Latest / The BioHub - by Avetix / Episode 163 - Ken Macnamara - CEO at Trogenix

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Episode 163 - Ken Macnamara - CEO at Trogenix · The BioHub - by Avetix

0:06
So welcome back to another episode of the Bio Hub.
0:08
Today we're delighted to welcome on Ken McNamara, a scientist and
0:12
CEO working at the cutting edge of genetic medicine.
0:15
Ken is the Co founder and CEO of Trojenix, where he's driving the
0:19
development of next generation genetic therapies designed to
0:22
tackle serious diseases, including cancer at their root
0:26
cause. Before launching Trojenix, Ken
0:29
served as Chief Product Officer at Ask Bio, a pioneer in gene
0:32
therapy and now a part of Bayer. So join us today as we'll
0:36
discuss Trojenix's recent $95 million Series A round, the pros
0:41
and cons have operated as a biotech company based out of
0:44
Edinburgh and what the next 12 to 24 months looks like for
0:48
Trojenix. So Ken, thanks so much for
0:51
coming on. How are you?
0:51
Yeah. Very well.
0:54
Thanks, Tom. Excited to be here.
0:56
Yeah, look, it's a pleasure to have you on.
0:58
So thanks for for coming on and helping us out with this.
1:02
And let's let's just start off with with your your story, your
1:05
journey through the field. So you started your career as a
1:07
chemist at Edinburgh and obviously now leading trogenics.
1:12
What was that journey like to get to where you are today?
1:15
And how did your way of thinking about science changed?
1:18
I guess it's as you moved into a leadership position.
1:23
Yeah, so, so my PhD was chemistry and, and I guess I've
1:27
taken a journey that's, you know, stretched from chemistry
1:30
to biology to engineering, marketing, sales, manufacturing,
1:36
all sorts of things. But do you know, I have to say
1:40
when, when, when I got Trogenics off the ground, it seemed that
1:45
everything I'd ever done was leading me to this point.
1:50
So, you know, a PhD is quite narrow and focused, right?
1:55
But what I quickly realized was that the skills around, you
2:00
know, forming A hypothesis, experimenting, problem solving,
2:04
innovating, that's, that's common across everything, you
2:09
know. So whilst in a PhD you're
2:11
focused on that, you know, my first company, I quickly moved
2:15
away from chemistry into biology, into engineering, into
2:19
sales. But it's the same problem
2:21
solving skills, the same people skills of, of, you know,
2:25
understanding that you, you don't know all the answers and
2:28
bringing people together that maybe there's, maybe there's the
2:32
lesson that you know, you don't do it alone, you never do.
2:37
And that is as important in science as it is in terms of
2:42
finding cures to cancer, running businesses, getting getting
2:46
drugs to patients. It's all about problem solving
2:49
at the end of the day. Yeah, nice.
2:51
And just take us back to when I guess you first had Co founded
2:55
Trojenix. So when did you realize that the
2:57
science behind the company wasn't just interesting
3:00
research, but something that you could actually build a company
3:03
around here? Just talk us through that,
3:06
through that moment. That's that's easy.
3:08
It was as soon as I met Steve. So Steve is CSO of Trojenix and,
3:14
and developed a foundational science.
3:17
So he's professor of stem cell and cancer biology here in here
3:20
in Edinburgh. What Steve did that really
3:25
inspired me was he took a very patient centric approach, right.
3:29
So in, in our lead program in glioblastoma, it's an area of
3:37
huge unmet need, but it's also an area of huge amounts of
3:40
failure. But, but that failure is, is
3:43
informed us. So we looked at what Steve had
3:48
done and, and what inspired me was he'd looked at every kind of
3:51
angle of where things had struggled.
3:57
You know, the, the, the micro environment, the, the delivery,
4:03
the, the right patient group, the right child design and, and
4:06
quite systematically worked his way through those to develop a
4:11
therapeutic that is for every patient and is thinking about
4:16
the potential for curative outcomes.
4:20
The the models that he'd developed the product in were
4:26
translational. So he developed the world's
4:28
biggest buy Bank of patient derived primary cell lines.
4:33
He developed our method to take tissue straight from surgery so
4:37
we could then test our drug products in in human tissue and
4:44
developed a syngeneic mouse model that was was actually
4:46
representative of the patient presentation So highly
4:50
suppressive tumor microenvironment.
4:53
And with all of those things that, I mean, the, the results
4:56
are curative in the animal model, we see the drug is
5:02
incredibly selective in human tissue.
5:05
So we have that precision. And yeah, I mean, I just
5:09
screamed we've we've got to get this to patients.
5:11
We've got to try it in the clinic.
5:13
It's the only only next step to take it.
5:16
Nice. And we can get into the the
5:18
pipeline a little bit further on, but it's that many companies
5:22
that are doing this sort of stuff that you guys are doing.
5:24
Or is this quite an uncharted field of of science that you
5:27
guys are in at the moment? So in terms of glioblastoma,
5:31
it's our lead program. It's a new huge unmet needs and
5:37
I would say it's been of significant interest from for
5:41
pharma, biotech over over decades now.
5:47
So I think whenever there's such an unmet need, of course there's
5:51
there's people interested, but what we are doing is, is really
5:56
transformational in terms of the approach.
6:00
So in, you know, to take a step back maybe in, in cancer care,
6:07
there's there's been a revolution in terms of targeted
6:11
agents. So be that, you know, going
6:13
after a surface tumor antigen or a specific genetic pathway.
6:17
We have seen drugs being developed, they're really
6:20
offering significant extensions to life.
6:22
But in all of those cases got, you know, going after a single
6:28
target is often creating challenges.
6:32
You know, we we we don't truly have the differential between
6:35
the disease tissue and healthy tissue.
6:38
So you're always in some sort of compromise of balancing potency
6:43
with off target side effects. And then going after that single
6:48
target means that the ultimately the the therapeutic is, you
6:54
know, the cancer evolves around that pathway and we see relapse.
7:00
Now what Trogenics is doing is, is turning that on its head.
7:03
We're not going after a genetic target, we're not going after a
7:06
surface tumor antigen. We're going after the
7:09
fundamental unit of cancer and that's the cell.
7:12
So whilst we see heterogeneity across patients at the genetic
7:16
level, at the phenotypic level we see homogeneity and that
7:21
actually gives us a handle where we can develop a therapeutic for
7:26
every patient. OK, not a subset of, you know, 1
7:29
genetic subtype, but every patient there.
7:32
And in glioblastoma, we created the world's biggest patient
7:37
biobank of samples. That's fifty different patients
7:42
across the full heterogeneity of the disease now fully
7:47
characterized. And indeed what you see is, you
7:49
know, a lot of heterogeneity, but at the phenotypic level.
7:52
So that's the described by a master transcriptional network.
7:57
So transcription factors are up regulated that give for you
8:01
might think of as a barcode of that disease cell.
8:06
And it's that where we're going after and it's common across all
8:09
patients some sort in GBM that's socks to socks, 9 cell signaling
8:15
factors all describing that disease cell state.
8:19
And we've developed a technology that harnesses that as a genetic
8:24
switch to a promoter that is harnessing that barcode of the
8:29
disease and only switching on in that disease cell state.
8:34
Now with that specificity and cancer, we know what we want to
8:38
do, right? You want to kill, kill the cell
8:42
and you want to train the immune system so it doesn't come back
8:44
again. Those pills have all been in the
8:47
clinic. So it's that precision is the is
8:49
the real differentiator and going after that precision
8:53
within that cell context. So it's for every patient.
8:57
So for us that's really transformational in terms of
9:01
where we are with the field. So whilst everyone's interested
9:04
in GPM, we've got a very differentiated approach that we
9:08
can start thinking about potential to move away from
9:13
chronic disease management and the potential for one and done
9:16
creative responses. Yeah, amazing.
9:19
It just to dive into a little bit more into the Odysseus
9:22
platform which targets tumor cell identity rather than
9:26
individual mutations. Can you just give us a run
9:30
through and explain why or why you're particularly excited
9:34
about that approach? Because I know it's in quite a
9:36
crowded field of, of cancer therapies.
9:40
And you mentioned the differentiation then just like
9:42
what, what sets you guys truly apart from maybe others that are
9:46
that are trying to that are out there as well?
9:48
Yeah. So, so for me it's around the
9:50
precision, right. So precision of that phenotypic
9:54
level at the cellular level and harnessing that.
9:59
And that's that's what we have from the Odysseus platforms, the
10:01
underlying platform behind Trogenics.
10:05
So Odysseus is our AI guided. So it's bioinformatics, machine
10:10
learning, all of those hot topics, understanding the
10:14
genomics, but but it was super important to understand about
10:18
the this is, it's not just the the bioinformatics and machine
10:22
learning AI element. It's the combination of that in
10:27
context with synthetic biology tools.
10:29
So we can design 50 a hundred different fragments of synthetic
10:36
super enhancers, as we call them to create this genetic switch,
10:40
but we're able to then build those as drug products.
10:45
So the DNA, the virus, and then actually test that in meaningful
10:54
models. So translational, you know,
10:56
patient drive cell lines, patient tissue syngenate mouse
11:00
models, and we're able to do that in incredible throughput.
11:03
So it's a combination of those three things that the AI
11:07
synthetic biology tools and the meaningful models that we can do
11:11
in an iterative synthetic biology type development cycle
11:15
in screen 5000 different therapeutic drug candidates and,
11:20
and know incredibly quickly that we have that precision to do
11:24
what we need to do. And as I said, with with
11:28
precision, we in cancer, we know what we want to do, we want to
11:30
kill and we want to train the immune system.
11:32
And there's, there's lots of, you know, validated in the
11:36
clinic drug products out there that, that, that they show that
11:42
it can work if you have the precision, which is what we
11:45
bring. And with our lead program, we
11:48
have that in GBM. But underlying platform is for
11:51
for every solid tumor, every, every disease cell type really.
11:55
So, So what we're really looking to now is and rolling that out
11:59
across multiple different programs.
12:02
Nice. And just to go into the the
12:05
glioblastoma space, it's obviously been a very difficult
12:09
space to be in over, over previous times.
12:12
Why did you start here instead of a more friendly tumor type?
12:15
And what just maybe give us a bit of a run through some of the
12:18
preclinical results, What, what did that tell you about the
12:21
potential for durable responses in patients as well?
12:25
Yeah, so, so, so GBM is certainly not friendly.
12:28
I mean it's the it's the worst of it's the worst of cancer is
12:31
the biggest killer of the under 40s shoot unmet need.
12:36
But it's but it's also been an area where there's been a lot of
12:39
failure. They've been been in 20 years.
12:43
The standard of care has not really progressed, but equally
12:49
there are signs out there from from current clinical trials
12:53
that immunotherapy can work if you can hit the tumor hard and
12:57
early. There's this plenty signs out
13:00
there that to show that immunotherapy can work.
13:02
And that's it. That's exactly what we do.
13:05
Because of the precision that we bring, both the FDA and the MHRA
13:10
have approved us to go ahead of standard of care.
13:14
Now that's really important for two things, right #1 you want to
13:20
treat people early when they've still got an immune system to
13:23
respond. It's an immunotherapy at the end
13:25
of the day, so you want to treat people early.
13:28
But two, in terms of the drug trial, that means we doze and
13:34
then three weeks later, we'll reset what's left of the tumor
13:39
and that. And from a drug development
13:40
point of view, that's incredible position to be in.
13:42
Now that I've been involved in Parkinson's and Huntington's
13:45
where you're looking at 2 CRN points within a few weeks.
13:48
We have that biological material in our hand and that really
13:53
propels the the, the clinical trial forward and we can make
13:57
informed decisions. Have we got the dosing right?
13:59
Have we got the volume right? And that that, yeah, that
14:04
propels us through the clinic. And I guess one of the recent
14:08
milestones that you guys announced was your fundraising
14:10
round. So you announced a $95 billion
14:13
or £70 million Series A round, which is an amazing milestone,
14:18
particularly given how tough the biotech arc it's been over over
14:22
the past few years. What do you think was the key to
14:25
convincing investors to to take a leak with Trojenix and you?
14:29
And how important was some of the backing from companies like
14:31
Eli Lilly in terms of both credibility and and validation
14:35
as well? Yeah.
14:37
So, so it has been a difficult funding environment, but I, I
14:41
guess the message is that when the right components are there,
14:44
then then the the funding finds you.
14:47
We have a team that been there and done it.
14:51
The, the science is utterly compelling and the opportunity
14:56
to, to commercialize and actually get this to patients
15:00
is, is really advanced. So I think all of those things
15:06
were very compelling for the VCs, for the, for the pharma
15:10
partners and we were able to provide to, to complete an
15:16
upsized funding round. And we did that because number
15:22
one, it allows us to take the lead program in GBM through to
15:26
what I think can be registrational data.
15:28
But Elite really allows us to to put in the pipeline and bring
15:32
our next programs into the clinic as well.
15:39
But you know, to go back to your point about, you know, the
15:42
investors and the team and board, what's what was great for
15:48
us as, as a, as a company was then to, to be able to choose
15:52
the right partners to bring into that, into that boardroom, into
15:55
the, into the team that can help propel this forward.
15:58
And, and I think all of those partners support us in that
16:02
mission to to bring this to patients as quickly and
16:05
effectively as possible. Yeah, nice.
16:08
And I think like obviously the oncology ecosystem is, is
16:13
definitely crowded within immunotherapy, gene therapies
16:15
and cell therapies. If you just look at like the
16:18
broader landscape, how, how do you see Trojanix fitted in that,
16:22
Yeah, that, that, that space. So in GBM, you know for for us
16:27
it's the perfect for perfect indication to go after first.
16:32
OK. And there's there's a number of
16:34
reasons for that. Number one, the huge unmet
16:36
needs. Two, we understand the
16:40
pathophysiology of the disease. 3, we have the differentiated
16:44
technology and four, there's a really supportive regulatory
16:48
environment, so we can move it through the clinic quickly and
16:52
and in very formed ways as I was explaining, we can leverage that
16:58
then you know, we can leverage that clinical data in GBM into
17:02
another entire pipeline programs.
17:04
So in liver and other indications in the brain and the
17:08
lung, they all benefit from that, that first product moving
17:14
through. So we can bring that through
17:16
faster in terms of the differentiation.
17:20
I mean, as I said, we have seen a cancer cure revolution, but
17:24
but really I think we can be so much more ambitious now.
17:28
We have the tools to move beyond chronic cancer care and think
17:34
about curative one and done therapies.
17:36
And that's that's the space we're in.
17:38
And not many people have really made that that kind of next step
17:44
in terms of that revolution. And so I think we're leading the
17:47
way there, particularly in solid tumours of huge unmet need for
17:53
we desperately need to make that next time.
17:57
Sounds so exciting and this next question, I'll break it up into
18:00
two. But what So what the company is
18:03
based out of Edinburgh, Why did you choose to base Trojanix in
18:07
Edinburgh versus maybe moving the company to a more a bigger
18:12
hub maybe across the US or wherever that is?
18:16
Just talk us through what some of the advantages of operating
18:18
in Scotland of you in terms of talent research and
18:22
collaborations. Yeah.
18:24
So, so I guess when when thinking about company, I mean,
18:26
number one has to be the people, right.
18:29
Have you got the best possible people to deliver and the the
18:34
mission and the vision of the of the business.
18:36
And then here and I remember we we certainly have that.
18:40
I mean, it's a huge strategic advantage for us.
18:44
The the company draws on advances in a number of
18:49
different key fields. So genomics, we're a world
18:52
centre in genomics, synthetic biology, we're the in the world
18:56
centre and synthetic biology, bioinformatics, machine learning
19:02
and oncology, of course. So immunotherapy oncology, we
19:07
are based in Edinburgh, the Institute for Regeneration and
19:11
Repair. It's the world's biggest of its
19:12
kind. It's over 1000 researchers
19:14
focused on the genomics and the bioinformatics on the synthetic
19:19
biology tools. And the second part is we we are
19:25
within the Cancer Research UK network.
19:28
So Cancer Research UK is the world's biggest research cancer
19:32
charity, $500 million annually into fundamental Cancer
19:37
Research. So that that's, that's been
19:41
transformational. I mean that's been over decades
19:43
and decades. So that the quality of the, the
19:47
fundamental science and cancer here is absolutely stunning.
19:51
So we have access to all of the best translational models and
19:56
the, and the people to really drive that vision forward.
20:00
So I think that's, that's a tremendous strategic asset to be
20:04
based here. And then of course on on a
20:07
personal level, I cycle a run to work everyday.
20:12
My kids walk to school. It's the most beautiful city to,
20:17
to live and work in. But of course I have, you know,
20:21
for the C-Suite. I have direct flights to Boston,
20:25
to New York. I have the sleeper train to
20:27
London. I can be in London for a 7:00 AM
20:29
meeting. So it's ideally located as far
20:33
as I'm concerned. Definitely.
20:34
And and just I guess on the flip side, what is there any
20:38
challenges that come with be being based up in Scotland and
20:42
being away from maybe some of the more typical biotech hubs?
20:46
Like what's some of the disadvantages of of being where
20:48
you are, if if any that is? I don't see any to be honest.
20:53
I mean like, like I say, I mean, I mean, so the, the core R&D
20:58
team, the the clinical development team are all based
21:00
here. Terrific talent.
21:04
And then for those of us in the C-Suite, that's so easy to go
21:08
anywhere in the world. I'm off to China on Sunday, so
21:11
direct flight from London, you know, I have direct flights to
21:16
Boston, NY or wherever I need to be.
21:18
So I don't see any disadvantages.
21:22
Yeah, nice. And correct me if I'm wrong, but
21:24
I, I assume that like being based up in Scotland, obviously
21:27
you're probably not paying the salaries that you would maybe in
21:29
London, like you probably have a a much healthier cash burn rate
21:33
as well. I would assume just being where
21:34
you are, salaries are lower, all of that sort of stuff, and
21:38
correct me if I'm wrong. With that, yeah, yes, yes, I
21:41
know. I mean, I like to think we we're
21:43
a global company, so we compete globally, but we have been very
21:50
capital efficient I would say. But I think that's more around
21:55
decision making and clarity of intent than it is about some of
22:00
the fundamentals. And but I'm yes, I'm sure our
22:03
lab costs are cheaper than they are in Boston.
22:09
But I think capital efficiency for me is driven by the clarity
22:13
of intent. And I think one of my learnings
22:16
through my career and and particularly in this business is
22:21
that you have to start with the end in mind, OK?
22:23
I think too often it's been a race to the clinic and that's
22:28
not the end goal. The end goal is getting this to
22:30
patients is to commercialize and we make better decisions on that
22:34
journey if we're if we're thinking about it from the very
22:38
beginning. So one of the things I did early
22:41
doors was bring on my chief strategy officer, T Salamilla.
22:44
He was Chief patient access officer for Novartis gene
22:47
therapy. He rolled out Kim Raya, Carl
22:50
Ginn, first car T have roll out Zoljesma.
22:55
I mean blockbuster AAV gene therapy.
23:00
We did that preclinically and we did it because we're always
23:05
thinking with the end of mind. How do we bring this to
23:06
patients? And I think that with that
23:10
thought process, you become capital efficient.
23:18
Yeah, definitely that, that's something that I, I get asked a
23:20
lot, I guess from someone on the other side of the feds to
23:23
recruitment, like at what point should we bring commercial into
23:26
the into the business? And often companies think about
23:29
that earlier and earlier, which which obviously makes sense just
23:32
given that you have that angle that you're trying to trying to
23:34
get to. So, yeah, so when, when, when I
23:37
was in big pharma, you know, we always said, you know, you've
23:41
got to plan C years ahead at least your commercial strategy.
23:44
Now because of the unmet need and because of I think the
23:50
transformational results we we can bring.
23:55
I think that's, that's exactly where we are.
23:57
I think we can bring registrational data and and
23:59
commercialize in a very short time frame.
24:03
So we have to be thinking about it early.
24:05
And like as you look ahead to the next sort of 12 to 24
24:08
months, just talk us through like what are the next major
24:10
milestones, inflection points that you guys are looking
24:13
forward to? And my guess is, is that after
24:16
the obviously had a successful fundraising round, there's a a
24:19
big focus on execution now. But what's some of the
24:21
operational or organizational goals that are coming up which
24:25
are critical for for Trogenix's future?
24:28
Yeah. So, so there's always a focus on
24:30
execution. That's that was one of the key
24:32
things that and I'll close that round so readily this year.
24:39
We're in the clinic UKUS and in GBM that the sad story is that
24:46
because it's such an an aggressive cancer, we, we reach
24:50
meaningful endpoints quickly. So we will be generating really
24:54
important clinical data this year in the lead program, but we
24:58
will be entering within within 1224 months.
25:00
We're entering the clinic with our follow on pipeline programs
25:04
as well. So I guess that's they're the,
25:08
they're the key value catalysts, you know, showing, you know,
25:13
first in class therapeutic in the clinic with meaningful, with
25:18
meaningful endpoints. Nice, exciting.
25:21
And then just to finish off a couple of more personal
25:24
questions. I think if you, you've obviously
25:27
had a of a superb, impressive career so far.
25:31
If you were to look back at your younger self and just give one
25:34
piece of advice at the start of your career, what what would
25:38
that be and why? I've been, I've been blessed
25:41
with with many mentors through my career.
25:45
I could quote with various bits of wisdom they passed on to me.
25:49
So I don't want it. I don't want it to kind of be my
25:52
own words in some ways. But I remember when I was first
25:56
promoted, my first leadership role and my mentor said, look,
26:01
can you, you don't have to be the smartest person in the room
26:04
now. And I find that very liberating.
26:09
You know, the idea that I say not bring in as many smart
26:15
people around you as you can. And you know, as a leader, your
26:18
role is just helping everyone else be as good as they can be.
26:24
I thought was OK, that's that's liberating.
26:27
I don't. It's all about the team.
26:32
And I guess, yeah, as a younger person, you maybe don't always
26:36
see that so clearly. Yeah, and if you were to have
26:40
dinner with any free people, past or present, who would you
26:44
go from? Why?
26:44
It doesn't necessarily need to be people in biotech, although
26:48
it can be if you like. But yeah, any three people you'd
26:51
like to just sit down and have a have a dinner with?
26:54
Yeah, that's, that's actually an easy one.
26:56
And one of them isn't biotech, but the, the, the answer is my
27:00
wife and three children, I guess building companies, getting
27:09
drugs to patients. It's it's quite time consuming.
27:11
It's, you know, the mission is so important.
27:14
It's definitely involves the whole family.
27:17
And I'd probably don't see them as much as I would like.
27:21
So if I had one night to go and go and after it I'd be my life,
27:27
it gets easy. Yeah.
27:29
Look, I love the answer and thanks again for coming on and
27:32
helping us out with this. It sounds like you know, what
27:35
you're building at Trogenics is super exciting and I'm looking
27:38
forward to seeing the next inflection points that you guys
27:40
will have and and following the company more closely.
27:43
So thanks for coming on and helping us out with this.
27:45
It was a pleasure to hear a bit more into Trogenics and and your
27:48
story as well. Well, thanks, Tom.
27:51
It's been a pleasure.