January 8, 2025 • 28 mins
In this week's episode of BioTech Nation, Dr. David Bearss, President and CEO of Halia Therapeutics, discusses inflammation and its reduction over a lifetime and in response to various incidents. He unveils the inflammasome, a recently discovered protein complex critical in regulating inflammatory responses and its potential in treating chronic diseases like myelodysplastic syndrome and Alzheimer's. Dr. Bearss shares insights into Halia's groundbreaking approach and his relentless pursuit of medical breakthroughs.
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Episode Transcript
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Dr. Moira Gunn (00:11):
Today on Tech Nation, we're talking about
inflammation, how it's there,and how we know it's being
reduced both over a lifetime andin response to the accidents and
incidents of living. DoctorDavid Bearss is the president
and CEO of Halia Therapeutics.And now, doctor David Beers.
(00:33):
Doctor Bearss, welcome to theprogram.
Dr. David Bearss (00:35):
Well, I'm excited to be here. Thank you.
Dr. Moira Gunn (00:37):
Now everyone is wary of inflammation, whether
it's in their joints, in theirgums, in wounds, anywhere in
their body. And you talk aboutthe inflammasome. That's like
inflammation, but it ends withzone, s o m e. What is the
inflammasome?
Dr. David Bearss (00:56):
Yeah. The the inflammasome is a a large
protein complex that formsinside of specific types of
cells in our body that regulatesthe immune inflammatory
response. And it's something,you know, I'm a cell biologist.
I have a PhD in cell biology andyou know, I've taught cell
biology at large, universitiesand I never have taught anybody
(01:19):
about this because it's a fairlynew discovery. We actually
didn't know this thing existedinside of ourselves until just a
few years ago, but it's, a we'restarting to find out that this
plays a major role in regulatingnot just not just the normal
healthy inflammation, but thekind of inflammation that that
is now associated with, a lot ofof chronic diseases and we call
(01:43):
it chronic inflammation.
Dr. Moira Gunn (01:45):
Now the inflammasome is part of, at
least, what it's made up of arethe red blood cells and the
white blood cells that we have.Right? Those are all together?
Dr. David Bearss (01:55):
That's that's correct. Yeah. So the the immune
cells are our white blood cellsin our body, and so so when we
produce immune, white bloodcells, they they can react to
different signals and canpropagate a signaling to say to
other cells, there's a problemhere. It's time to come and fix
this thing. And so that's partof our immune system is
constantly looking for what wecall danger or damage signals
(02:18):
that that tell the immune systemthere's a problem and when they
see that, certain immune cellswill activate this complex of
proteins that will then ask formore help to come to say more
more of these immune cells needto come here and need to fix
whatever whatever is wrong.
So so there's a there's aninterplay between all of our
blood cells and how they howthey get affected. So our blood
(02:41):
cells are all produced in ourbone marrow, and our bone marrow
is inside it's a tissue thatlives inside of our bones, and
it's maybe the hardest workingtissue in our body. It it it
replenishes all of our blood,both our red blood cells and
white blood cells, and even ourplatelets, which are are
involved in clotting. Itreplenishes those every single
(03:02):
day of our lives. So we'reconstantly turning over these
cells.
And so there's this thisinterplay, this connection in
interaction between red bloodcells, white blood cells,
platelets, all communicatingwith each other. And it's
remarkable that this this worksreally, really well for most of
our life. But just likeeverything, it's impacted, by
(03:25):
inflammation. It's impacted byas we age, it's impacted by our
aging as well.
Dr. Moira Gunn (03:31):
Now tell me what happens as you age.
Dr. David Bearss (03:33):
Yeah. So, you know, I think all of us,
especially, you know, as we getolder, But when we but when we
put a bunch of cells together inan organism, we we see that
every organism that that liveson the earth will age. And our
(03:54):
tissues you know, we used tothink that aging was just our
tissues got tired. They theythey just ran out of juice to be
able to do what they weresupposed to do and they quit
functioning properly. But agingis quite interesting and we've
learned a lot about it and oneof the areas that I've been
focused on is what happens toyour blood cells as you age.
So as I mentioned, our bonemarrow is a hardworking tissue.
(04:18):
It's turning over red bloodcells and white blood cells
every day of our life and, youknow, we used to think, oh, it
just runs out of gas as we getolder. It's not it's not as good
as it used to be. But what we'vediscovered is as we accumulate
damage over our lifetime, youknow, we we these bodies of ours
accumulate all kinds of of wearand tear. You know?
(04:39):
We we can feel it as we age. Ourour joints don't work as well as
they used to. Our and our andour bone marrow has the same
thing happening inside of it. Soso there are these signals that
I talked about, these thesedanger and damage signals that
tell our immune system there's aproblem here. And as we
accumulate that damage over ourlifetime, we start to see kind
of this this low smolderinginflammation.
(05:03):
So what we've discovered is thatwhen you're young, your red
blood cells and your white bloodcells are produced by a lot of
cells in your bone marrow. Youhave these cells called
progenitor cells, or we callthem stem cells sometimes, and
those cells are producing all ofyour blood cells. And when
you're young, there's lots ofthose kinds of progenitor stem
cells making all of your blood.As you get older, you start to
(05:26):
see that one clone, one singleprogenitor cell line inside your
blood is producing most of yourblood. And that that's
remarkable when we first, as ascientific community, when we
first discovered that a fewyears ago, it was just kind of
an oddity.
We said, oh, that's kinda weird.You know, why why does why does
one cell take over as we getolder? But what we've discovered
(05:48):
now is it is a part of the agingprocess that seems to be
predisposing us to a lot ofother other conditions. So when
we're young, our bone marrow'shealthy. It's producing lots of
blood cells from lots ofdifferent stem cells.
As we get older, one particularclone seems to take over and
produce most of our blood. Andwhat we've discovered is that
(06:11):
those clones are not normal. Andas we age, we start to see
accumulation of mutations. Andwhen you have mutations in blood
cells, they're not acting like anormal, healthy blood cell
should act and so we're we'restarting to ask the question,
what does that mean? What doesthat mean to human diseases?
Is there something significantabout that? And I think we can
(06:32):
say definitively there issomething significant about it.
It's having mutated blood cellsis not a positive thing. And as
we get older, we have more andmore of them.
Dr. Moira Gunn (06:41):
Now at any age, if there's a problem with those
cells that produce the the redand the white blood cells, you
have a problem. You have amedical condition. What would be
something we're familiar with?
Dr. David Bearss (06:56):
Yeah. So if you can't make blood cells, you
know, I think the most familiarthing to everybody is the word
anemia. And anemia just meansyou don't well, anemia means
you're you you have a deficiencyin red blood cells. So you're
not able to either produceenough red blood cells or
functionally, you're not able toto to make functional red blood
cells. So that's, you know, inanemia, we we we all probably
(07:19):
experience anemia at some pointin time in our life.
Women are more susceptible toit, than and children are
actually quite susceptible toit. But but I think all of us
are familiar with anemia. Andanemia, there's there's a lot of
causes. But as we've started tolook at it, we've realized that
that inflammation in our bonemarrow is one of the main causes
(07:40):
and drivers of anemia. So whenyou get inflammation, this
inflammatory signaling in yourbone marrow, it prevents the
differentiation of these stemcells into red blood cells.
And so we we can see a bigpercentage of the world's
population. We're talking aboutbillions of people, not not
millions, but literally billionsof people every year suffer from
(08:02):
anemia, and a good portion ofthat is connected to
inflammation.
Dr. Moira Gunn (08:06):
Now I have to say there's no doubt that you
really want this to be workingwell.
Dr. David Bearss (08:12):
That's right.
Dr. Moira Gunn (08:13):
And all kinds of things could cause it to not be
working well. And when itdoesn't, you know, it's related
to inflammation, andinflammation drives so many
things. But let's look at whatHalleah Therapeutics is focusing
on. What are you focusing on inthe inflammasome?
Dr. David Bearss (08:30):
So we discovered a few years ago that
the inflammasome, this bigprotein complex in your cells,
needs a lot of differentcomponents to come together at
the right place and the righttime to do what it's it does.
And we we discovered that thisgets messed up in different
diseases, and that's wherechronic inflammation that's
that's where it starts. So wediscovered a way to turn it off
(08:53):
by blocking the assembly of thiscomplex. And so we we have a
little drug that we we wedesigned. We actually designed
it on a computer.
We we used what's calledstructure based drug design. So
we we solved the structure ofthis protein that's part of the
inflammasome, and we designed adrug to go in and bind to this
this site on this protein thatblocks its ability to to form
(09:17):
this big complex. And when we dothat, we can show that that we
can dampen the signaling thatcomes from the inflammasome. And
in fact, even cells that havehad this this complex formed, we
can watch that complex go away.And so, you know, it's a general
mechanism that's associated withchronic inflammation.
And so, you know, when wediscovered this, we said, wow,
(09:39):
you know, what can we do withthis? Where is this important?
You know, where should we tryit? And, you know, because of my
background and things that I'veworked on in the past, I knew
that there was this veryspecific bone marrow disease
called myelodysplastic syndromeor MDS. So MDS is is a type of
leukemia that's that's containedin your bone marrow.
(10:02):
And, we know that it iscompletely dependent upon this
pathway, the inflammasome, to toactually form MDS and to
maintain MDS. And so it's adriver of this disease. So I
called some of my friends thatare experts in this area, some
doctors that treat thesepatients, and I said, what if I
had a way that I could turn thisthing off? Do you think that we
(10:25):
could look at that in humanpatients? And so we designed a
clinical trial where we couldtake MDS patients.
And right now, the way that wetreat MDS, by the way, is these,
these patients, they becausethey have such strong
inflammation happening in theirbone marrow, their bone marrow
cannot make red blood cells, andthey can't make good red white
(10:46):
blood cells. And so what whathappens is we call it a bone
marrow failure. So the bonemarrow just doesn't do what it's
supposed to do. And the best waythat we can treat it early on is
we just give peopletransfusions. So they come in,
they're very anemic, they feelterrible, and so we just give
them blood.
And and you can imagine that'sthat's not a great way to live
your life, having to come inevery week and get a
(11:07):
transfusion. Some of these someof these people, that's what
they have to do.
Dr. Moira Gunn (11:10):
So you're actually giving them red blood
cells and white blood cells eventhough they didn't create them
themselves.
Dr. David Bearss (11:17):
Exactly. So so we we just say, well, they can't
make them, so let's just givethem from somebody else. And so
that's that's kind of how we'rewe're trying to treat the
disease. It doesn't get at thecore of the disease. Right?
So that's not a really, aneffective therapy because we're
just trying to replace one ofthe problems. But but the real
problem, the driver of thisdisease happens in their bone
(11:38):
marrow, and it's driven byinflammation. So, obviously, we
studied it in the lab and wesaid, well, what would happen if
we treat it with our drug in amodel of this? And what we saw
was we could actuallydifferentiate. So we could take
marrow, bone marrow, and, youknow, we just stick a needle
into the into usually into thehip, the hip bone of of
somebody, and we pull out someof their marrow, and we can grow
(12:00):
them in the lab.
And so patients that have MDS,we can show that they're not
producing red blood cells andthey're not producing white
blood cells. And then we treatwith our drug and and we start
to see they're starting todifferentiate, and we can see
that they can move past thatblock that happened because of
inflammation. So that got usvery excited. And so, obviously,
(12:20):
we had to jump through all ofthe the experiments that need to
be done to get this ready to gointo people. But we, we're
actually treating real peoplewith this disease now.
We're asking the question, whatdoes this do, to their their,
ability to make red blood cellsif we can turn off inflammation
in their blood? And so we'rewe're excited about where we're
(12:40):
at. We just launched this studya couple months ago. And so we
hope by the end of this year, wecan release some data and say
this actually has an impact onon this disease. And by getting
rid of inflammation, we can wecan actually restore the body's
ability to produce, red redblood cells and white blood
cells normally again.
Dr. Moira Gunn (13:00):
So it's almost as if they still have the
capability to produce the redand white blood cells. But the
structure of the inflammasome,as it gets going, it stops it.
It counteracts it.
Dr. David Bearss (13:13):
That's exactly right. So so it's it basically
arrests these cells. So if youthink about a stem cell, that's
an undifferentiated cell. Itjust it can become all kinds of
things that So there's a commonprogenitor cell in your bone
marrow that can turn into whiteblood cells and red blood cells
(13:36):
and platelets. And when youinduce this inflammasome and
cause this inflammation, itstops it from being able to do
that.
So if I can take that away, allof a sudden, we start to see the
ability of these cells todifferentiate into red blood
cells and white blood cells andplatelets.
Dr. Moira Gunn (13:51):
Couple interesting stories here. One is
that so many of us have hadsurgeries. Small surgeries,
large surgeries, and around thewound and in our bodies, there's
inflammation. There's been aninsult to your body. Is that the
same kind of inflammation?
Is that affected by this?
Dr. David Bearss (14:09):
Yeah. So it's interesting. The the
inflammation that is triggeredby a surgery, your body sees
that as the same kind of damageresponse that it would if you,
you know, broke your leg or youcut your finger. And so so, you
know, obviously, we're going inand we're trying to excise out
or trying to fix somethingthat's wrong with a surgery, but
(14:30):
we induce all this information.And we used to think, you know,
back in the old days, 20, 30years ago, the old days are
scientifically Yeah.
That that that thatinflammation, that might be
really good. Right? I mean,there because your body's
responding to it and it's partof the healthy response to a
injury or an infection. But whatwe've discovered is is that most
(14:52):
of the inflammation after aprocedure is actually not
helping with the healingprocess. So so it actually, by
turning on this inflammasome,which is exactly what you do
when you have when you cause,damage, you're actually
preventing the healing process.
And that's why we try to, youknow, put ice on on you know,
when we have an injury is we tryto stop the the immune response
(15:15):
that's happening, and we take,you know, drugs like
nonsteroidal anti inflammatoriesor other types of drugs that
we've had available to us, butnone of those drugs will turn
off the inflammasome. And so sowe're we're just trying to stop
some of the downstream signalingthat comes. But until now, we've
never had something that couldturn off the real driver of the
(15:37):
inflammatory response. And sowe're super excited about the
idea. What happens if we justturn that thing off?
What if we stop it? Could weheal faster? And what we've seen
in the lab is it certainly lookslike we can. So we can go in and
do, you know, surgicalprocedures in the laboratory and
show that we can see healing isactually faster when you turn
(15:58):
off this this inflammasomesignaling.
Dr. Moira Gunn (16:00):
Now we're gonna try that in humans?
Dr. David Bearss (16:04):
Absolutely. That was like, you
Dr. Moira Gunn (16:05):
should be silent anytime
Dr. David Bearss (16:09):
soon. That's right. So in fact, as we're
we're recording this right now,we're we're actually treating
people today. We just got thefirst go ahead to treat some
people to see what happens postprocedure. And the the the the
nice thing about this is we canactually watch what happens in
their blood.
So after you have a a procedure,after you have a surgery done,
(16:31):
you will see induction ofinflammatory signaling in your
blood. You can actually monitorthat. So you'll see these
signals go up and we can seewhat happens. So what we're
doing is is we're seeing withwith patients, what happens
after their surgery when wedon't give them their therapy to
target the inflammasome and thenwhat happens when we give them
therapy to target theinflammasome and we see how
(16:54):
different that inflammatoryresponse is. And the nice thing
from a drug developmentstandpoint is that's a pretty
short study.
We we you know, we have acaptured population of people
that are having a procedure andthen we we watch just over the
course of a week what happens totheir inflammation. And so it it
can we can get a readout very,very quickly, which is exciting
(17:15):
for us because sometimes we wedesign clinical studies that
take literally years to figureout what's going on. In this
case, we we we hope that we cansee a signal very, very quickly.
Dr. Moira Gunn (17:25):
Now what are the first surgeries you're looking
at?
Dr. David Bearss (17:28):
So we have a very interesting, situation that
that exists where we arelocated. So we're our
headquarters is is in in Utah,right south of Salt Lake City.
And so the first surgeries thatwe're doing are actually
connected to where we're at inUtah. So So we have a population
of, young individuals that thatare, headed out as missionaries
(17:52):
for the, Church of Jesus Christof Latter day Saints or the
Mormon Church. And all of thosemissionaries that are going out,
they all have to have dentalexams and and they need to have
their wisdom teeth removed.
Dr. Moira Gunn (18:04):
Whether there's a problem or not.
Dr. David Bearss (18:05):
Whether there's a problem or not.
Dr. Moira Gunn (18:08):
We we can't handle this if there's a problem
when you're somewhere in theworld.
Dr. David Bearss (18:12):
That's right. We send them all over the world.
They go all over the place. Andso it was just decided that
prophylactically, it's a goodidea to take your wisdom teeth
out because for a young healthyperson, it's one of the things
that can actually cause acomplication if they're in
wherever, in Africa or, youknow, where you know, wherever.
We send them all over the place.
So so, what we decided and wedesigned this study to to ask
(18:36):
the question, well, when youwhen you pull your your 3rd
molars or your wisdom teeth out,you actually cause not just the
local inflammation in your jawwhere you pull that tooth out,
but it actually causes asystemic inflammatory response.
You activate that inflammasomeand your whole body says, hey.
We've got a problem here. Sowe're we're actually doing in in
(18:56):
literally today, we're we'rewe're dosing patients where we
can see what happens if weextract this tooth and we and we
turn off the inflammasome. Whathappens to the the signaling for
inflammation?
And the implications here arebig. So if we can show that we
can block by blocking theinflammasome, we can block that
systemic inflammatory response.We hope that leads to faster
(19:18):
recovery after a surgery bysuppressing inflammation. So we
can we we already know that thatif you can get back to work and
get back to, you know, activityquickly after surgery, your your
outcomes do are better. If youfeel lousy and you're just
laying around for a while, youactually do worse.
And so trying to get people backand and recover quickly is is a
(19:40):
really important important partof the recovery from, surgeries.
And inflammation plays a bigrole in people not feeling like
they they can get back and andget back to normal activity. So
so if it works there, the nextstep is, let's see where else it
works. Does it work in in, youknow, in in some of the standard
places that we look is bunionsurgery, tummy tuck surgery.
(20:03):
Those are those are also veryvery captured populations, but
but even, you know, in kneereplacements and hip
replacements and very commonsurgeries that we have all the
time.
We know that this pathway isactivated, and we're very, very
interested to see if we can wecan help people recover faster
by turning off that information.
Dr. Moira Gunn (20:23):
Well, I mispronounced the name of your
company when we first met. Isaid Halia, h a l I a. And I was
like, no. It's it's Halia, whichis which is Hawaiian. You guys
are all over the place.
Okay. How do you how did we getthis name halia?
Dr. David Bearss (20:40):
Yeah. Yeah. You know, I, it's, myself and,
one of our cofounders, aHawaiian scientist, and there's
not many scientists from Hawaii.So he's kind of a he's he's kind
of a unique individual, but, hisname is Keoni Kawe. And so Keoni
and I, got together to startCALIA with the idea that that we
(21:03):
could target inflammation in thebrain.
And we actually, discovered thisin a very interesting way. So,
Keone is a human geneticist. Sohe studies risk factors based
off of our genetics. So he looksat variations in in genes and
and what that does to risk fordifferent diseases. So he's
(21:23):
looking for, you know, the theplaces in our DNA where we have
differences and how that thatthat is correlated with our risk
for developing differentdiseases.
And his specific interest hasbeen in neurodegenerative
diseases like Alzheimer's. Andso he came to me and said, hey,
I discovered something reallyinteresting. So there's there's
(21:44):
a a very well known risk factorfor Alzheimer's disease. It's
called the APOE4, and it's ait's a polymorphism and you I
guess you call it a mutation,but it's a it's a it's a
different DNA sequence in thisgene called APOE. And if you
have this this flavor of thatthat, that gene, your risk for
Alzheimer's is quite high,relative to the rest of the
(22:07):
population.
So he was studying this, and heactually found a family. And
once again, it comes back toUtah. We we we have large
families in Utah usually. And hefound a family in Utah that had
this polymorphism, the APOE 4.But no nobody in their history,
their medical history, and theirfamily, nobody got Alzheimer's
disease.
So he actually organized afamily reunion, got all those
(22:32):
people to come, and and, theythey all consented to be studied
to see why with this thisgenetics that should should
predispose them to Alzheimer's,why none of them got
Alzheimer's. And so we were ableto sequence all we sequence over
200 individuals in this family.And we discovered they had
another unique DNA, very orpolymorphism or mutation that
(22:56):
actually looked like it wasassociated with preventing
Alzheimer's. And so when westarted the company, the whole
goal of the company was tofigure out, well, what does this
do? And we started the the thename of the company, Halea, is a
Hawaiian name that means fondmemories.
And so we started with the ideathat that, we could we could
target Alzheimer's. And in fact,we haven't given up on that. In
(23:18):
fact, very, very soon, we shouldbe, announcing that with our
second drug that we're movinginto the clinic is, is actually
targeting this exact pathwaythat we discovered and trying to
replicate what we discoveredgenetically in this family with
a new drug that can have thesame kind of activity. And in
fact, it right comes right backdown to inflammation as well. So
(23:40):
what we discovered is thisfamily has a mutation.
We call it a resilience mutationbecause they're resilient to a
lot of things. They they haveless heart disease. They have
less cancer. They have lessAlzheimer's. And it's
interesting that it's due totheir ability to have lower
response to inflammation.
So we're excited about, the ideathat we can take a genetic
(24:03):
discovery and translate thatinto something that we could
actually use as a therapeutic.
Dr. Moira Gunn (24:07):
You know, here we have Dave Beers, you know,
drug hunter. Drug discoverer,doctor Beers. Very impressive.
And I do have a question foryou, along these lines. I mean,
you have founded 8 biotechcompanies.
You've discovered many drugs. 16of those drugs have actually
(24:27):
moved into human clinicaltrials. Then I have to tell you,
that's an impressive record. Howis your current experience with
Halea the same, and how is itdifferent from your earlier
experience?
Dr. David Bearss (24:41):
Yeah. It's, you know, it's been it's it's
been an amazing career for me. II I love what I do. I get up
every morning thinking todaycould be the day we make a
discovery that changes the worldand and, you know, that's that's
not hyperbole. That's real.
Right? I mean, we can actuallyfind things that that change,
(25:01):
diseases in people, and that'sjust amazing to me. So so when I
first started, I was very naivein terms of of starting a
company. And and and really mymotivation to start a company is
I discovered I was a professor.I was, you know, in in the lab,
you know, doing research there,and and we discovered something
that we thought could be a newtherapy that could could help
(25:22):
people.
And I went to a mentor of minethat that, I learned a lot from
and and said to him, well, howdo I how do I take this from my
lab and turn it into somethingthat could help people? And he
said, well, you're probably theonly person in the world that's
gonna believe in this. And so ifif you wanna see it move
forward, you probably need to doit yourself. And so I actually
(25:43):
took the leap and and just said,okay. I walked away from a
tenure track faculty position ata major research university and
just decided I'm gonna start alittle company.
And I barely even knew what a aa stock was, a share in a
company. I hardly knew any ofthat. But thankfully, I I had a
great partner that that, helpedme, put together the first
(26:05):
company. But, you know, I had noidea how hard it was to raise
the money and to to go throughall the process of of, getting
the, supporting information toshow that the the drug could
could actually be safe andpotentially effective in people.
And so I guess what's differentabout Halia is that I had 7
(26:26):
other tries to learn a lot ofstuff that that, and make every
mistake that you can make.
And, hopefully, I'm not makingvery many anymore. But, I tell
people all the time, I, youknow, I I earned all the white
hair that I have because I, I'veI've probably made every mistake
that you can. But but what'skept me going is, you know, I I
really wanna make a differencein people's lives. I I lost my
(26:49):
grandfather the year I was born.Never had a relationship with
him.
Didn't don't know him. I haveone picture of me as a baby with
him holding me, and that's it.That's all I know about him. And
I lost my mom when when, whenstill when she was young, both
of cancer. And, I just decided,you know what?
If I can spend my life and makeit so other people's moms and
(27:12):
grandpas can be around a littlelonger, that's not a bad life to
live. And so so for me, that'swhat keeps me going every day is
is can I make a discovery thatcan keep people's grandmas and
grandpas and moms and dadsaround a little longer? And and,
you know, it's it's it's it'samazing to me that that, you
know, we've been able to to towork on projects that that, you
(27:35):
know, are now approved drugs,things that that people use, and
they have extended the life ofpeople. But it's, it's never
enough for me. I'd I I wannahave number 17, 18, 19, 20, you
know, to keep finding findingthe next one.
So, I I'm not gonna stop.
Dr. Moira Gunn (27:53):
Doctor Behar, I'm thrilled that you're not
gonna stop, personally.
Dr. David Bearss (27:57):
Thank you.
Dr. Moira Gunn (27:59):
I wanna thank you so much for coming on. I
hope you come back, visit usagain.
Dr. David Bearss (28:03):
I I'd love to. I'd love to tell you the the you
know, when we get some results,show you what's happened and and
what the next big thing is.
Dr. Moira Gunn (28:10):
You're on. You're on. Thanks again.
Dr. David Bearss (28:12):
Thanks a lot.
Dr. Moira Gunn (28:13):
Doctor David Bearss is the cofounder,
president, and CEO of HaliaTherapeutics. More information
is available at haliatx dotcom.That's haliatx.com.
Today on Tech Nation, we're talking about
inflammation, how it's there,and how we know it's being
reduced both over a lifetime andin response to the accidents and
incidents of living. DoctorDavid Bearss is the president
and CEO of Halia Therapeutics.And now, doctor David Beers.
(00:33):
Doctor Bearss, welcome to theprogram.
Dr. David Bearss (00:35):
Well, I'm excited to be here. Thank you.
Dr. Moira Gunn (00:37):
Now everyone is wary of inflammation, whether
it's in their joints, in theirgums, in wounds, anywhere in
their body. And you talk aboutthe inflammasome. That's like
inflammation, but it ends withzone, s o m e. What is the
inflammasome?
Dr. David Bearss (00:56):
Yeah. The the inflammasome is a a large
protein complex that formsinside of specific types of
cells in our body that regulatesthe immune inflammatory
response. And it's something,you know, I'm a cell biologist.
I have a PhD in cell biology andyou know, I've taught cell
biology at large, universitiesand I never have taught anybody
(01:19):
about this because it's a fairlynew discovery. We actually
didn't know this thing existedinside of ourselves until just a
few years ago, but it's, a we'restarting to find out that this
plays a major role in regulatingnot just not just the normal
healthy inflammation, but thekind of inflammation that that
is now associated with, a lot ofof chronic diseases and we call
(01:43):
it chronic inflammation.
Dr. Moira Gunn (01:45):
Now the inflammasome is part of, at
least, what it's made up of arethe red blood cells and the
white blood cells that we have.Right? Those are all together?
Dr. David Bearss (01:55):
That's that's correct. Yeah. So the the immune
cells are our white blood cellsin our body, and so so when we
produce immune, white bloodcells, they they can react to
different signals and canpropagate a signaling to say to
other cells, there's a problemhere. It's time to come and fix
this thing. And so that's partof our immune system is
constantly looking for what wecall danger or damage signals
(02:18):
that that tell the immune systemthere's a problem and when they
see that, certain immune cellswill activate this complex of
proteins that will then ask formore help to come to say more
more of these immune cells needto come here and need to fix
whatever whatever is wrong.
So so there's a there's aninterplay between all of our
blood cells and how they howthey get affected. So our blood
(02:41):
cells are all produced in ourbone marrow, and our bone marrow
is inside it's a tissue thatlives inside of our bones, and
it's maybe the hardest workingtissue in our body. It it it
replenishes all of our blood,both our red blood cells and
white blood cells, and even ourplatelets, which are are
involved in clotting. Itreplenishes those every single
(03:02):
day of our lives. So we'reconstantly turning over these
cells.
And so there's this thisinterplay, this connection in
interaction between red bloodcells, white blood cells,
platelets, all communicatingwith each other. And it's
remarkable that this this worksreally, really well for most of
our life. But just likeeverything, it's impacted, by
(03:25):
inflammation. It's impacted byas we age, it's impacted by our
aging as well.
Dr. Moira Gunn (03:31):
Now tell me what happens as you age.
Dr. David Bearss (03:33):
Yeah. So, you know, I think all of us,
especially, you know, as we getolder, But when we but when we
put a bunch of cells together inan organism, we we see that
every organism that that liveson the earth will age. And our
(03:54):
tissues you know, we used tothink that aging was just our
tissues got tired. They theythey just ran out of juice to be
able to do what they weresupposed to do and they quit
functioning properly. But agingis quite interesting and we've
learned a lot about it and oneof the areas that I've been
focused on is what happens toyour blood cells as you age.
So as I mentioned, our bonemarrow is a hardworking tissue.
(04:18):
It's turning over red bloodcells and white blood cells
every day of our life and, youknow, we used to think, oh, it
just runs out of gas as we getolder. It's not it's not as good
as it used to be. But what we'vediscovered is as we accumulate
damage over our lifetime, youknow, we we these bodies of ours
accumulate all kinds of of wearand tear. You know?
(04:39):
We we can feel it as we age. Ourour joints don't work as well as
they used to. Our and our andour bone marrow has the same
thing happening inside of it. Soso there are these signals that
I talked about, these thesedanger and damage signals that
tell our immune system there's aproblem here. And as we
accumulate that damage over ourlifetime, we start to see kind
of this this low smolderinginflammation.
(05:03):
So what we've discovered is thatwhen you're young, your red
blood cells and your white bloodcells are produced by a lot of
cells in your bone marrow. Youhave these cells called
progenitor cells, or we callthem stem cells sometimes, and
those cells are producing all ofyour blood cells. And when
you're young, there's lots ofthose kinds of progenitor stem
cells making all of your blood.As you get older, you start to
(05:26):
see that one clone, one singleprogenitor cell line inside your
blood is producing most of yourblood. And that that's
remarkable when we first, as ascientific community, when we
first discovered that a fewyears ago, it was just kind of
an oddity.
We said, oh, that's kinda weird.You know, why why does why does
one cell take over as we getolder? But what we've discovered
(05:48):
now is it is a part of the agingprocess that seems to be
predisposing us to a lot ofother other conditions. So when
we're young, our bone marrow'shealthy. It's producing lots of
blood cells from lots ofdifferent stem cells.
As we get older, one particularclone seems to take over and
produce most of our blood. Andwhat we've discovered is that
(06:11):
those clones are not normal. Andas we age, we start to see
accumulation of mutations. Andwhen you have mutations in blood
cells, they're not acting like anormal, healthy blood cell
should act and so we're we'restarting to ask the question,
what does that mean? What doesthat mean to human diseases?
Is there something significantabout that? And I think we can
(06:32):
say definitively there issomething significant about it.
It's having mutated blood cellsis not a positive thing. And as
we get older, we have more andmore of them.
Dr. Moira Gunn (06:41):
Now at any age, if there's a problem with those
cells that produce the the redand the white blood cells, you
have a problem. You have amedical condition. What would be
something we're familiar with?
Dr. David Bearss (06:56):
Yeah. So if you can't make blood cells, you
know, I think the most familiarthing to everybody is the word
anemia. And anemia just meansyou don't well, anemia means
you're you you have a deficiencyin red blood cells. So you're
not able to either produceenough red blood cells or
functionally, you're not able toto to make functional red blood
cells. So that's, you know, inanemia, we we we all probably
(07:19):
experience anemia at some pointin time in our life.
Women are more susceptible toit, than and children are
actually quite susceptible toit. But but I think all of us
are familiar with anemia. Andanemia, there's there's a lot of
causes. But as we've started tolook at it, we've realized that
that inflammation in our bonemarrow is one of the main causes
(07:40):
and drivers of anemia. So whenyou get inflammation, this
inflammatory signaling in yourbone marrow, it prevents the
differentiation of these stemcells into red blood cells.
And so we we can see a bigpercentage of the world's
population. We're talking aboutbillions of people, not not
millions, but literally billionsof people every year suffer from
(08:02):
anemia, and a good portion ofthat is connected to
inflammation.
Dr. Moira Gunn (08:06):
Now I have to say there's no doubt that you
really want this to be workingwell.
Dr. David Bearss (08:12):
That's right.
Dr. Moira Gunn (08:13):
And all kinds of things could cause it to not be
working well. And when itdoesn't, you know, it's related
to inflammation, andinflammation drives so many
things. But let's look at whatHalleah Therapeutics is focusing
on. What are you focusing on inthe inflammasome?
Dr. David Bearss (08:30):
So we discovered a few years ago that
the inflammasome, this bigprotein complex in your cells,
needs a lot of differentcomponents to come together at
the right place and the righttime to do what it's it does.
And we we discovered that thisgets messed up in different
diseases, and that's wherechronic inflammation that's
that's where it starts. So wediscovered a way to turn it off
(08:53):
by blocking the assembly of thiscomplex. And so we we have a
little drug that we we wedesigned. We actually designed
it on a computer.
We we used what's calledstructure based drug design. So
we we solved the structure ofthis protein that's part of the
inflammasome, and we designed adrug to go in and bind to this
this site on this protein thatblocks its ability to to form
(09:17):
this big complex. And when we dothat, we can show that that we
can dampen the signaling thatcomes from the inflammasome. And
in fact, even cells that havehad this this complex formed, we
can watch that complex go away.And so, you know, it's a general
mechanism that's associated withchronic inflammation.
And so, you know, when wediscovered this, we said, wow,
(09:39):
you know, what can we do withthis? Where is this important?
You know, where should we tryit? And, you know, because of my
background and things that I'veworked on in the past, I knew
that there was this veryspecific bone marrow disease
called myelodysplastic syndromeor MDS. So MDS is is a type of
leukemia that's that's containedin your bone marrow.
(10:02):
And, we know that it iscompletely dependent upon this
pathway, the inflammasome, to toactually form MDS and to
maintain MDS. And so it's adriver of this disease. So I
called some of my friends thatare experts in this area, some
doctors that treat thesepatients, and I said, what if I
had a way that I could turn thisthing off? Do you think that we
(10:25):
could look at that in humanpatients? And so we designed a
clinical trial where we couldtake MDS patients.
And right now, the way that wetreat MDS, by the way, is these,
these patients, they becausethey have such strong
inflammation happening in theirbone marrow, their bone marrow
cannot make red blood cells, andthey can't make good red white
(10:46):
blood cells. And so what whathappens is we call it a bone
marrow failure. So the bonemarrow just doesn't do what it's
supposed to do. And the best waythat we can treat it early on is
we just give peopletransfusions. So they come in,
they're very anemic, they feelterrible, and so we just give
them blood.
And and you can imagine that'sthat's not a great way to live
your life, having to come inevery week and get a
(11:07):
transfusion. Some of these someof these people, that's what
they have to do.
Dr. Moira Gunn (11:10):
So you're actually giving them red blood
cells and white blood cells eventhough they didn't create them
themselves.
Dr. David Bearss (11:17):
Exactly. So so we we just say, well, they can't
make them, so let's just givethem from somebody else. And so
that's that's kind of how we'rewe're trying to treat the
disease. It doesn't get at thecore of the disease. Right?
So that's not a really, aneffective therapy because we're
just trying to replace one ofthe problems. But but the real
problem, the driver of thisdisease happens in their bone
(11:38):
marrow, and it's driven byinflammation. So, obviously, we
studied it in the lab and wesaid, well, what would happen if
we treat it with our drug in amodel of this? And what we saw
was we could actuallydifferentiate. So we could take
marrow, bone marrow, and, youknow, we just stick a needle
into the into usually into thehip, the hip bone of of
somebody, and we pull out someof their marrow, and we can grow
(12:00):
them in the lab.
And so patients that have MDS,we can show that they're not
producing red blood cells andthey're not producing white
blood cells. And then we treatwith our drug and and we start
to see they're starting todifferentiate, and we can see
that they can move past thatblock that happened because of
inflammation. So that got usvery excited. And so, obviously,
(12:20):
we had to jump through all ofthe the experiments that need to
be done to get this ready to gointo people. But we, we're
actually treating real peoplewith this disease now.
We're asking the question, whatdoes this do, to their their,
ability to make red blood cellsif we can turn off inflammation
in their blood? And so we'rewe're excited about where we're
(12:40):
at. We just launched this studya couple months ago. And so we
hope by the end of this year, wecan release some data and say
this actually has an impact onon this disease. And by getting
rid of inflammation, we can wecan actually restore the body's
ability to produce, red redblood cells and white blood
cells normally again.
Dr. Moira Gunn (13:00):
So it's almost as if they still have the
capability to produce the redand white blood cells. But the
structure of the inflammasome,as it gets going, it stops it.
It counteracts it.
Dr. David Bearss (13:13):
That's exactly right. So so it's it basically
arrests these cells. So if youthink about a stem cell, that's
an undifferentiated cell. Itjust it can become all kinds of
things that So there's a commonprogenitor cell in your bone
marrow that can turn into whiteblood cells and red blood cells
(13:36):
and platelets. And when youinduce this inflammasome and
cause this inflammation, itstops it from being able to do
that.
So if I can take that away, allof a sudden, we start to see the
ability of these cells todifferentiate into red blood
cells and white blood cells andplatelets.
Dr. Moira Gunn (13:51):
Couple interesting stories here. One is
that so many of us have hadsurgeries. Small surgeries,
large surgeries, and around thewound and in our bodies, there's
inflammation. There's been aninsult to your body. Is that the
same kind of inflammation?
Is that affected by this?
Dr. David Bearss (14:09):
Yeah. So it's interesting. The the
inflammation that is triggeredby a surgery, your body sees
that as the same kind of damageresponse that it would if you,
you know, broke your leg or youcut your finger. And so so, you
know, obviously, we're going inand we're trying to excise out
or trying to fix somethingthat's wrong with a surgery, but
(14:30):
we induce all this information.And we used to think, you know,
back in the old days, 20, 30years ago, the old days are
scientifically Yeah.
That that that thatinflammation, that might be
really good. Right? I mean,there because your body's
responding to it and it's partof the healthy response to a
injury or an infection. But whatwe've discovered is is that most
(14:52):
of the inflammation after aprocedure is actually not
helping with the healingprocess. So so it actually, by
turning on this inflammasome,which is exactly what you do
when you have when you cause,damage, you're actually
preventing the healing process.
And that's why we try to, youknow, put ice on on you know,
when we have an injury is we tryto stop the the immune response
(15:15):
that's happening, and we take,you know, drugs like
nonsteroidal anti inflammatoriesor other types of drugs that
we've had available to us, butnone of those drugs will turn
off the inflammasome. And so sowe're we're just trying to stop
some of the downstream signalingthat comes. But until now, we've
never had something that couldturn off the real driver of the
(15:37):
inflammatory response. And sowe're super excited about the
idea. What happens if we justturn that thing off?
What if we stop it? Could weheal faster? And what we've seen
in the lab is it certainly lookslike we can. So we can go in and
do, you know, surgicalprocedures in the laboratory and
show that we can see healing isactually faster when you turn
(15:58):
off this this inflammasomesignaling.
Dr. Moira Gunn (16:00):
Now we're gonna try that in humans?
Dr. David Bearss (16:04):
Absolutely. That was like, you
Dr. Moira Gunn (16:05):
should be silent anytime
Dr. David Bearss (16:09):
soon. That's right. So in fact, as we're
we're recording this right now,we're we're actually treating
people today. We just got thefirst go ahead to treat some
people to see what happens postprocedure. And the the the the
nice thing about this is we canactually watch what happens in
their blood.
So after you have a a procedure,after you have a surgery done,
(16:31):
you will see induction ofinflammatory signaling in your
blood. You can actually monitorthat. So you'll see these
signals go up and we can seewhat happens. So what we're
doing is is we're seeing withwith patients, what happens
after their surgery when wedon't give them their therapy to
target the inflammasome and thenwhat happens when we give them
therapy to target theinflammasome and we see how
(16:54):
different that inflammatoryresponse is. And the nice thing
from a drug developmentstandpoint is that's a pretty
short study.
We we you know, we have acaptured population of people
that are having a procedure andthen we we watch just over the
course of a week what happens totheir inflammation. And so it it
can we can get a readout very,very quickly, which is exciting
(17:15):
for us because sometimes we wedesign clinical studies that
take literally years to figureout what's going on. In this
case, we we we hope that we cansee a signal very, very quickly.
Dr. Moira Gunn (17:25):
Now what are the first surgeries you're looking
at?
Dr. David Bearss (17:28):
So we have a very interesting, situation that
that exists where we arelocated. So we're our
headquarters is is in in Utah,right south of Salt Lake City.
And so the first surgeries thatwe're doing are actually
connected to where we're at inUtah. So So we have a population
of, young individuals that thatare, headed out as missionaries
(17:52):
for the, Church of Jesus Christof Latter day Saints or the
Mormon Church. And all of thosemissionaries that are going out,
they all have to have dentalexams and and they need to have
their wisdom teeth removed.
Dr. Moira Gunn (18:04):
Whether there's a problem or not.
Dr. David Bearss (18:05):
Whether there's a problem or not.
Dr. Moira Gunn (18:08):
We we can't handle this if there's a problem
when you're somewhere in theworld.
Dr. David Bearss (18:12):
That's right. We send them all over the world.
They go all over the place. Andso it was just decided that
prophylactically, it's a goodidea to take your wisdom teeth
out because for a young healthyperson, it's one of the things
that can actually cause acomplication if they're in
wherever, in Africa or, youknow, where you know, wherever.
We send them all over the place.
So so, what we decided and wedesigned this study to to ask
(18:36):
the question, well, when youwhen you pull your your 3rd
molars or your wisdom teeth out,you actually cause not just the
local inflammation in your jawwhere you pull that tooth out,
but it actually causes asystemic inflammatory response.
You activate that inflammasomeand your whole body says, hey.
We've got a problem here. Sowe're we're actually doing in in
(18:56):
literally today, we're we'rewe're dosing patients where we
can see what happens if weextract this tooth and we and we
turn off the inflammasome. Whathappens to the the signaling for
inflammation?
And the implications here arebig. So if we can show that we
can block by blocking theinflammasome, we can block that
systemic inflammatory response.We hope that leads to faster
(19:18):
recovery after a surgery bysuppressing inflammation. So we
can we we already know that thatif you can get back to work and
get back to, you know, activityquickly after surgery, your your
outcomes do are better. If youfeel lousy and you're just
laying around for a while, youactually do worse.
And so trying to get people backand and recover quickly is is a
(19:40):
really important important partof the recovery from, surgeries.
And inflammation plays a bigrole in people not feeling like
they they can get back and andget back to normal activity. So
so if it works there, the nextstep is, let's see where else it
works. Does it work in in, youknow, in in some of the standard
places that we look is bunionsurgery, tummy tuck surgery.
(20:03):
Those are those are also veryvery captured populations, but
but even, you know, in kneereplacements and hip
replacements and very commonsurgeries that we have all the
time.
We know that this pathway isactivated, and we're very, very
interested to see if we can wecan help people recover faster
by turning off that information.
Dr. Moira Gunn (20:23):
Well, I mispronounced the name of your
company when we first met. Isaid Halia, h a l I a. And I was
like, no. It's it's Halia, whichis which is Hawaiian. You guys
are all over the place.
Okay. How do you how did we getthis name halia?
Dr. David Bearss (20:40):
Yeah. Yeah. You know, I, it's, myself and,
one of our cofounders, aHawaiian scientist, and there's
not many scientists from Hawaii.So he's kind of a he's he's kind
of a unique individual, but, hisname is Keoni Kawe. And so Keoni
and I, got together to startCALIA with the idea that that we
(21:03):
could target inflammation in thebrain.
And we actually, discovered thisin a very interesting way. So,
Keone is a human geneticist. Sohe studies risk factors based
off of our genetics. So he looksat variations in in genes and
and what that does to risk fordifferent diseases. So he's
(21:23):
looking for, you know, the theplaces in our DNA where we have
differences and how that thatthat is correlated with our risk
for developing differentdiseases.
And his specific interest hasbeen in neurodegenerative
diseases like Alzheimer's. Andso he came to me and said, hey,
I discovered something reallyinteresting. So there's there's
(21:44):
a a very well known risk factorfor Alzheimer's disease. It's
called the APOE4, and it's ait's a polymorphism and you I
guess you call it a mutation,but it's a it's a it's a
different DNA sequence in thisgene called APOE. And if you
have this this flavor of thatthat, that gene, your risk for
Alzheimer's is quite high,relative to the rest of the
(22:07):
population.
So he was studying this, and heactually found a family. And
once again, it comes back toUtah. We we we have large
families in Utah usually. And hefound a family in Utah that had
this polymorphism, the APOE 4.But no nobody in their history,
their medical history, and theirfamily, nobody got Alzheimer's
disease.
So he actually organized afamily reunion, got all those
(22:32):
people to come, and and, theythey all consented to be studied
to see why with this thisgenetics that should should
predispose them to Alzheimer's,why none of them got
Alzheimer's. And so we were ableto sequence all we sequence over
200 individuals in this family.And we discovered they had
another unique DNA, very orpolymorphism or mutation that
(22:56):
actually looked like it wasassociated with preventing
Alzheimer's. And so when westarted the company, the whole
goal of the company was tofigure out, well, what does this
do? And we started the the thename of the company, Halea, is a
Hawaiian name that means fondmemories.
And so we started with the ideathat that, we could we could
target Alzheimer's. And in fact,we haven't given up on that. In
(23:18):
fact, very, very soon, we shouldbe, announcing that with our
second drug that we're movinginto the clinic is, is actually
targeting this exact pathwaythat we discovered and trying to
replicate what we discoveredgenetically in this family with
a new drug that can have thesame kind of activity. And in
fact, it right comes right backdown to inflammation as well. So
(23:40):
what we discovered is thisfamily has a mutation.
We call it a resilience mutationbecause they're resilient to a
lot of things. They they haveless heart disease. They have
less cancer. They have lessAlzheimer's. And it's
interesting that it's due totheir ability to have lower
response to inflammation.
So we're excited about, the ideathat we can take a genetic
(24:03):
discovery and translate thatinto something that we could
actually use as a therapeutic.
Dr. Moira Gunn (24:07):
You know, here we have Dave Beers, you know,
drug hunter. Drug discoverer,doctor Beers. Very impressive.
And I do have a question foryou, along these lines. I mean,
you have founded 8 biotechcompanies.
You've discovered many drugs. 16of those drugs have actually
(24:27):
moved into human clinicaltrials. Then I have to tell you,
that's an impressive record. Howis your current experience with
Halea the same, and how is itdifferent from your earlier
experience?
Dr. David Bearss (24:41):
Yeah. It's, you know, it's been it's it's
been an amazing career for me. II I love what I do. I get up
every morning thinking todaycould be the day we make a
discovery that changes the worldand and, you know, that's that's
not hyperbole. That's real.
Right? I mean, we can actuallyfind things that that change,
(25:01):
diseases in people, and that'sjust amazing to me. So so when I
first started, I was very naivein terms of of starting a
company. And and and really mymotivation to start a company is
I discovered I was a professor.I was, you know, in in the lab,
you know, doing research there,and and we discovered something
that we thought could be a newtherapy that could could help
(25:22):
people.
And I went to a mentor of minethat that, I learned a lot from
and and said to him, well, howdo I how do I take this from my
lab and turn it into somethingthat could help people? And he
said, well, you're probably theonly person in the world that's
gonna believe in this. And so ifif you wanna see it move
forward, you probably need to doit yourself. And so I actually
(25:43):
took the leap and and just said,okay. I walked away from a
tenure track faculty position ata major research university and
just decided I'm gonna start alittle company.
And I barely even knew what a aa stock was, a share in a
company. I hardly knew any ofthat. But thankfully, I I had a
great partner that that, helpedme, put together the first
(26:05):
company. But, you know, I had noidea how hard it was to raise
the money and to to go throughall the process of of, getting
the, supporting information toshow that the the drug could
could actually be safe andpotentially effective in people.
And so I guess what's differentabout Halia is that I had 7
(26:26):
other tries to learn a lot ofstuff that that, and make every
mistake that you can make.
And, hopefully, I'm not makingvery many anymore. But, I tell
people all the time, I, youknow, I I earned all the white
hair that I have because I, I'veI've probably made every mistake
that you can. But but what'skept me going is, you know, I I
really wanna make a differencein people's lives. I I lost my
(26:49):
grandfather the year I was born.Never had a relationship with
him.
Didn't don't know him. I haveone picture of me as a baby with
him holding me, and that's it.That's all I know about him. And
I lost my mom when when, whenstill when she was young, both
of cancer. And, I just decided,you know what?
If I can spend my life and makeit so other people's moms and
(27:12):
grandpas can be around a littlelonger, that's not a bad life to
live. And so so for me, that'swhat keeps me going every day is
is can I make a discovery thatcan keep people's grandmas and
grandpas and moms and dadsaround a little longer? And and,
you know, it's it's it's it'samazing to me that that, you
know, we've been able to to towork on projects that that, you
(27:35):
know, are now approved drugs,things that that people use, and
they have extended the life ofpeople. But it's, it's never
enough for me. I'd I I wannahave number 17, 18, 19, 20, you
know, to keep finding findingthe next one.
So, I I'm not gonna stop.
Dr. Moira Gunn (27:53):
Doctor Behar, I'm thrilled that you're not
gonna stop, personally.
Dr. David Bearss (27:57):
Thank you.
Dr. Moira Gunn (27:59):
I wanna thank you so much for coming on. I
hope you come back, visit usagain.
Dr. David Bearss (28:03):
I I'd love to. I'd love to tell you the the you
know, when we get some results,show you what's happened and and
what the next big thing is.
Dr. Moira Gunn (28:10):
You're on. You're on. Thanks again.
Dr. David Bearss (28:12):
Thanks a lot.
Dr. Moira Gunn (28:13):
Doctor David Bearss is the cofounder,
president, and CEO of HaliaTherapeutics. More information
is available at haliatx dotcom.That's haliatx.com.
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