March 13, 2025 • 46 mins
"The first decision I had to make when I joined was whether to continue this anito-cel progam that now looks to be potentially best-in-class in myeloma," Rami Elghandour, CEO of Arcellx, shares with Bloomberg Intelligence analyst Sam Fazeli. The company embodies the dream of biotech investors -- raising a small amount of capital while on the cusp of getting a drug to market with a highly credible partner. Arcellx and Gilead aim to take on the leader in multiple myeloma, Johnson & Johnson, targeting its engineered T-cell therapy (CAR-T) Carvykti with their own unique CAR-T, anito-cel. The discussion covers topics from the company's inception to Elghandour's journey through healthcare and how it has a real chance of launching a product after raising just $240 million. Oh, and Spider Man makes a cameo appearance too.
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Episode Transcript
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Speaker 1 (00:13):
Right.
Speaker 2 (00:13):
Welcome everybody to another episode of Bloomberg Intelligence Vanguards of
Healthcare podcast, where we speak with the leaders at the
forefront of change in the healthcare industry. My name is
Sam Fazelli and I'm a healthcare analyst at Bloomberg Intelligence,
the in house research arm of Bloomberg. There are several
reasons why I'm particularly excited to welcome Rame l gandur
(00:37):
CEO of Arselex to our podcast.
Speaker 3 (00:39):
Hi Rami, Hey Sam, It's a pleasure to be on.
Speaker 1 (00:42):
Thank you.
Speaker 2 (00:42):
Our Selex is one of the success stories of biotech.
Ipo'd about three years ago in one of the toughest
times for the biotech market, and I'll have to say
sadly those tough times are still here with us. The
shares didn't get off to a particularly strong start, falling
to as low as about seven dollars, I think after
a few months post IPO at fifteen dollars. But since
(01:06):
that loan it's been a strong performer, with the shares
up about four x relative to the IPO pressing and
nine x relative to that low that I mentioned in
May twenty twenty two. This is against the backdrop of
a very close to zero for the XBI, which is
the biotech ETF that a lot of people look at.
Speaker 1 (01:28):
The company has raised very little.
Speaker 2 (01:30):
Money, relatively speaking from the market by US biotech standards,
about one hundred and thirty million dollars at fifteen dollars
per share in feb twenty two with the IPO, and
then in quick succession one hundred and ten million dollars
in June of the same year at.
Speaker 1 (01:46):
A slightly higher price of sixteen dollars.
Speaker 2 (01:48):
And in December twenty two our SALEX raised three hunderd
twenty five million dollars in a code development a co
commercialization deal for Anita sell which we will talk about
with Kite now subsidiary of Gilead, followed by another twenty
eighty five million dollars in November twenty twenty three. Now,
these are obviously non dilutive numbers, right, They're not equity says,
(02:09):
although there was some equity element in some of these.
Killiad's ownership on that point is about thirteen percent of
the stock. So by all accounts, a biotech success story,
which is good to be talking about.
Speaker 1 (02:22):
There's too much doom of gloom in the sector.
Speaker 2 (02:24):
So let's start with a little background on Romie and
his personal journey, So I'm going to pass it on
to you to tell.
Speaker 3 (02:30):
Us Sure, Sam, Well, thanks again for having me. It's
a pleasure and honor to be on this with you. Yeah,
my journey is kind of interesting in that I always
joke I'm kind of not doing the right job. I'm
an electrical engineer by training, and I find myself running
a cell therapy company and maybe the toughest market that's
(02:52):
been around for a while in biotech. But the quick
kind of background personally is I am trained as an
electrical engineer year and I was actually about a third
of my way through my masters in w before I
went to the dark side and decided to go to
business school. From there, I got into venture capital for
a while. I was at janej in a corporate venture
(03:14):
group for about five years. And you know, my goal
was always to get into the when I at least
when I went to business school, to get into the
entrepreneurial side of management. And so I wound up jumping
to one of our portfolio companies where a couple of
years became CEO. I wound up being there for about
seven years, built that company from about thirty two, one
(03:35):
thousand people, took a public ran multiple successful studies. It
was really the experience of a lifetime. And then I
took a couple of years off, spent time with the kids,
went to car shows, did a lot of fun things,
and then I joined our sels about four years ago.
And I joked with my friends that, you know, biotech
had had an incredible run in the time that I
was in venture in mettech, and just as I arrived,
(03:58):
it seemed like the lights were turned off at the party.
Speaker 1 (04:02):
So not for our selcs though, now for our selecs.
Speaker 3 (04:07):
In fact, we actually just celebrated our tenth anniversary, which
is a pretty remarkable achievement for a biotech company.
Speaker 2 (04:13):
Yeah, yeah, no, I mean, I mean there are a
few who've been around a bit longer than that. We
just came off a call with another biotech CEO where
the company at least has been around for twenty years.
But in any case, the market cap is nowhere near
where our selex is today. And honestly, you know, there's
drug development things fail, right, So but I know you
(04:36):
also like telling the story of the company and how
the drug came about being So do you want to
just talk us through its funding history, the story of
the company's technology, and how hard has it been to
navigate these tough markets.
Speaker 3 (04:49):
Yeah, maybe I'll start with that first. I think one
of my proudest achievements is when we were in public
to the point you were talking about, there was a
headline in one of the publications that said biotech bear
market be damned. Our Selex ghost public anyway, and it
has been a really tough go. But sort of going back,
as I mentioned, we just celebrated our Kent anniversary. The
(05:11):
company was initially founded by David Hilbert. He's a brilliant scientist.
He really had the idea for taking this construct the didomain,
which is the foundational technology for our Selex, and testing
it as a binder in cell therapy, which turned out
to be a really brilliant idea. And Ali Babahani at
(05:32):
Nia is who David brought this idea to, and Ali
had the vision to see that this was in fact
a brilliant idea and something he would back very early on.
He then brought in Sime and George and sr I
and Novo Ventures, and the three of them founded were
the founding investors in the company. What David did really
(05:52):
well from an entrepreneurship perspective is he advanced the technology
very quickly and very efficiently, with very small amount of
capital into the clinic and got a proof of concept
within those first six years. And as I mentioned, I
joined four years ago and a really interesting time in
the company, partly because at the time we're in the
(06:13):
Altologous Cartes space, which I'm sure we'll talk about. But
what was all the rage back in twenty twenty one
when I joined was Allegeneic Cartes and all of a
myriad of other sort of newer technologies, and it was
sort of believed that Altologus would go to the wayside.
So that was kind of one dynamic we were contending with.
The other one was that there was a lot of
(06:35):
companies in the BCMA Cartes space, and so it seemed
like there wasn't a lot of space for another company.
And so actually the first decision I had to make
when I joined Ourselics was whether to continue this BCMA program,
this anito cell program that now looks to be potentially
best in class in my looma because there was a
lot of investor feedback that Autologus was kind of over
(06:59):
that there was two any other BCMA Cartes, and so
the company was thinking of not really investing more in
this program. And I think what I saw was, even
though it was only about six patients with very short
follow up, something that looked like it could be best
in class, and that the competitive landscape wasn't as strong
as people thought, that there was a lot of holes
(07:19):
in the other data sets, and that allegen at Cartes
and maybe this is the advantage of coming from outside
the space. While the hype was really high, the underlying
data didn't really support that hype. So we made a
bet that we thought this therapy could have could have legs,
and that bet has certainly paid off.
Speaker 2 (07:39):
Yeah, I mean ash was one of the big stories
of in twenty twenty four show price reaction was there
lots of questions, lots of discussion, But that's again the
story of Biotach. So you mentioned Cartes. I think the
majority of the audience who listens to these podcasts and
(08:00):
to know what they are, but just in case, do
you want to just tell us what they are and
what's the process that's used to make them and then
put them in the big picture of oncology.
Speaker 3 (08:12):
Yeah, it's a great question, particularly as a foundation for
the rest of our discussion. You know, cartes are basically
and this feel has only existed for about ten years
or so, and the core idea was could we use
our own immune cells to fight cancer. The way I
kind of think of it, particularly as an engineer, is
that we have cancer in our bodies all the time.
(08:33):
It's a copy paste error. We need to make new cells.
Every once in a while. When we're making those new cells,
there's an there are really an error that produces two
side effects that turn what we think about as cancer.
The first one is that the cells are able to
evade the immune system, so the immune system can't see
them and can't clear them. The second one is if
(08:54):
you're a Disney fan like me, Sam, you would have
gone on the Spider Man ride. And the problem on
the Spider Man and Ride is that the spider bots
get stuck in auto replication mode. They just continue to
make more and more of themselves until they overrun Avenger's campus.
And that's the same problem we have in our bodies,
that these cells, these cancer cells, start to auto replicate
(09:15):
and overtake our functioning organs. And so the genesis of
carte was if you could make our immune cells see
these cells, if they can bind to them, then they
could potentially clear them. And so what we do is
we take T cells from a patient and we genetically
modify them using a viral vector similar to kind of
(09:36):
how vaccines work, to express a binder that will actually
bind to the type of cancer that a patient has.
And that process is complex, and it's time consuming, and
it's somewhat expensive, and it's hard to do reliably at scale.
That's what's taken these ten years to kind of improve
and perfect this process. But that is essentially what cartes are.
(10:01):
It's harnessing a patient's on immune system by giving them
the visibility that they can see and bind to cancerselves
to actually clear their own cancer.
Speaker 2 (10:11):
That was an excellent little intro. So let's talk about
now some more specifics here. Now, this is not a drug.
This is a live product at the end of the day,
which therefore means that there is and also you're preparing it,
you're producing it out of the patient themselves. So took
us through the manufacturing steps that are involved, how complicated
(10:33):
they are, the time it takes, the success rates that
you've been seeing, and you can quote the latest numbers
if you like, getting into the patients, including getting their
T cells out and getting them back into an infusion
chair cost toxicity. I mean, I don't know how much
more do you want me to load in that. Just
take that one step at the time, starting from the patient,
(10:55):
and then how our selex is managing at the moment
in terms of getting these products produced.
Speaker 4 (11:03):
Yeah.
Speaker 3 (11:03):
No, it's a great question because there is definitely a
very hands on and logistical element of cart therapy that's
very different than any other therapy that you're going to
receive as a patient. So it starts with obviously, a
physician on college is determining that you're a candidate for
this kind of therapy, and part of it is that
(11:23):
you're fit enough to receive this therapy, right, because what
we're talking about here is again taking your immune cells
and kind of supercharging them. It's the ultimate and personalized
medicine and infusing them back in and that is going
to really rev up your immune system. Right, So you
have to be somewhat healthy enough and have enough disease
control to benefit from this therapy. So you will come
(11:45):
in once you're deemed fit and eligible for CARTI, and
will the site will perform what's called an aphoresis process.
They will actually withdraw these T cells from your body.
Those cells are then shipped to the manufacturing plant. They
are against transduced with that vector to express the right binder,
(12:06):
they're grown, and then they're shipped back to the site
so they can be infused into patient. That whole process
ideally would happen in a couple of weeks. Unfortunately, it
is a very difficult process to do. Why is it difficult, Well,
there's that logistical element that's involved that I mentioned that
you've got to actually, you know, book the patient, draw
(12:26):
the cells, ship them, you've got to manufacturing them. And
you're dealing with live cells. Like they're not easy to manufacture.
Different levels of health of these cells from these patients,
so there can be a lot of variability. There is
a manual element. You can automate these process as much
as you can, but there's always a manual element that
has to be done consistently, so it is hard to do.
(12:47):
I think what we're really excited about, which I'm sure
we'll get into, is partly that our construct at our
selics that binder, that magic thing that makes us different,
is super easy to express. I always say, you know,
from an engineering perspective, cells are like little manufacturing plants.
You ask them to make something, they're going to make it,
and the efficiency of how much they make it depends
(13:09):
on the complexity of the thing you're asking them to make.
So our binder is really simple, it's really easy to express,
which has led us to have one hundred percent manufacturing
success rate in our phase one and a ninety nine
percent manufacturing success rate in our phase two. When you
can combine that with our partnership with Kite, which you
mentioned at the outset, they are the best in the
world at manufacturing these cell therapies and producing them at scale,
(13:34):
and so we're excited to put in their hands that
sort of technology. And they've already demonstrated they're manufacturing and
executing our earlier line study right now and they're seeing
manufacturing times that are low in line with their commercial cartes,
which are around seventeen days.
Speaker 2 (13:54):
And so, Ronnie specifically on that point of manufacturing efficiency,
how does that com pa to your competitors based on
the information that you.
Speaker 3 (14:02):
Have, Yeah, the latest real world data that we're seeing
is our competitors can be in a four to six
week timeframe to return sales to a patient. Now, that
in and of itself, obviously is a lot longer than
the approximately seventeen days that Kite can manufacture app But
there's actually a nuance here that's even more important, which
is reliability. If you're running one of these centers, you
(14:24):
want to be able to maximize access. This is life
saving therapy. You want to be able to make sure
you offer it to as many patients as can benefit.
And if there is variability between three weeks, four weeks,
five weeks, six weeks, that makes it harder for you
to schedule and maximize the beds that you have. So
it's actually almost more important that you have reliability, which
Kite has at I believe in over ninety six percent
(14:47):
rate versus time. But both are important. But that reliability
of being able to produce at scale is something that
we believe is certainly enabled by the de domain and
our technology at our selings, but also by the world
class organization that KaiA is right.
Speaker 2 (15:05):
And then of course the element that we have to
think about here is that is the efficacy.
Speaker 1 (15:10):
Right, and then we'll get to cost and toxic later.
Speaker 2 (15:13):
So the beauty of these drugs, let's call them drugs, right,
of these drugs is the incredibly high response rates that
you're seeing. So of course in multiple miloma, the way
that people look at the response rates is how good.
Speaker 1 (15:29):
The put it as simple as possible.
Speaker 2 (15:32):
The car TI that the engineer tse you've delivered is
able to clear the offending miloid cells that are floating
around in your blood.
Speaker 1 (15:42):
Right now, talk to us a little bit about.
Speaker 2 (15:44):
The percentage of patients that you show complete clearance.
Speaker 1 (15:49):
We can talk about.
Speaker 2 (15:51):
Minimal RESI or measurable residual disease in a minute, but
in terms of the response rates, these are not far
from one hundred percent.
Speaker 3 (15:58):
Right, Yeah, I know it's a great question. Actually, maybe
dial this up a bit. You know, there's a couple
of factors that impact adoption of these therapies and their impact.
There's safety and efficacy, which you're getting into. We talked
about manufacturability and reliability a bit, but from a safety
and efficacy perspective, it is just rare to be able
to deliver across the board without trade offs on these
(16:20):
and I think that is really what's unique about our
SELX so on efficacy. If you look at MRD rates,
we're in the nineties. If you look at PFS rates,
it depends on kind of the time point that you
look at, but they start out in the nineties and
kind of go into the high seventies and eighties. The
cr rate, the complete response rates that you're talking about
in our phase one that was seventy nine percent in
(16:42):
a heavily pre treated population with you know, over about
two thirds of the patient's had high risk prognostic factor
and a median PFS of thirty months. Like that, those
results are really incredible. If you think of where my
LOOMA was ten years ago versus where it is now,
a really really incredible results. So I think we feel
(17:04):
like we can be just as good as anyone else
in efficacy. We have the potential to maybe be even
better in that we don't see a degradation in those
results that I mentioned between high risk groups with a
lot of other cartees. What you'll see is efficacy is
really strong if you get a really healthy patient, but
if you get a patient with bulky extramedullary disease, meaning
(17:27):
they have solid tumor nodules in addition to their blood
based myloma, they won't do as well, but we tend
to see not that there's no drop off, but pretty
consistent performance irrespective of the high risk nature of the patient.
From a safety perspective, there's even potentially a bigger differentiator
relative to what was kind of considered the best in
(17:50):
class data before our data was released. We have three
times as many patients with no CRS at all, which
is one of the most common side effects with therapy,
and fifty percent more patients with grade one or less CRS,
meaning that the therapy is very well tolerated, and most
importantly with some other cartes, we've seen delayed neurotoxicities which
(18:13):
are really strange. There are the presentation of parkinsonian like
CYS symptoms or colitis or palsy's that can be very
detrimental and in some cases irresolvable, and at the time
of our presentation at ASH in twenty twenty four, we
had seen none of those cases in one hundred and
fifty five patients treated. So when you kind of step
(18:35):
back and you think about the ability to deliver this
therapy at scale, to deliver it reliably to have efficacy
that is potentially best in class and a safety profile
that broadens the access to maximum number of patients that
can benefit. We feel like we're in a really strong
position here to hopefully help a lot of patients suffering
(18:57):
from island.
Speaker 1 (18:58):
It's interesting you say all these things.
Speaker 2 (18:59):
We've just in the process of fine fine publishing the
final report. It was a huge survey we did in
terms of number of questions we asked of my Looma physicians,
fifty in the US and fifty in Europe, and CRS
was the major thing that they were worried about in
(19:19):
terms of the side effect profile that that and then
of course I cans but that's one of the critical
things that that that turned out as, which of course
is understandable now just for those who don't know, CRS
is cyte kind release syndrome that's associated with the dynamics
of how when when T cells are actually get activated, right,
(19:41):
And so what's interesting to consider here is the other
two products that around the market are for want of
a better phrase, standard parties in that they use a
standard domain to bind or a fragment or antibody type
thing to bind to the antigen on the council cell
(20:02):
to allow then the cart to kill the council cell.
You use a synthetic approach, but how does that How
do you believe that's manifesting in the differences that you see.
Speaker 3 (20:15):
Yeah, it's a great question, and yeah, that is the
magic of our selics. We have this synthetic binder that
is not in nature. It's completely designed by us, and
it has a couple of benefits. So if I could
show you an image, which we can do on a podcast,
our binder is much smaller and simpler. And so back
to that analogy I used earlier of thinking of a
(20:37):
cell as a little manufacturing plant that you ask to
express one of these different structures. If you see the
other structures that Sam was referring to, the SEFV structure
that most cartes use, the bivalent camelid structure that another
CARTI uses, they're just very big and complex and they
have these really intricate folds in turns, and so it
(21:00):
is harder for cells to express them. So let me
put some numbers behind that that will help elucidate what
we mean. So with our binder, when we express, when
we transduce cells with our vector seventy percent of the
cells express the binder properly and our tumor clearing, which
is a really high percentage. If you look at one
(21:23):
of our other competitor cartes, only fifteen or sixteen percent
of their remaining cells are CAR positive and tumor binding
and clearing. That's a big delta between seven zero and
one six. So how does that manifest into some of
these things we talked about. Well, we can actually dose
twice as many of those effective cells as relative to
(21:44):
other cartes, which is why potentially we are able to
clear heavier disease without seeing an intenuation and efficacy. At
the same time, our total cell count could be a
half to a quarter of our competitors because of that efficiency. So,
for example, our target cell dose is one hundred and
fifteen million cells, we only need around one hundred and
(22:06):
forty million cells at a seventy percent efficiency to get
to that one fifteen where our competitors target dose is
only fifty million cells, but they may need three hundred
and fifty upwards of a billion cells at a fifteen
percent median efficiency to get that fifteen million. So we
believe that that has a lot to do Obviously, this
(22:26):
is all hypothesis at this point, and a lot more
work has to go into proving this out, but at
a very high level for this discussion, we believe the
efficiency of the D domain, its simplicity, its ease of expression,
does manifest, and how the cells are manufactured, how quickly
and reliably they're manufactured, how stable they are, and how
(22:48):
much how many fewer cells we need to dose while
still maximizing the effective cells, which speaks to all of
these benefits we discussed right now.
Speaker 2 (22:58):
On the efficacy front, we've got this. We've heard about
the upfront response rates, progression free survival numbers, measurable residual disease.
That's my favorite version of mr E. Other people say
different things which are all basically telling you how well
you're clearing the miloma cells or the tumor and how
(23:19):
long it takes for the patient to disease.
Speaker 1 (23:22):
To return progression free survival.
Speaker 2 (23:25):
So there's one element left here, of course, which you know,
these are supposed to be one undone, although I'm not
I don't know why they have to be one undone,
but let's say they're supposed to be one undone. Durability
is another one, right, So you've done the one shot
at the price point, whatever the price points are, When
(23:46):
will we get more durability? What is the timeline from
our selex in terms of showing continued durability in their
data sets, And of course the patient numbers are now
becoming quite meaningful combining the Phase one in the Phase two, etc.
Speaker 1 (24:02):
So what's the timelines on that.
Speaker 3 (24:04):
Yeah, I think that's a hard question to answer. Hopefully
it was going to take a long time. So our
Phase one, as I mentioned, had a thirty month PFS
and it took a couple of years for that to evolve. Obviously,
you need enough patients to go out longer, and the
longer it takes, the better the results are. So we
are in obviously in the early stages of Imagine one,
our pivotal study. We release preliminary data from that study
(24:27):
for the first time at ASH two months ago, so
we're hoping it's going to take a long time before
we hit a median there. But we're obviously very optimistic
given the results from our Phase one, which again was
in a heavier, pre treated, higher risk population relative to
Imagine one, and the reason for that, as an aside,
(24:47):
is Naturally, when you're running a Phase one, especially in oncology,
you're going to get the hardest patients because who's going
to go who else is going to go on a
phase one study for a new for a new asset
when there are other options available. But naturally, as you
move into a later into a larger study with a
more proven asset, you're able to recruit more patients that
(25:08):
are more representative of the general population, which is what
we have in Imagine one. So we're very hopeful. I think,
as you said, it's important to note, you know, when
you have MRD rates that are in the nineties, when
you have when you have CR rates that are climbing.
Our CR rate with only nine and a half months
of follow up with sixty two percent in our phase
one sorry, in Imagine one. I think all the trends
(25:33):
speak to that this is going to be, you know,
a long efficacious therapy, but we obviously need some time
to play that out.
Speaker 2 (25:41):
I think one of the other important things because the
types of patients, all patients in my limb will benefit
from these drugs, but the types of patients which you
mentioned earlier with bulky extramedullary disease. And again to remind folks,
extra military disease is when the cells have left the
(26:03):
bone marrow and are forming a solid tumor somewhere else.
Speaker 1 (26:06):
And the definition of this.
Speaker 2 (26:08):
Extra madulary disease is really important to keep an eye on,
right because most a lot of trials mentioned in so
called em D, but they don't all have the same
rules as to what counts as EMD. Some people in
some trials they use what is called paramedellary disease which
is closer to the bone or just jutting out of
(26:30):
the bone, and that perhaps doesn't have as much of
a difficulty to treat as a bulky true extra meditary disease.
So just to note that that is an important element
to keep an eye on whenever we look at these
comparative data sets. Right, So, in terms of coming to market,
you've got a registrational trial that's read out, and when
(26:52):
do you hope to be drinking that glass of champagne
for the first patient being commercially treated.
Speaker 3 (27:00):
Open to be on a market in twenty twenty six.
So obviously, with this pivotal data that's positive in hand,
are the next sort of big effort here between us
and our partners, Kaye is to get this BLA filed
and we expect to be our guidances to be on
the market next year, in twenty twenty six next year.
Speaker 2 (27:18):
Right now, coming to that point, obviously you're partner with Kite,
but Kite's part of Gillad. Gilliad is one of the
major CARTI players in not in myloma, but in b
cell diseases. So if we think about who you're coming
up against, you're going to come up against Johnson and Johnson,
which which you said you worked for right interesting now,
(27:42):
and they are they do have a very strong miloma franchise.
Speaker 1 (27:46):
It's not just Carti. They have bispecifics two of them.
Speaker 2 (27:50):
They have Darzalx, which by all accounts is going to
be one of the biggest at some point relative to
what rev Limid was, which was the Bristol Myers treatment.
So they have a you know, a pretty full bag
of drugs or treatments for maloma. And talk to us
through how does that feel going up against the competitor
(28:11):
like that, and what your challenges you think will be
in trying to get attention. Now again I have I'll
tell you at the end. Part of the questions we
asked in our survey, which is a data set that's
not been published yet but by the time this airs
it would have been published, is questioning academic community and
(28:31):
European centers as to how much awareness they have of
a need to sell and the number four academic centers
in the US was quite high. And then the next
question for them was of those that said, yes, we
do have experience, how many would you today start using
a need to sell immediately as soon as it's available.
And the answer today is twenty five percent now to me,
(28:55):
although a survey is a survey, right, If I did
it again, it'll be some other percent, But that's a
pretty good number for a company that hasn't even got
the product to the FDA, let alone being on the market,
I think.
Speaker 1 (29:07):
Right, So I'd love your comment on this is the
sort of numbers.
Speaker 2 (29:11):
I'm sure you've done the same kind of surveys or not,
I don't know, But tell us about this upcoming competition.
Speaker 3 (29:19):
Yeah, I know, Like, well, thank you for sharing that. Yeah,
I think. Look, the awareness around anito Cell I think
is high and continues to grow, and we're very happy
about that because, as you said, it's not We're not commercial,
we're not on the market, we're not promoting. This is
purely through scientific presentations who have captured I think the
attention of the of the myloma community. And as you said,
(29:41):
I am an exchange A guy. It's a great company.
I have a lot of respect for J and J.
They have a life saving therapy that they've partnered, and
we certainly wish that they do very well. I think
it's great that we have multiple companies building this market
in JJBMS as well as US AND and Gilead. I
(30:01):
believe this market is certainly there's a lot of patients
who can benefit from these therapies, So I think it's
great that I look at it less as competition, to
be honest, and more is like there's an opportunity here
to save a lot of lives. And I think we
obviously have something that's compelling and differentiated relative to our competitors,
but there's also a lot of opportunity to help a
lot of patients here.
Speaker 2 (30:23):
And I think the.
Speaker 3 (30:23):
Nature of CARTI therapy I shouldn't use this analogy since
planes are falling out of the sky right now, but
it would be hard to say that one airline can
sort of handle all all flights in the US right
because it is effectively a just in time sort of
production business. You need to be able to take people
from point A to point B, and I think cart
(30:44):
is a little bit like that. I think it's actually
helpful to have multiple companies in this space. Now, being
a competitive guy, I also have to say, I feel
like we have the best therapy here. I think we
have the best partner in Kite Gilead. That ability to scale,
manufact and deliver reliably is going to matter a lot.
And I think one thing that's interesting in biotech that
(31:05):
I've noticed this is coming from outside the space, is
I don't feel like people often appreciate as much how
much execution matters. I think there's always a belief like
it kind of if you build it, they will come,
And there is an element of that to the point
you just talked about that the data is good, it
attracts a lot of attention, but you ultimately have to
(31:26):
be able to deliver, you know, I always use an
analogy like, think about the difference. I'm a big Disney
guy if you haven't noticed, but there's a big difference
between Disney and Universal Studios, not just because the IP
is different, but because the experience is different. The way
Disney trains people, the reliability. You can go to anybody
in any Disney park and ask a question and they
will be friendly, They will be knowledgeable, be able to
(31:47):
direct you in the right direction. It isn't always the
case with other theme parks. I think you look at
best buys still around, but Circuit City isn't right. Very
similar businesses. Why did one survive and the other one
didn't Because execution matters. So I can't state enough that
we're very confident in our ability to execute, partly because
of Kite, but partly because of the experiences we bring
(32:08):
as well. In my last company, we launched against the
three largest tech companies in the world and captured about
twenty twenty five percent market share in three and a
half years in a much harder market. I believe in
the market we're entering here, and so execution does matter
a lot. I think we're confident in our profile and
being differentiated for the reasons we talked about. We're confident
(32:31):
in our partner, and we're confident in our ability to execute.
Speaker 2 (32:34):
Great Now, just a couple more questions on here, and
then we go to a bit of a broader conversation
and see where we end up. Obviously, you've got not
just carties that are going to be out there competing
for the same patient poof. You've got other drugs, particularly
by specifics.
Speaker 1 (32:53):
That try and do the same thing, get the t
sell to the disease.
Speaker 2 (33:00):
You've got other ones such as GSK coming with a
drug called blend rep, which has got good deficacy data.
Speaker 1 (33:07):
Good survival data.
Speaker 2 (33:08):
It's got a side effect issue that is significant and
needs to be addressed and dealt with. But how do
you see this spectrum if you imagine, let's not worry about.
Speaker 1 (33:20):
Fourth line patients, i e.
Speaker 2 (33:22):
Those who've had two or three Let's go to the
early patients where you were coming off of your first
after being newly diagnosed, you've relapsed, and let's think about
this future where our selex.
Speaker 1 (33:34):
Is also available, need to sell is also available.
Speaker 2 (33:36):
How do you think the world's going to look at
these options in treating And of course myloma is one
of those that proves that you can have twenty drugs,
ten drugs and they all either combine or they're going series.
So just took us through where you think you're approved
in earlier lines, not necessarily newly diagnosed with the earlier lines.
Speaker 1 (34:01):
How does that world look like from your perspective.
Speaker 3 (34:03):
Yeah, I think that's a great question. I think the
point you just made is a really excellent one too, Sam.
This is a bit of a polyform macee market, right,
and that patients are likely to go on multiple drugs,
so it's not one or the other. The way I
believe that this market's going to evolve is that cartes
are going to have a segment of frontline, so they're
going to take some share from transplant, even which is
the gold standard front line treatment for many patients today.
(34:27):
I think obviously, and I would say that anito cell
will likely take the majority of that share just because
of the safety element that we talked about.
Speaker 1 (34:36):
And that's a big patient population that matters.
Speaker 3 (34:38):
That is as earlier Yeah, that is a big patient population.
Speaker 2 (34:42):
And it matters more.
Speaker 3 (34:43):
Safety matters more and more as you move earlier and
earlier lines. Right, This risk of Parkinson's that we talked about,
it may be not something people want to deal with,
but it may be a manageable risk for a fifth
sixth line patient. It is not an acceptable risk in
a second or a front line patient. So we believe that,
you know, I believe that frontline we're going to get
the majority of that share. I'd say the same is
(35:03):
true if second line and second line. If you put
us sign frontline right now, second line is probably half
of the overall population that we expect to be treated
with cartes between second and second line, plus, half of
the patients are in second line, So we believe we're
going to get the lion's share, if not the majority
of those second line patients as well. For the same reason,
(35:24):
from the safety reason, I think as you get into
third line, maybe you start to get some other cartes
getting shared in third line just because of logistics and
capacity and all those kind of things. And then fourth
line maybe you have the other cartes taking most of
the fourth line share, and then by specifics I think
would be fifth line plus. That's the way I would
(35:45):
see the world. So for that reason, we and I
are very confident that we're going to be the share
leader by a good margin here in this market. But
we do also again believe that it's a big enough
market that it's going to accommodate multiple players again, and
the combination safety, efficacy, manufacturer ability, brand awareness from Kite
all those reasons that we should be able to capture
(36:08):
the majority of the kind of you know, second part
of third second, first line component of the market and
then maybe the other cartes kind of play in later
and then buy specifics down the line.
Speaker 4 (36:21):
Right right.
Speaker 2 (36:23):
I mean, there's it's quite interesting in that in the
world where folks don't get a transplant, some of that
is because they delay it. And I wonder whether those patients,
if they were offered a safer car tie or a
safe cartee, would actually not want to delay. But we'll
see how that number shifts out.
Speaker 1 (36:41):
Now.
Speaker 2 (36:43):
Last question on therapies et cetera, what where to after
after my looma?
Speaker 1 (36:48):
And we have a lot of work to do, a
lot of wood to chop still on my looma?
Speaker 2 (36:52):
But where where where else is our sels pointing its concept?
Speaker 3 (36:57):
Yeah, Like, we really believe that this technology is differentiator.
It's obviously had a profound effect in myloma, and we
are pushing hard to explore where else it can help patients.
So we currently have a study in AML which has
been a really challenging area, as you know, targeting CD
one twenty three, we actually disclose that we're going to
(37:19):
have a second antigen target in AML going into the
clinic this year as well, so continuing to invest in
that space obviously, we feel like I think many people agree,
there's a huge unmet need there and we'd love to
really make a dent in AML. We also just launched
a study in autoimmune in my cia gravis. I think
(37:40):
we've seen some research that suggests that there's some activity,
particularly for plasma cell mediated disease like myesthenia, and so
we're excited about that and seeing where the potential is.
And then lastly, we have a number of solid tumor
programs that are in development, and again I think we
see some promise in the extra madullary disease point we
(38:01):
both talked about earlier. The fact that we can clear
that gives us some hope that there is something about
THED domain that allows it to operate in that suppressive
solid tumor environment. All you know, acknowledging that that's not
exactly the same as some other solid tumors, but it's
certainly a prelude. And so we're excited about the solid
tumor programs and seeing if we can again kind of
(38:22):
move the needle and you know, step back. We're trying
to build a generational company, and certainly the Myloma program
is a great foundation to do that, but for us
to truly do that, we feel like we are hopeful
that we can make a dent in some of these
other conditions, and we're investing appropriately.
Speaker 2 (38:40):
And then if we looked at say you're back in
this same seat in twenty four months, in two years time,
would we be able to talk more about the AML
and the solid tumor data and the my senior GRAVIS data.
Speaker 4 (38:54):
I hope.
Speaker 3 (38:54):
So, I mean, we don't have guidance on those on
when we'd release data from those programs, but based on
the pace of enrollment and progress in those programs, I
would be hopeful that in the next two years we
can really see the potential of those programs and be
able to talk about them.
Speaker 2 (39:12):
Well, you do realize you have to start going to
more of the solid tumor type conferences.
Speaker 1 (39:18):
Not just hematology conferences. But that's a good reason for
us to be able to see again.
Speaker 2 (39:22):
So let's get towards wrapping up electrical engineering background, so
you must have quite a lot of interest in all
the evolution and the discussions going around machine learning and
large language models, small language models, small machine learning, tiny
machine learning. I've been listening to tiny machine learning recently.
And how does that I mean, you're a biotech company.
(39:45):
We talked about how much money you've raised, and these
are things that cost a lot of money to do.
Speaker 1 (39:50):
How does that fit into your current thinking.
Speaker 3 (39:53):
Yeah, it's not going to surprise you, Sam, but you know,
aside from oursels, I looked at a lot of CEO
roles and aiml back in twenty nineteen, twenty twenty when
I started looking at opportunities again. So I know it's
kind of all the hype now and it's become a
part of the sort of general lexicon, but it's definitely
something I was very early on. So actually, one of
the first things I did when I joined our selex
(40:15):
is to challenge our team to start working on this.
So we've been working on it for a couple of
years now, and look, I think there's a lot of
potential there. I think I would say the easier parts.
None of it is that easy, But the easy part
is to use it to help you accelerate development to
be able to go from a target to a clinical
(40:36):
candidate nomination much faster. I think that is one sort
of area where we use it. I think the second
one is to engineer binders that are generally harder to engineer,
to come up with alternatives where are traditional methods of
identification and refinement haven't yielded results. We found it to
(40:57):
be useful where it's ultimately probably most valuable. But it's
going to be hard to prove, whether for us or
anyone else, is can it help you predict what will
ultimately work in the clinic, because that would obviously have
massive ramifications from a fundraising timeline for patients, etc. Perspective.
(41:17):
I think that's a much harder thing to prove out.
I think it's very early days, so I do think
it's going to be very impactful. We have to have
probably a separate podcast for us to talk about my
concerns about AI to general society and disruption to jobs
and all that kind of stuff, because I'm definitely more
(41:38):
on the bearish side of its general impact to society.
I don't think that's going to be a negative. I
think it'll be a net positive for biotech. I worry
about the overall impact to society from an employment perspective,
because it is just it's a tool that drives efficiency.
You can do a lot more with a lot less
(41:59):
people using it. And I feel like from a government
and a policy perspective, we need to support our people
in society as we kind of manage through this disruption.
Speaker 1 (42:10):
Would you start another car tea company? Now?
Speaker 3 (42:12):
Well, I always joke I'm not the founding type. I'm
more of the scaling type, So I wouldn't start one,
But I think could someone start? Could someone start one?
I think sure? Like yes, the funding environment is really tough,
and you know, I can tell you so many stories
from the IPO and some of these and the bad
deal and all these things that were hard. But you know,
(42:32):
I feel like the core thing is isn't whether you
start a carte company now, is it? Like is it
differentiated right?
Speaker 2 (42:38):
Like?
Speaker 3 (42:38):
Do you have some path to being best in class
or one of the best companies in your space? Is
the market attractive enough? Or where you're pointing like, can
you capture share? Ultimately? Do you have the right team
that can really carry this thing forward and position this
story well, I think those are the things that ultimately
made a difference in our sellings. Even though times were
(43:02):
really tough, we've been able to be really successful. So
I think if people can answer yes to those questions,
then I think, yeah, you can start a company. I
don't think there's a reason to do.
Speaker 2 (43:12):
What you've just described is what anyone starting a y
it's a company needs to think about. Yeah.
Speaker 3 (43:17):
Yeah, So I wouldn't say like carties is an exclusion criteria.
I think sometimes we get too like wrapped around the axle.
I'll tell you from a BD perspective. For example, I
got asked all the time, like, what are you guys
interested in? Is it cartes in oncology, We're interested in
what I just said. We're interested in things that are
differentiated in attractive markets with that are the right stage
(43:40):
of development, that have good phase one data, kind of
similar to what our Selex was when I joined, Like
we have what we're good at is taking an asset
from those early stages and making it successful. It's not
like we had a ton of my Looma or oncology
experience when I started here, Like, we built that experience, right,
so we can build that experience in any space. It's
(44:00):
more like the asset has to be the right asset.
So I think if people have a great asset, they'll
find a way.
Speaker 1 (44:06):
Right.
Speaker 2 (44:07):
Last question, if you were not doing this Rommy and
you weren't in biotake, what would you be?
Speaker 3 (44:12):
Oh man, that's a good question. Like when I was
kind of going, I'm a very you know, top down,
first principles kind of person. So when I was thinking
about what to do before I joined our selics, I'm
also a very impact rive in person, So I was like,
what is going to change the world in the next
ten years? So I came up with selling gene therapies,
artificial intelligence, virtual reality, autonomous driving, and fintech. So those
(44:37):
are the spaces I generally i'm interested in. I spent
a lot of time thinking about but I think, you know,
I may do those things. I may. I work with
nonprofits a lot to spend time trying to make the
world a better place. Yeah, I don't know, but I
love what I'm doing now, so I don't think about it.
As you can tell you caught me by surprise. It's
not something I think about. I'm a very like I'm
(44:59):
doing what I'm doing, and that's all I think about.
I don't do boards, I don't do anything else really.
I go to the gym, I spend time with my kids,
and I work, and those are the things I enjoyed.
Speaker 1 (45:08):
I had to do something that was offscript, so.
Speaker 2 (45:13):
Okay, Robmie Elegan dud thank you very much for your
time and talking to us about the story of our selex,
which I'm really excited to be following and continue to follow.
And I wish you the best success because what that
means is that there's a good product on the market
for multiple my lower patients. So thank you very much
(45:35):
for joining us, and thanks for your time.
Speaker 3 (45:36):
Thanks so much, Sam, It's been a pleasure and I
really enjoyed the time with you.
Speaker 4 (45:40):
Cheers Moss as
Speaker 2 (46:08):
Usual, uses
Right.
Speaker 2 (00:13):
Welcome everybody to another episode of Bloomberg Intelligence Vanguards of
Healthcare podcast, where we speak with the leaders at the
forefront of change in the healthcare industry. My name is
Sam Fazelli and I'm a healthcare analyst at Bloomberg Intelligence,
the in house research arm of Bloomberg. There are several
reasons why I'm particularly excited to welcome Rame l gandur
(00:37):
CEO of Arselex to our podcast.
Speaker 3 (00:39):
Hi Rami, Hey Sam, It's a pleasure to be on.
Speaker 1 (00:42):
Thank you.
Speaker 2 (00:42):
Our Selex is one of the success stories of biotech.
Ipo'd about three years ago in one of the toughest
times for the biotech market, and I'll have to say
sadly those tough times are still here with us. The
shares didn't get off to a particularly strong start, falling
to as low as about seven dollars, I think after
a few months post IPO at fifteen dollars. But since
(01:06):
that loan it's been a strong performer, with the shares
up about four x relative to the IPO pressing and
nine x relative to that low that I mentioned in
May twenty twenty two. This is against the backdrop of
a very close to zero for the XBI, which is
the biotech ETF that a lot of people look at.
Speaker 1 (01:28):
The company has raised very little.
Speaker 2 (01:30):
Money, relatively speaking from the market by US biotech standards,
about one hundred and thirty million dollars at fifteen dollars
per share in feb twenty two with the IPO, and
then in quick succession one hundred and ten million dollars
in June of the same year at.
Speaker 1 (01:46):
A slightly higher price of sixteen dollars.
Speaker 2 (01:48):
And in December twenty two our SALEX raised three hunderd
twenty five million dollars in a code development a co
commercialization deal for Anita sell which we will talk about
with Kite now subsidiary of Gilead, followed by another twenty
eighty five million dollars in November twenty twenty three. Now,
these are obviously non dilutive numbers, right, They're not equity says,
(02:09):
although there was some equity element in some of these.
Killiad's ownership on that point is about thirteen percent of
the stock. So by all accounts, a biotech success story,
which is good to be talking about.
Speaker 1 (02:22):
There's too much doom of gloom in the sector.
Speaker 2 (02:24):
So let's start with a little background on Romie and
his personal journey, So I'm going to pass it on
to you to tell.
Speaker 3 (02:30):
Us Sure, Sam, Well, thanks again for having me. It's
a pleasure and honor to be on this with you. Yeah,
my journey is kind of interesting in that I always
joke I'm kind of not doing the right job. I'm
an electrical engineer by training, and I find myself running
a cell therapy company and maybe the toughest market that's
(02:52):
been around for a while in biotech. But the quick
kind of background personally is I am trained as an
electrical engineer year and I was actually about a third
of my way through my masters in w before I
went to the dark side and decided to go to
business school. From there, I got into venture capital for
a while. I was at janej in a corporate venture
(03:14):
group for about five years. And you know, my goal
was always to get into the when I at least
when I went to business school, to get into the
entrepreneurial side of management. And so I wound up jumping
to one of our portfolio companies where a couple of
years became CEO. I wound up being there for about
seven years, built that company from about thirty two, one
(03:35):
thousand people, took a public ran multiple successful studies. It
was really the experience of a lifetime. And then I
took a couple of years off, spent time with the kids,
went to car shows, did a lot of fun things,
and then I joined our sels about four years ago.
And I joked with my friends that, you know, biotech
had had an incredible run in the time that I
was in venture in mettech, and just as I arrived,
(03:58):
it seemed like the lights were turned off at the party.
Speaker 1 (04:02):
So not for our selcs though, now for our selecs.
Speaker 3 (04:07):
In fact, we actually just celebrated our tenth anniversary, which
is a pretty remarkable achievement for a biotech company.
Speaker 2 (04:13):
Yeah, yeah, no, I mean, I mean there are a
few who've been around a bit longer than that. We
just came off a call with another biotech CEO where
the company at least has been around for twenty years.
But in any case, the market cap is nowhere near
where our selex is today. And honestly, you know, there's
drug development things fail, right, So but I know you
(04:36):
also like telling the story of the company and how
the drug came about being So do you want to
just talk us through its funding history, the story of
the company's technology, and how hard has it been to
navigate these tough markets.
Speaker 3 (04:49):
Yeah, maybe I'll start with that first. I think one
of my proudest achievements is when we were in public
to the point you were talking about, there was a
headline in one of the publications that said biotech bear
market be damned. Our Selex ghost public anyway, and it
has been a really tough go. But sort of going back,
as I mentioned, we just celebrated our Kent anniversary. The
(05:11):
company was initially founded by David Hilbert. He's a brilliant scientist.
He really had the idea for taking this construct the didomain,
which is the foundational technology for our Selex, and testing
it as a binder in cell therapy, which turned out
to be a really brilliant idea. And Ali Babahani at
(05:32):
Nia is who David brought this idea to, and Ali
had the vision to see that this was in fact
a brilliant idea and something he would back very early on.
He then brought in Sime and George and sr I
and Novo Ventures, and the three of them founded were
the founding investors in the company. What David did really
(05:52):
well from an entrepreneurship perspective is he advanced the technology
very quickly and very efficiently, with very small amount of
capital into the clinic and got a proof of concept
within those first six years. And as I mentioned, I
joined four years ago and a really interesting time in
the company, partly because at the time we're in the
(06:13):
Altologous Cartes space, which I'm sure we'll talk about. But
what was all the rage back in twenty twenty one
when I joined was Allegeneic Cartes and all of a
myriad of other sort of newer technologies, and it was
sort of believed that Altologus would go to the wayside.
So that was kind of one dynamic we were contending with.
The other one was that there was a lot of
(06:35):
companies in the BCMA Cartes space, and so it seemed
like there wasn't a lot of space for another company.
And so actually the first decision I had to make
when I joined Ourselics was whether to continue this BCMA program,
this anito cell program that now looks to be potentially
best in class in my looma because there was a
lot of investor feedback that Autologus was kind of over
(06:59):
that there was two any other BCMA Cartes, and so
the company was thinking of not really investing more in
this program. And I think what I saw was, even
though it was only about six patients with very short
follow up, something that looked like it could be best
in class, and that the competitive landscape wasn't as strong
as people thought, that there was a lot of holes
(07:19):
in the other data sets, and that allegen at Cartes
and maybe this is the advantage of coming from outside
the space. While the hype was really high, the underlying
data didn't really support that hype. So we made a
bet that we thought this therapy could have could have legs,
and that bet has certainly paid off.
Speaker 2 (07:39):
Yeah, I mean ash was one of the big stories
of in twenty twenty four show price reaction was there
lots of questions, lots of discussion, But that's again the
story of Biotach. So you mentioned Cartes. I think the
majority of the audience who listens to these podcasts and
(08:00):
to know what they are, but just in case, do
you want to just tell us what they are and
what's the process that's used to make them and then
put them in the big picture of oncology.
Speaker 3 (08:12):
Yeah, it's a great question, particularly as a foundation for
the rest of our discussion. You know, cartes are basically
and this feel has only existed for about ten years
or so, and the core idea was could we use
our own immune cells to fight cancer. The way I
kind of think of it, particularly as an engineer, is
that we have cancer in our bodies all the time.
(08:33):
It's a copy paste error. We need to make new cells.
Every once in a while. When we're making those new cells,
there's an there are really an error that produces two
side effects that turn what we think about as cancer.
The first one is that the cells are able to
evade the immune system, so the immune system can't see
them and can't clear them. The second one is if
(08:54):
you're a Disney fan like me, Sam, you would have
gone on the Spider Man ride. And the problem on
the Spider Man and Ride is that the spider bots
get stuck in auto replication mode. They just continue to
make more and more of themselves until they overrun Avenger's campus.
And that's the same problem we have in our bodies,
that these cells, these cancer cells, start to auto replicate
(09:15):
and overtake our functioning organs. And so the genesis of
carte was if you could make our immune cells see
these cells, if they can bind to them, then they
could potentially clear them. And so what we do is
we take T cells from a patient and we genetically
modify them using a viral vector similar to kind of
(09:36):
how vaccines work, to express a binder that will actually
bind to the type of cancer that a patient has.
And that process is complex, and it's time consuming, and
it's somewhat expensive, and it's hard to do reliably at scale.
That's what's taken these ten years to kind of improve
and perfect this process. But that is essentially what cartes are.
(10:01):
It's harnessing a patient's on immune system by giving them
the visibility that they can see and bind to cancerselves
to actually clear their own cancer.
Speaker 2 (10:11):
That was an excellent little intro. So let's talk about
now some more specifics here. Now, this is not a drug.
This is a live product at the end of the day,
which therefore means that there is and also you're preparing it,
you're producing it out of the patient themselves. So took
us through the manufacturing steps that are involved, how complicated
(10:33):
they are, the time it takes, the success rates that
you've been seeing, and you can quote the latest numbers
if you like, getting into the patients, including getting their
T cells out and getting them back into an infusion
chair cost toxicity. I mean, I don't know how much
more do you want me to load in that. Just
take that one step at the time, starting from the patient,
(10:55):
and then how our selex is managing at the moment
in terms of getting these products produced.
Speaker 4 (11:03):
Yeah.
Speaker 3 (11:03):
No, it's a great question because there is definitely a
very hands on and logistical element of cart therapy that's
very different than any other therapy that you're going to
receive as a patient. So it starts with obviously, a
physician on college is determining that you're a candidate for
this kind of therapy, and part of it is that
(11:23):
you're fit enough to receive this therapy, right, because what
we're talking about here is again taking your immune cells
and kind of supercharging them. It's the ultimate and personalized
medicine and infusing them back in and that is going
to really rev up your immune system. Right, So you
have to be somewhat healthy enough and have enough disease
control to benefit from this therapy. So you will come
(11:45):
in once you're deemed fit and eligible for CARTI, and
will the site will perform what's called an aphoresis process.
They will actually withdraw these T cells from your body.
Those cells are then shipped to the manufacturing plant. They
are against transduced with that vector to express the right binder,
(12:06):
they're grown, and then they're shipped back to the site
so they can be infused into patient. That whole process
ideally would happen in a couple of weeks. Unfortunately, it
is a very difficult process to do. Why is it difficult, Well,
there's that logistical element that's involved that I mentioned that
you've got to actually, you know, book the patient, draw
(12:26):
the cells, ship them, you've got to manufacturing them. And
you're dealing with live cells. Like they're not easy to manufacture.
Different levels of health of these cells from these patients,
so there can be a lot of variability. There is
a manual element. You can automate these process as much
as you can, but there's always a manual element that
has to be done consistently, so it is hard to do.
(12:47):
I think what we're really excited about, which I'm sure
we'll get into, is partly that our construct at our
selics that binder, that magic thing that makes us different,
is super easy to express. I always say, you know,
from an engineering perspective, cells are like little manufacturing plants.
You ask them to make something, they're going to make it,
and the efficiency of how much they make it depends
(13:09):
on the complexity of the thing you're asking them to make.
So our binder is really simple, it's really easy to express,
which has led us to have one hundred percent manufacturing
success rate in our phase one and a ninety nine
percent manufacturing success rate in our phase two. When you
can combine that with our partnership with Kite, which you
mentioned at the outset, they are the best in the
world at manufacturing these cell therapies and producing them at scale,
(13:34):
and so we're excited to put in their hands that
sort of technology. And they've already demonstrated they're manufacturing and
executing our earlier line study right now and they're seeing
manufacturing times that are low in line with their commercial cartes,
which are around seventeen days.
Speaker 2 (13:54):
And so, Ronnie specifically on that point of manufacturing efficiency,
how does that com pa to your competitors based on
the information that you.
Speaker 3 (14:02):
Have, Yeah, the latest real world data that we're seeing
is our competitors can be in a four to six
week timeframe to return sales to a patient. Now, that
in and of itself, obviously is a lot longer than
the approximately seventeen days that Kite can manufacture app But
there's actually a nuance here that's even more important, which
is reliability. If you're running one of these centers, you
(14:24):
want to be able to maximize access. This is life
saving therapy. You want to be able to make sure
you offer it to as many patients as can benefit.
And if there is variability between three weeks, four weeks,
five weeks, six weeks, that makes it harder for you
to schedule and maximize the beds that you have. So
it's actually almost more important that you have reliability, which
Kite has at I believe in over ninety six percent
(14:47):
rate versus time. But both are important. But that reliability
of being able to produce at scale is something that
we believe is certainly enabled by the de domain and
our technology at our selings, but also by the world
class organization that KaiA is right.
Speaker 2 (15:05):
And then of course the element that we have to
think about here is that is the efficacy.
Speaker 1 (15:10):
Right, and then we'll get to cost and toxic later.
Speaker 2 (15:13):
So the beauty of these drugs, let's call them drugs, right,
of these drugs is the incredibly high response rates that
you're seeing. So of course in multiple miloma, the way
that people look at the response rates is how good.
Speaker 1 (15:29):
The put it as simple as possible.
Speaker 2 (15:32):
The car TI that the engineer tse you've delivered is
able to clear the offending miloid cells that are floating
around in your blood.
Speaker 1 (15:42):
Right now, talk to us a little bit about.
Speaker 2 (15:44):
The percentage of patients that you show complete clearance.
Speaker 1 (15:49):
We can talk about.
Speaker 2 (15:51):
Minimal RESI or measurable residual disease in a minute, but
in terms of the response rates, these are not far
from one hundred percent.
Speaker 3 (15:58):
Right, Yeah, I know it's a great question. Actually, maybe
dial this up a bit. You know, there's a couple
of factors that impact adoption of these therapies and their impact.
There's safety and efficacy, which you're getting into. We talked
about manufacturability and reliability a bit, but from a safety
and efficacy perspective, it is just rare to be able
to deliver across the board without trade offs on these
(16:20):
and I think that is really what's unique about our
SELX so on efficacy. If you look at MRD rates,
we're in the nineties. If you look at PFS rates,
it depends on kind of the time point that you
look at, but they start out in the nineties and
kind of go into the high seventies and eighties. The
cr rate, the complete response rates that you're talking about
in our phase one that was seventy nine percent in
(16:42):
a heavily pre treated population with you know, over about
two thirds of the patient's had high risk prognostic factor
and a median PFS of thirty months. Like that, those
results are really incredible. If you think of where my
LOOMA was ten years ago versus where it is now,
a really really incredible results. So I think we feel
(17:04):
like we can be just as good as anyone else
in efficacy. We have the potential to maybe be even
better in that we don't see a degradation in those
results that I mentioned between high risk groups with a
lot of other cartees. What you'll see is efficacy is
really strong if you get a really healthy patient, but
if you get a patient with bulky extramedullary disease, meaning
(17:27):
they have solid tumor nodules in addition to their blood
based myloma, they won't do as well, but we tend
to see not that there's no drop off, but pretty
consistent performance irrespective of the high risk nature of the patient.
From a safety perspective, there's even potentially a bigger differentiator
relative to what was kind of considered the best in
(17:50):
class data before our data was released. We have three
times as many patients with no CRS at all, which
is one of the most common side effects with therapy,
and fifty percent more patients with grade one or less CRS,
meaning that the therapy is very well tolerated, and most
importantly with some other cartes, we've seen delayed neurotoxicities which
(18:13):
are really strange. There are the presentation of parkinsonian like
CYS symptoms or colitis or palsy's that can be very
detrimental and in some cases irresolvable, and at the time
of our presentation at ASH in twenty twenty four, we
had seen none of those cases in one hundred and
fifty five patients treated. So when you kind of step
(18:35):
back and you think about the ability to deliver this
therapy at scale, to deliver it reliably to have efficacy
that is potentially best in class and a safety profile
that broadens the access to maximum number of patients that
can benefit. We feel like we're in a really strong
position here to hopefully help a lot of patients suffering
(18:57):
from island.
Speaker 1 (18:58):
It's interesting you say all these things.
Speaker 2 (18:59):
We've just in the process of fine fine publishing the
final report. It was a huge survey we did in
terms of number of questions we asked of my Looma physicians,
fifty in the US and fifty in Europe, and CRS
was the major thing that they were worried about in
(19:19):
terms of the side effect profile that that and then
of course I cans but that's one of the critical
things that that that turned out as, which of course
is understandable now just for those who don't know, CRS
is cyte kind release syndrome that's associated with the dynamics
of how when when T cells are actually get activated, right,
(19:41):
And so what's interesting to consider here is the other
two products that around the market are for want of
a better phrase, standard parties in that they use a
standard domain to bind or a fragment or antibody type
thing to bind to the antigen on the council cell
(20:02):
to allow then the cart to kill the council cell.
You use a synthetic approach, but how does that How
do you believe that's manifesting in the differences that you see.
Speaker 3 (20:15):
Yeah, it's a great question, and yeah, that is the
magic of our selics. We have this synthetic binder that
is not in nature. It's completely designed by us, and
it has a couple of benefits. So if I could
show you an image, which we can do on a podcast,
our binder is much smaller and simpler. And so back
to that analogy I used earlier of thinking of a
(20:37):
cell as a little manufacturing plant that you ask to
express one of these different structures. If you see the
other structures that Sam was referring to, the SEFV structure
that most cartes use, the bivalent camelid structure that another
CARTI uses, they're just very big and complex and they
have these really intricate folds in turns, and so it
(21:00):
is harder for cells to express them. So let me
put some numbers behind that that will help elucidate what
we mean. So with our binder, when we express, when
we transduce cells with our vector seventy percent of the
cells express the binder properly and our tumor clearing, which
is a really high percentage. If you look at one
(21:23):
of our other competitor cartes, only fifteen or sixteen percent
of their remaining cells are CAR positive and tumor binding
and clearing. That's a big delta between seven zero and
one six. So how does that manifest into some of
these things we talked about. Well, we can actually dose
twice as many of those effective cells as relative to
(21:44):
other cartes, which is why potentially we are able to
clear heavier disease without seeing an intenuation and efficacy. At
the same time, our total cell count could be a
half to a quarter of our competitors because of that efficiency. So,
for example, our target cell dose is one hundred and
fifteen million cells, we only need around one hundred and
(22:06):
forty million cells at a seventy percent efficiency to get
to that one fifteen where our competitors target dose is
only fifty million cells, but they may need three hundred
and fifty upwards of a billion cells at a fifteen
percent median efficiency to get that fifteen million. So we
believe that that has a lot to do Obviously, this
(22:26):
is all hypothesis at this point, and a lot more
work has to go into proving this out, but at
a very high level for this discussion, we believe the
efficiency of the D domain, its simplicity, its ease of expression,
does manifest, and how the cells are manufactured, how quickly
and reliably they're manufactured, how stable they are, and how
(22:48):
much how many fewer cells we need to dose while
still maximizing the effective cells, which speaks to all of
these benefits we discussed right now.
Speaker 2 (22:58):
On the efficacy front, we've got this. We've heard about
the upfront response rates, progression free survival numbers, measurable residual disease.
That's my favorite version of mr E. Other people say
different things which are all basically telling you how well
you're clearing the miloma cells or the tumor and how
(23:19):
long it takes for the patient to disease.
Speaker 1 (23:22):
To return progression free survival.
Speaker 2 (23:25):
So there's one element left here, of course, which you know,
these are supposed to be one undone, although I'm not
I don't know why they have to be one undone,
but let's say they're supposed to be one undone. Durability
is another one, right, So you've done the one shot
at the price point, whatever the price points are, When
(23:46):
will we get more durability? What is the timeline from
our selex in terms of showing continued durability in their
data sets, And of course the patient numbers are now
becoming quite meaningful combining the Phase one in the Phase two, etc.
Speaker 1 (24:02):
So what's the timelines on that.
Speaker 3 (24:04):
Yeah, I think that's a hard question to answer. Hopefully
it was going to take a long time. So our
Phase one, as I mentioned, had a thirty month PFS
and it took a couple of years for that to evolve. Obviously,
you need enough patients to go out longer, and the
longer it takes, the better the results are. So we
are in obviously in the early stages of Imagine one,
our pivotal study. We release preliminary data from that study
(24:27):
for the first time at ASH two months ago, so
we're hoping it's going to take a long time before
we hit a median there. But we're obviously very optimistic
given the results from our Phase one, which again was
in a heavier, pre treated, higher risk population relative to
Imagine one, and the reason for that, as an aside,
(24:47):
is Naturally, when you're running a Phase one, especially in oncology,
you're going to get the hardest patients because who's going
to go who else is going to go on a
phase one study for a new for a new asset
when there are other options available. But naturally, as you
move into a later into a larger study with a
more proven asset, you're able to recruit more patients that
(25:08):
are more representative of the general population, which is what
we have in Imagine one. So we're very hopeful. I think,
as you said, it's important to note, you know, when
you have MRD rates that are in the nineties, when
you have when you have CR rates that are climbing.
Our CR rate with only nine and a half months
of follow up with sixty two percent in our phase
one sorry, in Imagine one. I think all the trends
(25:33):
speak to that this is going to be, you know,
a long efficacious therapy, but we obviously need some time
to play that out.
Speaker 2 (25:41):
I think one of the other important things because the
types of patients, all patients in my limb will benefit
from these drugs, but the types of patients which you
mentioned earlier with bulky extramedullary disease. And again to remind folks,
extra military disease is when the cells have left the
(26:03):
bone marrow and are forming a solid tumor somewhere else.
Speaker 1 (26:06):
And the definition of this.
Speaker 2 (26:08):
Extra madulary disease is really important to keep an eye on,
right because most a lot of trials mentioned in so
called em D, but they don't all have the same
rules as to what counts as EMD. Some people in
some trials they use what is called paramedellary disease which
is closer to the bone or just jutting out of
(26:30):
the bone, and that perhaps doesn't have as much of
a difficulty to treat as a bulky true extra meditary disease.
So just to note that that is an important element
to keep an eye on whenever we look at these
comparative data sets. Right, So, in terms of coming to market,
you've got a registrational trial that's read out, and when
(26:52):
do you hope to be drinking that glass of champagne
for the first patient being commercially treated.
Speaker 3 (27:00):
Open to be on a market in twenty twenty six.
So obviously, with this pivotal data that's positive in hand,
are the next sort of big effort here between us
and our partners, Kaye is to get this BLA filed
and we expect to be our guidances to be on
the market next year, in twenty twenty six next year.
Speaker 2 (27:18):
Right now, coming to that point, obviously you're partner with Kite,
but Kite's part of Gillad. Gilliad is one of the
major CARTI players in not in myloma, but in b
cell diseases. So if we think about who you're coming
up against, you're going to come up against Johnson and Johnson,
which which you said you worked for right interesting now,
(27:42):
and they are they do have a very strong miloma franchise.
Speaker 1 (27:46):
It's not just Carti. They have bispecifics two of them.
Speaker 2 (27:50):
They have Darzalx, which by all accounts is going to
be one of the biggest at some point relative to
what rev Limid was, which was the Bristol Myers treatment.
So they have a you know, a pretty full bag
of drugs or treatments for maloma. And talk to us
through how does that feel going up against the competitor
(28:11):
like that, and what your challenges you think will be
in trying to get attention. Now again I have I'll
tell you at the end. Part of the questions we
asked in our survey, which is a data set that's
not been published yet but by the time this airs
it would have been published, is questioning academic community and
(28:31):
European centers as to how much awareness they have of
a need to sell and the number four academic centers
in the US was quite high. And then the next
question for them was of those that said, yes, we
do have experience, how many would you today start using
a need to sell immediately as soon as it's available.
And the answer today is twenty five percent now to me,
(28:55):
although a survey is a survey, right, If I did
it again, it'll be some other percent, But that's a
pretty good number for a company that hasn't even got
the product to the FDA, let alone being on the market,
I think.
Speaker 1 (29:07):
Right, So I'd love your comment on this is the
sort of numbers.
Speaker 2 (29:11):
I'm sure you've done the same kind of surveys or not,
I don't know, But tell us about this upcoming competition.
Speaker 3 (29:19):
Yeah, I know, Like, well, thank you for sharing that. Yeah,
I think. Look, the awareness around anito Cell I think
is high and continues to grow, and we're very happy
about that because, as you said, it's not We're not commercial,
we're not on the market, we're not promoting. This is
purely through scientific presentations who have captured I think the
attention of the of the myloma community. And as you said,
(29:41):
I am an exchange A guy. It's a great company.
I have a lot of respect for J and J.
They have a life saving therapy that they've partnered, and
we certainly wish that they do very well. I think
it's great that we have multiple companies building this market
in JJBMS as well as US AND and Gilead. I
(30:01):
believe this market is certainly there's a lot of patients
who can benefit from these therapies, So I think it's
great that I look at it less as competition, to
be honest, and more is like there's an opportunity here
to save a lot of lives. And I think we
obviously have something that's compelling and differentiated relative to our competitors,
but there's also a lot of opportunity to help a
lot of patients here.
Speaker 2 (30:23):
And I think the.
Speaker 3 (30:23):
Nature of CARTI therapy I shouldn't use this analogy since
planes are falling out of the sky right now, but
it would be hard to say that one airline can
sort of handle all all flights in the US right
because it is effectively a just in time sort of
production business. You need to be able to take people
from point A to point B, and I think cart
(30:44):
is a little bit like that. I think it's actually
helpful to have multiple companies in this space. Now, being
a competitive guy, I also have to say, I feel
like we have the best therapy here. I think we
have the best partner in Kite Gilead. That ability to scale,
manufact and deliver reliably is going to matter a lot.
And I think one thing that's interesting in biotech that
(31:05):
I've noticed this is coming from outside the space, is
I don't feel like people often appreciate as much how
much execution matters. I think there's always a belief like
it kind of if you build it, they will come,
And there is an element of that to the point
you just talked about that the data is good, it
attracts a lot of attention, but you ultimately have to
(31:26):
be able to deliver, you know, I always use an
analogy like, think about the difference. I'm a big Disney
guy if you haven't noticed, but there's a big difference
between Disney and Universal Studios, not just because the IP
is different, but because the experience is different. The way
Disney trains people, the reliability. You can go to anybody
in any Disney park and ask a question and they
will be friendly, They will be knowledgeable, be able to
(31:47):
direct you in the right direction. It isn't always the
case with other theme parks. I think you look at
best buys still around, but Circuit City isn't right. Very
similar businesses. Why did one survive and the other one
didn't Because execution matters. So I can't state enough that
we're very confident in our ability to execute, partly because
of Kite, but partly because of the experiences we bring
(32:08):
as well. In my last company, we launched against the
three largest tech companies in the world and captured about
twenty twenty five percent market share in three and a
half years in a much harder market. I believe in
the market we're entering here, and so execution does matter
a lot. I think we're confident in our profile and
being differentiated for the reasons we talked about. We're confident
(32:31):
in our partner, and we're confident in our ability to execute.
Speaker 2 (32:34):
Great Now, just a couple more questions on here, and
then we go to a bit of a broader conversation
and see where we end up. Obviously, you've got not
just carties that are going to be out there competing
for the same patient poof. You've got other drugs, particularly
by specifics.
Speaker 1 (32:53):
That try and do the same thing, get the t
sell to the disease.
Speaker 2 (33:00):
You've got other ones such as GSK coming with a
drug called blend rep, which has got good deficacy data.
Speaker 1 (33:07):
Good survival data.
Speaker 2 (33:08):
It's got a side effect issue that is significant and
needs to be addressed and dealt with. But how do
you see this spectrum if you imagine, let's not worry about.
Speaker 1 (33:20):
Fourth line patients, i e.
Speaker 2 (33:22):
Those who've had two or three Let's go to the
early patients where you were coming off of your first
after being newly diagnosed, you've relapsed, and let's think about
this future where our selex.
Speaker 1 (33:34):
Is also available, need to sell is also available.
Speaker 2 (33:36):
How do you think the world's going to look at
these options in treating And of course myloma is one
of those that proves that you can have twenty drugs,
ten drugs and they all either combine or they're going series.
So just took us through where you think you're approved
in earlier lines, not necessarily newly diagnosed with the earlier lines.
Speaker 1 (34:01):
How does that world look like from your perspective.
Speaker 3 (34:03):
Yeah, I think that's a great question. I think the
point you just made is a really excellent one too, Sam.
This is a bit of a polyform macee market, right,
and that patients are likely to go on multiple drugs,
so it's not one or the other. The way I
believe that this market's going to evolve is that cartes
are going to have a segment of frontline, so they're
going to take some share from transplant, even which is
the gold standard front line treatment for many patients today.
(34:27):
I think obviously, and I would say that anito cell
will likely take the majority of that share just because
of the safety element that we talked about.
Speaker 1 (34:36):
And that's a big patient population that matters.
Speaker 3 (34:38):
That is as earlier Yeah, that is a big patient population.
Speaker 2 (34:42):
And it matters more.
Speaker 3 (34:43):
Safety matters more and more as you move earlier and
earlier lines. Right, This risk of Parkinson's that we talked about,
it may be not something people want to deal with,
but it may be a manageable risk for a fifth
sixth line patient. It is not an acceptable risk in
a second or a front line patient. So we believe that,
you know, I believe that frontline we're going to get
the majority of that share. I'd say the same is
(35:03):
true if second line and second line. If you put
us sign frontline right now, second line is probably half
of the overall population that we expect to be treated
with cartes between second and second line, plus, half of
the patients are in second line, So we believe we're
going to get the lion's share, if not the majority
of those second line patients as well. For the same reason,
(35:24):
from the safety reason, I think as you get into
third line, maybe you start to get some other cartes
getting shared in third line just because of logistics and
capacity and all those kind of things. And then fourth
line maybe you have the other cartes taking most of
the fourth line share, and then by specifics I think
would be fifth line plus. That's the way I would
(35:45):
see the world. So for that reason, we and I
are very confident that we're going to be the share
leader by a good margin here in this market. But
we do also again believe that it's a big enough
market that it's going to accommodate multiple players again, and
the combination safety, efficacy, manufacturer ability, brand awareness from Kite
all those reasons that we should be able to capture
(36:08):
the majority of the kind of you know, second part
of third second, first line component of the market and
then maybe the other cartes kind of play in later
and then buy specifics down the line.
Speaker 4 (36:21):
Right right.
Speaker 2 (36:23):
I mean, there's it's quite interesting in that in the
world where folks don't get a transplant, some of that
is because they delay it. And I wonder whether those patients,
if they were offered a safer car tie or a
safe cartee, would actually not want to delay. But we'll
see how that number shifts out.
Speaker 1 (36:41):
Now.
Speaker 2 (36:43):
Last question on therapies et cetera, what where to after
after my looma?
Speaker 1 (36:48):
And we have a lot of work to do, a
lot of wood to chop still on my looma?
Speaker 2 (36:52):
But where where where else is our sels pointing its concept?
Speaker 3 (36:57):
Yeah, Like, we really believe that this technology is differentiator.
It's obviously had a profound effect in myloma, and we
are pushing hard to explore where else it can help patients.
So we currently have a study in AML which has
been a really challenging area, as you know, targeting CD
one twenty three, we actually disclose that we're going to
(37:19):
have a second antigen target in AML going into the
clinic this year as well, so continuing to invest in
that space obviously, we feel like I think many people agree,
there's a huge unmet need there and we'd love to
really make a dent in AML. We also just launched
a study in autoimmune in my cia gravis. I think
(37:40):
we've seen some research that suggests that there's some activity,
particularly for plasma cell mediated disease like myesthenia, and so
we're excited about that and seeing where the potential is.
And then lastly, we have a number of solid tumor
programs that are in development, and again I think we
see some promise in the extra madullary disease point we
(38:01):
both talked about earlier. The fact that we can clear
that gives us some hope that there is something about
THED domain that allows it to operate in that suppressive
solid tumor environment. All you know, acknowledging that that's not
exactly the same as some other solid tumors, but it's
certainly a prelude. And so we're excited about the solid
tumor programs and seeing if we can again kind of
(38:22):
move the needle and you know, step back. We're trying
to build a generational company, and certainly the Myloma program
is a great foundation to do that, but for us
to truly do that, we feel like we are hopeful
that we can make a dent in some of these
other conditions, and we're investing appropriately.
Speaker 2 (38:40):
And then if we looked at say you're back in
this same seat in twenty four months, in two years time,
would we be able to talk more about the AML
and the solid tumor data and the my senior GRAVIS data.
Speaker 4 (38:54):
I hope.
Speaker 3 (38:54):
So, I mean, we don't have guidance on those on
when we'd release data from those programs, but based on
the pace of enrollment and progress in those programs, I
would be hopeful that in the next two years we
can really see the potential of those programs and be
able to talk about them.
Speaker 2 (39:12):
Well, you do realize you have to start going to
more of the solid tumor type conferences.
Speaker 1 (39:18):
Not just hematology conferences. But that's a good reason for
us to be able to see again.
Speaker 2 (39:22):
So let's get towards wrapping up electrical engineering background, so
you must have quite a lot of interest in all
the evolution and the discussions going around machine learning and
large language models, small language models, small machine learning, tiny
machine learning. I've been listening to tiny machine learning recently.
And how does that I mean, you're a biotech company.
(39:45):
We talked about how much money you've raised, and these
are things that cost a lot of money to do.
Speaker 1 (39:50):
How does that fit into your current thinking.
Speaker 3 (39:53):
Yeah, it's not going to surprise you, Sam, but you know,
aside from oursels, I looked at a lot of CEO
roles and aiml back in twenty nineteen, twenty twenty when
I started looking at opportunities again. So I know it's
kind of all the hype now and it's become a
part of the sort of general lexicon, but it's definitely
something I was very early on. So actually, one of
the first things I did when I joined our selex
(40:15):
is to challenge our team to start working on this.
So we've been working on it for a couple of
years now, and look, I think there's a lot of
potential there. I think I would say the easier parts.
None of it is that easy, But the easy part
is to use it to help you accelerate development to
be able to go from a target to a clinical
(40:36):
candidate nomination much faster. I think that is one sort
of area where we use it. I think the second
one is to engineer binders that are generally harder to engineer,
to come up with alternatives where are traditional methods of
identification and refinement haven't yielded results. We found it to
(40:57):
be useful where it's ultimately probably most valuable. But it's
going to be hard to prove, whether for us or
anyone else, is can it help you predict what will
ultimately work in the clinic, because that would obviously have
massive ramifications from a fundraising timeline for patients, etc. Perspective.
(41:17):
I think that's a much harder thing to prove out.
I think it's very early days, so I do think
it's going to be very impactful. We have to have
probably a separate podcast for us to talk about my
concerns about AI to general society and disruption to jobs
and all that kind of stuff, because I'm definitely more
(41:38):
on the bearish side of its general impact to society.
I don't think that's going to be a negative. I
think it'll be a net positive for biotech. I worry
about the overall impact to society from an employment perspective,
because it is just it's a tool that drives efficiency.
You can do a lot more with a lot less
(41:59):
people using it. And I feel like from a government
and a policy perspective, we need to support our people
in society as we kind of manage through this disruption.
Speaker 1 (42:10):
Would you start another car tea company? Now?
Speaker 3 (42:12):
Well, I always joke I'm not the founding type. I'm
more of the scaling type, So I wouldn't start one,
But I think could someone start? Could someone start one?
I think sure? Like yes, the funding environment is really tough,
and you know, I can tell you so many stories
from the IPO and some of these and the bad
deal and all these things that were hard. But you know,
(42:32):
I feel like the core thing is isn't whether you
start a carte company now, is it? Like is it
differentiated right?
Speaker 2 (42:38):
Like?
Speaker 3 (42:38):
Do you have some path to being best in class
or one of the best companies in your space? Is
the market attractive enough? Or where you're pointing like, can
you capture share? Ultimately? Do you have the right team
that can really carry this thing forward and position this
story well, I think those are the things that ultimately
made a difference in our sellings. Even though times were
(43:02):
really tough, we've been able to be really successful. So
I think if people can answer yes to those questions,
then I think, yeah, you can start a company. I
don't think there's a reason to do.
Speaker 2 (43:12):
What you've just described is what anyone starting a y
it's a company needs to think about. Yeah.
Speaker 3 (43:17):
Yeah, So I wouldn't say like carties is an exclusion criteria.
I think sometimes we get too like wrapped around the axle.
I'll tell you from a BD perspective. For example, I
got asked all the time, like, what are you guys
interested in? Is it cartes in oncology, We're interested in
what I just said. We're interested in things that are
differentiated in attractive markets with that are the right stage
(43:40):
of development, that have good phase one data, kind of
similar to what our Selex was when I joined, Like
we have what we're good at is taking an asset
from those early stages and making it successful. It's not
like we had a ton of my Looma or oncology
experience when I started here, Like, we built that experience, right,
so we can build that experience in any space. It's
(44:00):
more like the asset has to be the right asset.
So I think if people have a great asset, they'll
find a way.
Speaker 1 (44:06):
Right.
Speaker 2 (44:07):
Last question, if you were not doing this Rommy and
you weren't in biotake, what would you be?
Speaker 3 (44:12):
Oh man, that's a good question. Like when I was
kind of going, I'm a very you know, top down,
first principles kind of person. So when I was thinking
about what to do before I joined our selics, I'm
also a very impact rive in person, So I was like,
what is going to change the world in the next
ten years? So I came up with selling gene therapies,
artificial intelligence, virtual reality, autonomous driving, and fintech. So those
(44:37):
are the spaces I generally i'm interested in. I spent
a lot of time thinking about but I think, you know,
I may do those things. I may. I work with
nonprofits a lot to spend time trying to make the
world a better place. Yeah, I don't know, but I
love what I'm doing now, so I don't think about it.
As you can tell you caught me by surprise. It's
not something I think about. I'm a very like I'm
(44:59):
doing what I'm doing, and that's all I think about.
I don't do boards, I don't do anything else really.
I go to the gym, I spend time with my kids,
and I work, and those are the things I enjoyed.
Speaker 1 (45:08):
I had to do something that was offscript, so.
Speaker 2 (45:13):
Okay, Robmie Elegan dud thank you very much for your
time and talking to us about the story of our selex,
which I'm really excited to be following and continue to follow.
And I wish you the best success because what that
means is that there's a good product on the market
for multiple my lower patients. So thank you very much
(45:35):
for joining us, and thanks for your time.
Speaker 3 (45:36):
Thanks so much, Sam, It's been a pleasure and I
really enjoyed the time with you.
Speaker 4 (45:40):
Cheers Moss as
Speaker 2 (46:08):
Usual, uses
Host
Jonathan Palmer
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