start to, you know, at least cut down the costs, but at the part where you have to customize, there's no way you can do anything about it.
That's where the cost factor comes in. Now, that's the reason that this particular drug that we are working on is available in the US. Okay. It is available in the US.
And there if your kid is 60 kgs, okay, 60 kgs for one year, you have to be $300,000. That's the cost of the drug in the US. We have brought it down to six lakhs in India. Now, six compared to $300,000, six lakhs is nothing, but in India, six lakhs is huge and a lot of our parents are not in the financial means to do that.
Right. So we want to make it even more less. But the problem is in other places, the more you produce, the less is of course. But in this case, we can't do that because we are at the least known.
So currently what we're trying to figure out is some way of making sure that the process is as inexpensive as possible. But all certain, how many of the diseases you take, that bit that it's customization comes. That's where the money part plays a huge role. And like you said, if you had different types of facilities, which all get a different example, we work with neuroma sliders, that's a particular type of diabetes called a diabetes called mori maturity on to diabetes, which is because of mutation in either HNF4, or HNF1 alpha gene.
So now we don't deal with diabetes. But if somebody wants to deal with that, they can start it. We can pass on the technology, we can do this and they can work on that. But we don't have the bandwidth or the thing to work on that.
A future that hopefully in about 10 years and a decade India is ready for. We were responsible, like for example, okay, fun story. Sorry, just before we get to it. I think we need to digest this.
Let's take a break and catch you on the other side. But these fine story and much more. Are you looking for finance products and services that can enhance your personal finance experience? Are you looking for a space to talk about your financial product or service?
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Welcome back to Simplified, where we are discussing Dart with Bertie and how they always skate the bullseye. We are not discussing as much as just listening with the jaws open as Bertie tells us what he's doing. So I'm going to view myself and just also that I'm listening to Bertie's podcast. I must say you are a natural teacher and I can see by all the characters.
Yeah, I mean not just about it, if you thought like science. I'm still wondering. Great. I do take classes.
There is a Marathi humorist, Nomor now named P.L. Deshpande. So P.L. Deshpande will add.
So he said that someone who can take a 50 minute discussion and put it down in 10 lines as a journalist. And someone who can take 10 lines of discussion and pump it up into a 50 minute lecture as a professor. So he is, yeah, both actually. You saw of Squish now.
Really, part of me is jumping up and down because I'm going to be the coolest guy at all parties. I'm going to often talk about more than a disease. And I'm somebody who can take no content at all and turn into 50 minutes of our first podcast. By the way, yes, I do take classes.
Do the panama guy. I will learn the alphabet from you. That's where Chuck, there's something else to do. I also like making P.B.D.s.
But compared to the other P.B.D.s, the teacher's make mine school of memes. It's very kind of the current. There are times when a professor, a couple of professors are sitting there and I put up something and the professors have no idea what it's about. No idea.
Instead of you talking about this, how I can put up a picture. For example, one does not cross into more than one does not walk into more than that. I was simply walking into more than that. So I put up that picture of Sean Bean and put up a small thing about what is a semi permeable membrane.
For example, a molecule has to put out energy to work. I put that and I put ATP next to it. Every student got it immediately. This is where I'm like, scientists.
Everybody got it. And then they're like, that's it. And when I use those memes, it becomes much more engaging for students and they get it. And the teachers don't.
And there's this big generation gap. I have to point of view. You should. I mean, at least three of those textbooks.
I mean, I wanted for my daughter for sure. Actually, the thing is this. I do believe that the age of the textbook has gone. I mean, textbooks are required, but not as a primary.
It's more like a repository of information than a disseminator of knowledge or each other. It is basically audio visual, which is I am telling you, I am a mechanical engineer. I spent all my life in a differential equation and, you know, all kinds of transform Laplace transform, Fourier transform, without really knowing what a Laplace really did. I saw YouTube videos which graphically explained them.
And then I said, oh, wow, this is what it is. And that's a beauty, right? So now I have a great mental picture. Now it's cool for me because I don't know.
I have all respect for Laplace in the 17th century. If you got it out without YouTube and everything. He kind of invented the thing. That's why he's also pointed.
If I make a quickie, ask three of you. Why do you think you got the word meme from? I know. Which of the audience?
Yes, it's the selfish gene. 1936. So if you guys use the word meme, thank us. You're responsible for that.
Yeah. Cooler that you thought. Okay. Actually, you are in real memetics.
Exactly. Yeah. The story which I had for you guys. So when you first started Dart and when I came in, I was doing some work and I was also the grant writer.
Firstly, because apparently my English was good for writing so they made me grant a writer but then I realized I had the ability to actually write grants. So then I wrote a grant and we actually got through and the government was excellent. You're going to work on grad, DCCs. You're working on BMT.
This sounds cool. How much money you want? X lakhs. They're like, okay, cool.
We're going to set up a so the government of India, CCRI, CMR. They have a very strict way. They have a set panel. 12 people who are experts in your line of work decide whether your project is good enough, is useful and it's worth the Indian amount putting the money in, which makes sense.
The Indian government is not going to give up money to anybody in any video or any other project. So we submitted and then we made it and we made it and they're like, listen, we have an issue. First of all, they couldn't find 12 experts in DMD in India. Then they said, okay, 12 is an arbiter number, make it eight.
And they found eight people. But six of the experts who know everything about it were already scientific arises with us. So you have conflict of interest. So they can't be on the board because they are part of our board.
So they have only two people and those two people already knew us and they were like, yeah, we already know that they're doing great, we can't help you. So technically they couldn't find people who were not invested in us who could say, yes, give them the money. So that became a long discussion and finally they did something and said, okay, even if they're conflict of interest, they are experts. So we just take for granted that they're doing it in the right sense and all the way around and finally they said, yes, now then it is a little second part.
Now I got a grant, which means I get the money to work on it. So that leads to me doing a clinical trial. Now, till 2016, India has had a very, very strict clinical trial section. If you make a note, if you make a medicine, clinical phase one, you give to at least 200 different people who have the disease, you give the same incentive to 100 people who don't have the disease.
Those who have the disease should feel better, at least not all maximum amount of it should feel better. Those don't have the disease. Nothing should happen to them. Right.
That's the plan. That's how any medicine you make in the world that's what it has to clinical trial phase one, phase two, phase three, phase one, phase five, phase one, two, two, three, that's how it will go through all these systems. And finally, we're going to take all the data from our patients, what the brain is doing in the past, the brain and the brain is losing this possibility. So you have the ability to make your immune patients.
What is it going through, and what kinds of, like, so I've got a29 per cent to get a 10 per cent, because essentially, this is the first in the world, it's not going to end. It's not going through it. Because the first in the world, it's going through the process. And I think that a couple of patients are going through it.
And the first thing is that one of our patients is that a couple of patients are looking to have that type of medicine. Of course, in the first case, we're going to have a couple of patients problem. Like we have, we have a– So they're like, we can't say because all of this is not like, you know, right? And now it's all, you know, on the computer, you can do this one line.
So when you say online and Facebook, you have to select the number of 200 parts from the and actually I can't. So there was physically no way to start the clinical trials first because it doesn't exist. So for probably two years, me, Arun and I see, oh, we kept traveling to Delhi, talking to people, talking to experts and trying to convince them that clinical trials, like what you said, we can't do it because it's impossible. Finally, in 2016, 2017, Dr.
Samya Swaminathan, who at that time was said, I was like, Oh, she's like, double it. So she came down, she met us. And she was like, guys, I know what you want. I know what you mean, but we need to make a change at the basic level.
So then they sat in and then in 2017, they finally got everybody together and said, okay, in the case of genetic therapy, we will say that you can do something called a investigative lead trial, which means you can use it on one person, only one person, only and then give us two years of data. And that led us to saying, oh, finally we can do it. And that opened up the clinical trial thing to anybody who does genetic therapy in India in the future. So until then nobody had ever tried it.
And we saw huge, it's a huge breakthrough. And, you know, had to have to even the bureaucrat spot this thing. That's not easy. It's not all easy to get this from.
Actually, not a problem. So you basically made a change at the molecular level. Yes. Yeah.
But DNA of clinical trial. I'm amazing. But what I want to ask you was, you said, then, I mean, part of what you are responsible for is to make sure that, you know, the child doesn't get worse. Yeah.
How do you like, what's the, how do you figure that out for administering the? Okay. So you're like, so right now all my data is based on one kid who we started taking trial to coordinate it. Yeah.
So it's all because so far we have, we have permission for more, but we haven't started to get into the cancer. So I'm going to run it. Nothing is this. First of all, again, clinical trials, pre clinical trials is what is called, is done on two things.
One is on the cell, right? We do toxicity tests. They take all his muscles. They have a million cells and he added a little bit of drugs.
None of the cells should die. Okay. So that's what it talks about. Then you have an increased dosage toxicity test.
Okay. If you give five milligrams per kg of the kid, what is it? Then you give 10 milligrams, then 100. So we keep upping up the dosage till something bad happens.
Okay. And then we know that, okay, the toxicity till this level, and it was a huge amount. Like for a 60 kg, you have to give about 4 kg of medicine or something. So that was okay.
That's fine. But you have to prove that at that point. So what is therapeutic and what is fatal? So you have to escalate dose, isolated dose and like that, you have to do.
And other than cell work, we also have to do animal studies. We have we had to genetically make MDX mice, which have DMB. And very interesting, Zebrafish, which India does not right now, right now, recognize whatever deals in the world are going to this. Zebrafish, which are basically from the Himalayan Springs, are the only fish in the world, which has DMB.
Wow. Yeah. And the interesting thing is, unlike other animals, which, for example, golden retrievers also get DMD. Okay.
But the poor things is that they can't walk and they go through the usual thing and the life also gets shot down and we don't want to. I mean, fluff, who wants to hurt fluff? The Zebrafish, if they have DMB, there's a small drink in that tail. That's it.
It does not affect the swimming. It does not. It's misshapen tail, but it's DMD. It's literally the same distrofen protein and Zebrafish is life is about two or three months.
So we can do experiments on that. So that's how we prove that this works and you know, we have different animal studies and all this. And finally, with the permission of the ICMR and the BCGI and the kid became 18 years old. So he became a major, his mom dad, his grandpa, grand mother, everybody signed.
And finally, we got the kid and we do follow three things. One is a heart, the lungs and his distrofen levels in the blood. So so far, what we thought or what we expected was his cardiac efficiency and his partner efficacy was dropping slowly at the age of 10 or 12. We thought it would stop.
This is all we wanted. If something's going bad, all we wanted is to stop. What we did not realize and very happy to show to ICMR and how to tell everybody is over the last 12 months or 18 months, we've seen it increased by 0.5%. So that is an increase, which we did not want to think.
But it is the actual positive thing. And psychologically also, that is the difference. The kid himself is feeling more vibrant. He's saying I can hold a pen for longer.
I can I can roll around in my sleep. But as a scientist, I can't take that because it's also that he didn't try it before. Maybe now he feels he can do any more. But but psychologically, it makes him feel like that he's doing better as well.
So we are seeing empirical evidence of him getting better for his particular condition. So that getting better is 0.5%. Okay, it's not a big thing. He's not going to walk.
He's not his heart is not going to be 100%. We wanted to stop it from going to zero. We managed to get from 50 to 50.5, which is a huge thing for us. So that's where we are.
Amazing. I still have nothing to say. I have nothing to say. I'm looking at audacity recording and there's nothing like it's like one time.
And we they must be like, oh, produce, we finally think like fuck, we finally managed to get a guest as manager, shut this lot more. But simplified host being simplified host, we can talk for an hour on how speechless we are. But he's so how is this administered on the on the kid? Like what's the question?
I mean, there are different versions, but ours, we figure out the best way is called a slow IV. So what we get is a small white powder and it gets dissolved in saline and then it's run into your IV for 30 to 40 minutes, once in two weeks. That's what's going on for that kid. Right.
I mean, for a year, that's what happened. So very slow IV. So things is there are six billion, seven billion cells in your body. Right.
Oh, yeah. So every cell in your body has the same DNA. We need to change it. Right.
Now, thing is this, once a particular cell has been influenced by our molecule and it's changed, then every consequence time it reproduces, like it becomes too dine, it is carried on. So you don't have to change that. Right. So the thing is this, we just have to get to a cell.
We just have to get to some cell once we change it. Then the problem every time after that it is going to continue, normally, but to get to some billion cells is a long time. That's why we have to keep doing this over a point. But it also means that over a course of, let's say, two or two and a half years, we might be able to meet 90% of the cells in the body, which means that it becomes more resilient.
That is why our future thing is to start this as early as possible. This kid is 18 years old. Right. It's hard to learn.
So I've already suffered a lot. Hopefully when the ICMR sees the result that we have from our next clinical trial, which has a little younger kids, like about 11 or 12, they finally say, okay, you can go for little kids. Then the kid was like three or four who just has difficulty getting up, but can run and can walk and have if we put him on a two or a three year therapy, then when he's about six or seven, he's 90% normal. Wow.
The best case scenario, which I genuinely wish we could do, but because of the billions of ethical issues are there is to have this therapy at a fetal stage. Wow. Okay. So let's say there's a married couple, right?
And the mother says that suddenly from a rural side of mother comes and says, my mother's younger brother died when he was 11 years old and he couldn't walk. And we're like, wait a minute. Your mother's younger brother, that means DMD. That means your mother could be a carrier.
That means you could have that. Let's get you tested. And then we find out that she is a carrier of that gene. If she's never suffered because she's a carrier, but then there's a 50% chance of a kid.
If it's a boy having the same disease. Oh, let's say that also comes to and you have a kid who we have a genetic test and we know that that kid has DMD and we know exactly which eggs on at the fetal stage. If we could make a change to it and the kid when he's born, he's born without DMD. Of course, this is highly unethical and illegal as of now in India.
We can't even think about that. That's what I'm doing. But that is where the problem is coming. If you can do this, what other things you can do.
Yeah. Then people start asking questions like, huh? Can we make it stronger? So that's the thing when theoretically this is possible.
This is the kind of stuff which I am also, but I have my difference of opening with my friends and family and everybody else is that when I was in school, I was a big fan of the X-Files and Star Trek and Star Wars. And when I read about DNA, it was science fiction to me. Right. And now just a few years later, very few years later, for those who are wondering about me age, I can say that I'm part of this process.
Right. But having grown up with those hypothetical situations, I won't think of it as very different from the good that we can do. The problems are that, the internal problems are there. But then what is the line?
Where do we go? That is where the thing is. So yeah, we are one of the very few people who have this kind of a term right now, but we are not, that's a bit busy to come to when we come to be part of the cycle. You said it's illegal in India, at least.
That's somewhere around the world that it is legal. I'm feeling the excess is not one of them. That's very nice. Well, the thing is, people don't, because people don't realize that it can be done to have made it illegal, which is what the problem was in China.
Right. So they have a couple of Christopher Gashnai babies who are immune to AIDS, but whose lives have been shortened because of this problem. It was not illegal because they didn't realize that it was illegal. Yeah.
And now it's illegal there. Yeah. Because we know that it happens only in voice, right? It's illegal to even reveal the gender of the baby before being born.
So because of that particular rule itself. Wow. Yeah. So it's a very, it's like a unseen, like I would say, like an unseen effect of what was supposed to be a good policy.
Yeah. So an archaic female infinitesite rule stops us from doing all the risks. It's fine. Right now, yeah, I mean, even if I had the British, I can't do it, but you can't do it.
But you can't do it. Yeah. Clean the clearance. Like, but you don't know the parents are potentially carriers before.