September 26, 2025 • 52 mins
Tonight on The Brian Crombie Hour, Brian interviews Murat Croci. Murat is the co-founder and co-CEO of Ibex Biosciences and brings two decades of biotech leadership and five patents to advancing breakthrough treatments. Founded in 2015, Ibex is developing two transformative drugs: a single-dose malaria cure that blocks parasites from entering red blood cells, showing strong effectiveness in animal models, and an antibody drug conjugate targeting chemoresistant colorectal cancer. Using alpaca-based antibodies against CD147, this ADC achieves 100% efficacy in mouse models, eliminating tumors that typically recur in 35% of patients. The company focuses on colon cancer first, with potential expansion to melanoma and ovarian cancer. Brian closes this episode with some thoughts of his six year anniversary of the Brian Crombie Radio Hour.
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Speaker 1 (00:00):
The views expressed in the following program are those of
the participants and do not necessarily reflect the views of
Saga nine sixty am or its management.
Speaker 2 (00:18):
Believing Everyone and Welcome to the Brian Crombie Radio wom
I've got a really interesting gentleman company and at least
two fascinating innovative pharmaceutical medical products to introduce you to. Tonight.
Marat Karachi is with us, said tonight, he is the
co founder and co CEO of Ibex Biosciences. It's an
innovative biotechnology company and what they're all about is they
(00:40):
want to discover, validate, and produce potential solutions to a
multitude of serious challenges facing human health by investing in
exploratory projects and processes that may not have been validated
with the public research community. He's just told me a
little bit out and I think he's going to tell
you about two products that he's taken through the process
and now he's struggling to find the money to comerualize them. Madatt,
(01:01):
Welcome to the show.
Speaker 3 (01:02):
Sir, Thank you, Brian, welcome to be here. Great to
be here.
Speaker 2 (01:06):
So tell me about these two products that you've done
a lot of work.
Speaker 3 (01:10):
With if you could, certainly. So you know, as you said,
the company's trying to go after stuff that's very difficult
to cure. So we decided to go after malaria. But
unlike other drugs in the market, we found an Achilles heel.
So you have these parasites and they basically I won't
(01:31):
go into the details, and maybe your listeners would care,
but I'll do it in thirty seconds. Let's say you're
bitten by an infected mosquito. That mosquito goes from your
blood into your liver, it hangs out there for about
ten days and it comes out of deliver. Now, you
get no symptoms from this. It's asymptomatic. Once it goes
(01:52):
into bloodstream, that's when the symptoms occur. That's when they
start attacking red blood cells. So what they do is
red blood cells reproduce, red blood cells explode, and they
infect new red blood cells. And this goes on and
on and on until either the immune system clears infection
or you have organ failure and you die. So our
(02:14):
innovative solutions extremely simple. We found out how to plug
the whole so they can't get into a red blood cell. Well,
guess what they have thirty seconds to a minute to
get into a red blood self. If they don't do that,
they perish and infection ends. And that's that's simple, and
it solves the problem both prophylactically, and it also serves
a purpose secure. This has been tested in mice with
(02:37):
human blood, so it replicates the human state. So that's
how we've solved malaria. So that's what we're doing. We're
trying to seek funds to get this through a human trial.
Human trial would be very simple. You affect the patient
and you administer the drug or vice versa, and you
see if it works. You know, in three days, if
(02:59):
it clears infect then it works, and you basically solved
one of the world's most difficult problems in medical humanity,
which is which is malaria killed six hundred people every year.
It's killed millions throughout history, if not billions.
Speaker 2 (03:15):
So tell us a little bit about a malaria just
to take a step back, if you could. It's carried
it's carried by mosquitoes.
Speaker 3 (03:22):
Yeah, it's a parasite. It's called plost Minium fel superium,
and it's doesn't infect all mosquita. So people know you
can get been by mosquito. Right, you can get malaria. Right,
that's not the case. The mosquito would have to be
infected with the parasite in order to get malaria. And
it's pretty much nonexistent in the US. It has been eradicated.
(03:44):
You might hear one or two cases here and there.
Most cases are people who come back from Africa and
are infected because it won't show up until like ten days.
In fact, there's a.
Speaker 2 (03:53):
Fox housendicated in North America versus not in Africa.
Speaker 3 (03:58):
Well, it was here in the US in America like
a long time ago, right.
Speaker 2 (04:02):
How is it better eradicated? What was there?
Speaker 3 (04:05):
I mean through through through excessive uses of pesticides which
have killed everything. Plus we don't have wet seasons like
they do in Africa, so the climate's a little different.
It's warmer there, it's wetter there.
Speaker 2 (04:18):
Okay, So still a big problem in in Africa obviously.
Speaker 3 (04:22):
Right, Africa, Indonesia, some places in the Middle East, South America.
Uh so yeah, you have you have fatalities and and
not only death. You have you have loss of work hours,
you have to take care family members, you have to
stay home for weeks, you have you have massive headaches, fevers, shivers,
(04:42):
it's symptoms can be severe that and you take a
drug and you're also going to get you you can
get side effects from the current drugs that are available.
So it's not a pretty sight.
Speaker 2 (04:54):
There's no there's no vaccine from hilaria, is that correct?
Speaker 3 (04:58):
So there vaccines from here area, and they're about seventy
percent effective and you need four shots and they're seasonal.
A parasite can invade vaccines more so than other types
of infections. That's that's their hallmark. They can do that,
but the current vaccines are woefully inadequate. Even the ones
(05:21):
that have come out, they're again seventy percent effective four injections.
Speaker 2 (05:27):
So and if you're infected and you get sick, what
what do you take?
Speaker 3 (05:32):
Then? Like artemisson in is a standard of care right
now that people use for severe malaria, and that may
or may not work. It's not one hundred percent effective,
it has side effects, and you know it's inadequate, and
the mosquitoes have developed resistance to that drug right now,
(05:56):
so now they're trying to find another drug to replace
it because it's not as a active it was like
ten years ago.
Speaker 2 (06:02):
So it sounds like your your invention, your product is
world changing.
Speaker 3 (06:08):
Yeah, I mean they can't evolve, it's impossible. You have
to exist to evolve. They can't get into a red
blood cell. They die. So it's pretty straightforward. It's extremely simple.
It's a simple solution. This is a huge problem. You know,
maybe Bill Gates is listening here and says, oh, I
want to go and invest in ibacs and solve this problem.
I mean it's just sitting there, and you know, I
(06:30):
say these things with certainty because if your listeners having
to go to site, they can actually see these reports
that were generated. I actually published them that were done
by third parties and they're research organizations that actually work
with Bill Gates and Gates Foundations partners like MMV Medicines
from Malaria Vengers. They're the ones independent lab that did
(06:54):
these tests that has validated in the actual report cure
word one shot cure.
Speaker 2 (07:03):
Now, did you come up with this technology? Is this
your invention? Is this from an academic institution? Is this
how do you come up with this idea to stop
them from being able to go into the red blood cells?
Speaker 3 (07:14):
Great idea, A great question, Brian. Look, when we started
the company, we wanted to do things very differently than
everyone else. So we actually commissioned these experiments from scratch.
We didn't license these from anywhere else. We didn't license
it from another university institution. I went and I basically
(07:35):
found scientists who are would take risks and chances and
who are innovative. Our chief scientific officer, doctor Vidal Dolla Cruz,
invented the phase display technology, a technology that won the
Nobel Prize. I have doctor Norman Lai, who worked for
NIH under Roscoe Brady. His lab generated programs products that
(07:57):
generated in the billions of dollars when they were licensed
to large pharma. So I sought these scientists. I asked
them to conceptualize ideas to solve major problems. And we
came up with this solution for malaria, and we came
up with another solution for cancer, and I guess we'll
(08:17):
talk about that a little later.
Speaker 2 (08:20):
Yeah, let's leave that for just a second. And so
you've been doing this, you said, for eight years, ten years,
ten years? And how much money have you raised so far?
Speaker 3 (08:29):
So we've raised between equity investments and loans, it's close
to twenty million dollars.
Speaker 2 (08:39):
And how much are you trying to raise right now,
because this would be a substantial change to take it
out of animal testing into human testing.
Speaker 3 (08:46):
Would it now absolutely absolutely huge? So we were trying
to raise in total twenty five million, and that would
cover colon cancer, refractory colon cancer, and malaria in a
phase one study. So we're doing two indicatas. Were trying
to raise twenty five million in a reg D five
O six uh C offering. And so the malaria would
(09:09):
be very quick because it's an acute indication. Cancer would
take a little longer time. But but our drug and
I don't jump the gun here, it's probably probably jumped
a lot of guns to your ryne. But I mean, look,
the cancer, we'd probably go after patients who are very
sick maybe uh maybe who are they're they're they're fit,
(09:31):
but you know, they're they're basically you know, on their
last leg in terms of trying other new drugs that
are out there, and uh, and so that we go
after those sick patients in that clinical trial. So we'd
hope to to get that done as you know, as
quickly as possible as well.
Speaker 2 (09:49):
So so let's stay with millary just for another minute.
If I could please explain to everyone, if you could,
what the process to commercialization would be. You're talking about
funding the phase one. Would you need then to do
a phase two and a phase three before you can
submit to the FDA to get approval? And how many
people would be in your phase one? What would the
phase two do? And how many people? And what would
(10:11):
the phase three do? And how many people? And how
long would that take before you would likely get approved
by the FDA? Give us the roadmap if you could.
Speaker 3 (10:18):
Great, great questions, great question. Look, there are three places
in the world that you can do a challenge model,
and one of them is in our backyard at Natural
Institutes of Health, and they will run a challenge model
that means they actually raise plasmonium foul ciprium, they culture it,
(10:39):
and basically through a cro contract research organization who has
worked with them in the past and have worked with
many phase one clinical trials dealing just with malaria, we
would contract them and they would seek volunteers, which they
tell me is not very difficult for malaria, believe it
or not. And these individuals will get our drug administered
(11:02):
and we'll get live malaria injected into them, so they
will get infected and then and at which point, within
two or three days, it will be determined whether the
drug works or not. And then of course there's the
you know, the there's filings that go along with the
results that would be similar to the FDA, and if
(11:24):
it cures these patients, like we think the drug will,
you know, we essentially pass phase one studies.
Speaker 2 (11:30):
And so phase one is efficacy in a small population?
Is that correct?
Speaker 3 (11:35):
Correct? I would say twenty people? Twenty? OK?
Speaker 2 (11:39):
So then what's what's Phase two?
Speaker 3 (11:41):
Would be a field test ran that would we we
would need we would need to go to Africa or
another place in an endemic region, and we would we
haven't done the study designed there, but basically it would
at this point we wouldn't. We would raise additional funds,
so that would be easy. If we pass a phase
(12:02):
one we can get institutional funds from almost anywhere, so
that wouldn't be a problem.
Speaker 2 (12:09):
But fairly short, I know you haven't done this the
study design, you say, but is that a large population
and a long time or is that again a short
popular small population a short time.
Speaker 3 (12:21):
Yes, so there's no shortage of those who are infected.
If you go to Africa I wouldn't. I couldn't tell
you the exact timeline, but I would say that probably
going to be it's going to be not twenty, but
maybe one hundred patients that would be injected with our
drug ibex thirteen to see if it works with them,
(12:41):
and we would monitor those patients. And again, the drug
is supposed to clear the infection in two to three days,
so the clinical trial shouldn't take a long time, okay.
Speaker 2 (12:52):
And then the Phase three I've always been told the
phase three are the big, long, big population expensive ones.
Would you probably have that situation as well?
Speaker 3 (13:01):
I mean, if it depends on the indication, right, this
is an acute indication, so you have the you have
the infection, and after the drug is administery, you shouldn't
have it. So you're again talking per patient maybe three
four days, and then you'll monitor them several weeks afterwards.
So I wouldn't think that would be very expensive either.
(13:24):
But at that point it's kind of moot because they
know the drug works and you have no shortage of investors.
But in terms of timeline, I would probably say that
that would probably take probably about a year to do
a Phase three from start to finish and most of
its paperwork. I would say, it's not actually administering the
drug to patients and monitor.
Speaker 2 (13:45):
So you're talking about what three years to five years
before this product would come to the market.
Speaker 3 (13:51):
Yeah, I would say like probably three to five is correct.
That's a great range, okay.
Speaker 2 (13:57):
And how many people did you say, parish are ye
from malaria?
Speaker 3 (14:01):
It's about six hundred thousand.
Speaker 2 (14:04):
Six hundred thousand. Yeah, And everything else you say is
either seventy percent effective or doesn't actually solve the problem.
And what you're looking for is twenty five million dollars
to do the phase one that starts the process, gets
the proof of efficacy, and then after that you got
to prove that it's safe. You got to do it
(14:24):
in the in the in the in the in the
in Africa, and you've got to do the phase three,
and you've got to submit it to the FDA and
get approval. So there's processes to go through, but the
real nut is getting this twenty five million dollars to
do the phase one to prove its efficacious. And you've
proven already that it's efficacious with human blood, albeit in mice.
Speaker 3 (14:42):
Is that correct? That's absolutely right? And Just to clarify,
it's five million just for malaria. The rest the twenty
The rest is for the cancer program.
Speaker 2 (14:52):
So there's two five million dollars that effectively, what this
is is an option on solving problems for six hundred
thousand people a year.
Speaker 3 (15:02):
Yeah, I mean that's what I'm saying. I mean, like
Bill Gates is spending much more than this to resolve this,
and if he want it solved, here we go. You
can do it immediately. I mean anyway, it doesn't have
to be a Bill Gates. You know Elon Muscott malariy
he almost died from it, actually well reported in South Africa.
Could be anyone of these guys they want to solve
(15:23):
this problem. This is the way to do it. It's
a definitive solution to malaria. They cannot circumvent, you know,
the blockade, and we happen to find the drug that
pinpoints at exact point where it can't enter. They just perish.
So it's remarkable that we discovered it and validated it
like we have. We're going to file a publication next year.
(15:46):
We're submitting a manuscript for this. Approximately it takes a
while to publish, but all the data is available online
in our website.
Speaker 2 (15:57):
So yeah, fascinating. We're going to take break for some
messages and be back in just two minutes, and I'm
gonna ask Pierre Jean, the banker to talk a little
bit about the challenge of raising money and what he
thinks of this product and this company. Stay with us,
everyone back in just two minutes.
Speaker 1 (16:20):
No Radio, No Problem stream is live on Sagay nine
six am dot C.
Speaker 2 (16:25):
A Welcome back everyone to the brand Crimey Radio Hour.
I've got Madat Parrocchi from Ibex. We've been just chatting
about his product for malaria that sounds actually fascinating. And
(16:47):
I've got Pierre Jean. I always love mispronounce your last name.
I apologize Fournier. I think it is who is the
investment banker that's taking a Morot and his company to
the market. We've had the pleasure of chatting with Pierre
Jean for short before. He runs an investment bank out
of Paris, France. But he's got operations in London, England
(17:08):
and in the United States, and he raises money for
people around the world that are fascinating companies up here.
And why is Murat having challenges raising twenty five million
dollars with you on the assignment. It should be easy. No, seriously,
like tell us how challenging it is for biotech companies
to raise money.
Speaker 4 (17:26):
I went swer to it, but in one minute, I
want to tell you why is it that I took
the challenge to work with Murat and ibex.
Speaker 5 (17:33):
Please is.
Speaker 4 (17:36):
A very intelligent individual. For sure, he has no, if
any scientific background. Still, if you follow what he said
during the first half of the presentation, it was very
easy to follow. He takes the right verb for you
to understand. So I took the challenge of fundraising for
Miura because he's a good interview. Also, he wants to
change the He wants to change the world, and that's
(17:59):
what is to do not only malaria but also in
cancer Colorata concert. So it's challenging because the time I'm
very difficult. We published a research in my bank about
two weeks ago and we demonstrate that it takes about
twenty two months to raise funds in the biotech world.
That is the current time now, So no surprise, we
(18:19):
made some time. Now we got traction on the cancer
part of the business. But it is expensive, that a
lot of money to put it on the table. We
have to raise twenty million dollars, but we have some
strong mark of interest. Besides is working the segment of
biotech which is called ADC. ADC. Well, you know, my friend,
(18:40):
I have cancer and when I was treated, when I
was first treated with cancer, I did chemotherapy. Chemotherapy is
like bleach that goes into your blood and kill all
the cell that I'm moving too fast, like your hair,
like your cancer cells. And in this case, this technology
select the cancer cells and try to destroy the cancer
(19:05):
cells very selectively and effectively. That's why I was very
interested into the project.
Speaker 2 (19:11):
Why don't you tell us a little about this cancer
product then if you could?
Speaker 3 (19:15):
Okay, And anybody drug conjugate isn't anybody with a linker.
At the end of the linker, there's a drug like
a chemo agent, and anybody is objective is to bind
to the cell surface of the of the tumor and
then enter the tumor. And when it enters a tumor,
(19:37):
they call that endocytosis. That's the process where the Anybody
drug conjugate enters the tumor cell surface and then once
it's inside, it releases its payload. Enzymes clip the payloads,
so the payloads a chemo agent, and the chemo agent
disperses inside the tumor and destroys it. So that's what
(20:00):
an ADC is. Now, this is a relatively new area
of therapeutics and they've shown to be very effective. Most
recently they talked a lot about in her to for
low hur to breast cancer, which is an ADC. And
(20:20):
so you're going to see a lot of these drugs
that are going to come out into the market, but
they're not all the same. Some of these drugs are
achieved something called by standard effect, so not all if
the conjugate gets inside the tumor. Some are released early
on and the chemo agent that is near the tumor
(20:42):
happens to kill the tumor cell. They call that a
bystandard effect. In our case, we're working with alpaka based antibodies.
They're called VHH, so they're considerably smaller than a traditional
heavy light chain and so that provides a benefit for
targeting small crevices on proteins that may be difficult to
(21:04):
bind to. And then there's another advantage that our drug has, okay,
and that is it endos cytosis. That means it really
goes into tumor cells much readily than other proteins. So
it's called CD one forty seven. You don't have to
remember that. But because it's targeting that CD one forty
cent protein, it happens to go inside cancer cells very
(21:26):
very very effectively. But I mean effectively, I mean have effectively.
Well we've done. The most recent study was they grafted
a human tumor into a mouse. They call these xenograph models,
and then they administered the ADC intravenously into the mouse,
(21:49):
and then they monitor the size of the tumor because
these tumors will get very very large. They have no
immune systems in these mice, so it's continuing to grow, grow, grow, grow, well.
In the administration of the IBEX thirteen ADC, there was
no tumor left. It didn't just suppress tumor growth, it
(22:11):
eliminated the tumor. They couldn't find anything there. It was
one hundred percent. And just like the malaria study, I
you know, I upload these reports publicly on our website
through the portal, and so because it's very difficult to believe,
it's almost incredulous. When you say something to someone and
(22:34):
he says, well, here's the independent data. This is what
this drug achieved. I didn't say, the independent party says,
says it. And what's even more interesting here is that
the drug, the cancer type that we tested was highly
chemo resistant to all the to all the five floor
(22:57):
of your skill and oxaliplatin. These are keymo drugs that
are standard care drugs given to colon cancer patients. And
you know when it becomes refractory. So those drugs work. Okay,
don't get me wrong, right, sixty five percent of those
patients that receive it going to complete remission and in
five years it doesn't come back. But when it comes back,
(23:18):
those cells become resistant. And then the thirty five percent
struggle to get better and they go on different regimens
and the cells keep on coming back. That was the
celts that were implant in this animal model, those chemo
resistance cells, and it took the tumor into zero. So
(23:40):
we're going into a refractory colon cancer. And as I
said earlier, which I jumped in, we want to target
patients that are terminal that because they expressed this target
more than patients who could receive chemo.
Speaker 2 (23:57):
Fascinating. So let me ask you a couple of questions
if I could. So it's sounds like you're not actually
changing what you call the payload. The payload is still chemo.
You've got what something that is the carrier of the
payload that can get into the cell, into the tumor
more effectively. Is that correct?
Speaker 3 (24:17):
That's correct.
Speaker 5 (24:18):
So it's a.
Speaker 2 (24:19):
Technology that you've got rather than a new drug.
Speaker 3 (24:23):
Well, the antibody is the antibody is a carrier and
you're using a standard payload, which is correct. But together
they called an a d C and anybody drug conjugate.
So the type of drug we're using Brian will not
work unless it enters the cell. If it doesn't enter
(24:44):
this cell, it won't work. So the carrier is extremely important.
Speaker 2 (24:50):
Into the cell is the key. And so tell me
why are so many cells chemo resistant?
Speaker 3 (24:57):
Well, one of the mechanisms is exactly why our drug
works so well, because it over expresses CD one forty seven.
The literature is huge on this. This is a mechanism
by which the cancer cells resist traditional chemo agents, and
(25:18):
we're exploiting that. We're noticing that. We looked at the
publications and cells that are chemo resistant, and we determine, like,
what are these cells over expressing to defend themselves against
chemo agents, and we noticed expression levels of one forty
seven on the cell surface was tremendously high, particularly in
(25:40):
chemo resistant colon cancer. And so that's what we targeted
and it works wonderfully.
Speaker 2 (25:48):
I mean, you're focused right now on colon cancert refractory
colon cancer. To be exact, I think you said, is
this technology and this this drug combination effective in other
cancers as well? Or we don't know yet.
Speaker 3 (26:05):
Yes, it would be effective in other cancers. We tested
in melanoma, we tested in ovarian cancer, and they were
both effective. But we just have to choose one indication
to begin with and then move from there.
Speaker 2 (26:19):
And did I understand what you said a couple minutes
ago that that thirty five percent of the people, So
sixty five per chemo works in sixty five percent of people,
but not in thirty five percent of people, and in
thirty five percent of people it comes back within five years.
Is that that's what you said.
Speaker 3 (26:35):
That's right, that's right, that's incredible.
Speaker 2 (26:38):
I've never heard that before. That's that's terribly scary.
Speaker 3 (26:43):
If you look at the numbers for poling cancer. You'll
see they're not that great survival. If it comes back
and it's it's underserved, it's an underserved cancer.
Speaker 2 (26:59):
And if it comes back, you're saying that these tumors
are more chemo resistant than they were before.
Speaker 3 (27:06):
Absolutely, absolutely, they are far more chemo resistant.
Speaker 2 (27:10):
And your product solves that. It's all it's actually it's
it's focused on those chemo resistant tumors. There's something in
that chemo resistant tumor that is expressed that actually attracts
your product.
Speaker 3 (27:26):
It's like on the surface of the tumor, there is
just more doors that open, and that door is CET
one forty seven, and it's more resistance. The more doors
are are on the surface and the better it works.
Speaker 2 (27:41):
Fascinating. So tell us you've now told us sort of
how it works. Tell us where you are in the
study approval process. Have you've done any studies in humans yet?
Speaker 3 (27:52):
So we want to go into a human study. We've
done multiple animal studies and we've come to a point
where we were trying to raise money for again a
phase one human study, and I just pointed out, we
want to work with patients that are terminal, which is
very unusual. I mean I have to work with my
chief scientific officer and chief medical officers see if they
(28:15):
can design this. They think that it's possible to do
terminal fit patients for this drug instead of doing this
slow way, just because we see this like remarkable results
we have in mice. So again, the twenty five M
covers malaria, which is five M and the rest goes
to pull rectal cancer.
Speaker 2 (28:36):
So how many patients would you have in this twenty
million dollar study?
Speaker 3 (28:42):
So I didn't look at the study design that's still
being planned, but my guess is it's somewhere between like
thirty and forty patients is probably standard for a face.
Speaker 2 (28:53):
And how long how long you know, you've already said
that they would be terminable terminal, so you know how
long is your Do they injected once? How many times?
Speaker 5 (29:03):
Like?
Speaker 2 (29:03):
Tell me about what the course of the medication is.
Speaker 3 (29:07):
So I don't know the injection protocol, but you could
inject it more than once. Uh, it's so many milligrams
per kilogram that's administered over so many weeks. But again,
if it reflects the same efficacies it did in the
animal models, I mean it should be highly effect against
these patients. It shouldn't go on for months and months.
(29:29):
I mean, the God willing, they'll be sent home earlier
and they'll be removed from their terminal state. If the
drug works as well as it has transid if.
Speaker 2 (29:39):
The phase one works, you'd have to do the same thing,
go through a phase two and a phase three.
Speaker 3 (29:43):
We would, we would. There are certain exemptions you can
get to allow the drug to be utilized during the
clinical trial if it has exemplary results like this. Now
I'm not a regulatory expert, so I'm gonna I'm going
to leave that questions to maybe part two here with you.
Speaker 2 (30:00):
But it seems to me that if what you're doing
is actually delivering the chemo payload more effectively, that some
of the people that might be interested in this are
the companies that that produce the chemo payload, because they,
you know, would look at your drug as a better
way to deliver their drug. Is that is that a possibility.
Speaker 3 (30:21):
Well, the payloads that we use are off patent and
they're produced by many many companies. It's not one. So
like it's like I think this, I think a lot
of people would be interested in this drug, but it's
nothing proprietary to to like get this payload, there are
(30:41):
many CROs that will conjugate it to the antibody became
it becomes like you know, buying a loaf of bread
at a grocery store at some point, so there's nothing
proprietary to it.
Speaker 2 (30:55):
So you know, I'm familiar with the process called a
five H five five oh one two process that would
take a formally generic product through the approval process more
quickly if you've changed the delivery mechanism but not change
the efficacy of the payload. Is that a potentiality of
a way that you could actually get approval more quickly.
Speaker 3 (31:16):
So I'm not a regulatory expert, but I would say no,
because I think the regulatory agencies deemed this as a
totally new drug because anybody binding specifically to an antigen
on the surface would be considered unique on its own,
irrespective of the payload. So I don't think that's possible. Again,
(31:39):
I'm not a regulatory agency, but I would say that
if that's true, many other ADC companies would have done.
Speaker 2 (31:44):
That, right, So you've got to start from scratch, and
so the phase one, Phase two, Phase three would be
what the same three to five year timeframe that we
talked about before.
Speaker 3 (31:54):
Yeah, I'd say that's correct.
Speaker 2 (31:57):
I'd say that, and you're going to have to you know,
once you prove the efficacy in the phase one, you're
gonna have to come back to raise more money for
the phase two, in the phase three, But it becomes
a lot easier because you got the proof of efficacy
in the phase one.
Speaker 3 (32:09):
Is that correct exactly? I mean, if you pass a
phase one like this and show efficacy, you'll have investment
bankers knocking at your door and large large you know,
almost every VC would want to be on that deal.
Speaker 2 (32:23):
So tell me take a step back, and you know
you're you seem to be an incredibly smart guy. Took
a look at your resume. You've got a great background.
You know, why would someone like you get motivated to
get invested in and committed to two products They're going
to take, you know, three to five years to come
to the market. You got to get twenty five million
dollars to prove efficacy before you even get sort of
(32:46):
people saying you're right, why take such a big risk?
Speaker 3 (32:49):
Well, you know, I involved myself in this business without
understanding those risks. So I'm i didn't understand the risk.
My business partner didn't understand the risks. And how long
it took. I mean, we've been at it for ten years.
But we're here now. So we try not to look
back and we look look at look what we've accomplished
to date, which is phenomenal, like like we could have
(33:12):
failed right up to this point. I think we've already
succeeded because a few drug companies can even manage the
type of efficacy that we're seeing in this period of
time with the little bit of money that we did spend.
So I say, we've actually succeeded. But you're right, then
here's the Here's the last stage is getting the human
(33:36):
data funds raised. And I think that's a product of
the environment right now, not not It doesn't reflect on
the performance of our biologic it's just environment right now.
You have to you have to understand that these funds
are are scared that they're going to run out of
(33:56):
cash and they can't raise new funds because everyone on
the sideline waiting to see what's happening with all these
tariffs and you know, these adversarial trade agreements that are
coming across these are creating you know, nervousness for investors.
They want to see what happens. They want the dust
(34:18):
to settle. Especially the Health and Human Services director in
our country. You know, they're they're making policies that create uncertainty.
They want to know exactly what's happening before people invest.
It's just human nature to pause. And so that's not
a reflection of how good our drug is. It's just
the environment that we're in.
Speaker 2 (34:38):
It seems that some people internationally that Robert K. Jr.
Is Is almost questioning new technologies, new products, new new ideas,
and so that there's a cloud over you know, clearly
new vaccines, but but like new new science. Is that
the part of your problem?
Speaker 3 (34:58):
Well, well, so far we don't have an mRNA product.
Even though our malaria drug could be an mRNA, it
could be that may not be affecting us directly. I mean,
there's also a flip side. There's also something good to
say about his policies. I mean, he recently announced that
they are trying to move away from animal testing, monkey testing,
(35:22):
primate testing, and in that respect it could be helpful
to us because we can test these in mice. We
don't have to do primates. So sometimes it's a double
edged sword. It depends on the industry you're in, and
it also depends on what you want to have achieved,
(35:44):
but you have to be very careful and look at
each thing independently.
Speaker 2 (35:49):
The Big John's we're going to take a break for
some messages and we're going to come back with PJ
and Marot and chat a little bit about how he
actually raise money. We're going to go from the science
to actually bring money. Stay with us that one back
in two minutes.
Speaker 1 (36:07):
No Radio, No Problem stream is live on SAGA nine
sixty am dot col.
Speaker 2 (36:23):
Welcome back everyone to the Bran Crimey Radio Hour. I've
got Maroc Crochey with us today. He's the co founder,
the co CEO of Ibex's Bio. They've got two fascinating
products that have gone through animal testing. He's ready and
poised to take them into humans in phase one studies.
He's trying to raise twenty five million dollars five million
for a study on malaria and twenty million dollars for
(36:45):
a study on refractory colon cancer. And it sounds very
promising and he's talking about the challenges in the marketplace.
We've also got his investment banker, Pierre Jean Fournier of
Fournier Investment Banker of Paris, France, who who's an expert
in raising money for biotech companies, et cetera, and has
been involved in this business both in Europe as well
(37:07):
as North America for what two decades now, I guess
PJ if not more. Frankly, let's talk a little bit
about the process. So you're a private company, Marat, I
presume I am, yes, And so you've got to go
to private investors and raise money. I presume you've got
a website that's got all of your science and an
(37:29):
investor deck on it. But people are going to be
making not an investment in a public company through a
public security. So what is it they're doing. They're taking
a look at what your investor deck and is there
an information memorandum there or a prospectives or something like that.
Speaker 3 (37:45):
So it's a five to six C offering and basically,
if you're an accredited investor, you can look at this
investment agreement and all the information and make an investment
right on the website.
Speaker 2 (38:01):
And an a credit investor is what someone that makes
a certain amount of income or certain networth and so
therefore is deemed to be sophisticated.
Speaker 3 (38:08):
That's correct, that's correct.
Speaker 2 (38:10):
And you have to do a compliance type application to
prove that you're in a credit investor before you get
access to the information.
Speaker 3 (38:17):
So if they don't have a lawyer letter, if they
don't have an accountant letter, we would help pay for
that certification. So they just click on the website, please
help me certify, and we would send it to a
third party to help them get certified, very cooch.
Speaker 2 (38:35):
So then once they get certified as an a credit investor,
they can get access to the information and they go
through it. And then what you're asking for twenty five million,
But I'm not one person putting in twenty five million?
How much have I got the right to put in?
Speaker 3 (38:47):
Five k? That's the investment.
Speaker 2 (38:50):
Five k is the minimum investment, okay, And of the
total twenty five million dollars, does that by one hundred
percent of the company or fift percent of the company.
Speaker 3 (39:01):
So the valuation two parts the offering is thirty seven
and a half million is a pre money valuation thirty
seven So fifty percent goes into the thirty seven and
a half million. The other fifty percent is a convertible note,
which is at twelve percent, and it gives the investor
the option to convert at a twenty percent discount their
(39:22):
principle and interest.
Speaker 2 (39:24):
So that's interesting. So twelve and a half million dollars
goes into a convertible note. Take a step back and
explain the convertible note. Why that makes sense?
Speaker 3 (39:33):
Okay, so half of the if someone invests ten k
as an example, five k goes into equity at thirty
seven and a half million. The other five k is
a convertible note. It's again twelve percent with a twenty
percent discount. It makes sense for a couple of reasons.
If the valuations off the investor can make it up.
(39:56):
They get also precedents over equity positions because it is
it is a kind of debt form of debt. So again,
if we if the evaluation doesn't go higher, then they
can make up the difference with the convertible note in
the discorder.
Speaker 2 (40:12):
So it's a twenty percent discount to the next offering.
Is that correct?
Speaker 3 (40:15):
Correct? That's right.
Speaker 2 (40:16):
So that's interesting. So you've got downside protection with the
convertible note and some upside exposure with the equity and
in a complete sort of failure, you're in a debt position,
so you've got some security in the debt position. If
it's a down round where the next round has a
(40:37):
lower price, you've got the protection of you can convert
at a twenty percent discount to the next round, and
then if things look spectacular, you can convert. Is the
conversion right at my choice, the investor's choice or can
you force me to convert?
Speaker 3 (40:51):
It's at the investor's choice, and it's at the next
rounds valuation whenever that is.
Speaker 2 (40:57):
And how long does the debt, how long is the
data outstanding, and how long is the conversion?
Speaker 3 (41:03):
Right there, it's it's within a four year period.
Speaker 2 (41:08):
Sounds fascinating, And then you know what would be your intention?
You would go out obviously after phase one and do
another private round, or would you be going public at
some point in time in the future.
Speaker 3 (41:17):
We'd love to We'd love to go public if the
public markets open up. We'd love to list this on
a public exchange and get it get an exit for
our investors in that manner. PJ.
Speaker 2 (41:29):
What do you think the chances are of not being
successful in this?
Speaker 4 (41:34):
Well, I'm going to move the result of one hundred percent.
You know, you asked me about how I did going
to raise funds. In the case of ibex, you have
to understand that the ADC market is very very recent,
so much so that I signed five deals in this
sector over the three months. So it's a very recent market,
(41:55):
very effective against cancer, and again so the public. The
mechanism of action is very simple. It kills the cancer
cell selectively, okay, targeting the sales. So I'm very very
optimistic because.
Speaker 2 (42:07):
You don't lose your hair.
Speaker 6 (42:09):
No.
Speaker 4 (42:09):
I didn't lose my hair because I put a hat
with with ice on it, so it prevents, uh, the
hair to fall down.
Speaker 5 (42:18):
No.
Speaker 2 (42:18):
But with with this drug that Marat's got, you don't
lose your hair because it's selective and it doesn't kill
hair hair cells.
Speaker 4 (42:27):
Makes you love Marat?
Speaker 3 (42:28):
I don't know.
Speaker 2 (42:32):
Well, it sounds like it's fascinating.
Speaker 4 (42:33):
Rot.
Speaker 2 (42:34):
Is there a website people should go to if they're interested.
Speaker 3 (42:37):
Ibexx dot bio I b e X dot bio. They
can click to invest button and they can get more
information from there. But they can see the website at
I B e X dot b i O And.
Speaker 2 (42:51):
If you want any information for me. Just contact me
at Brian at Briancrombie dot com and I'd be happy
to uh to forward your your your interest to to PJ.
PJ before I let you go, I understand you've just
published a new book. What's the new book? This is fascinating.
Speaker 4 (43:08):
Yeah. The title is How I Beat Goldman Sachs.
Speaker 2 (43:13):
How I Beat Goldman Sachs. You beat Goldman Sachs.
Speaker 3 (43:16):
Yeah.
Speaker 4 (43:16):
It happened five times in the late nineties, and one
of them I got them the big deal of the year.
Speaker 7 (43:23):
It was the PMC Philip Morris Scope, which was the
biggest company on Earth at that tage, and I took
the deal which was ten billion dollars in the writing
against Goldman and DLJ and Citibank. And I was amazing
because I was on my desk dealing with five hundred
investors in the world.
Speaker 4 (43:44):
A lot of fun. You should check the book. It's
very funny to read.
Speaker 2 (43:47):
How I Beat Gorman? And how do I get it
through Amazon?
Speaker 4 (43:51):
Or what Amazon? Do you take? My name?
Speaker 2 (43:54):
Excellent? PJ. Thank you so much for joining us. I
really appreciate it, and thank you for the introduction to
a fascinating gentleman and a really innovative company Ibex that
I'm I'm hopeful gets the money because I think this
is going to make us some important moves forward in
life and uh and health. And so Marata Crotchy, thank
you so much for joining us and telling us a
(44:15):
little about your your your product for malaria that is
right now killing six hundred thousand people a year, and
this product sounds like it could really solve that. And
also your product for factory colon cancer that that takes
the chemo payload and delivers it far more effectively, particularly
(44:36):
to two people that have got colon cancer, that that
come back five years later with the cancer all over again,
and really need your products. So thank you so much.
Ibex dot com is the website to go to, or
Brian at biocomb dot com got bio great, ibas bio.
I apologize, thanks for correcting me. That's our show for tonight.
(44:59):
I'm going to come back a couple of completing comments
in just a minute. Thanks very much. Everybody.
Speaker 1 (45:07):
Stream us live at SAGA nine to sixty am dot C.
Speaker 6 (45:22):
Talking back everyone to the brinkromby radio wire. So tonight
is six years that I've been doing this show. I
can't believe that it's been that long. It's been an
incredible opportunity. And I have been passionate to movie people
for a long period of time and also been passionate
but really getting to know people with in depth conversations.
Speaker 5 (45:40):
Some people who criticized me in the past.
Speaker 6 (45:41):
Today, I'd like to really sit down with people and
get to know what they're all about and not participate
in those really quick ten or fifteen or thirty second,
you know, quick shit handshakes.
Speaker 5 (45:52):
I'd like to sit down with people and get to
know what they're all about.
Speaker 6 (45:55):
And you've given me that opportunity, and so thank you
very much for that, and for those of you that
have tuned in and several occasions over the course of
the last the last six years, three thousand shows, over
two thousand interviewees. It's just been an incredible opportunity and
thank you for that. I'm on every night Monday through
Friday at six o'clock on nine to sixty AM. But
(46:15):
in addition to on average getting about thirty thousand listeners,
I have the opportunity to post on podcast servers on YouTube,
on social media. I get a lot of following on LinkedIn,
and I therefore get a breadth of exposure and people listening.
Speaker 5 (46:34):
To me, frankly, from around the world and from a lot.
Speaker 6 (46:36):
Of my different business contacts and political contacts and other
contacts really you know, across the Greater Toronto, Werry, across Canada,
across North America, across the world, and it is really
an incredible experience. I've been lucky enough to interview some
of my heroes in business and politics, from.
Speaker 5 (46:53):
Jim Pattison, David Peterson, John Torrey, Hayes mckellyan, the list
goes on, and it's been.
Speaker 6 (47:01):
A unique opportunity for me to spend fifty minutes with
interesting people.
Speaker 5 (47:04):
Asking them about their life, their career.
Speaker 6 (47:06):
I've interviewed business people, developers, people head of different associations
high tech biotech from France, from Israel, from Canada, from
the United States about their passion, their business, their scientific
develops and.
Speaker 5 (47:23):
Interest and that's been a huge opportunity for me to.
Speaker 6 (47:26):
Really delve into what makes these people excited about their business,
their prospects, their scientific inventions, etc.
Speaker 5 (47:34):
And that's been a great opportunity. I also get an
opportunity to rant and.
Speaker 6 (47:38):
Have been encouraged by my broadcaster to close my shows
and or open my shows with my own little rant
or my own five or seven or ten point plan
on how I would solve problems, so that you get
to know me and I get an opportunity to chat
about the things that I'm so passionate about. I ended
up talking about politics often earlier in the week, and
(48:01):
to our international affairs. I've been very interested obviously what's
going on in the Middle East, in Ukraine, and I've
been able to reach out to people that are very
knowledgeable in Ukraine, in Eastern Europe, in the Middle East,
and or people that are aware of it, former ambassadors
of the like, and really delve into what caused the problem,
what is causing the problem, what the potential solutions are,
(48:21):
and some of the more negative side of things in
regards to abductions, kidnappings, hostages.
Speaker 8 (48:30):
Right.
Speaker 5 (48:30):
And it's been.
Speaker 6 (48:32):
Fascinating for me the individuals that I get from key
from different parts of Israel that are willing to and
interested in talking to me.
Speaker 5 (48:40):
I've interviewed people from South Africa. I've interviewed people from China,
I've interviewed people from Japan. I've interviewed people from across
Canada and in the United States.
Speaker 2 (48:47):
And in France in the UK.
Speaker 6 (48:50):
From Ireland, I've ended up connecting up with some of
my long distance cousins that are in either Scotland or
Ireland and had the opportunity interviewed in them, as well
as some of my cousins from the United States as
well as across Canada.
Speaker 5 (49:06):
Later in the week. I haven't talked about arts or
lifestyle issues.
Speaker 6 (49:09):
I am passionate about that. I have been presidents of
the Mississiga Arts Council. I've been chair of the Mississiti
City Summit. I worked for the Walt Disney Company, not
necessarily in entertainment.
Speaker 5 (49:20):
I was doing amusement parks. I did movies at the TVs,
I did hotels, at the restaurants.
Speaker 6 (49:25):
But I really got exposed to the entertainment business and
loved it, and so I get the opportunity to delve
into that at a far greater degree. And I've also
been very interested in social capital and building communities. I've
started and got halfway through a doctoral thesis on social capital,
and so therefore it's a real pleasure of mine to
delve into some of these people that you know, some
people would call culches or lifestyle people and what they
(49:46):
think makes people take you know, you know, a professor
of empathy on several occasions that I just think is
fascinating people on happiness.
Speaker 5 (49:56):
That is obviously very interesting.
Speaker 6 (49:59):
And I I get to therefore interview people from all
walks of life, from across the world and come to
you every night and try to get my message and
my interviewees to you through radio, through podcasts, through video,
on social media and on YouTube. And it's an incredible experience.
And I get to listen to them all, synthesize what
(50:22):
they have to say, think about them in regards to
my own points of view, and turn around and give
you often my rent, my ten point plan.
Speaker 5 (50:32):
And it's an incredible opportunity.
Speaker 6 (50:33):
And for those of you that reach out and I
get comments every day, people recommending great topics, great interviews,
people criticizing some of the comments, people suggesting what new
topic I should be focused on, people trying to get on.
Speaker 5 (50:48):
My show, and it's an incredible opportunity.
Speaker 8 (50:50):
I really enjoy that opportunity to interact with you and
have the opportunity, if you're interested, get to know you
over fifty minutes of a very long, in depth conversation,
which I think is what we don't have enough of
in our world today.
Speaker 5 (51:05):
So thank you for the opportunity.
Speaker 6 (51:07):
To spend six years, five nights a week, over any
days that is fifty two times five, so over two
hundred days a year in chatting with you.
Speaker 5 (51:18):
I appreciate it.
Speaker 6 (51:19):
Thank you for listening, thank you for watching, thank you
for your participation, and thank you to starting at sixty
for the opportunity. It's a unique one and great one
one that I'm very very happy that I've had the
privilege to host, to interview, to spout my own point
of view and interact with.
Speaker 5 (51:39):
All the people. Thanks, good night, and to repeat.
Speaker 6 (51:42):
Which I often close my show by saying, I'm on
every night, five nights a week.
Speaker 5 (51:47):
I did a Friday I'm nine to.
Speaker 6 (51:48):
Sixty AM in stream online at Triple W, SAVY at
sixtym dot All my podcasts and the videos go up
on my website, Brian Promy dot com as soon as
the radio show goes to air, as well. I put
them on several different podcast servers, on YouTube, on LinkedIn, etcetera.
Speaker 5 (52:03):
So if you missed my show on the radio, you
can get me a whole bunch of otherways, thanks.
Speaker 1 (52:08):
For six years good Night, no Radio, no problem. Stream
is live on SAGA nine sixty am dot c a
The views expressed in the following program are those of
the participants and do not necessarily reflect the views of
Saga nine sixty am or its management.
Speaker 2 (00:18):
Believing Everyone and Welcome to the Brian Crombie Radio wom
I've got a really interesting gentleman company and at least
two fascinating innovative pharmaceutical medical products to introduce you to. Tonight.
Marat Karachi is with us, said tonight, he is the
co founder and co CEO of Ibex Biosciences. It's an
innovative biotechnology company and what they're all about is they
(00:40):
want to discover, validate, and produce potential solutions to a
multitude of serious challenges facing human health by investing in
exploratory projects and processes that may not have been validated
with the public research community. He's just told me a
little bit out and I think he's going to tell
you about two products that he's taken through the process
and now he's struggling to find the money to comerualize them. Madatt,
(01:01):
Welcome to the show.
Speaker 3 (01:02):
Sir, Thank you, Brian, welcome to be here. Great to
be here.
Speaker 2 (01:06):
So tell me about these two products that you've done
a lot of work.
Speaker 3 (01:10):
With if you could, certainly. So you know, as you said,
the company's trying to go after stuff that's very difficult
to cure. So we decided to go after malaria. But
unlike other drugs in the market, we found an Achilles heel.
So you have these parasites and they basically I won't
(01:31):
go into the details, and maybe your listeners would care,
but I'll do it in thirty seconds. Let's say you're
bitten by an infected mosquito. That mosquito goes from your
blood into your liver, it hangs out there for about
ten days and it comes out of deliver. Now, you
get no symptoms from this. It's asymptomatic. Once it goes
(01:52):
into bloodstream, that's when the symptoms occur. That's when they
start attacking red blood cells. So what they do is
red blood cells reproduce, red blood cells explode, and they
infect new red blood cells. And this goes on and
on and on until either the immune system clears infection
or you have organ failure and you die. So our
(02:14):
innovative solutions extremely simple. We found out how to plug
the whole so they can't get into a red blood cell. Well,
guess what they have thirty seconds to a minute to
get into a red blood self. If they don't do that,
they perish and infection ends. And that's that's simple, and
it solves the problem both prophylactically, and it also serves
a purpose secure. This has been tested in mice with
(02:37):
human blood, so it replicates the human state. So that's
how we've solved malaria. So that's what we're doing. We're
trying to seek funds to get this through a human trial.
Human trial would be very simple. You affect the patient
and you administer the drug or vice versa, and you
see if it works. You know, in three days, if
(02:59):
it clears infect then it works, and you basically solved
one of the world's most difficult problems in medical humanity,
which is which is malaria killed six hundred people every year.
It's killed millions throughout history, if not billions.
Speaker 2 (03:15):
So tell us a little bit about a malaria just
to take a step back, if you could. It's carried
it's carried by mosquitoes.
Speaker 3 (03:22):
Yeah, it's a parasite. It's called plost Minium fel superium,
and it's doesn't infect all mosquita. So people know you
can get been by mosquito. Right, you can get malaria. Right,
that's not the case. The mosquito would have to be
infected with the parasite in order to get malaria. And
it's pretty much nonexistent in the US. It has been eradicated.
(03:44):
You might hear one or two cases here and there.
Most cases are people who come back from Africa and
are infected because it won't show up until like ten days.
In fact, there's a.
Speaker 2 (03:53):
Fox housendicated in North America versus not in Africa.
Speaker 3 (03:58):
Well, it was here in the US in America like
a long time ago, right.
Speaker 2 (04:02):
How is it better eradicated? What was there?
Speaker 3 (04:05):
I mean through through through excessive uses of pesticides which
have killed everything. Plus we don't have wet seasons like
they do in Africa, so the climate's a little different.
It's warmer there, it's wetter there.
Speaker 2 (04:18):
Okay, So still a big problem in in Africa obviously.
Speaker 3 (04:22):
Right, Africa, Indonesia, some places in the Middle East, South America.
Uh so yeah, you have you have fatalities and and
not only death. You have you have loss of work hours,
you have to take care family members, you have to
stay home for weeks, you have you have massive headaches, fevers, shivers,
(04:42):
it's symptoms can be severe that and you take a
drug and you're also going to get you you can
get side effects from the current drugs that are available.
So it's not a pretty sight.
Speaker 2 (04:54):
There's no there's no vaccine from hilaria, is that correct?
Speaker 3 (04:58):
So there vaccines from here area, and they're about seventy
percent effective and you need four shots and they're seasonal.
A parasite can invade vaccines more so than other types
of infections. That's that's their hallmark. They can do that,
but the current vaccines are woefully inadequate. Even the ones
(05:21):
that have come out, they're again seventy percent effective four injections.
Speaker 2 (05:27):
So and if you're infected and you get sick, what
what do you take?
Speaker 3 (05:32):
Then? Like artemisson in is a standard of care right
now that people use for severe malaria, and that may
or may not work. It's not one hundred percent effective,
it has side effects, and you know it's inadequate, and
the mosquitoes have developed resistance to that drug right now,
(05:56):
so now they're trying to find another drug to replace
it because it's not as a active it was like
ten years ago.
Speaker 2 (06:02):
So it sounds like your your invention, your product is
world changing.
Speaker 3 (06:08):
Yeah, I mean they can't evolve, it's impossible. You have
to exist to evolve. They can't get into a red
blood cell. They die. So it's pretty straightforward. It's extremely simple.
It's a simple solution. This is a huge problem. You know,
maybe Bill Gates is listening here and says, oh, I
want to go and invest in ibacs and solve this problem.
I mean it's just sitting there, and you know, I
(06:30):
say these things with certainty because if your listeners having
to go to site, they can actually see these reports
that were generated. I actually published them that were done
by third parties and they're research organizations that actually work
with Bill Gates and Gates Foundations partners like MMV Medicines
from Malaria Vengers. They're the ones independent lab that did
(06:54):
these tests that has validated in the actual report cure
word one shot cure.
Speaker 2 (07:03):
Now, did you come up with this technology? Is this
your invention? Is this from an academic institution? Is this
how do you come up with this idea to stop
them from being able to go into the red blood cells?
Speaker 3 (07:14):
Great idea, A great question, Brian. Look, when we started
the company, we wanted to do things very differently than
everyone else. So we actually commissioned these experiments from scratch.
We didn't license these from anywhere else. We didn't license
it from another university institution. I went and I basically
(07:35):
found scientists who are would take risks and chances and
who are innovative. Our chief scientific officer, doctor Vidal Dolla Cruz,
invented the phase display technology, a technology that won the
Nobel Prize. I have doctor Norman Lai, who worked for
NIH under Roscoe Brady. His lab generated programs products that
(07:57):
generated in the billions of dollars when they were licensed
to large pharma. So I sought these scientists. I asked
them to conceptualize ideas to solve major problems. And we
came up with this solution for malaria, and we came
up with another solution for cancer, and I guess we'll
(08:17):
talk about that a little later.
Speaker 2 (08:20):
Yeah, let's leave that for just a second. And so
you've been doing this, you said, for eight years, ten years,
ten years? And how much money have you raised so far?
Speaker 3 (08:29):
So we've raised between equity investments and loans, it's close
to twenty million dollars.
Speaker 2 (08:39):
And how much are you trying to raise right now,
because this would be a substantial change to take it
out of animal testing into human testing.
Speaker 3 (08:46):
Would it now absolutely absolutely huge? So we were trying
to raise in total twenty five million, and that would
cover colon cancer, refractory colon cancer, and malaria in a
phase one study. So we're doing two indicatas. Were trying
to raise twenty five million in a reg D five
O six uh C offering. And so the malaria would
(09:09):
be very quick because it's an acute indication. Cancer would
take a little longer time. But but our drug and
I don't jump the gun here, it's probably probably jumped
a lot of guns to your ryne. But I mean, look,
the cancer, we'd probably go after patients who are very
sick maybe uh maybe who are they're they're they're fit,
(09:31):
but you know, they're they're basically you know, on their
last leg in terms of trying other new drugs that
are out there, and uh, and so that we go
after those sick patients in that clinical trial. So we'd
hope to to get that done as you know, as
quickly as possible as well.
Speaker 2 (09:49):
So so let's stay with millary just for another minute.
If I could please explain to everyone, if you could,
what the process to commercialization would be. You're talking about
funding the phase one. Would you need then to do
a phase two and a phase three before you can
submit to the FDA to get approval? And how many
people would be in your phase one? What would the
phase two do? And how many people? And what would
(10:11):
the phase three do? And how many people? And how
long would that take before you would likely get approved
by the FDA? Give us the roadmap if you could.
Speaker 3 (10:18):
Great, great questions, great question. Look, there are three places
in the world that you can do a challenge model,
and one of them is in our backyard at Natural
Institutes of Health, and they will run a challenge model
that means they actually raise plasmonium foul ciprium, they culture it,
(10:39):
and basically through a cro contract research organization who has
worked with them in the past and have worked with
many phase one clinical trials dealing just with malaria, we
would contract them and they would seek volunteers, which they
tell me is not very difficult for malaria, believe it
or not. And these individuals will get our drug administered
(11:02):
and we'll get live malaria injected into them, so they
will get infected and then and at which point, within
two or three days, it will be determined whether the
drug works or not. And then of course there's the
you know, the there's filings that go along with the
results that would be similar to the FDA, and if
(11:24):
it cures these patients, like we think the drug will,
you know, we essentially pass phase one studies.
Speaker 2 (11:30):
And so phase one is efficacy in a small population?
Is that correct?
Speaker 3 (11:35):
Correct? I would say twenty people? Twenty? OK?
Speaker 2 (11:39):
So then what's what's Phase two?
Speaker 3 (11:41):
Would be a field test ran that would we we
would need we would need to go to Africa or
another place in an endemic region, and we would we
haven't done the study designed there, but basically it would
at this point we wouldn't. We would raise additional funds,
so that would be easy. If we pass a phase
(12:02):
one we can get institutional funds from almost anywhere, so
that wouldn't be a problem.
Speaker 2 (12:09):
But fairly short, I know you haven't done this the
study design, you say, but is that a large population
and a long time or is that again a short
popular small population a short time.
Speaker 3 (12:21):
Yes, so there's no shortage of those who are infected.
If you go to Africa I wouldn't. I couldn't tell
you the exact timeline, but I would say that probably
going to be it's going to be not twenty, but
maybe one hundred patients that would be injected with our
drug ibex thirteen to see if it works with them,
(12:41):
and we would monitor those patients. And again, the drug
is supposed to clear the infection in two to three days,
so the clinical trial shouldn't take a long time, okay.
Speaker 2 (12:52):
And then the Phase three I've always been told the
phase three are the big, long, big population expensive ones.
Would you probably have that situation as well?
Speaker 3 (13:01):
I mean, if it depends on the indication, right, this
is an acute indication, so you have the you have
the infection, and after the drug is administery, you shouldn't
have it. So you're again talking per patient maybe three
four days, and then you'll monitor them several weeks afterwards.
So I wouldn't think that would be very expensive either.
(13:24):
But at that point it's kind of moot because they
know the drug works and you have no shortage of investors.
But in terms of timeline, I would probably say that
that would probably take probably about a year to do
a Phase three from start to finish and most of
its paperwork. I would say, it's not actually administering the
drug to patients and monitor.
Speaker 2 (13:45):
So you're talking about what three years to five years
before this product would come to the market.
Speaker 3 (13:51):
Yeah, I would say like probably three to five is correct.
That's a great range, okay.
Speaker 2 (13:57):
And how many people did you say, parish are ye
from malaria?
Speaker 3 (14:01):
It's about six hundred thousand.
Speaker 2 (14:04):
Six hundred thousand. Yeah, And everything else you say is
either seventy percent effective or doesn't actually solve the problem.
And what you're looking for is twenty five million dollars
to do the phase one that starts the process, gets
the proof of efficacy, and then after that you got
to prove that it's safe. You got to do it
(14:24):
in the in the in the in the in the
in Africa, and you've got to do the phase three,
and you've got to submit it to the FDA and
get approval. So there's processes to go through, but the
real nut is getting this twenty five million dollars to
do the phase one to prove its efficacious. And you've
proven already that it's efficacious with human blood, albeit in mice.
Speaker 3 (14:42):
Is that correct? That's absolutely right? And Just to clarify,
it's five million just for malaria. The rest the twenty
The rest is for the cancer program.
Speaker 2 (14:52):
So there's two five million dollars that effectively, what this
is is an option on solving problems for six hundred
thousand people a year.
Speaker 3 (15:02):
Yeah, I mean that's what I'm saying. I mean, like
Bill Gates is spending much more than this to resolve this,
and if he want it solved, here we go. You
can do it immediately. I mean anyway, it doesn't have
to be a Bill Gates. You know Elon Muscott malariy
he almost died from it, actually well reported in South Africa.
Could be anyone of these guys they want to solve
(15:23):
this problem. This is the way to do it. It's
a definitive solution to malaria. They cannot circumvent, you know,
the blockade, and we happen to find the drug that
pinpoints at exact point where it can't enter. They just perish.
So it's remarkable that we discovered it and validated it
like we have. We're going to file a publication next year.
(15:46):
We're submitting a manuscript for this. Approximately it takes a
while to publish, but all the data is available online
in our website.
Speaker 2 (15:57):
So yeah, fascinating. We're going to take break for some
messages and be back in just two minutes, and I'm
gonna ask Pierre Jean, the banker to talk a little
bit about the challenge of raising money and what he
thinks of this product and this company. Stay with us,
everyone back in just two minutes.
Speaker 1 (16:20):
No Radio, No Problem stream is live on Sagay nine
six am dot C.
Speaker 2 (16:25):
A Welcome back everyone to the brand Crimey Radio Hour.
I've got Madat Parrocchi from Ibex. We've been just chatting
about his product for malaria that sounds actually fascinating. And
(16:47):
I've got Pierre Jean. I always love mispronounce your last name.
I apologize Fournier. I think it is who is the
investment banker that's taking a Morot and his company to
the market. We've had the pleasure of chatting with Pierre
Jean for short before. He runs an investment bank out
of Paris, France. But he's got operations in London, England
(17:08):
and in the United States, and he raises money for
people around the world that are fascinating companies up here.
And why is Murat having challenges raising twenty five million
dollars with you on the assignment. It should be easy. No, seriously,
like tell us how challenging it is for biotech companies
to raise money.
Speaker 4 (17:26):
I went swer to it, but in one minute, I
want to tell you why is it that I took
the challenge to work with Murat and ibex.
Speaker 5 (17:33):
Please is.
Speaker 4 (17:36):
A very intelligent individual. For sure, he has no, if
any scientific background. Still, if you follow what he said
during the first half of the presentation, it was very
easy to follow. He takes the right verb for you
to understand. So I took the challenge of fundraising for
Miura because he's a good interview. Also, he wants to
change the He wants to change the world, and that's
(17:59):
what is to do not only malaria but also in
cancer Colorata concert. So it's challenging because the time I'm
very difficult. We published a research in my bank about
two weeks ago and we demonstrate that it takes about
twenty two months to raise funds in the biotech world.
That is the current time now, So no surprise, we
(18:19):
made some time. Now we got traction on the cancer
part of the business. But it is expensive, that a
lot of money to put it on the table. We
have to raise twenty million dollars, but we have some
strong mark of interest. Besides is working the segment of
biotech which is called ADC. ADC. Well, you know, my friend,
(18:40):
I have cancer and when I was treated, when I
was first treated with cancer, I did chemotherapy. Chemotherapy is
like bleach that goes into your blood and kill all
the cell that I'm moving too fast, like your hair,
like your cancer cells. And in this case, this technology
select the cancer cells and try to destroy the cancer
(19:05):
cells very selectively and effectively. That's why I was very
interested into the project.
Speaker 2 (19:11):
Why don't you tell us a little about this cancer
product then if you could?
Speaker 3 (19:15):
Okay, And anybody drug conjugate isn't anybody with a linker.
At the end of the linker, there's a drug like
a chemo agent, and anybody is objective is to bind
to the cell surface of the of the tumor and
then enter the tumor. And when it enters a tumor,
(19:37):
they call that endocytosis. That's the process where the Anybody
drug conjugate enters the tumor cell surface and then once
it's inside, it releases its payload. Enzymes clip the payloads,
so the payloads a chemo agent, and the chemo agent
disperses inside the tumor and destroys it. So that's what
(20:00):
an ADC is. Now, this is a relatively new area
of therapeutics and they've shown to be very effective. Most
recently they talked a lot about in her to for
low hur to breast cancer, which is an ADC. And
(20:20):
so you're going to see a lot of these drugs
that are going to come out into the market, but
they're not all the same. Some of these drugs are
achieved something called by standard effect, so not all if
the conjugate gets inside the tumor. Some are released early
on and the chemo agent that is near the tumor
(20:42):
happens to kill the tumor cell. They call that a
bystandard effect. In our case, we're working with alpaka based antibodies.
They're called VHH, so they're considerably smaller than a traditional
heavy light chain and so that provides a benefit for
targeting small crevices on proteins that may be difficult to
(21:04):
bind to. And then there's another advantage that our drug has, okay,
and that is it endos cytosis. That means it really
goes into tumor cells much readily than other proteins. So
it's called CD one forty seven. You don't have to
remember that. But because it's targeting that CD one forty
cent protein, it happens to go inside cancer cells very
(21:26):
very very effectively. But I mean effectively, I mean have effectively.
Well we've done. The most recent study was they grafted
a human tumor into a mouse. They call these xenograph models,
and then they administered the ADC intravenously into the mouse,
(21:49):
and then they monitor the size of the tumor because
these tumors will get very very large. They have no
immune systems in these mice, so it's continuing to grow, grow, grow, grow, well.
In the administration of the IBEX thirteen ADC, there was
no tumor left. It didn't just suppress tumor growth, it
(22:11):
eliminated the tumor. They couldn't find anything there. It was
one hundred percent. And just like the malaria study, I
you know, I upload these reports publicly on our website
through the portal, and so because it's very difficult to believe,
it's almost incredulous. When you say something to someone and
(22:34):
he says, well, here's the independent data. This is what
this drug achieved. I didn't say, the independent party says,
says it. And what's even more interesting here is that
the drug, the cancer type that we tested was highly
chemo resistant to all the to all the five floor
(22:57):
of your skill and oxaliplatin. These are keymo drugs that
are standard care drugs given to colon cancer patients. And
you know when it becomes refractory. So those drugs work. Okay,
don't get me wrong, right, sixty five percent of those
patients that receive it going to complete remission and in
five years it doesn't come back. But when it comes back,
(23:18):
those cells become resistant. And then the thirty five percent
struggle to get better and they go on different regimens
and the cells keep on coming back. That was the
celts that were implant in this animal model, those chemo
resistance cells, and it took the tumor into zero. So
(23:40):
we're going into a refractory colon cancer. And as I
said earlier, which I jumped in, we want to target
patients that are terminal that because they expressed this target
more than patients who could receive chemo.
Speaker 2 (23:57):
Fascinating. So let me ask you a couple of questions
if I could. So it's sounds like you're not actually
changing what you call the payload. The payload is still chemo.
You've got what something that is the carrier of the
payload that can get into the cell, into the tumor
more effectively. Is that correct?
Speaker 3 (24:17):
That's correct.
Speaker 5 (24:18):
So it's a.
Speaker 2 (24:19):
Technology that you've got rather than a new drug.
Speaker 3 (24:23):
Well, the antibody is the antibody is a carrier and
you're using a standard payload, which is correct. But together
they called an a d C and anybody drug conjugate.
So the type of drug we're using Brian will not
work unless it enters the cell. If it doesn't enter
(24:44):
this cell, it won't work. So the carrier is extremely important.
Speaker 2 (24:50):
Into the cell is the key. And so tell me
why are so many cells chemo resistant?
Speaker 3 (24:57):
Well, one of the mechanisms is exactly why our drug
works so well, because it over expresses CD one forty seven.
The literature is huge on this. This is a mechanism
by which the cancer cells resist traditional chemo agents, and
(25:18):
we're exploiting that. We're noticing that. We looked at the
publications and cells that are chemo resistant, and we determine, like,
what are these cells over expressing to defend themselves against
chemo agents, and we noticed expression levels of one forty
seven on the cell surface was tremendously high, particularly in
(25:40):
chemo resistant colon cancer. And so that's what we targeted
and it works wonderfully.
Speaker 2 (25:48):
I mean, you're focused right now on colon cancert refractory
colon cancer. To be exact, I think you said, is
this technology and this this drug combination effective in other
cancers as well? Or we don't know yet.
Speaker 3 (26:05):
Yes, it would be effective in other cancers. We tested
in melanoma, we tested in ovarian cancer, and they were
both effective. But we just have to choose one indication
to begin with and then move from there.
Speaker 2 (26:19):
And did I understand what you said a couple minutes
ago that that thirty five percent of the people, So
sixty five per chemo works in sixty five percent of people,
but not in thirty five percent of people, and in
thirty five percent of people it comes back within five years.
Is that that's what you said.
Speaker 3 (26:35):
That's right, that's right, that's incredible.
Speaker 2 (26:38):
I've never heard that before. That's that's terribly scary.
Speaker 3 (26:43):
If you look at the numbers for poling cancer. You'll
see they're not that great survival. If it comes back
and it's it's underserved, it's an underserved cancer.
Speaker 2 (26:59):
And if it comes back, you're saying that these tumors
are more chemo resistant than they were before.
Speaker 3 (27:06):
Absolutely, absolutely, they are far more chemo resistant.
Speaker 2 (27:10):
And your product solves that. It's all it's actually it's
it's focused on those chemo resistant tumors. There's something in
that chemo resistant tumor that is expressed that actually attracts
your product.
Speaker 3 (27:26):
It's like on the surface of the tumor, there is
just more doors that open, and that door is CET
one forty seven, and it's more resistance. The more doors
are are on the surface and the better it works.
Speaker 2 (27:41):
Fascinating. So tell us you've now told us sort of
how it works. Tell us where you are in the
study approval process. Have you've done any studies in humans yet?
Speaker 3 (27:52):
So we want to go into a human study. We've
done multiple animal studies and we've come to a point
where we were trying to raise money for again a
phase one human study, and I just pointed out, we
want to work with patients that are terminal, which is
very unusual. I mean I have to work with my
chief scientific officer and chief medical officers see if they
(28:15):
can design this. They think that it's possible to do
terminal fit patients for this drug instead of doing this
slow way, just because we see this like remarkable results
we have in mice. So again, the twenty five M
covers malaria, which is five M and the rest goes
to pull rectal cancer.
Speaker 2 (28:36):
So how many patients would you have in this twenty
million dollar study?
Speaker 3 (28:42):
So I didn't look at the study design that's still
being planned, but my guess is it's somewhere between like
thirty and forty patients is probably standard for a face.
Speaker 2 (28:53):
And how long how long you know, you've already said
that they would be terminable terminal, so you know how
long is your Do they injected once? How many times?
Speaker 5 (29:03):
Like?
Speaker 2 (29:03):
Tell me about what the course of the medication is.
Speaker 3 (29:07):
So I don't know the injection protocol, but you could
inject it more than once. Uh, it's so many milligrams
per kilogram that's administered over so many weeks. But again,
if it reflects the same efficacies it did in the
animal models, I mean it should be highly effect against
these patients. It shouldn't go on for months and months.
(29:29):
I mean, the God willing, they'll be sent home earlier
and they'll be removed from their terminal state. If the
drug works as well as it has transid if.
Speaker 2 (29:39):
The phase one works, you'd have to do the same thing,
go through a phase two and a phase three.
Speaker 3 (29:43):
We would, we would. There are certain exemptions you can
get to allow the drug to be utilized during the
clinical trial if it has exemplary results like this. Now
I'm not a regulatory expert, so I'm gonna I'm going
to leave that questions to maybe part two here with you.
Speaker 2 (30:00):
But it seems to me that if what you're doing
is actually delivering the chemo payload more effectively, that some
of the people that might be interested in this are
the companies that that produce the chemo payload, because they,
you know, would look at your drug as a better
way to deliver their drug. Is that is that a possibility.
Speaker 3 (30:21):
Well, the payloads that we use are off patent and
they're produced by many many companies. It's not one. So
like it's like I think this, I think a lot
of people would be interested in this drug, but it's
nothing proprietary to to like get this payload, there are
(30:41):
many CROs that will conjugate it to the antibody became
it becomes like you know, buying a loaf of bread
at a grocery store at some point, so there's nothing
proprietary to it.
Speaker 2 (30:55):
So you know, I'm familiar with the process called a
five H five five oh one two process that would
take a formally generic product through the approval process more
quickly if you've changed the delivery mechanism but not change
the efficacy of the payload. Is that a potentiality of
a way that you could actually get approval more quickly.
Speaker 3 (31:16):
So I'm not a regulatory expert, but I would say no,
because I think the regulatory agencies deemed this as a
totally new drug because anybody binding specifically to an antigen
on the surface would be considered unique on its own,
irrespective of the payload. So I don't think that's possible. Again,
(31:39):
I'm not a regulatory agency, but I would say that
if that's true, many other ADC companies would have done.
Speaker 2 (31:44):
That, right, So you've got to start from scratch, and
so the phase one, Phase two, Phase three would be
what the same three to five year timeframe that we
talked about before.
Speaker 3 (31:54):
Yeah, I'd say that's correct.
Speaker 2 (31:57):
I'd say that, and you're going to have to you know,
once you prove the efficacy in the phase one, you're
gonna have to come back to raise more money for
the phase two, in the phase three, But it becomes
a lot easier because you got the proof of efficacy
in the phase one.
Speaker 3 (32:09):
Is that correct exactly? I mean, if you pass a
phase one like this and show efficacy, you'll have investment
bankers knocking at your door and large large you know,
almost every VC would want to be on that deal.
Speaker 2 (32:23):
So tell me take a step back, and you know
you're you seem to be an incredibly smart guy. Took
a look at your resume. You've got a great background.
You know, why would someone like you get motivated to
get invested in and committed to two products They're going
to take, you know, three to five years to come
to the market. You got to get twenty five million
dollars to prove efficacy before you even get sort of
(32:46):
people saying you're right, why take such a big risk?
Speaker 3 (32:49):
Well, you know, I involved myself in this business without
understanding those risks. So I'm i didn't understand the risk.
My business partner didn't understand the risks. And how long
it took. I mean, we've been at it for ten years.
But we're here now. So we try not to look
back and we look look at look what we've accomplished
to date, which is phenomenal, like like we could have
(33:12):
failed right up to this point. I think we've already
succeeded because a few drug companies can even manage the
type of efficacy that we're seeing in this period of
time with the little bit of money that we did spend.
So I say, we've actually succeeded. But you're right, then
here's the Here's the last stage is getting the human
(33:36):
data funds raised. And I think that's a product of
the environment right now, not not It doesn't reflect on
the performance of our biologic it's just environment right now.
You have to you have to understand that these funds
are are scared that they're going to run out of
(33:56):
cash and they can't raise new funds because everyone on
the sideline waiting to see what's happening with all these
tariffs and you know, these adversarial trade agreements that are
coming across these are creating you know, nervousness for investors.
They want to see what happens. They want the dust
(34:18):
to settle. Especially the Health and Human Services director in
our country. You know, they're they're making policies that create uncertainty.
They want to know exactly what's happening before people invest.
It's just human nature to pause. And so that's not
a reflection of how good our drug is. It's just
the environment that we're in.
Speaker 2 (34:38):
It seems that some people internationally that Robert K. Jr.
Is Is almost questioning new technologies, new products, new new ideas,
and so that there's a cloud over you know, clearly
new vaccines, but but like new new science. Is that
the part of your problem?
Speaker 3 (34:58):
Well, well, so far we don't have an mRNA product.
Even though our malaria drug could be an mRNA, it
could be that may not be affecting us directly. I mean,
there's also a flip side. There's also something good to
say about his policies. I mean, he recently announced that
they are trying to move away from animal testing, monkey testing,
(35:22):
primate testing, and in that respect it could be helpful
to us because we can test these in mice. We
don't have to do primates. So sometimes it's a double
edged sword. It depends on the industry you're in, and
it also depends on what you want to have achieved,
(35:44):
but you have to be very careful and look at
each thing independently.
Speaker 2 (35:49):
The Big John's we're going to take a break for
some messages and we're going to come back with PJ
and Marot and chat a little bit about how he
actually raise money. We're going to go from the science
to actually bring money. Stay with us that one back
in two minutes.
Speaker 1 (36:07):
No Radio, No Problem stream is live on SAGA nine
sixty am dot col.
Speaker 2 (36:23):
Welcome back everyone to the Bran Crimey Radio Hour. I've
got Maroc Crochey with us today. He's the co founder,
the co CEO of Ibex's Bio. They've got two fascinating
products that have gone through animal testing. He's ready and
poised to take them into humans in phase one studies.
He's trying to raise twenty five million dollars five million
for a study on malaria and twenty million dollars for
(36:45):
a study on refractory colon cancer. And it sounds very
promising and he's talking about the challenges in the marketplace.
We've also got his investment banker, Pierre Jean Fournier of
Fournier Investment Banker of Paris, France, who who's an expert
in raising money for biotech companies, et cetera, and has
been involved in this business both in Europe as well
(37:07):
as North America for what two decades now, I guess
PJ if not more. Frankly, let's talk a little bit
about the process. So you're a private company, Marat, I
presume I am, yes, And so you've got to go
to private investors and raise money. I presume you've got
a website that's got all of your science and an
(37:29):
investor deck on it. But people are going to be
making not an investment in a public company through a
public security. So what is it they're doing. They're taking
a look at what your investor deck and is there
an information memorandum there or a prospectives or something like that.
Speaker 3 (37:45):
So it's a five to six C offering and basically,
if you're an accredited investor, you can look at this
investment agreement and all the information and make an investment
right on the website.
Speaker 2 (38:01):
And an a credit investor is what someone that makes
a certain amount of income or certain networth and so
therefore is deemed to be sophisticated.
Speaker 3 (38:08):
That's correct, that's correct.
Speaker 2 (38:10):
And you have to do a compliance type application to
prove that you're in a credit investor before you get
access to the information.
Speaker 3 (38:17):
So if they don't have a lawyer letter, if they
don't have an accountant letter, we would help pay for
that certification. So they just click on the website, please
help me certify, and we would send it to a
third party to help them get certified, very cooch.
Speaker 2 (38:35):
So then once they get certified as an a credit investor,
they can get access to the information and they go
through it. And then what you're asking for twenty five million,
But I'm not one person putting in twenty five million?
How much have I got the right to put in?
Speaker 3 (38:47):
Five k? That's the investment.
Speaker 2 (38:50):
Five k is the minimum investment, okay, And of the
total twenty five million dollars, does that by one hundred
percent of the company or fift percent of the company.
Speaker 3 (39:01):
So the valuation two parts the offering is thirty seven
and a half million is a pre money valuation thirty
seven So fifty percent goes into the thirty seven and
a half million. The other fifty percent is a convertible note,
which is at twelve percent, and it gives the investor
the option to convert at a twenty percent discount their
(39:22):
principle and interest.
Speaker 2 (39:24):
So that's interesting. So twelve and a half million dollars
goes into a convertible note. Take a step back and
explain the convertible note. Why that makes sense?
Speaker 3 (39:33):
Okay, so half of the if someone invests ten k
as an example, five k goes into equity at thirty
seven and a half million. The other five k is
a convertible note. It's again twelve percent with a twenty
percent discount. It makes sense for a couple of reasons.
If the valuations off the investor can make it up.
(39:56):
They get also precedents over equity positions because it is
it is a kind of debt form of debt. So again,
if we if the evaluation doesn't go higher, then they
can make up the difference with the convertible note in
the discorder.
Speaker 2 (40:12):
So it's a twenty percent discount to the next offering.
Is that correct?
Speaker 3 (40:15):
Correct? That's right.
Speaker 2 (40:16):
So that's interesting. So you've got downside protection with the
convertible note and some upside exposure with the equity and
in a complete sort of failure, you're in a debt position,
so you've got some security in the debt position. If
it's a down round where the next round has a
(40:37):
lower price, you've got the protection of you can convert
at a twenty percent discount to the next round, and
then if things look spectacular, you can convert. Is the
conversion right at my choice, the investor's choice or can
you force me to convert?
Speaker 3 (40:51):
It's at the investor's choice, and it's at the next
rounds valuation whenever that is.
Speaker 2 (40:57):
And how long does the debt, how long is the
data outstanding, and how long is the conversion?
Speaker 3 (41:03):
Right there, it's it's within a four year period.
Speaker 2 (41:08):
Sounds fascinating, And then you know what would be your intention?
You would go out obviously after phase one and do
another private round, or would you be going public at
some point in time in the future.
Speaker 3 (41:17):
We'd love to We'd love to go public if the
public markets open up. We'd love to list this on
a public exchange and get it get an exit for
our investors in that manner. PJ.
Speaker 2 (41:29):
What do you think the chances are of not being
successful in this?
Speaker 4 (41:34):
Well, I'm going to move the result of one hundred percent.
You know, you asked me about how I did going
to raise funds. In the case of ibex, you have
to understand that the ADC market is very very recent,
so much so that I signed five deals in this
sector over the three months. So it's a very recent market,
(41:55):
very effective against cancer, and again so the public. The
mechanism of action is very simple. It kills the cancer
cell selectively, okay, targeting the sales. So I'm very very
optimistic because.
Speaker 2 (42:07):
You don't lose your hair.
Speaker 6 (42:09):
No.
Speaker 4 (42:09):
I didn't lose my hair because I put a hat
with with ice on it, so it prevents, uh, the
hair to fall down.
Speaker 5 (42:18):
No.
Speaker 2 (42:18):
But with with this drug that Marat's got, you don't
lose your hair because it's selective and it doesn't kill
hair hair cells.
Speaker 4 (42:27):
Makes you love Marat?
Speaker 3 (42:28):
I don't know.
Speaker 2 (42:32):
Well, it sounds like it's fascinating.
Speaker 4 (42:33):
Rot.
Speaker 2 (42:34):
Is there a website people should go to if they're interested.
Speaker 3 (42:37):
Ibexx dot bio I b e X dot bio. They
can click to invest button and they can get more
information from there. But they can see the website at
I B e X dot b i O And.
Speaker 2 (42:51):
If you want any information for me. Just contact me
at Brian at Briancrombie dot com and I'd be happy
to uh to forward your your your interest to to PJ.
PJ before I let you go, I understand you've just
published a new book. What's the new book? This is fascinating.
Speaker 4 (43:08):
Yeah. The title is How I Beat Goldman Sachs.
Speaker 2 (43:13):
How I Beat Goldman Sachs. You beat Goldman Sachs.
Speaker 3 (43:16):
Yeah.
Speaker 4 (43:16):
It happened five times in the late nineties, and one
of them I got them the big deal of the year.
Speaker 7 (43:23):
It was the PMC Philip Morris Scope, which was the
biggest company on Earth at that tage, and I took
the deal which was ten billion dollars in the writing
against Goldman and DLJ and Citibank. And I was amazing
because I was on my desk dealing with five hundred
investors in the world.
Speaker 4 (43:44):
A lot of fun. You should check the book. It's
very funny to read.
Speaker 2 (43:47):
How I Beat Gorman? And how do I get it
through Amazon?
Speaker 4 (43:51):
Or what Amazon? Do you take? My name?
Speaker 2 (43:54):
Excellent? PJ. Thank you so much for joining us. I
really appreciate it, and thank you for the introduction to
a fascinating gentleman and a really innovative company Ibex that
I'm I'm hopeful gets the money because I think this
is going to make us some important moves forward in
life and uh and health. And so Marata Crotchy, thank
you so much for joining us and telling us a
(44:15):
little about your your your product for malaria that is
right now killing six hundred thousand people a year, and
this product sounds like it could really solve that. And
also your product for factory colon cancer that that takes
the chemo payload and delivers it far more effectively, particularly
(44:36):
to two people that have got colon cancer, that that
come back five years later with the cancer all over again,
and really need your products. So thank you so much.
Ibex dot com is the website to go to, or
Brian at biocomb dot com got bio great, ibas bio.
I apologize, thanks for correcting me. That's our show for tonight.
(44:59):
I'm going to come back a couple of completing comments
in just a minute. Thanks very much. Everybody.
Speaker 1 (45:07):
Stream us live at SAGA nine to sixty am dot C.
Speaker 6 (45:22):
Talking back everyone to the brinkromby radio wire. So tonight
is six years that I've been doing this show. I
can't believe that it's been that long. It's been an
incredible opportunity. And I have been passionate to movie people
for a long period of time and also been passionate
but really getting to know people with in depth conversations.
Speaker 5 (45:40):
Some people who criticized me in the past.
Speaker 6 (45:41):
Today, I'd like to really sit down with people and
get to know what they're all about and not participate
in those really quick ten or fifteen or thirty second,
you know, quick shit handshakes.
Speaker 5 (45:52):
I'd like to sit down with people and get to
know what they're all about.
Speaker 6 (45:55):
And you've given me that opportunity, and so thank you
very much for that, and for those of you that
have tuned in and several occasions over the course of
the last the last six years, three thousand shows, over
two thousand interviewees. It's just been an incredible opportunity and
thank you for that. I'm on every night Monday through
Friday at six o'clock on nine to sixty AM. But
(46:15):
in addition to on average getting about thirty thousand listeners,
I have the opportunity to post on podcast servers on YouTube,
on social media. I get a lot of following on LinkedIn,
and I therefore get a breadth of exposure and people listening.
Speaker 5 (46:34):
To me, frankly, from around the world and from a lot.
Speaker 6 (46:36):
Of my different business contacts and political contacts and other
contacts really you know, across the Greater Toronto, Werry, across Canada,
across North America, across the world, and it is really
an incredible experience. I've been lucky enough to interview some
of my heroes in business and politics, from.
Speaker 5 (46:53):
Jim Pattison, David Peterson, John Torrey, Hayes mckellyan, the list
goes on, and it's been.
Speaker 6 (47:01):
A unique opportunity for me to spend fifty minutes with
interesting people.
Speaker 5 (47:04):
Asking them about their life, their career.
Speaker 6 (47:06):
I've interviewed business people, developers, people head of different associations
high tech biotech from France, from Israel, from Canada, from
the United States about their passion, their business, their scientific
develops and.
Speaker 5 (47:23):
Interest and that's been a huge opportunity for me to.
Speaker 6 (47:26):
Really delve into what makes these people excited about their business,
their prospects, their scientific inventions, etc.
Speaker 5 (47:34):
And that's been a great opportunity. I also get an
opportunity to rant and.
Speaker 6 (47:38):
Have been encouraged by my broadcaster to close my shows
and or open my shows with my own little rant
or my own five or seven or ten point plan
on how I would solve problems, so that you get
to know me and I get an opportunity to chat
about the things that I'm so passionate about. I ended
up talking about politics often earlier in the week, and
(48:01):
to our international affairs. I've been very interested obviously what's
going on in the Middle East, in Ukraine, and I've
been able to reach out to people that are very
knowledgeable in Ukraine, in Eastern Europe, in the Middle East,
and or people that are aware of it, former ambassadors
of the like, and really delve into what caused the problem,
what is causing the problem, what the potential solutions are,
(48:21):
and some of the more negative side of things in
regards to abductions, kidnappings, hostages.
Speaker 8 (48:30):
Right.
Speaker 5 (48:30):
And it's been.
Speaker 6 (48:32):
Fascinating for me the individuals that I get from key
from different parts of Israel that are willing to and
interested in talking to me.
Speaker 5 (48:40):
I've interviewed people from South Africa. I've interviewed people from China,
I've interviewed people from Japan. I've interviewed people from across
Canada and in the United States.
Speaker 2 (48:47):
And in France in the UK.
Speaker 6 (48:50):
From Ireland, I've ended up connecting up with some of
my long distance cousins that are in either Scotland or
Ireland and had the opportunity interviewed in them, as well
as some of my cousins from the United States as
well as across Canada.
Speaker 5 (49:06):
Later in the week. I haven't talked about arts or
lifestyle issues.
Speaker 6 (49:09):
I am passionate about that. I have been presidents of
the Mississiga Arts Council. I've been chair of the Mississiti
City Summit. I worked for the Walt Disney Company, not
necessarily in entertainment.
Speaker 5 (49:20):
I was doing amusement parks. I did movies at the TVs,
I did hotels, at the restaurants.
Speaker 6 (49:25):
But I really got exposed to the entertainment business and
loved it, and so I get the opportunity to delve
into that at a far greater degree. And I've also
been very interested in social capital and building communities. I've
started and got halfway through a doctoral thesis on social capital,
and so therefore it's a real pleasure of mine to
delve into some of these people that you know, some
people would call culches or lifestyle people and what they
(49:46):
think makes people take you know, you know, a professor
of empathy on several occasions that I just think is
fascinating people on happiness.
Speaker 5 (49:56):
That is obviously very interesting.
Speaker 6 (49:59):
And I I get to therefore interview people from all
walks of life, from across the world and come to
you every night and try to get my message and
my interviewees to you through radio, through podcasts, through video,
on social media and on YouTube. And it's an incredible experience.
And I get to listen to them all, synthesize what
(50:22):
they have to say, think about them in regards to
my own points of view, and turn around and give
you often my rent, my ten point plan.
Speaker 5 (50:32):
And it's an incredible opportunity.
Speaker 6 (50:33):
And for those of you that reach out and I
get comments every day, people recommending great topics, great interviews,
people criticizing some of the comments, people suggesting what new
topic I should be focused on, people trying to get on.
Speaker 5 (50:48):
My show, and it's an incredible opportunity.
Speaker 8 (50:50):
I really enjoy that opportunity to interact with you and
have the opportunity, if you're interested, get to know you
over fifty minutes of a very long, in depth conversation,
which I think is what we don't have enough of
in our world today.
Speaker 5 (51:05):
So thank you for the opportunity.
Speaker 6 (51:07):
To spend six years, five nights a week, over any
days that is fifty two times five, so over two
hundred days a year in chatting with you.
Speaker 5 (51:18):
I appreciate it.
Speaker 6 (51:19):
Thank you for listening, thank you for watching, thank you
for your participation, and thank you to starting at sixty
for the opportunity. It's a unique one and great one
one that I'm very very happy that I've had the
privilege to host, to interview, to spout my own point
of view and interact with.
Speaker 5 (51:39):
All the people. Thanks, good night, and to repeat.
Speaker 6 (51:42):
Which I often close my show by saying, I'm on
every night, five nights a week.
Speaker 5 (51:47):
I did a Friday I'm nine to.
Speaker 6 (51:48):
Sixty AM in stream online at Triple W, SAVY at
sixtym dot All my podcasts and the videos go up
on my website, Brian Promy dot com as soon as
the radio show goes to air, as well. I put
them on several different podcast servers, on YouTube, on LinkedIn, etcetera.
Speaker 5 (52:03):
So if you missed my show on the radio, you
can get me a whole bunch of otherways, thanks.
Speaker 1 (52:08):
For six years good Night, no Radio, no problem. Stream
is live on SAGA nine sixty am dot c a
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