Matthew Oki O'Connor on Cyclodextrins & RAADfest 2025 Activist Panel

Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Greetings and welcome to the United States Transhumanist Party Virtual
Enlightenment Salon. My name is Jannati Stolieroth the second and
I am the Chairman of the US Transhumanist Party. Here
we hold conversations with some of the world's leading thinkers
in longevity, science, technology, philosophy, and politics. Like the philosophers

(00:22):
of the Age of Enlightenment, we aim to connect every
field of human endeavor and arrive at new insights to
achieve longer lives, greater rationality, and the progress of our civilization. Greetings,
ladies and gentlemen, and welcome to our US Transhumanist Party
Virtual Enlightenment Salon. Today we have a special conversation in

(00:44):
store for you about some emerging scientific research that could
help to remove ourterial plaque by clearing the nondegradable cholesterol
that accumulates within cells in the arterial walls. Certainly, the
cardiovascular disease is still the leading cause of death, and

(01:04):
if we want to overcome aging and death, this is
a problem that needs to be fought with a lot
of the available resources. So joining us today we have
our Director of Community and Citizen Science and twenty twenty
four US vice presidential candidate Daniel Tweed. We also have

(01:28):
doctor Bill Andrews, who is our technology advisor and founder
and CEO of Sierra Sciences. And we have our Legislative Director,
Jason Geringer joining us as well. And our special guest
today is doctor Matthew O'Connor, who also goes by OK.

(01:48):
He is the CEO of Scientific Affairs at Cyclarity Therapeutics.
He was awarded his master's degree in neuroscience from Northwestern
Medical in nineteen ninety nine and his PhD and biochemistry
from Baylor College of Medicine in two thousand and five.
His post doctoral research includes work at UC Berkeley on

(02:08):
muscle stem cells and aging. He is also the former
vice president of Research at the Sens Research Foundation, where
he oversaw a broad swath of research projects spanning many
aspects of rejuvenation biotechnology, from which he authored many papers
and patents. So Cyclarity Therapeutics and its work will be

(02:30):
the focus of Matthew's presentation today, and then we'll have
time for a discussion, some questions, a deeper dive into
that work. So Matthew, welcome, thank you very much, and
please feel free to begin your presentation.

Speaker 2 (02:48):
Okay, Thanks so much, Trinnedy, and thanks everyone for coming
to speak with me today. So thanks for the kind introduction.
As Jennity said, I co founder of Cyclarity Therapeutics and
our technology spun out of the Sense Foundation, which is
now emerged as the Longevity Research Institute, But a few

(03:12):
years ago we moved up to the Buck Institute for
Research on Aging up in Nevado, California, which is where
we are headquartered now. And one main point that I
want to make big picture about our approach and about
our technology is that we're remediating something that we believe

(03:37):
is a fundamental, basic part of the aging process, which
is part of oxidative stress and oxidative stress to one
of the fundamental building blocks of life, which is cholesterol.
And so when we say that we're developing a cardiovasco
disease drug, really we've developed a drug that tar gets

(04:00):
a fundamental aging molecule, and we're targeting cardiovascular disease as
a disease indication first, but I believe that our drug
will have applications in many aspects of aging and aging
biology and medicine. So to take a quick step back,
the type of technology, the technology platform that we're using

(04:23):
to develop next generation therapeutics at cyclarity is these scavenging molecules,
and so we developed these scavenging molecules to encapsulate small
toxic biomolecules that accumulate with age and various cells and

(04:43):
tissues and then float away with them, and we settled
on these type of molecule called cyclodextrins. Cyclodextrins are cyclic carbohydrates.
They've been used in many aspects of industry chemistry over

(05:04):
the years, but most in the last couple of decades.
In medicine, they've been used mostly as delivery tools to
deliver drugs as a part of drug formulations. But in
twenty fifteen, the first cycled extro based drug was approved
and it was acquired by merk It's now called Britian

(05:25):
otherwise known as Sugarmaducks, and what it is is it's
an antidote or reversal agent for a anesthesia agent, a paralytic,
and so it grabs on to after when you're going
to get surgery, you get dosed with the paralytics so
that you don't move around during surgery, and then the
anesthesiologist gives you Britian after they're done with the surgery,

(05:49):
and the Britian sweeps through, grabs up all of the paralytic,
pulls it out of your bloodstream and upee the Britian
and the paralytic out and you wake up right away
and you have no side effects from the paralytic and
you're better off. Britain is a blockbuster drug. It's sold

(06:11):
one point eight billion dollars last year, which is more
than all of anesthesia combined. And this is the same
type of approach that we want to take with our drugs,
is to make things that are specific for a certain
target that you don't need any more of. Right, you
don't need any of that paralytic in your body after
the surgery is done, so you just get rid of

(06:33):
all of it, and the optimal amount of it to
be in your body after the surgery is zero. So
we developed this the cycled extra in technology, which is
a dimerization technology where we stick to cycled extrints together.
And that's pretty much the core of our intellectual property,
which is the ability to encapsulate whatever it is that

(06:53):
we build to target with one of our cyclic extrien dimers.
And we've been granted serve patents in this area. So
most of what I'll talk about today is targeting the
oxidized form of cholesterol called seven keto cholesterol. I'll talk
more about that in a minute. We're also working on

(07:15):
targeting junk that accumulates in your eye with age and
causes the major form of macular degeneration. We're also looking
at nanoplastics, which is a good use case for our technology,
as well as you know, some other things like an
asusure reversal, which obviously there's there's many other anesthetics that

(07:35):
we could build reversal agents for. So we started out
pretty early on doing some pretty intense computational chemistry with
cyclodextrins and as opposed to other groups, which there's many
many groups doing computational chemistry simulations these days, not enough.
I think it's a growing field and something that everyone

(07:59):
needs to invest more in. But instead of going really
general with computational chemistry or specializing in what most people
specialize in, which is protein either protein protein interactions or
ligand receptor ligand binding interactions, we focused on an only

(08:19):
modeling cyclodextrins and their bonding with whatever target that we
wanted to go after and we do increasing levels of
sophistication of simulations until we get to the level where
we can actually predict an affinity constant for a given
target before we even synthesize it. And now what we're

(08:41):
doing is layering on AI and machine learning so that
we can actually take the human out of the process
of designing the drug and let the AI iterate until
it comes up with the ideal binding partner for whatever
kind of molecular junk that we're trying to get rid of.
So we did a lot of that to come up

(09:02):
with our lead drug candidate, and then we synthesized a
number of prototypes and iterated back and forth between the
chemistry and the bench until we came up with our
first drug that I'll tell you a little bit more
about in a minute. But first of let me take
a step back and talk about the free radical oxidation

(09:25):
process that causes the kind of oxidized cholesterol that we're
worried about. So you've probably all heard free radicals. Free
radicals have been around aging, medicine and biology for decades,
and when you have an oxygen free radical, they can
react with a lot of different molecules in negative ways.

(09:45):
They can react with your DNA, with your mitochondria. When
they react with regular cholesterol, which is pictured here in
yellow in the middle, then you add a oxygen molecule on. Typically,
so this is a non asomatic process. It's a random process,
but it's not so random because more often than not,
the chemistry prefers that it adds it in the seventh position,

(10:08):
which means that you get seven ketocholesterol or seven KC,
and I'll sort of use oxidizedcholesterol or a seven k
C interchangeably in the rest of my presentation. And so
oxidized cholesterol has been implicated in many aspects of aging,

(10:28):
including aging in the eye and liver, aging and brain aging.
Most of what I'm going to talk about today revolves
around how it causes atheroscrosis in your blood vessels and
how it does that. So this a lot of the

(10:50):
concept behind cholesterol oxidation, how it happens and where it
happens and when it happens, was worked out. A lot
of it was working out in the nineties in vitro
and in mice, but it's only in the last decade
that we've started to see some really convincing evidence that
oxidized cholesterol as well associated with cardiovascular disease, which with

(11:15):
negative outcomes and with severity of disease. So there's a
growing awareness of oxidized cholesterol's involvement in heart disease and atheroscrosis.
So how does it do that? So when you get
a alesion in your blood vessel wall, like a fatty

(11:37):
streak that you start developing in your teenage years, a macrophage,
part of your immune system, is supposed to come along
and eat up that lesion. But when it runs into
oxidized cholesterol, it can't digest it, and it can't it
can't recycle it, it can't transport it back out into the bloodstream. Now,

(11:59):
macrophage is a really good at recycling cholesterol. When they
get regular cholesterol in the form of LDL, they take
it apart and then repackage it into HDL and if
they don't need it, and then return it back into
circulation where it can go back to your liver for
recycling back into the rest of the body where you

(12:20):
might need more cholesterol. But with the oxidized forms of cholesterol,
it can't do that. It can't do the reverse cholesterol transport,
and so it just eats more and more of it.
And this is the oxidized cholesterol as highly toxic and
it causes the macrophage to start sequestering lipid and balloon

(12:41):
up into something called the foam cell. And foam cells
are these big blobby cells. They're kind of LIKEX and
essence cells. But it's not caused by by the over
division like with fibroblasts or something like you might have
heard of, but it's caused by toxicity from things like oxidizedcholesterol.

(13:04):
And foam cells build plaque. They are the driver of
the mass of the plaque accumulation that you get, and
it's an early and continuous stage in the plaque building process.
What we wanted to do was ask ourselves, could we
design a drug to specifically bind the common oxidized form

(13:26):
of cholesterol, could we remove it from cells and tissues,
and could removing that reverse the foam cell phenotype and
potentially rescue atheroscrosis. So we built this drug, which we're
calling udp zeror zero three, which we trained first computationally
and then synthetically to prefer binding oxidized cholesterol and to

(13:52):
ignore regular cholesterol, which you need to survive. And so
we built this first drug and it has a very
high affinity for the oxidized form of cholesterol and it
leaves regular cholesterol alone. And we've done a great deal
of work to characterize this drug and get it ready

(14:19):
to be a drug. So first up here at the top,
you have macrophages, just normal healthy macrophages grown, and then
you give them a little bit of oxidized cholesterol and
they bloon up into nasty looking foam cells. And then
when we give our drug, they turn back into healthy

(14:40):
macrophages without those blobby lipids in their in their cytosols.
And your quantification of that here.

Speaker 1 (14:51):
So if you go back for a moment, I just
want to see the quantities here. So it's ten micromolar
sevn ketocholesterol.

Speaker 2 (15:01):
Yes, yeah, in this particular case. We've done it many
different permutations of this, many different ways, and you can
see how how that's working here. And so that's just
how the macrophages look. How they look better, They look younger, right,
they were nasty and old looking. But do they go
back to doing their job? And the answer is yes.

(15:22):
If you poison them with the oxidized cholesterol, their ability
to eat, their ability to do phagocytosis drops, and then
we give them our drug. The phagocytic capabilities come back
multiple different ways with both human and mouse cells that

(15:43):
we did this with. Perhaps more importantly I mentioned earlier
reverse cholesterol transport, and that's a big part of the
job of the macrophages in your blood vessels is to recycle,
is to get rid of the excess cholesterol. But when
you give them oxidized cholesterol, like over here on the left,
the reverse cholesterol transport activity goes down to almost zero.

(16:08):
And then when you give our drug, just very briefly
for a short amount of time, it goes back up
quite significantly, which we think means that our drug is
restoring the ability the macrovisions to do their job not
just in eating, but also in metabolizing cholesterol transporting cholesterol.

(16:34):
And that's a pretty key aspect of atheroscrosis. So then
we went through and did a good amount of characterization
of the phenomenon and looked at gene expression. And I'll
just show a few examples from our recent publication on this.
One is the CD forty seven, which is being targeted
by a competitor of ours with a therapeutic antibody, which

(17:01):
is kind of like in a tumor where the tumor
evades the immune system. The foam cells do the same thing,
so they turn up this don't eat me signal called
CD forty seven. And what we've shown is that our
treatment with our drug brings that back down a bit,

(17:23):
so that the cells should be able to be cleared,
the foam cells should be able to be cleared by
other macrophages. Another, various aspects of lipid transport get done
regulated and then go back to normal when we treat
with our drug, and and and then various other aspects

(17:43):
of inflammation of scavenging genes that are either upregulated or
downregulated in response to the insult, which is the oxidized cholesterol,
and then get reverted variously by treatment with our drug.

(18:04):
Out of the weeds a little bit. What happens to
animals when you give them our drug, Well, it's it's
it's still early days with really fully investigating this, but
this is the most exciting data that I think. I
think generally that rodent models of cardiovascar disease of atheroscorosis

(18:27):
are are pretty artificial and unrealistic, and so I don't
really like them and I don't like working in them.
But in in normal healthy rats, if you give them
our drug, our drug is designed to be cleared very

(18:48):
quickly and to be cleared through the urine. And that's
exactly what we see. I'm not showing the data here,
but actually when we dose with our drug, we see
the target of our drug, wich is the oxidized olesterol
coming out in the urine. And we see it coming
out in the same time scale as we see our
drug being excreted in the urine. And so this suggests

(19:09):
that our drug is doing its job, and it's doing
it very fast. And so the the animals are are
peeing out their their oxidized cholesterol within a couple of
hours of administration of the drug.

Speaker 3 (19:26):
Uh.

Speaker 2 (19:26):
And so this, this story that I just told you,
was just recently published in the journal athos Crosis. And
I should add in here that we just a professor
in the field, without talking to us about it, wrote
a nice commentary about our paper, and that was just
published this past week. So we wanted to turn this

(19:51):
into a clinical stage drunk, so we worked on the
chemistry and the manufacturing. We scaled the process to kilogram
scale manufacturing, We made large scale batches, we put it
into single use sterile files. We had many meetings with
regulators in many countries in the UK, in the US

(20:12):
and in Australia. And then earlier this year we launched
our Phase one clinical trial in Australia. And I'll tell
you more about that in a minute, but first here's
the leadership of our team, me and Mike Cope, co
founders the company, Noah Rosenberg, the chief medical officer, and

(20:36):
the clinical advisory board that he recruited to to help
us turn our drug into into something that could go
into people. So PK. Shaw was the main guy who
dissected in the nineteen nineties the cholesterol oxidation process. And

(20:56):
Steve Nichols is argue, the world's expert on how blaque
is built. He's got about I think eight hundred publications
on the subject and he is leading our clinical trial
now in Australia. So we're doing what's called the traditional

(21:17):
sad MAD trial, which is single ascending dose, multiple ascending
dose trial. So we've just completed the single ascending dose
portion of our trial and so healthy volunteers have received
the highest dose of our drug that we intend ever
to give to humans, and it's preliminarily seems to be safe.

(21:43):
And now we've started in the first stage of the
multiple ascending dose. And one innovation that we're doing is
our phase one trial is being run in Australia, which
isn't particularly innovative. Probably a third of all phrase phase
one trials are being run in Australia these days because

(22:03):
it's a great place to run early stage clinical trials.
But our trial is actually instead of being run by
a private company, it's being run by an academic research organization,
the Victorian Heart Institute, which is headed up by Steve Nichols,
and he has the country's foremost heart hospital and he's

(22:28):
it's just we're super lucky. This is the type of
guy that the big drug companies call to get their
drugs over the final stages, like the help You Little
Aid drugs in phase three. He's worked on those bempaedoic
acid he get those approved. So to have somebody like
him taking an interest in our drug at at such

(22:52):
an early stage is really we're really lucky to have him.
So a little bit more detail about the design of
our trial. We started out at an extraordinarily low dose
of our drug, only one twenty fifth of what we
were eventually intending to dose and scale it up until
we got to where we are now. And we've just

(23:14):
gotten past which is the highest dose, which is twenty
five miligram per kilogram of the recipient. And like I said,
we've started the multiple dose. So of course, the main
outcome that we're looking for is safety, you know, vital signs, reactions,
hearing tests, looking at the pharmacokinetics, how fast the drug

(23:39):
is cleared from from circulation. And then what I'm most
excited about and what the data then I'm really looking
forward to seeing in the coming weeks is the pharmaco
dynamics of the target engagement to see if our drug
is actually grabbing the oxidized cholesterol and pulling it out
of the human patients, out of their blood and into

(24:01):
their urine. So we already have permission. Another nice thing
about doing trials in Australia is that they're quite flexible
with trial design and they've already given us permission once
if our drug has proven to be safe and healthy
young volunteers, we can go straight into a what's called

(24:22):
like a Phase one B type trial in a small
number of human patients who have coronary artery disease. They
have plaque in their cornary artery, and we can dose
them with our drug. We can look for that target engagement,
see if they're peeing out the seven KC. And then
we can look and at blood inflammation markers, which we'd

(24:44):
expect to go down based on some of the data
that I showed you before, and we can do non
invasive imaging of their plaque using CTA aigrams, look at
their plaque before and after treatment and see if if

(25:05):
it improves, see if it gets reduced, see if it
looks less than flamed, that kind of thing. Next is
our phase two plan, which is a scaled up version
of exactly what I just described for late stage phase one,
which will be in about one hundred and fifty patients
who already have a qute cornary arter disease, and we'll

(25:31):
look again at the oxide cholesterol in their blood and
the urine will look at their blood work, see if
it improves, and do the imaging, and then of course
we'll monitor them for heart attacks and strokes, and hopefully
that gets better over the short duration of the phase
two trial. So I want to take a little bit
of a step back before I wrap up and talk.

(25:54):
Just remind you what I said before, which is that
oxided cholesterol plays a role in brain aging because where
do you have the most cholesterol, the highest density of
cluster in your body, It's in your brain. So we're
looking at using our trug for various aspects of aging
in dementia. So we're looking at al Shimer's disease, we're
looking at stroke recovery, and like I said before, we're

(26:16):
interested in macula de generation, and we've recently become interested
in looking at at liver failure. So we're we've raised
a good amount of money so far to run our
phase one. We're closing on a round of that now
and then we're going to start raising money for our
phase two as so if anybody listening is interested in

(26:40):
investing in Cyclarity Therapeutics, please please reach me. And we're
expecting to make a ideal with a large pharma company
post phase two where we would license out our drug
UDPS year zero three and basically hand it off to

(27:05):
a large pharmaceutical partner to shepherd it through phase three
clinical trials and approval. And marketing and all of that,
and at that point we expect to have a big
return for our investors in three or four years. So
this is the team of amazing people that make this
happen at at psych Clarity here in California. But we've

(27:30):
actually got a team of over one hundred collaborators and
consultants and CROs all around the world and many too
many to thank here. So I'll stop show my disclaimers
and I can stop here and take any questions that

(27:53):
you all have.

Speaker 1 (27:54):
Yes, thank you very much Matthew for that very informative presentation,
and we do have some questions from our panel thus far,
So Daniel Tweet wonders, is injection of your drug UDP
zero zero three the only administration route so far? Or
are there other possibilities as well?

Speaker 2 (28:14):
There's various aspects of injection that we're looking at. So
all the data that we have so far and all
the work that we've done so far is intervenous. But
we've tested it in animals subcutaneously and it works very well,
and so we're envisioning that it will eventually be released
as either as subcutaneous or intramuscular injection. It could be

(28:40):
like a patch or a pump. It won't. It's unlikely
to be a pill.

Speaker 1 (28:49):
Yes, thank you for that answer. And Bill has two questions.
The first question is why CCTA instead of c I
M T. And Bill, I'll let you elaborate on that
question for the laypersons in the audience just a moment. Bill,
you need to unmute.

Speaker 4 (29:12):
Why a CTN G Graham instead of a CIMT since
you're looking at the plaque before it's ruptured.

Speaker 2 (29:23):
So the CIMT is generally done by ultrasound and CTA
is done by X ray. Just for the audience, I
know you know this, Bill, And you get a better
resolution with CTA and you can look more more deeply
into more hidden blood vessel walls as opposed to being

(29:47):
somewhat restricted to more surface level blood vessels with ultrasound,
so that the most quantitative And this isn't this is
and all coming from me. It's mostly from a cardiologist who
who insists that that CTA is the gold standard right

(30:08):
now in terms of doing really quantitative measurements, uh, you know,
down to the single percent different measurements in plaque thickness
and also being able to see the fat Attenuation Index
UH and which is how dense the plaque is, which

(30:30):
which tells you a lot about the characteristics. So even
if the plaque volume isn't changing, you can tell if
the plaque is getting ready to rupture or if it's
if it's getting less likely to rupture. And you can
also tell things about the inflammation using ai UH layered
on top of the CTA imaging these days, so there's
a lot a lot of data you can get out

(30:51):
of the ct A. The bad thing is that that
that you're exposed to X rays and it's not as
fast and cheap. I wish we were doing both, and
I'd like to move into doing both at some point
in the not too distant future.

Speaker 4 (31:03):
Okay, I was misinformed. I guess about c I t
I know you can only do it on the karateid arteries,
but I was thinking that people.

Speaker 2 (31:11):
Are less interested. I get into arguments with with the
you know, vascular surgeons and such about this. They I
think the karated is a great place just as a
marker to look to see if a drug like ours
is working. But they say, oh, why do you want
to look at the crodit It's so easy to do
to do surgery and fix the crowded artery. Uh, so

(31:34):
you know there's no there's no market for for treating
crowded stenosis, just to you know, go after a major
artery like like the cornary artery. And I agree with
you that it's a really nice, easy place to look
for plaque and see it really easily and non invasively.

(31:54):
But I get kind of shouted down by the cardiologists
when I try to make that argument.

Speaker 4 (32:00):
Okay, I was actually super impressed, So I take your
word for PCSK nine inhibitors with statins have been shown
to turn salt plaque into hard plaque. It's hard plaque
can to be still filled with oxidized cholesterol. I'm not
sure about that. And will your psyclogextrons get rid of
oxidated cholesterol in hard plack if it is.

Speaker 2 (32:21):
Sort yeah, I don't have I have a I have
an answer for you. I don't have a perfectly scientifically
satisfying answer to you. I was really worried about that
when we first developed our drug, about whether or not
it was going to be able to penetrate plaque at all.
And so we got samples of hardened plaque tissue from

(32:41):
patients that it was taken out of surgically, and we
soaked our drug in hardened plaque tissue and it pulled
tons of oxidz cholesterol out of the hardened plau tissue.
I don't know the mechanism by which it penetrates so well. Uh,
there's there's not a good explanation for why our drug

(33:02):
penetrates hardened plaque tissue well. But in our hands, you know,
very preliminarily, it looks like it does, and so I
am optimistic that it will in patients. But it's something
we need to look into more. And I wish there
were better animal models to look at that kind of question.

Speaker 4 (33:22):
Again, I was super so the other question I had
was just combined with the first one. I was super impressed.
I was asking these questions because I've been led to
believe from some clinical studies that I'm trying to get
going that these were the top things to be doing.
But I'm actually thinking what you're doing here might be
better than PCSK nine inhibitors with statins for reducing plaque.

Speaker 3 (33:45):
Yeah.

Speaker 2 (33:46):
I mean the problem is that those are what's available today, right,
So what's on the market now are LDL lowering drugs.
Statins and PCSK nine inhibitors and the cananighbors might be
working slightly better than status, but they're both doing basically
the same thing, lowering your LDL cholesterol, which has you know,

(34:07):
this bad reputation as being the bad cholesterol, but you
actually need ald L cholesterol. It's how you distribute cholesterol
through your body. Most of the cells in your body
wouldn't have any cholesterol if it wasn't for LDL cholesterol,
so you can't just get rid of it. That's why
I like the oxidized cholesterol as a target, because the
optimal amount of it and your body is zero. If
I could like get rid of It's like lead, right,

(34:29):
what's the optimal amount of lead in your body? It's zero.
So if you could just get rid of all your
lead and all of your oxide cholesterol, you'd just be
better off. And so that's why I like it as
a drug target. And I think it's it's a progression,
it's the next generation. We're going to start seeing the
LP little A drugs coming out I think in the
next year or two, but those are only going to work,

(34:51):
and it's basically a different kind of LDL cholesterol, and
I think to really move the needle towards reversing disease
rather than just slowing it down, which is basically what
the lipid lowering drugs do, We're going to need something
more aggressive that can reverse disease.

Speaker 4 (35:08):
So did you just say you're targeting you have something
that's going to be targeting LP little A.

Speaker 2 (35:13):
No, no, No, I was just saying the next big
heart disease drugs that are going to be released. I'm
predicting because there's several big drug companies that have them
in late stage phase three clinical trials and they seem
to be working reasonably well. Are going to be LP
little A lowering drugs, and we will be the next

(35:35):
generation of drugs after those, I believe.

Speaker 1 (35:39):
Yes, very interesting. So that gives rise to a hypothetical
question for me. So, if cholesterol exists in the bloodstream
but it doesn't get oxidized, if you take care of
all of the oxidized cholesterol, does the non oxidized cholesterol
pose any risk of atherosclerosis or can the macrophages that

(36:03):
you mentioned digest any other cholesterol to render it harmless.

Speaker 2 (36:10):
Yeah, I mean that's a big part of the job
of the macrophage is is to collect the cholesterol and
recycle it send it back to your liver. So that's
what that's what should happen. The issue is that you
always have oxygen free radicals around, so it's just it's

(36:30):
like rusting. It literally is rusting, right, it's the rusting
process of oxygen reacting in this case with cholesterol instead
of like metal on your car or something like that.

Speaker 3 (36:39):
Right.

Speaker 2 (36:40):
But it's a similar process, and so it's going to
keep happening. And so if you have elevated cholesterol, it's
and you have the same amount of oxidation. If you
increase either oxidation or cholesterol, you're going to end up
with more oxidized cholesterol. So people with elevated cholesterol tend

(37:02):
to have more oxidized cholesterol in their system. It's not
a one to one because you can have more oxidation
in your system for various reasons. And we don't exactly
understand why there are people walking around with like normal
levels of cholesterol but really high levels of oxidized cholesterol.

Speaker 1 (37:18):
And is it possible to have the opposite scenario where
someone has high levels of cholesterol overall but low levels
of oxidized cholesterol for whatever reason, or do we not
observe that unless that person has been treated with something
like UDP zero zero three.

Speaker 2 (37:36):
You know, there are people who do seem to be
somewhat resistant to walking around with high cholesterol. I don't
think it's well studied enough to say that they aren't
accumulating oxidized cholesterol in various places in their bodies, whether
or not they develop atheroschrosis at a young age like

(37:56):
most of them do. I think they're probably building up
oxized cholesterol someplace where we're not looking, like in the brain,
which is really hard to buyopsy. You can only look
at it pretty much after somebody dies, and other tissues
as well.

Speaker 1 (38:15):
Yes, thank you for that answer. And Bill has a question.
Do antioxidants reduce the levels of oxidized cholesterol or can
some antioxidants do that?

Speaker 2 (38:28):
You know, I it's something that some groups have looked
into a little bit. It, I mean mostly antioxidants have
been kind of a disappointment in general in medicine and
anti aging medicine.

Speaker 5 (38:41):
Right.

Speaker 2 (38:41):
They haven't proven to be very effective. Now, the counter
argument to that is that we haven't built good enough
antioxidants yet. We haven't targeted them for the right places
or something like that. So I think there's potential room
for that. But you can't reduce your oxygen free radicals

(39:02):
to zero. You can't like completely prevent all oxygen free
radicals from forming, no matter how many antioxidants you take.
So that's why I follow this kind of damage repair
philosophy philosophy approach. You know, Generally, my approach to studying

(39:25):
and trying to remediate the aging process and and therapeutically
is that I think it's the best place to intervene.
But there is potential to see I haven't seen yet
a convincing study showing that that there's good antioxidant evidence
showing reduction in oxidized cholesterol levels in a person, but

(39:46):
I don't think it's been studied enough, and I think
better studies with better antioxidants could work to some extent
with it. And perhaps we've started a small project looking
at some kind of combin therapy in that realm, in
a model system that we're looking at that maybe it
could be helpful, especially since you get when you have

(40:10):
high inflammation in someplace like a plaque, you also get
high levels of oxidation and so if you combine, if
you combine antioxidation with getting rid of oxidized cholesterol, maybe
we'll get a synergistic effect.

Speaker 1 (40:26):
Very interesting, Thank you very much. And we have a
number of questions from Daniel Tweed as well. Let's start
with the questions that focus on the name of the drug,
and Daniel is curious about the origins of the name
u DP zero zero three. Is that a chemical name
shorthand of some sort.

Speaker 2 (40:46):
It's so UDP stands for Underdog Pharmaceuticals, which was the
original name of our company, and then we changed our
company named as Cyclarity Therapeutics a few years ago. So
we just we did the kind of boring but efficient thing,
which was numbering our compounds from starting from one as

(41:12):
we invented them. And yeah, it'll get a more exciting
name at some point. I didn't want to give it
a sexy name too early, because what I see happening
is that you get your favorite name and you name it,
and then you get a partnership or you get a
new big investor and they don't like your name and

(41:33):
they make you change the name. And then you see
drugs go through like three, four or five different names
before they actually get you know, widespread on the market,
and I figured out just wait a little while before we,
you know, get get married to a name. But if
people have ideas for names for us, send them to me,
and we're starting to make a list.

Speaker 1 (41:56):
Yes, So for those viewers watching this virtual Enlightenment salon,
please put any ideas you have for a name for
UDP zero zero three that might eventually be used in
our YouTube chat and we will relay them to OK

(42:17):
And in the meantime, Daniel has another question. He notes
this scavenging therapy molecule sounds like it has benefits for
both new as well as long term users, and he
wants to know if that's correct given that this process
of oxidation happens continuously. So would you expect that this

(42:39):
is a drug that could also be administered over the
long term for someone to prevent the formation of atherosclerotic plas.

Speaker 3 (42:48):
Yeah.

Speaker 2 (42:49):
I think it can be a preventative as well as
a reversal agent. And I hope we see a day
when based on a biomarker task like sized cholesterol in
your blood or in a tissue sample, you can take
our drug and that you don't have to wait until
you're one of your blood vessels is like more than

(43:10):
fifty percent included when you start having trouble you know,
climbing stairs or breathing or getting chest pain or something
like that, or having a know hour attack before you
ever get diagnosed with having atheroscrosis. So yeah, so I
think it can be preventive as well as a reversal.
I don't think that you will need to take it continuously,

(43:32):
like every day or something like that. I think you
can take it intermittently and we hope that you will
just have to take approximately six doses in a row
over a couple of weeks. Our current protocol is over
the course of sixteen days, every third day you get
a dose and that that should get rid of the

(43:54):
vast majority of the oxidzed cholesterol in your system. And
that's taken decades for it to build up. Hopefully you
don't have to come back for another five or ten
years for another course of treatment. So maybe people are
going to start getting this when they're symptomatic in their sixties, say,
but later on, maybe we'll be taking it in you know,

(44:17):
our thirties or forties, every you know, five or ten
years to make sure you don't get sick from that stuff.

Speaker 1 (44:23):
Yes, indeed, and would you pair that with some sort
of diagnostic tests, say a blood test to measure the
oxidized cholesterol, the seven keto cholesterol, rather than just the
total cholesterol or the LDL.

Speaker 2 (44:40):
Eventually, we're not developing a there's not a commercially available
seven k C. There's two kinds of blood tests you
can do for oxidized cholesterol. One is for oxidized LDL,
which there is a test for and you can you
can go and get Our drug should not not directly

(45:01):
remove ox LDL. Our drug isn't meant to attack LDL
or HDL. It's meant to attack cells and tissues. So
what ox LDL does is it delivers seven k C
to the blood vessel walls and two macrophases, and so
then our drug can go into the macrophages and pull

(45:22):
it out after it's been delivered. So you can get
a test for ox LDL, but our drug shouldn't be
lowering ox l dl. We can test in our clinical trial.
We are testing people for blood and you're in oxidized
cholesterol seven keto cholesterol. But we're not developing a diagnostic

(45:43):
that we're intending to know to release and sell to
the public. I think that the world will be better
off if and when there is such an approved diagnostic.
We're doing a little bit of work trying to invent
a faster, cheaper method of measuring seven keto cholesterol so
that US or somebody else, a diagnostics company could could

(46:07):
take that and turn it into a diagnostic test that
patients could take. To your question about what it will
be paired with when it's first released, it will probably
be paired with with with andiogram. So you'll get a
scan of your of your say, coronary artery, and it'll
be blocked, and you'll take our drug and you'll come

(46:27):
back in six months or a year and get another
scan and hopefully it will have improved, and maybe it'll
have improved, but it won't have improved as much as
your cardiologist wants, and so they'll give you another course
of treatment.

Speaker 6 (46:39):
Uh.

Speaker 2 (46:40):
And they could do that, you know, once every year
or so until they're satisfied that you're better. But I
eventually I hope that it gets reduced to an easier
biomarker like a blood test. Yes, thank you.

Speaker 1 (46:55):
And that leads into the question from Daniel tweet. How
affordable would this therapy be in vision to.

Speaker 2 (47:03):
Be well, we expected to be covered by insurance. We're
planning to two uh to to release it you know
widely in uh in all the you know markets around

(47:25):
the world.

Speaker 7 (47:26):
Uh.

Speaker 2 (47:27):
It's not going to be you know, uh a dollar
or ten dollars a treatment. It's probably going to be
at least a few thousand dollars for a treatment. And
that we don't know the market economics get it's probably
going to be thousands of dollars for a treatment.

Speaker 6 (47:46):
Uh.

Speaker 2 (47:47):
And but you know, I think that's it's more expensive
than like a statin, but it's going to be cheaper
than a gene therapy or and competitive with the therapeutic antibiodies.

Speaker 1 (48:02):
Yes, and as you said, hopefully the few thousand dollars
per treatment will be administered every fairly large number of years,
like five or ten years, rather than say, every year.
So thank you for that answer. And Bill also wonders
with regard to the comment about the angiogram, will you

(48:23):
DP zero zero three reduce clocks also or at least
have that tendency to do that.

Speaker 4 (48:30):
Let me say I was miss I was thinking differently
when I asked that question. I was forgetting that regular
angigrams can detect large plaque bulges too, so, but but yeah,
is there any chance that this would help with ruptured
plaques When a clock gets formed.

Speaker 2 (48:47):
Our drug acts quickly in terms of removing oxide cholesterol,
but it acts slowly in terms of allowing the macrophage
then to go back to doing its job and cleaning
up the plaque. So our drug isn't designed to work
like draino and flush out your arteries in in minutes.

(49:08):
It's meant to flush out all your oxidized cholesterol and
then for it to heal over the course of weeks
and months. So you wouldn't want to rely on our
drug if you were like in an ambulance needing like
a cloudbuster, you know, because you're the you know, the
blood flow to your brain has been been blocked. That said,

(49:33):
there's clouding, there's clotting that happens inside of plaque, and
and ruptured plaque can get stuck places where it's not
very easy to remove surgically, and you know, sometimes there's
decisions about whether to leave it alone or monitor it,
or go in and remove it. And so in some

(49:56):
of those edge cases where it's where a wait and
see uh approach might work better than maybe our drug
with help. But I'm just sort of I'm kind of
rambling because I'm thinking about this on the flat, because
I haven't thought about that question before.

Speaker 4 (50:12):
About There's another question I had, and that's because I
was doing some Google searches while you were answering some
other questions. But on cyclodextrons, I saw that there's two
hydroxy propyle beta cyclodextrin that's already available for getting rid
of oxidized cholesterol. Is that is yours comparable to that?

(50:34):
And it didn't look like that's used as a dimer
like yours is.

Speaker 2 (50:38):
Yeah, so what you're Yeah, well, you're the two hydroxypropyle
beta cyclodextrin or just hydroxyprople beta cyclod extrin or h
pbc D. It's been around for decades. It's it's used
in in foods, it's used in I think it's in
for breeze. It's it's it's used to deliver drugs. It's

(51:00):
it's very safe, you can inject it at very high doses,
you can eat it. There's there's food grid hydroxy public
beta cyclodextra and so should you get injected with it
in order to get treated safe for you know, aging
or atheroschrosis something like that, or or other diseases. There
are actually two companies that are trying to use that

(51:24):
substance to treat Niemann Pick type CE disease, which is
a rare licens almost storage disorder, which is a cholesterol
transporter disorder. Now, hydroxy probably beta cyclodextrin doesn't bind cholesterol
very well at all. It's a very very weak, if
at all, binder of cholesterol. But they figure this stuff

(51:45):
is so safe and it's approved for like anything that
you want to use it for. Uh, So we're going
to take these kids and dose them with like enormous
enormous quantities of this stuff and see if it helps.
Because it did help in animal model. So if you
give an animal with this name and Pick disease, this

(52:06):
hydroxy prople beta cyclduxtrain when they're very young, it helps.
It does help a lot. I suspect it is helping
the patients. It's been a little difficult for these companies
to prove that it's helping because these patients are so
sick and have so much brain damage that it's hard
to tell if they're getting better. I think they're living

(52:27):
longer with a very poor standard of living. I think
the drug is very weak but probably effective at extraordinarily
high doses. And the kind of doses that you need
to make it effective since it's such an inactive compound,
is like having one of these kids trying to lie
still on a table getting a IB for like six
hours or something like that. So I think our drug

(52:51):
would work better for name and Pick disease. We're not
working on that, but I'd love to be working on
that someday. And I think it would be this same
kind of thing if HPbCD could help you with others races,
I think you would need to be getting an IV
bag full of it frequently in order for it to
have an effect. It's just not a drug. It's you know,

(53:14):
it's it's something that is a very weak binder of
a lot of things. So I don't know what else
it's binding when it's going in there, But you know,
it's pretty safe stuff, so it probably doesn't hurt. But
I mean it's been shown to cause hearing loss at
very high doses in rodents, so that's something that some
people are concerned about. You just need to stay clear

(53:37):
of those hearing loss toxic doses.

Speaker 1 (53:41):
Interesting. Thank you very much, and we've got a few
questions from Daniel. He wonders could this be used to
externally process a patient's blood in a kind of dialysis
modality or would that not make sense? I think Daniel,
what you're considering is perhaps taking a patient's blood and

(54:02):
applying the drug to it outside of the patient's body
and then doing some sort of like therapeutic plasma exchange
where you pump in the clean blood and replace the
existing blood with it. Or would that not really take
care of the problem, which would be that cholesterol accumulating
in the arteries.

Speaker 2 (54:23):
Yeah, it's a good question, and it's something we thought
about for a while. So one problem with the approach
is the last thing that you just said, Jenity, which
is that you could pull all of the oxide. Using
a method like that, you could pull all the oxides
cholesterol out of the blood stream, but you couldn't. You
wouldn't be delivering your drug to the system and letting

(54:46):
our drug go into your blood vessel walls and any
other tissues where it might be able to pull oxide
cholesterol out of now, that doesn't mean we haven't thought
about it and that it might not be a good
therapeutic approach. What we haven't been able to think of
a way to do is, so you know, you take
the drug, you take the blood out of the body,

(55:08):
and then you put our drug in there. Presumably you
want to pull the drug out before putting it back
into the body or else like why did you go
through this process rather than just delivering it into the body.
So we haven't been able to think of a way
to clear our drug out of the blood stream as

(55:29):
a part of that process.

Speaker 5 (55:30):
Yet.

Speaker 2 (55:31):
If there's people listening who are interested in the in
how that might work, or think they might understand something
about the how to make that work in a kind
of like a sort of a dialysis sort of approach,
we're interested in that as approach, but we haven't started
playing with it yet, but it's it's a cool idea
that we want to work on sometime.

Speaker 1 (55:52):
Yes, thank you very much for that answer. And Daniel's
other question is could targeted cyclodextrins be created did using
a suitably genetically engineered cell, such as perhaps an E.
Coli bacterium that could be harnessed for that purpose, like,
could you reconfigure one of those to produce the cyclodextrons.

Speaker 2 (56:14):
So the core building blocks are built by by microbes,
but I've never heard of a microbe building a modified cyclodextrin.
Like the example that Bill was asking me about earlier
is a hydroxy propylated cyclodextrin. So you take a hydroxypropyle
chemical group and stick it onto a onto a cyclodextrin.

(56:36):
Which is part of the power of cyclodextrins is how
you could there's potentially hundreds or you know, theoretically infinite
different types of chemical groups that you could stick onto
a cyclodextrin and then a cyclodextrian. There's three different sizes
of cyclodextrians. The cyclodextrins that we're using are the medium size,
and we're making dimers of them. Our dimers have forty

(57:00):
sites on them where you could potentially put any of
these chemical groups that you want, so they're kind of
infinitely engineerable. Now I've never heard of a microbe figuring
out how to do that chemistry on its own, but
they're very good at producing the core building blocks, and

(57:21):
that's how they're how the building blocks are made that
we buy and then use to do our synthetic chemistry
on top of that, But I've never heard of somebody
figuring out how to how to culture, how to like
grow substituted We call them substituted cyclodextrons like in a vat.

Speaker 1 (57:41):
Yes, thank you for that answer. And Daniel wonders, a
dimer is a chemical pairing of identical molecules. Yes, that's
the definition. Essentially, a molecule or molecular complex consisting of
two identical molecules or subunits that are link together.

Speaker 2 (58:01):
But you don't necessarily, so you could have the dimer,
and you could imagine that on one side of the
dimer you have one kind of chemistry and on the
other dimer you have another kind of chemistry. And we
can do that kind of chemistry. Uh, when we engineer
our dimers, and that is part of our intellectual property

(58:21):
is making the two different halves different, so that if
you have an asymmetrical target, you could engineer one side
to grab one side of your target in a certain
way and the other side so you could work on
you know, the charge, So if you're looking at a
charged target, you could put the opposite charge on one

(58:44):
side of the cycled extrin and not on the other side.
If if once, if your target is like has like
a skinny and a fat side like that, you could
make your your cycled extra more more narrow on one
side and fatter on the other. Those are all things
that we play with a lot when we're in the
early stages of engineering our cyclic extrons at the computational

(59:05):
and then synthetic level very interesting.

Speaker 1 (59:07):
So the dimers are more versatile than they may appear
at first glance, at least with your approach. Now, one
question that I'm curious about is in regard to your
future plans. In the event that the phase two trials
are successful, you stated you would make a deal with
a large pharma company to essentially manufacture and sell this drug.

(59:31):
Would you plan for a deal where Cyclarity would maintain
the intellectual property and then the pharma company would pay
you royalties over time to use it. Or would you
just sell the intellectual property in one lump sum and
let the pharma company do what it pleases thereafter.

Speaker 2 (59:50):
There's a lot of potential ways that could play out,
and you know, I may or may not be in
a position to get my perfect wish. So my perfect
wish is that we would do a partnership with a
large pharma company, either a joint venture where we share
responsibility for the further development, for the carrying out of

(01:00:12):
the phase three, so that we could have influence over
how the phase three is developed, what kind of patients
it gets used, and how it's being tested so that
they don't mess it up, that kind of thing. And
then you know, going into the marketing, likely the big
pharma company, we do all the marketing, and then we
would get royalties from that. So we would get upfronts
and royalties, likely in either the scenario where it was

(01:00:32):
a joint venture or where we just sold the drug
to a partner and they just took it over from there.
And then you know, another possibility is that our whole
company would get acquired by a large drug company. That's
not really my favorite idea because what I really want
to do is take the proceeds from that equity event
when they buy the drug from us. So they do

(01:00:53):
a deal and we get upfronts, and then we pour
that money back into the company, into our platform so
that we can develop our next ten drugs with those funds,
which might not happen if we get acquired.

Speaker 1 (01:01:06):
Yes, indeed, I think it would be a preferable outcome
if you continue to have input and involvement and an
income stream from how that drug gets developed and used,
in particular, because then you could ensure that it actually
gets rolled out to patients. Sometimes pharmaceutical companies will acquire

(01:01:30):
intellectual property and sit on it, and that's not necessarily
the best outcome for patients who could benefit from the
drug in clinical settings. Bill Wonders, would DP zero zero
three qualify for fast track clinical studies.

Speaker 2 (01:01:49):
I think that to be fast track, it would have
to be rare disease. I am envisioning it more angling
towards accelerated approval, which is what FDA uses for disease indications,
where you may be able to get a tentative approval
and then need to keep doing studies to prove that

(01:02:09):
you're having the outcome effects like effects on heart attacks
or strokes. That's really my dream for this is that
we would get approved on the basis of plaque regression,
rather than doing what is traditionally done, which is due
like a long five year study with thousands of patients
waiting for people to have heart attacks and strokes, and
then you count bodies and you see if people on

(01:02:31):
the active group die less or have fewer heart attacks
than the people on the placebo group, which I think
is we're going to look back on those kinds of
studies someday and think they're barbaric. I hope that we
can get accelerated approval on the basis of their plaque
regression and then show the reduction in heart attacks and
strokes in the following years after initial approval.

Speaker 1 (01:02:53):
Yes, indeed, that would definitely be more humane and better
for the patients. So I know we're past the hour.
Do you have time for a couple more questions just
the ones that have been post?

Speaker 2 (01:03:05):
Let's say two more questions and then I got to run.

Speaker 1 (01:03:07):
All right, So, Daniel Wonders, is the Victorian Hard Institute
funding most or all of the trials now taking place.

Speaker 2 (01:03:17):
No, Cyclarity Therapeutics is funding one hundred percent of the
trials taking place. Almost all of the money has come
from private investment into Cyclarity therapeutics.

Speaker 3 (01:03:29):
All right.

Speaker 1 (01:03:30):
And Daniel's comment, after which I will pose his last question,
is this is almost like a precursor to what cellular
nanomachines might one day accomplish and I hope we all
live to see the day when that happens. And his
final question is he sees that it's interesting that the
blockbuster drug Britian out sells the anesthesia drugs or did

(01:03:54):
he hear that incorrectly? Does it actually outsell the common
anesthesia drug.

Speaker 2 (01:04:01):
Yeah, it outsells all of anesthesia put together. Now that said,
that's a little bit misleading because Britian is still unpatent
and so Merk can charge a lot of money for it,
whereas most traditionally used anesthesia agents are generic and pretty cheap.
But it's still pretty impressive to me that this one

(01:04:21):
reversal agent, it's so incredibly valuable and profitable because anesthesiologists
love it. It's incredibly safe and effective, and even if
they accidentally were on purpose, anesthesiologists are getting lazy and
dosing their patients with an excess of Britian. And I
was a study done recently trying to bring them to

(01:04:43):
task and looking for the consequences of giving your patients
too much Britian, and they couldn't find any consequences from
giving patients, like you know, two or three times as
much Britian as they needed to clear out the paralytics.
The anesthesiologists are just strigging their shoulders and like not
doing the math to figure out exactly how much they

(01:05:05):
should give their patients and just taking a you know,
a bunch off of the shelf and giving them the
whole bial rather than calculating how much they should be
getting their patient. Because it's it's a next generation drug.
It only grabs onto something bad that you want to
get rid of and then you pee it out and
you pee out you know, whatever extra that you that
you get. So it's really a perfect drug, and you

(01:05:27):
know that's that's how we want our drug to work
as well.

Speaker 1 (01:05:31):
Yes, that sounds like a great drug essentially no adverse
side effects. So thank you Matthew for all of your
answers and for your time today. That was a fascinating
and enlightening presentation. Do you have any final words for
our audience, any comments that you wish you could have made,
or anything else that you want to say before we close.

Speaker 2 (01:05:54):
I just want to say thanks so much for having
me here to present to the transhuman to a party
and people have more ideas, you know, whether they're about
the name, or about the science, or if you're in
science and you want to collaborate with Cyclarity, if you
know you're in a research lab and do you have
a model system that you think our drug could work in,

(01:06:15):
we'd love to collaborate with you and get to the
finish line together. It takes a huge number of people
to get a drug approved, and there's so many wonderful
supporters out there, and I invite everyone to get in touch,
get in touch with me on LinkedIn, follow up Cyclarity
on social media, and we'll try to keep you all

(01:06:37):
updated on how things are going.

Speaker 1 (01:06:40):
All right, thank you very much, Okay for your time today.
This was quite an enlightening presentation. Please to all of
our viewers, share your ideas with us in the chat
or reach out to ok and to Cyclarity on social media.
And I hope that we can all live long and prosper.

Speaker 2 (01:07:05):
Thank you.

Speaker 8 (01:07:06):
Indeed, thanks Cody and Ghanadi. We want to get rid
of this guy. As you know, our purpose here at
Redfast Revolution against Agent and Death is to kill death. Right, So, uh, Joe,
how are we going.

Speaker 3 (01:07:26):
To kill death?

Speaker 5 (01:07:27):
I mean together, that's the whole thing.

Speaker 9 (01:07:30):
Together together in a coordinated, collaborative fashion where we feel
like we feel we feel our life more than we
feel that.

Speaker 8 (01:07:42):
Okay, and Cody, how are we going to kill death?
How is it I mortally is going to kill death?

Speaker 10 (01:07:47):
Well, everything Joe just said. But also we need to
free the geniuses of society who are working on the
science end of it, and we do that together.

Speaker 3 (01:07:57):
Good, So, Ghannadi tell us your view.

Speaker 11 (01:08:00):
We need to get the public to recognize that killing
death is both feasible and desirable. They need to see
a plausible path for getting from here to there, and
that's actually one way in which games like lev the
Game can help to get them to see it's not
going to be a single moment in time. It's not

(01:08:21):
going to be a single magic pill or panacee. It's
going to be a process. But it's a process that
each person, even if you're sixty five or seventy five
or eighty or ninety, has a chance in undergoing successfully.

Speaker 8 (01:08:37):
Okay, I will play Devil's advocate and I will ask Death, Death,
what did you think about that?

Speaker 12 (01:08:44):
I was quite inspired by Joe's talk, and it's been
quite lonely as the only ageless character. Maybe you should
join them.

Speaker 8 (01:08:54):
Wow, that's good. That's good. Uh, but uh, how about
if we killed you?

Speaker 12 (01:09:01):
That would not be pleasant at all? Although I am
so busy of late, I could use the rest.

Speaker 3 (01:09:09):
Ah. Good.

Speaker 8 (01:09:10):
At least we could freeze you. Okay, we can keep
you frozen forever.

Speaker 12 (01:09:16):
That would be quite peaceful.

Speaker 3 (01:09:19):
But I think you like more the hit than the cold.
What do you like more?

Speaker 12 (01:09:23):
The cold is quite fine. These bonds don't care.

Speaker 8 (01:09:27):
Okay, Before we sacrifice death, is there a question from
the public to death?

Speaker 13 (01:09:35):
No?

Speaker 3 (01:09:39):
I like that, that's a good question. What is your
last male?

Speaker 12 (01:09:42):
I prefer souls?

Speaker 8 (01:09:45):
Okay, we have a question here also ruddy No, okay,
So why don't you come in front death here and
see how we can sacrifice you?

Speaker 3 (01:10:02):
So I grab that we are all going to punch
him Halloween.

Speaker 5 (01:10:09):
Halloween.

Speaker 3 (01:10:10):
So yeah, we.

Speaker 8 (01:10:14):
Are here to kill death before death kills us. So
for immortality, Viva Revolution, Viva. Okay, now, Death you can go,
and let's go for the questions. How we want people?

(01:10:37):
This is a fantastic panel. We have incredible people working
on different projects. I'm so excited to be here. This
is our family. So questions from our family members, Okay,
all the way, Okay, first one that is closer.

Speaker 3 (01:10:54):
This is a This is more of a just an observation.

Speaker 14 (01:10:57):
I thought the points you made, Joe were just truly
deep and profound and hit me in my heart. I
think all of us struggle with various things and including
lack of influence and frustration and ego and all that.
But if we can collaborate and basically put our private

(01:11:20):
concerns aside and think bigger and think real, longer range,
we'll all be better off.

Speaker 3 (01:11:25):
So thank you for that.

Speaker 9 (01:11:27):
Yeah, we're I mean a lot of people in this room,
a lot of people. The people who put rat Fest
together are from people unlimited and and we sort of
have we have the strength and the focus to do
that because we have we have one another.

Speaker 5 (01:11:43):
Okay, so we're not working. We're not solo agents.

Speaker 9 (01:11:46):
It's it's tough to be a solo agent immortalist in
you know, in this world.

Speaker 3 (01:11:52):
Okay, we have a question here in the bank.

Speaker 5 (01:11:55):
Thank you, Jove.

Speaker 13 (01:11:57):
He's very inspiring to hear you all the time. Understanding
human being unbelievable. I treasure you. You talked recently about
he's going to need a new faith. That touched me
very deeply. Can you explain a little bit to the audience, Well,

(01:12:17):
you mean by having this new faith.

Speaker 9 (01:12:19):
Yeah, I think I think, Uh, a lot of us
have felt like, oh, something was gonna happen, there's gonna
be a particular breakthrough before now, and have gotten discouraged.
Horrible things happened. I lost Bernie. I mean, that's the
fucking worst thing that can happen.

Speaker 5 (01:12:38):
And and uh, and.

Speaker 9 (01:12:41):
So these there's a faith that's basically we're externalizing.

Speaker 3 (01:12:45):
Uh.

Speaker 5 (01:12:45):
And this is the faith we learn it.

Speaker 9 (01:12:46):
We actually learned this from religion, which is really we're
like and I mean to.

Speaker 5 (01:12:52):
We do.

Speaker 9 (01:12:53):
But but even if even if you're keep your religion,
we're we have we have to modify. Okay, we have to.
We have to develop here. And and so there's a
faith that's innate. It's innate to the human body. It's
a feeling of it's a feeling, a core gut feeling
of life. It's not really it's not really dependent on
what's happening out here. It's not really dependent on is

(01:13:14):
this breakthrough gonna happen, Is this piece of funding gonna happen?
It's it is what is It's not faith that's just
core in our bodies. That is it's not part of
our mentality. We're not really, we can't really measure it.
We're not really, we're not. It's not dependent on anything
out here, because good things happen and bad things happen.
And that's how we keep going because we just because it,

(01:13:36):
because it's it's something physical, it's something I wish Rose
was here. Michael Rose, you probably have something to say
about it, because it's something innate to the human form
that we're tapping into. That isn't it's not doctrinaire, it's
just organic.

Speaker 3 (01:13:52):
Okay.

Speaker 8 (01:13:52):
We have balloons for the people with questions. Uh it
says a stop agent in Spanish, stop and be simeon.
So you have a question or you one double or both?

Speaker 5 (01:14:07):
What can we do? What can we do to.

Speaker 15 (01:14:12):
Double this attendance of Bradfest this year, double it again
next year, double again, keep doubling it every year.

Speaker 9 (01:14:22):
Yes, thank you. We need help. We need we need help.
We work our asses off. We have some We have
about seven hudred registrations here. It's a little bit more
than last year, which is which is nice. But but
but that's really what we want to do. That really
is our vision and and and we need help, like
we need we need other organizations to to see this

(01:14:45):
vision and and and share this share this opportunity with us,
and we need people to do it. We need people
to bring people and we say this every year and
and and the truth is it doesn't happen. So so
so we just shift in mindset. And I mean part
of it is just me being more direct, like I
am here. I don't think we've been this direct, but.

Speaker 5 (01:15:03):
We need help. You know, people come up to us
and we're gonna help, We're gonna do it.

Speaker 9 (01:15:06):
And a lot of times they're marketers and they're just
selling us their services. That's not really what I'm talking about.
I'm talking about like, I'm talking about people who want
to who want to share this vision and this mission
with us. Yeah, because it's for everybody.

Speaker 3 (01:15:20):
Actually, Okay, okay, here another question in the front.

Speaker 15 (01:15:24):
Yes, So this room is full of change agents.

Speaker 3 (01:15:29):
Right.

Speaker 15 (01:15:31):
When I work to create the Health Spent Action Coalition,
which as two hundred and seventy five cross sector organizations,
I worked with a wonderful operator that helped manage Props
seventy one and Prop fourteen and got fifteen billion dollars
of California taxpayer money for an agency for regenerative medicine.

(01:15:54):
That was the work of advocates, and that was the
work of narratives of people, right, narratives of people. So
before I took this on as a stem cell advocate,
in the background in law, a person that inspired me
was a young woman, Sabrina Cohen. She became a quadriplegic

(01:16:18):
and an accident when fourteen years old from Miami Beach.
I met her at the Miami Project to Cure Paralysis
when I was giving a talk. She looked just like
Sandra Bullock in a wheelchair. She became the first associate
director of my organization, a nonprofit organization that created the
World stem Cell Summit, and before we launched the health

(01:16:40):
Span Action Coalition, which was founded on an idea between
Aubrey and I to bring this world together. Health span
should be a fundamental human right. I asked Sabrina, who
has gone on in a top realtor and created Sabrina
Cohen Foundation Adaptive Beach Days in Miami. Each Sabrina does immortality.

(01:17:03):
Does a long life, a long lifespan matter to people
in your community, meaning the sci spinal cord injury community. Yes, Bernie,
we in our community know we're aging faster, We know
we are going to die young for all the things
that we go through day by day. And I will

(01:17:26):
join you and the spinal cord injury world will do
it be a part of this. This is cross sector
and it's and you are the spark. I mean, I
am really inspired by being here. I was nervous about
coming to this because I heard about Ratfest and it
might be like a rave and you know grave, you know,

(01:17:47):
but this is really the real deal. So I just
want to say how inspired I am and proud to
be associated with.

Speaker 8 (01:17:54):
You and Barney those words coming from you are very
important to all of us, huh and all you have
been doing for so long.

Speaker 11 (01:18:06):
So okay, yes, First of all, Bernie, I'd like to
thank you for the heroic work that you and Melissa
King have done over the decades and advocating for stem
cell research, which is a crucial pathway toward life extension
and curing deadly diseases that could kill people in the meantime.

(01:18:29):
And I also wanted to echo what you said in
terms of encouraging people to find initiatives that already exist
that they could contribute to And this also goes along
the lines of what Joe articulated, because even when I
was looking out to see how I could contribute to

(01:18:49):
the field, I was thinking about what endeavors were already
in progress that needed help. And you are important, as
Joe said, one person can make a difference within that
collaborative approach. Like with led the game, I saw that
there was a previous team that had tried to develop
it but didn't have the funds, and I didn't want

(01:19:11):
that project to just languish. I didn't want it to
disappear down the memory hole, since there wasn't even the
source code for the original game remaining. So I brought
it to a playable state. But I needed another individual
Y'ari starin Vukotich to program it. I needed the community
to provide feedback. Likewise with the Transhumanist Party, when Zoltenischwan

(01:19:31):
founded it, he ran for president. He had the Immortality
Bus campaign. In twenty sixteen, he decided he wanted to
move on to other endeavors, so he stepped down from
the leadership role of the Transhumanist Party. Really, he's more
like a serial startup founder than someone who keeps an
initiative going for years, but he wanted it to go

(01:19:52):
on for years. He wanted it to outlast his tenure.
So he asked me to be the chairman, and I decided, well,
this is my opportunity to contribute to something longer lasting
and perhaps something that would last beyond my own tenure
as chairman. So think about those kinds of initiatives, those
that are already in progress that you could make a
difference and you could carry to the next level.

Speaker 8 (01:20:15):
Okay, good point, eleanor a balloon, I'm a question.

Speaker 16 (01:20:19):
I want I want to ask the question for the balloon,
So thank you so much. No, but so you were talking,
Joe about numbers matter and which is true, but there's
something about passion and having such a conviction of moving
this initiative forward, and I was wondering, if you this
is a good time maybe to tell all these activists

(01:20:41):
here what it takes to create Radfist and how even
one more person that jumps in in the way that
they can contribute can make a difference, because I don't
know if people here know what kind of team you
guys have and how long it takes to actually produce
this of So maybe you can give a little bit
of detail.

Speaker 9 (01:21:03):
Yeah, we have a really small, really good team. Uh
of I want to say, you know, Michelle Andrews uh,
Jeene Wideman, uh, Marianna Cellis and Daniella Escobar is the
team with Jim and I and you know they're working
on that, uh you know, most of the year, most

(01:21:27):
of the year and so so. But but the vision
is of a platform, and that's and that's where we
can do something that doesn't really have a limit in
size and and we basically do it on like a
zero budget. Like we basically do it on on uh

(01:21:51):
there's there's no extra money in this, so we you know,
and and Jim doesn't get paid, you know, and I
get paid a little bit.

Speaker 5 (01:21:59):
You know.

Speaker 9 (01:22:00):
That's why I'm doing uh uh messaging strategy for you know,
boring companies, but which I try to help them.

Speaker 5 (01:22:06):
But yeah, so so.

Speaker 9 (01:22:11):
And this is a little bit, this is a little
bit where we are because because we're on the cutting
edge of longevity, right, I mean that's and and this
is where this is where the space is right now
and it doesn't need to be like we could have
we could have volunteers that have superb capability that could really,
as you're saying, really expand what we're doing. We could

(01:22:32):
have a chunk of money that isn't even that big
of a chunk of money that could change how we
function so so and it's time for that. Honestly, it's
time for that. So you guys love rat Fest. We
love rat Fest, but you know we don't honestly, we
don't want to keep just doing it like this.

Speaker 5 (01:22:50):
We don't.

Speaker 9 (01:22:51):
We we we we we want it. We have to
go uh in a more. I want to say bigger,
but it's not just about bigger. It's it's just an
ex we have to expand. That's that's, that's what has
to happen.

Speaker 10 (01:23:05):
I add that one person with a passion is more
powerful than one hundred people with an interest. So whatever
we can do to increase passion in ourselves, we need
to do that. And we need to bring more people
in who have passion more so than interest.

Speaker 8 (01:23:23):
Yeah, just let me add we need to collaborate internationally.
Like for example, I'm very happy that every year I
bring friends. In fact, here is a Spanish friend Elena,
and there is as a Mexican friend Dorris, and then
also Cody.

Speaker 3 (01:23:40):
Cody always brings friends.

Speaker 8 (01:23:42):
We have Mark Hamilton, we have well as behind all
of us bring people.

Speaker 3 (01:23:47):
We need to bring more people.

Speaker 8 (01:23:48):
We need to collaborate, and we need to keep this
growing growing, and also in different places. Because I organize
something in Spain as well. On my public is mostly
Spanish and then some of those come here as well.
So we need to keep on collaborating and also experiment
different things like we are doing this march in the

(01:24:11):
Centers of Power of Spain. That is why I think
it's so important that we have a rally for Longevity
in Washington, d C.

Speaker 3 (01:24:18):
Washington d C has to see this.

Speaker 8 (01:24:20):
As Gennadi mentioned the Immortality Bones the coffin, it was
a coffin in front of the US Capitol that actually
should have had more media coverage. And you know, the
Coalition for Radical Eve Extension can do it and better
because I like Sultan Isban, but it was one man show.

(01:24:45):
Here we are hundreds of people from all over the world.
And then before giving you the word gym, because there
are other initiatives we need to adapt.

Speaker 3 (01:24:55):
And I want.

Speaker 8 (01:24:56):
To ask, because Cody hasn't spoken too much, where we
are going to be next month and what we are
going to do next month.

Speaker 9 (01:25:05):
Yeah, let me let me just jump in just quickly. Look,
we're not just like immortality entrepreneurs. We're not just like
starting something and moving on to the next thing.

Speaker 5 (01:25:20):
That's not what we're doing. We're we're we're.

Speaker 9 (01:25:22):
In this and we're not going to quit on this,
and we're actually not going to quit on you.

Speaker 5 (01:25:26):
And that's the difference. You know.

Speaker 9 (01:25:29):
It's it's one thing to have a campaign and do
something and then disappear into something else. That's not what
That's not what we're about. We're we're on this and
I and we've shown that because ten years is ten years.
We're we're we're on this to stay. That's that's why, honestly,
that's why you should support us.

Speaker 8 (01:25:45):
Well, we are here to kill death. Look at it
death there. We are here to kill you.

Speaker 7 (01:25:51):
Uh.

Speaker 8 (01:25:52):
And there are different approaches. So so what are we
going to do? Who are we going to meet where?

Speaker 3 (01:25:57):
Cody?

Speaker 10 (01:25:58):
Okay, Well, first I wanted to say, Immortalis is kind
of doing slightly what Radfast is doing, but on a
different stage. So Radfest gives the scientists and the researchers
of longevity the stage and the voice to the public
and immortalis is giving the stage to those same people
to move forward faster and what they're doing. So next

(01:26:20):
month we are going with jose To. He's going to
introduce us to one of his friends in Argentina, Javier Malay.

Speaker 8 (01:26:27):
The President of Argentina, is going to meet with us
with Mark Wallas, I mean Mark Hamilton Wallas and Cody
and myself because we are proposing to have Immortalists in
Buenos Aires, south of Buenos Aires, and we want competition.
Also the USA has to get in there. Of course,
the USA has to be there.

Speaker 10 (01:26:48):
Argentina is one of three or four governments we're in
talks with right now.

Speaker 8 (01:26:54):
So okay, Jim here is the father of the beast.

Speaker 3 (01:27:00):
Thank you. I'll thank you.

Speaker 17 (01:27:01):
A great job. You guys, great John, thank you, thank
you all of it. You're great, You're fantastic. I just
want to make one thing simple here that I'm feeling
about all this and uh oh oh, you guys look great,
by the way, is that I want to keep it
simple in the context that when we talk about companies
and everything, uh, you know, helping and expanding and helping
and expand you don't have we're not talking about anybody

(01:27:21):
stopping what you're doing. What you're doing is great, what
your cody, all you guys Janati, But but make Radfest
your home and the context that make it your base. Uh,
make it. Make it that you're telling your people, all
your members from the big right when Radfest ends, that
they need to be at Radfest, not just sitting back
and waiting for you know, your different meetings you have,

(01:27:42):
get them, get them, You're already doing that in some state.
But this is really what we're talking about. This is
the simplicity of it. This is how we're going to double.
This is how we're going to triple. In fact, everybody
here talking to your friends, your family, everybody, get into
this conversation, get into this life speaking, speak it up
and making it that simple. Uh, you know, we're we're
we're come many. Thank you Joe for your presentation. All
you guys, like I said, you're amazing. But let's keep

(01:28:04):
it also to this point simple that we talked to
our people right when you're right, when Radfest ends, you're
setting them up, and you do a great job setting
them up now to be here and it will be
this then Radfest will build something that will be a
springboard for all of us.

Speaker 18 (01:28:19):
It will build everybody.

Speaker 17 (01:28:21):
That's the point. By us focusing together and this initiative,
we will build then everybody's initiative along with that. But
if we don't have that one focus, we're scattered, and
that's what happens.

Speaker 3 (01:28:30):
Thank you, Uh one, two and three.

Speaker 19 (01:28:39):
Yes, My wife is the president of our vice president
of ALICE, which is the Latin American Sociology Association. They
have their conferences every two years. So what they do
in the meantime is they have pre ALICE conferences all
over Latin America. There might be three or four or
five of them in Mexico alone, And optimally you want

(01:29:02):
those people coming to your main conference, but in truth,
they're not all going to go there. So what would
happen is you would invite just a few speakers from
the main conference to go to all these different locations
you're promoting it. My wife's the president of ten universities
in Mexico. We would hold one our university that would
give us, and we make it very an expensive for
the students to come. So the students, you know, pay

(01:29:23):
the expenses of the conference, and most of those you know,
ninety percent of those students and other people don't go
to the main conference, but you're still spreading the word.

Speaker 20 (01:29:37):
Okay, so I don't even know where to start. To
your point, what I tell my friends, just to simplify,
is I'm going to the first largest conference in the
world on longevity. Your presentation was right on. I'm a

(01:29:58):
global marketing comunication expert and I'm not selling anything. I
want to collaborate and help. I told lis Perish that
I moved to Mexico because I believe that access to
the things that people need are much easier being in Mexico.
I speak Spanish, so unfortunate. So whatever is needed, I'm there.

(01:30:24):
I'm in Tijuana.

Speaker 5 (01:30:25):
I'm right on the border.

Speaker 20 (01:30:27):
One of the things that I think is critical in
my opinion of teaching at MBA programs, working and marketing
all my life is you need to think from the
outside and versus inside out. What does that mean when
I talk to people, regular people? To your point, how

(01:30:48):
do you double attendance? You need to get people excited
and passionate. The people that I talk to about this
concept are afraid. They're afraid, and what are they afraid of?
You'll never guess. They're afraid of loneliness. They're like, if

(01:31:09):
I outlive, I look at my mother.

Speaker 5 (01:31:11):
Two of her friends just died. It's very sad.

Speaker 20 (01:31:16):
So when you're talking, when you're excited, because you've already
bought into the concept, you cannot get through people. And
I'll tell you this as a marketer for many years,
you will just people will just be negative or they'll
just shut down. You will not convince them in that way.

(01:31:38):
So what's needed is to your point, this is a
time for strategy. This is a time to sit down
and figure out all of the strategic elements of driving
this movement forward. One with collaboration, one with messaging, one
with outreach, very clear, simple messages that can help people

(01:31:59):
get over the fear, look at the benefits, sell them
on the benefits so that you can bypass either misinformation
or just get them thinking in a more positive way.
And I'm also open to helping in any way with that.
That is one of my expertises as well. But I

(01:32:19):
believe there's so much that can be done at this moment.
There's a lot of momentum, but it is a time
to collaborate and be strategic so that you limit the
resources and with less energy, you can do more and it's.

Speaker 5 (01:32:36):
Hard, but it's doable.

Speaker 20 (01:32:37):
You have amazing people. There's amazing people here that I'm
just like, I've never expected to see all of this.
I've been in touch with Jose, I knew about all
of these conferences. But there's so much more that I
think can be done just to move all of these forwards.
So again, thank you for that presentation. I think it

(01:32:57):
was wonderful.

Speaker 9 (01:32:59):
Yeah, thank you, thank you for your comments, and we'd
like to connect more with you. I do want to
say that the more obvious opportunity is people who are
already into longevity. Okay, we're talking about travel, We're talking
about paying a registration fee, We're talking about spending a
couple of days somewhere. That's the obvious target. It is
It is the transhumanists. Okay, there's like this, there's there's

(01:33:24):
actually a significant number of transhumanists. There's actually a significant
number of longevity people. I'm not saying we shouldn't reach
out expand the market. We one hundred percent want to
do that, but let's mobilize the people who are already
into this to actually, you know, fucking do something.

Speaker 15 (01:33:44):
I have some.

Speaker 18 (01:33:45):
Feedback that might help us improve our message. There's an
organization called this Stage. It's an international organization of forty
five thousand CEOs and thirty seven countries. I'm a speaker
to them on sales and also longevity. My astartmental longevity
presentation will ask raise your hand if you would like
to live forever. About half raise their hand. Then I'll say, okay,

(01:34:10):
raise your hand if you'd like to live forever with
great health, a sharp mind, unhitted mobility. Now we're at
three quarters. And then if I ask, raise your hand
if you and your family and your friends could live
forever with great hell, almost everybody raises their hands. So
we might think about that and somehow it might help

(01:34:31):
us improve the message. The second of feedback I get
this negative is this is against God's will. God has
determined how long we're gonna live, and there's nothing we
can do about it. So there's no need for me
to get involved. I don't have an answer for that myself. Well,
I will tell you my wife's Catholic and that's how

(01:34:52):
she feels. So there's two philosophies of life determinism. So
I just mentioned that she believes in and the others
you will. That means I'm in charge of how long
I'm gonna live, and number one by what I do.
And number two, if I'm doing good for the world
like I think I'm trying to do, then the man

(01:35:12):
upstairs will see that and keep you a life longer.
So I just want to make sure those two main
pushbacks so it might help us improve our message.

Speaker 3 (01:35:22):
A beautiful guess.

Speaker 5 (01:35:23):
I just just a piggyback on that.

Speaker 9 (01:35:25):
I do think I know I did a little bit,
but I do think we need to stop this like
boxing match with religion. Like let's let's uh yeah, yeah,
you know, if you believe in a god, just believe
in a god who wants you to live.

Speaker 5 (01:35:38):
You know. Yeah, let's welcome everybody.

Speaker 9 (01:35:41):
It's actually for it's actually for everybody, Yeah, because because
we want to live. It's not about a doctor, a doctor,
an agreement in doctrine. That's that's not it's not really
about that. It's about it's about human beings living.

Speaker 5 (01:35:55):
Right.

Speaker 11 (01:35:56):
Yes, So, uh, I agree with you, Joe. I think determinism,
irrespective of religious or philosophical roots, as a kind of
evolved coping mechanism that various traditions of thought have developed
over the course of millennia when mortality really was unavoidable

(01:36:19):
because the technology just wasn't there, So people figured out
a way to make peace with death instead of trying
to fight it. The problem with that mindset is right
now we are on the cusp of being able to
kill death, but it will be dependent on our efforts.
So any sort of determinism or fatalism will undermine those efforts,

(01:36:40):
and we ultimately need the religious communities of the world
to align with us on this. As I've said yesterday,
religions evolved too, and we can hopefully influence them to
evolve in a positive direction without requiring people to give
up something that's valuable to them. So I'm an atheist,
but I don't want to convert anybody. If you are

(01:37:02):
a Christian or a Jew, or a Muslim, or a
Hindu or a Buddhist, I want you to be a
Christian or Jew, or a Muslim or Hindu or Buddhist
who believes in immortality or radical life extension.

Speaker 5 (01:37:12):
In this world.

Speaker 11 (01:37:14):
Yes, and that's that's how we can get to it together.
And then we could argue about theology or philosophy all
we want. Once we have immortality, and then we could
actually drill deeply into what we believe and why without
running out of time to do it.

Speaker 2 (01:37:28):
We argue about it forever if we wanted.

Speaker 3 (01:37:31):
So.

Speaker 10 (01:37:31):
I don't understand the argument of it's against God's will
for longevity, because the Bible says we're created in God's image,
and I haven't heard about God dying.

Speaker 3 (01:37:39):
So that's right.

Speaker 9 (01:37:44):
It's the Hebrews Btseilla Melohem, right, So that's in the
It's in the image of God.

Speaker 3 (01:37:49):
The Gospel of longevity.

Speaker 8 (01:37:52):
Jim, Okay, we have a question here, Bob under balloon.

Speaker 21 (01:37:56):
Yeah, I think we need to walk our I had
my fifty year service celebration at the Boeing Company about
three months ago, and it happened to be in the
middle of one of my fasting periods.

Speaker 5 (01:38:12):
I thought, I'm not going to break my fast for this.

Speaker 3 (01:38:14):
Hell.

Speaker 22 (01:38:14):
No, you gotta take charge of yourself and say I'm
going to be different.

Speaker 5 (01:38:20):
You gear are different.

Speaker 22 (01:38:21):
You know, do the things and do not pay attention
to what the masses who follow the sheep expectation follow.
You're going to retire, not to death, but to do
more things. When you have your fifty year self fast
if you can fast, you know, don't stop.

Speaker 8 (01:38:41):
Okay, we have time for two more questions, and also
remember after this we're going to have a very nice meal.

Speaker 3 (01:38:49):
Life is also to be enjoyed.

Speaker 8 (01:38:51):
That is why we want to be immortal, because we
want to have fun. We have to enjoy life, so
the food will be nice. But we have time for questions.
One question here, Taylor.

Speaker 23 (01:39:04):
Yeah, I have a couple of questions. One is actually
for you, Jose in Madrid, are you are your speakers
that you have planned? Are they actually going to be
there in person and not over zoom because that's a
far away to travel for a lot of us. And
another is for Ganadi.

Speaker 5 (01:39:21):
And we've had a lot.

Speaker 23 (01:39:22):
Of exciting protocols announced here on the main stage and
in some of the clinics, and are you considering incorporating
any of those into your game, as you know things
that might pop up if you're advocating for anti aging.

Speaker 8 (01:39:38):
Okay, the first question, yes, I like to do like
in Radfast, the speakers have to be there because I
want also the people to talk with the speakers.

Speaker 3 (01:39:47):
This is important.

Speaker 8 (01:39:48):
And yesterday there was a beautiful VIP reception with the
speakers and those participants who wanted to go, and so
I want them to be in touch.

Speaker 3 (01:39:57):
There are certain exceptions.

Speaker 8 (01:39:58):
Last year I had Brian Joe, but Brian Johnson tries
to avoid international trouble because of his Arcadian rhythm and
he's sleep and this year so he didn't come in person.
He was by zoom. This year I also have one
person byzom who is George. George Church is no longer
traveling internationally and so it's Ray Kersweil. He doesn't travel internationally.

(01:40:20):
But otherwise, all the people are coming to Madrid. Yes,
this is a real conference and I have tours for them.
I want them to enjoy life, to see how beautiful
life is and how fantastic the Mediterranean diet is.

Speaker 11 (01:40:34):
Yes, So Taylor, to answer your question, I'm of course
still open to feedback on LV the game.

Speaker 5 (01:40:41):
We're currently unbuild.

Speaker 11 (01:40:43):
Zero point nine to one, so we're not at one
point zero yet. The game is open to iteration and
refinement now in terms of how specific do we want
to get. There's a reason why I had a singular
selection for fitness regimen and the singular selection for improve nutrition.
It's supposed to be whatever you think works or whatever

(01:41:05):
works for you or whatever ends up working in practice.
And the reason why I did that was because I
wanted to show at least the approximate scale of effects.

Speaker 5 (01:41:15):
So if you engage in the.

Speaker 11 (01:41:18):
Best possible fitness regimen, whatever that happens to be, that
could reverse your aging somewhat, that could rejuvenate you somewhat,
make you healthier, make you live longer. It's not going
to make you live to one fifty. Likewise, if you
have the best diet in the world, it could help
you live longer, it could help you avoid certain diseases.
It's not going to make you live to one fifty

(01:41:38):
or one thousand or a million years. So within the game,
I'm less focused on being minutely accurate. I'm more focused
on accuracy and relative.

Speaker 5 (01:41:50):
Terms, like what is it that you would really need
to do?

Speaker 11 (01:41:52):
What kinds of interventions to reach that indefinite, open ended
lifespan immortality if you will. And that's why I not
only include the rejuvenation therapies. I include other causes of
death too, and the opportunity to fight those, which you
will have more time to do if you're ageless. So

(01:42:13):
think about all the risks facing humanity and the effect
size of each of them.

Speaker 8 (01:42:20):
Okay, if there is one question, and also I want
death to ask a question. Death, come here, I want
you to ask a question to our panelies. So think
about that question. Well we have a quick one, right,
quick one, and then death think about it because it
is a matter of life or death.

Speaker 7 (01:42:41):
He said, we don't want to boxing match with the religion,
but what if that religion wants to fight us, and
particularly they if they like they oppose cryonics for example.

Speaker 11 (01:42:52):
Yes, what if those who are religious or of certain
religious persuasions want to fight us?

Speaker 5 (01:43:00):
That's the question, Joe, go ahead, and I have some
thoughts to it.

Speaker 9 (01:43:04):
Yeah, it's still it's still not a good strategy. Okay,
we you know, there's there's a lot of people who
it's just not the way we want to go. There's
there's a lot of people like in the middle ground
that we just want to bring around to our our
to understand what we're doing. And that's what we need
to keep going with. And yeah, yes, it's still the
best way to go. And my view is fight the dogmatism.

Speaker 11 (01:43:27):
Don't fight the core of their faith or their religious tradition,
but fight against the fact that they want to impose
their views on others. And I have a rather strong
libertarian strict small L, not capital L.

Speaker 5 (01:43:41):
But I believe in individual freedom.

Speaker 11 (01:43:44):
I believe in your right to make the choices that
you want to make for your life and your well
being as a patient, as a health and wellness enthusiast,
as a cryonicist. So the argument from individual rights will
resonate with a lot of both secular and religious individuals.
And you can appeal to a lot of people who

(01:44:05):
might even be say, fundamentalists, but tell them, well, what
about the US Constitution?

Speaker 5 (01:44:10):
What about the Bill of Rights?

Speaker 11 (01:44:11):
What about what the founders wanted individuals.

Speaker 5 (01:44:14):
To enjoy us their freedom?

Speaker 10 (01:44:16):
Okay, now I want to say something to okay quickly. Also,
you got to look at the silver lining of people
fighting us, because that's actually progress because first things are ridiculed,
then they're violently opposed, and then is widely accepted as truth.

Speaker 2 (01:44:31):
So we're making progress when they're fighting us.

Speaker 3 (01:44:34):
Yeah, very good. Sir Arthur S.

Speaker 8 (01:44:37):
Clark who said that anyway, death has the final question,
so it must be an immortal question.

Speaker 12 (01:44:45):
I realize I strike a lot of your hearts with
anxiety and fear. How death do you want to ameliorate that.

Speaker 2 (01:44:58):
I didn't understand it?

Speaker 11 (01:45:00):
Well, I don't know if I want to alleviate the
fear of death as long as you exist, because fear
can be a powerful motivator. Now, I've been asked this
question a lot since I published Death Is Wrong.

Speaker 5 (01:45:13):
Well, aren't you doing all this just because you're afraid
to die?

Speaker 11 (01:45:18):
I don't deny that I'm afraid to die, but I
have to go deeper than that, and I have to ask, well,
if I'm afraid of something, why is it that I'm afraid?
What is it that I'm afraid to do or become?
I'm afraid to lose something good. I'm afraid to lose
life because life is good. Why am I afraid to

(01:45:39):
lose life?

Speaker 3 (01:45:39):
Because I love life?

Speaker 11 (01:45:40):
So I think fear of death isn't something to be
ashamed of. Fear of death stems from love of life,
and love of life is something that should be embraced.

Speaker 2 (01:45:50):
Well.

Speaker 6 (01:45:50):
As people, we need adapt to adapt to some kind
of catalyst in life, and we've really don't.

Speaker 24 (01:46:00):
And so I would say, let's not make death the
catalyst of our movement. Uh, you know, I I think
that what Jim was talking about on the main stage.
I think it was Opening Night about about being.

Speaker 6 (01:46:11):
Drawn to to because to consider ourselves pre human, about
being drawn to what will be our true human state,
which is which is what would be considered heaven on Earth.

Speaker 5 (01:46:24):
But it's really it's really what Earth should be.

Speaker 3 (01:46:27):
Ha ha yeah yeah, yeah yeah. Don't don't take it,
don't take it wrong. But uh.

Speaker 15 (01:46:35):
I read the folks enjoy abundance.

Speaker 3 (01:46:37):
And beautiful, beautiful Jim.

Speaker 8 (01:46:40):
Actually, when people say that what gives meaning to life
is death, that is so stupid. It's like saying, what
gives meaning to marriage is divorce. No, what gives meaning
to marriage is marriage. What gives meaning to life is
life more life. So we are going, fine, we are

(01:47:01):
going to lunch. We are go and take some pictures
because this is for immortality and he's a very good
look in death.

Speaker 3 (01:47:09):
So have some pictures with death.

Speaker 8 (01:47:11):
Also, Happy lunch, Sa

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