Latest / The BioHub - by Avetix / Episode 73 - Tatiana Novobrantseva - CSO of NextPoint Therapeutics

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Episode 73 - Tatiana Novobrantseva - CSO of NextPoint Therapeutics · The BioHub - by Avetix

0:04
So welcome back to the episode of the Bio Hub.
0:07
Today, we're excited to host Tatiana Nova Brand to Sava, a
0:11
scientist and biotech leader who's been at the forefront of
0:13
some of the most exciting breakthroughs in immunology.
0:16
Tatiana is the CSO at Next Point Therapeutics, where she's
0:19
driving innovation in precision immuno oncology and developing
0:23
new therapies to harness the immune system in cancer.
0:26
Tatiana's career spans leadership roles at companies
0:29
like Modern Giants Therapeutics and Al Nylon, and she's also Co
0:34
founded Versao Therapeutics. So join us today as we'll talk
0:39
through Tatiana's journey, next points pipeline and Tati's
0:42
Tatiana's role in business development as ACSO.
0:46
So Tatiana, thanks so much for coming on.
0:48
How are you? I'm doing well.
0:50
Thank you very much for having me.
0:52
It's really a pleasure to be here.
0:54
Yeah. It's a pleasure to have you on
0:56
as well. So thanks so much for coming on.
0:58
So look, let's start off with a little bit about your journey
1:01
then. So you've had a career that
1:03
spans across academia, pharma, biotech, and now cutting edge
1:07
immunotherapy. Can you walk us through your
1:10
journey into immunology and what's kept you excited about
1:13
the field over the years? It's, it's, it's a wonderful
1:17
question, right? Because immunology has not
1:21
always been a wonderful field to be in from the external
1:26
perspective, but for me, it has always been really the
1:30
centerpiece of how everything has evolved.
1:35
I always like to tell the very beginning of the story, right?
1:38
So I have hay peepers and they were pretty violent.
1:44
And there were absolutely no drugs, right?
1:48
No antihistamines back, back back then.
1:51
So after very long winters in Moscow, right, when everyone was
1:55
outside and enjoying the sunshine, that finally was
1:58
there, right, I was absolutely stuck inside, right?
2:01
With my nose against the window thinking, I mean, what the hell,
2:04
Like, why, why is this happening, right?
2:07
So that was really a very personal, very simple, I guess
2:11
reason to start wondering how the immune system works at all,
2:15
right? And we're really talking about
2:17
about school, right? So elementary school.
2:21
And that's how it sort of eventually led me to become an
2:25
immunologist, right? So I did my PhD in at the
2:30
University of Cologne with Klaus Raevski in B cell immunology and
2:34
really digging into what makes our immune system react, right?
2:39
What is the enemy and how does it clear out?
2:43
That enemy becomes a very, very interesting question.
2:46
And now you know, with a lot more that I know, a lot more
2:52
that the field knows, right? It's really not a simple
2:56
question and we don't always have the answers, especially
2:59
when designing drugs that we try to target a very precise
3:04
populations of immune cells to either attack cancer or to help
3:07
fighting an infectious disease or try to revert fibrotic
3:12
disease. I mean any, any type of
3:14
inflammatory consequences, right?
3:18
It's, it is still a complicated not 100% answered question, but
3:23
nevertheless, that's, that's how my interest in immunology came
3:29
together right and stayed for years, right.
3:33
So my, but obviously my PhD and postdoc were very basic, very
3:40
fundamental B cell immunology with a lot of genetic
3:44
manipulations and making mice that express only one possible
3:50
receptor specificity on B cells and seeing how those B cells
3:53
actually behave if they failed the whole Organism.
3:58
Then I went into industry and my first industry job was at
4:02
Biogen, and that was involvement in a lot of inflammatory type
4:08
projects. There were a couple projects
4:10
that really concerned B cell development, but we also studied
4:13
a lot of inflammatory and fibrotic conditions and found
4:17
super interesting insights there.
4:19
And then I went to Alnylam, and Alnylam was first and foremost
4:24
about making nucleic acids a drug, right?
4:29
So a serenade as a new therapeutic modality.
4:32
And back then, no one believed it could be a therapeutic
4:36
modality, right? So being an immunologist, there
4:38
was an interesting proposition because it certainly brought a
4:41
unique perspective. And we have beautiful projects.
4:44
I'm trying to deliver outside liver, but that was certainly
4:47
before its time because it's only now becoming popular and
4:53
back then, you know, I've heard many different opinions.
4:56
So come on, focus on some real organs like liver, right?
5:01
That is there, you know where to find it.
5:04
What are those floating immune cells?
5:08
And then actually immuno oncology responses came right in
5:15
the field. So CTLA 4 blocking antibodies,
5:18
PD1 PDL one blocking antibodies started to produce amazing long
5:22
lasting responses in cancer patients.
5:28
And that's when suddenly immunotherapy brought immunology
5:31
to the forefront. And now we are really in a mini
5:35
renaissance of of immunology because both immunotherapy and
5:40
out union research are really thriving.
5:42
So has been a long journey. I hope I explained how I got
5:46
interested, but then there has been so much happening that it
5:49
was impossible not to stay interested.
5:53
Yeah, good. You, you've obviously been in
5:56
both academia and the industry. What do you think the big
6:00
differences and similarities are between an academic and industry
6:04
approach to immunology? Well.
6:07
So, you know, it's a, it's a, it's a, it's a question really
6:11
that many, many, many people ask because everyone who starts in
6:16
science starts in academia, right?
6:18
There is no other way to start. You start with getting some
6:22
education, right? That doesn't matter which degree
6:24
you get. And then you either switch or
6:28
stay, right, or collaborate. And now, actually, I think that
6:32
with time, a lot of the boundaries blur, which is a
6:36
wonderful thing, and a lot more people are involved in both or
6:40
have been switching back and forth.
6:42
But again, when I was graduating from my PhD program, it was
6:49
still pretty frowned upon to go into industry research because
6:54
if you were a real scientist, right, you needed to stay in
6:57
academia and sort of dig very, very deep into that particular
7:04
discipline and set of questions. So there has always been a
7:12
little bit of maybe higher meaning in academic research,
7:17
right? Which I certainly was under the
7:21
spell of, right? And when I got a phone call
7:24
asking me if I'm interested in interviewing for a position
7:28
budget, and I actually said that I was not right.
7:32
Thank God I was convinced to go and interview.
7:35
And when I came into the building, I started talking to
7:39
people who actually worked at Biogen, right?
7:41
They I realized they were absolutely phenomenal scientists
7:45
with great publication records. But in addition to driving
7:51
science and getting to the publication, they had a
7:55
possibility to actually develop something that will change how
7:59
we treat disease and it will change people's lives, right?
8:02
So for me, that was such an eye opening experience and I was
8:06
absolutely naive to what industry is especially in the US
8:13
because you know, I still think that and, and there is a lot
8:18
less biotech in Europe still today, even though the field has
8:23
expanded and flourished. And there it's it, it, it is
8:26
absolutely amazing. But just by by sheer volume,
8:30
right, there's still more here. Obviously there is huge
8:34
competition now coming from Asia, in particular China and
8:38
Singapore and Korea, right? So there is a lot happening
8:44
everywhere. So this is, this is all
8:46
wonderful, but just having that. So I think that that's the main
8:49
difference really, right, That your project can contribute to
8:55
making something that people use within your lifetime rather than
9:01
contributing to the fundamental knowledge, which is incredibly
9:04
important, right? And without that, pretty much
9:08
nothing would have been possible today, right?
9:11
But might not contribute to anything that people can use.
9:16
So this is not, I think that both are incredibly fulfilling
9:20
careers. And at the end of the day, it's
9:23
a personal choice and 1 can be involved in both, which is
9:27
wonderful. But that's that's for me maybe
9:31
the only difference. Yeah, very good.
9:36
So you joined Next Point as Chief Scientific Officer in
9:39
2024. What drew you to the company and
9:43
what made this opportunity stand out to you at this stage of your
9:45
career? Yes, I joined in January 24,
9:50
right after JP Morgan conference was over.
9:53
I didn't want to participate in JP Morgan conference two days
9:56
after joining the company. So next point, as as as usual,
10:03
as with every opportunity in life, right, the important thing
10:07
for me is science and people, not necessarily in that
10:12
sequence, but those are the two driving things, right?
10:17
So what is done at the company, right?
10:21
What is it based on and what the company is developing and the
10:24
team surrounding that. And the team of course is
10:28
involving everyone, right, founders, investors, the actual
10:34
operational team. And next point manages to
10:37
combine all of that. It's, it's super innovative
10:41
science, great execution, phenomenal investor support and
10:46
absolutely wonderful founders. So it was, it was just an
10:52
amazing opportunity. And so I, I, I was very, very
10:57
lucky to have had that in front of me and for their ability to
11:01
join. Yeah, very good.
11:05
So next points pipeline includes 2 clinical stage programs and
11:09
two Imds on the horizon. Can you tell us more about these
11:13
programs, what makes them different and where you see them
11:17
making the biggest impact? So next point is all around the
11:24
7H7, which is also called HLA 2 and the two receptors to the
11:29
molecule and while being centered around that pathway,
11:35
which is not found in in Roden, so not found in mice and rats,
11:41
but is present in primates, both non human primates and humans.
11:49
It's it's an incredibly innovative space because people
11:54
didn't have their body to study that in my.
11:57
So it's always was very difficult to actually get to
12:00
studying that because you have to be within human systems.
12:05
And the two programs that are in the clinic are immunotherapeutic
12:10
programs because B7H7 through those two receptors, 1 is CARE
12:15
3DL3 and another one is TMIT D2 is either inhibiting or
12:21
stimulating different immune populations and regulating the
12:25
immune responses. So the first two programs are
12:28
really immunotherapeutic approaches.
12:30
The first one to inhibit your 3DL3, which is an inhibitory
12:33
receptor if you like an analog of PD1, even though it's
12:38
expressed in a completely non redundant and independent
12:44
setting and on different cells. But the second program is really
12:50
inhibiting B7H7 on the tumor cells, but also by that
12:55
inhibition limiting the interaction with care 3DL3, but
12:59
opening up the interaction with team HD two, which is a cost
13:02
stimulatory receptor. So trying to activate the
13:05
immune, both approaches try to activate the immune system to
13:10
attack cancer. Whereas the first program is
13:17
what we call a pure antibody that has just the blocking
13:23
ability as much as we can stay within one mechanism.
13:27
The second antibody also has enhanced ADCC activity.
13:31
So it can through the FC receptor activate in key cells
13:36
and macrophages to really kill the tumor directly in addition
13:41
to blocking the inhibitory mechanism through B7H7 and
13:46
activating the activatory mechanism.
13:48
So those are the two programs in the clinic, right.
13:51
But then while working and the when the company was really
13:56
started, it was an immunotherapeutic company that
14:01
deals with an independent chip point, right that is heavily
14:07
present in PD1 non responsive populations of of patients and
14:15
has completely non redundant regulation in the immune system.
14:19
However, while working on this within the company, we realized
14:23
that B77 can also be used as a tumor target because it is
14:29
highly upregulated on a big, big array of human tumors and it's
14:35
only expressed really on one tissue.
14:38
And this is got epithelial cells got associated epithelial cells
14:43
in the normal tissue. So there is a lot to be said
14:48
that we can actually target that molecule and cause direct tumor
14:52
disruption and also potentially add immunotherapeutic effects to
14:57
that destruction. So while destroying the tumor,
14:59
we can stimulate the immune system to recognize what's being
15:02
destroyed to keep the responses really long term.
15:05
So that's, that's, that's, that's the pipeline and it's a
15:10
pretty amazing combination within one pathway to be able to
15:15
to do both and potentially combine those in one molecule.
15:20
Yeah. And you've worked on both tumour
15:23
target targeted therapies and immune modulating strategies.
15:28
From your perspective, what do you think the strengths and
15:30
limitations are of each approach, and how do you think
15:33
they can complement each other in cancer treatment?
15:37
So I just told you that we can actually combine them with one
15:42
molecule potentially. But let's maybe take a step back
15:47
and talk a little wider than just next point approaches
15:51
because your question is just to compare tumor targeting versus
15:54
immunomodulation. And then we'll circle back to
15:57
next point approaches because I think it illustrates a very,
16:00
very interesting approach and example of how they can be
16:04
combined. Anyhow.
16:05
So tumor targeting is very difficult because tumor is
16:10
derived from normal tissue and it's extremely difficult to find
16:15
something which is super specific on the tumor, but is
16:19
never present anywhere else. But if we find something like
16:23
that, then of course we can just directly destroy those cells by
16:29
targeting a toxic payload, by targeting the immune system to
16:33
those cells to destroy them, right?
16:35
So that becomes easy. But that distinction is very,
16:38
very difficult. And people are using now very
16:41
different approaches, right, Either identifying tumor
16:45
associated antigens, which has been probably 150 years, maybe
16:51
more now long effort and it has produced some wonderful results,
16:58
but not that many. And now people are looking at
17:03
what can be even more specific. Can there be a peptide which is
17:08
presented by MIC complexes on tumor cells that is only
17:11
produced by those tumor cells? And there are some, right?
17:14
They can be derived from rearranged genes within the the
17:19
tumor itself, right, from aberrant expressed genes, maybe
17:23
from what is called dark genome, so from non coding regions rate,
17:28
but that are activated in the tumor specifically.
17:31
So those approaches are wonderful if you have something
17:34
that is super direct, but it's very difficult to find something
17:39
super specific, right? And the second limitation of the
17:42
approach is that the more specific you get, typically you
17:46
get to smaller and smaller patient population basically
17:53
already coming to very individualized care, which again
17:57
is, is, is becoming possible because we are becoming better
18:01
and better at analyzing whole genome, whole exome, whole
18:08
metabolism, whatever, what whatever we, we need to rate
18:12
things, but they, they are expensive.
18:14
And if you can have a wider approach, it's always good if
18:20
it's specific enough, right. So that's on the tumor targeting
18:23
side. On the immunotherapy side, you
18:26
are really trying to use the immune system and its natural
18:31
ability to recognize the tumor and to re stimulate responses.
18:34
Because by the time the patient is diagnosed, the immune system
18:37
is losing the battle, right, that the tumor is growing.
18:40
So immune system cannot control it anymore.
18:45
So immunotherapeutic approaches are wonderful in a sense that
18:49
they can typically be applicable to very wide patient populations
18:53
and that generally very safe because you're trying to
18:58
reactivate pre-existing immune responses and generate new ones.
19:02
But they are really generated in the most natural way.
19:08
Of course, it also has the drawback that if you activate
19:13
too many immune cells or not specific enough to the tumor,
19:18
they start destroying healthy tissue.
19:21
And autoimmune type responses are probably the main side
19:29
effects of immunotherapy, right. So we are dealing with narrower
19:36
populations versus wider populations, right, In tumor
19:40
targeting versus immunotherapy, we're dealing with different
19:43
side effects because of different payloads we use.
19:48
But ideally, right, we all would like to see cancer just go away,
19:56
meaning we want to destroy the tumor.
19:58
And if the tumor burden is very, very large, you'll likely need
20:03
something that directly destroys the tumor.
20:06
Even if it's used for a very short period of time, but then
20:10
you need the immune system to clear out the remains and keep
20:15
the tumor from coming back. So ideally, we would want to
20:18
combine those approaches, right? And for that we need sort of a
20:22
good arsenal of tumor targeting approaches so that hopefully
20:28
every patient would have something that targets his or
20:31
her tumor and then immunotherapy to really give the long lasting
20:39
responses that will keep the patient tumor free, right.
20:44
So and coming back to next points programs, we have a
20:48
chance. Of course, unfortunately it will
20:51
not work for every patient because the patients for which
20:54
it will work, hopefully we'll need to express B7H7 on the
20:57
tumor, just a large population, but not every cancer patient
21:02
does. But if we manage that, that we
21:06
can actually target the tumor with CD3 Engager or an ADC, but
21:11
then within that very same molecule we can stimulate the
21:14
immune system, enhance the recognition of doing cancer and
21:17
keep the long term responses. So that's that's the hope
21:21
working with a unique molecule that can serve both as
21:25
immunomodulator and a tumor target.
21:28
Yeah. Very good.
21:30
The immuno oncology field has evolved rapid evolved rapidly in
21:35
the last decade. Where do you think the field
21:37
stands today and what do you think the next frontier looks
21:40
like in immuno oncology? This is, this is an amazing
21:46
question coming now right in mid 2025 because right now the
21:52
immuno oncology field is not the most popular, I would say
21:57
compared to several years ago especially.
22:03
But so if we go back some 10-15 years ago, right, immuno,
22:12
oncology, immunotherapy, tumor immunology, all were really
22:19
unpopular, very niche, small disciplines, right?
22:27
Very few people involved and no one believed it could be done
22:33
because immune system is having such broad mechanisms, you can
22:38
do nothing to it that will be tumor destructive and safe at
22:42
the same time. You're either not stimulating
22:44
enough and not doing anything to the tumor or everything will
22:47
just blow up. Then CDLA 4 inhibition and then
22:53
on its heels, PD1 inhibition came and started showing long
22:57
term responses and Melanoma, which before that was a death
23:01
sentence, right? Late stage Melanoma.
23:05
Basically people were told to just go and put their pairs in
23:10
order, right? And suddenly we, we, we, we
23:13
found immunotherapy that that caused responses unfortunately
23:17
not in majority of patients, but the combination of CTLA 4 and
23:21
PD1 probably can do very meaningful things for 40 ish
23:26
percent of those patients, right.
23:28
So that's what created this humongous popularity.
23:34
Everything was immuno oncology. We can do a lot more.
23:39
Let's build on that momentum. Let's try to get to the patients
23:44
were not affected by this right. The field has exploded, but then
23:52
within that explosion, right, people were trying to combine
23:55
everything with PD1 inhibition or use molecules that look
23:59
exceedingly similar to PD one and are expressed in very, very
24:03
similar populations of immune cell that compared to PD 1.
24:07
So until today, there is no second PD one, right, which is
24:13
broadly applicable, reasonably safe and effective.
24:19
So people started saying, OK, is it immuno oncology or is it just
24:23
PD one. And obviously I strongly believe
24:28
that this is immuno oncology and we just need to change the
24:31
approach where we're looking and there are a lot of approaches
24:34
targeting different cells targeting receptors that are
24:37
independently regulated from what causes up regulation of PD1
24:42
and PDO 1. So we we will find something
24:46
which is very broad. But right now the, the tumor
24:52
targeting approach is maybe with a little bit of immunomodulation
24:55
and T cell engagers, which by the near the fact that they
25:00
engage T cells directly, they become immunotherapy because T
25:03
cells are part of the immune system.
25:05
But in essence they have tumor targeting approaches, right?
25:07
Because we bring T cells via tumor associated antigen
25:11
directly to the tumor cell. So they're really taking center
25:16
stage and as I just said within the last five minutes or so,
25:21
right, They that makes the, the therapeutic approach is very
25:26
narrow, right, because you need a very good targeting agent,
25:30
which is difficult to find, especially for wider population.
25:34
So I think that the field is wide open and we're really
25:38
waiting for the next thing. Maybe I will comment on one more
25:46
relatively recent development, PD1 or PDO, one that Jeff by
25:50
specifics have been all the rage for the last year or so on the
25:56
heels of clinical data. So seeing responses and people
26:00
who failed every available therapy, including PD.
26:03
One, the jury's still out there. We haven't yet seen the full
26:11
data sets that lead to approvals, so we're still
26:16
waiting. But that combination engages the
26:21
Jeff pathway in addition to PD1 pathway.
26:24
And the Jeff pathway is certainly touching a lot on
26:28
innate immunity as well as blood vessel formation and and then
26:32
tumor supply. So this is venturing outside of
26:36
just T cell reactivation or activation.
26:42
So hopefully that will pan out or at least that will pave a way
26:48
for differentiated approaches beyond PD, one in very, very
26:54
different patient populations and then very different
26:57
immunological mechanisms. So I really think that all types
27:03
of bispecifics as well as just monoclonal antibodies activating
27:09
other than just T cells. So either multiple cell types at
27:14
the same time or activating myeloid cells or activating and
27:17
K cells will bring something that will be wide, effective and
27:25
safe. Yeah, good.
27:29
So your role currently as CSO, you're not just leading science,
27:32
but you're also involved in shaping partnerships and
27:35
strategic direction as well. What's your role in business
27:39
development at Next Point, and how do you see science driving
27:42
those conversations? So yes, I am very, very actively
27:48
involved in both internal strategy shaping as well as
27:54
external conversations with potential partners and or
27:57
investors. It's a fascinating asset to have
28:04
in sort of in, in, in your position to be able to talk
28:09
science to very, very wide array of people.
28:14
And at least when I was going through formal education, I was
28:20
never taught how to talk to people who are not trained in
28:24
science, right. So we are all trained to present
28:28
to fellow scientists and to people who are really super well
28:33
versed in exactly that field that you are studying, which is
28:38
necessary because again, if you need to do something novel at at
28:44
the very least you need to be able to explain why it matters
28:48
and why it's novel to people who have been studying similar
28:51
things, right. On the other hand, when you're
28:54
talking to potential partners and investors, it's a very
28:58
different conversations. It's, it's a different set of
29:04
people with the interest to see where this program can take you,
29:11
right. How can we solve an unmet
29:15
clinical need? And if we do that well, is there
29:21
potential to also do well financially if we're talking
29:24
about investors in particular, right, but also for farmer
29:29
partners right at, at at the end of the day, every company is a
29:33
business. So they need to be able to sell
29:36
the drug, right, and get the profit that will continue
29:41
driving innovation and generation of the novel drugs.
29:44
So it's, it's, it's, it's fascinating from that
29:49
perspective, right? But also bringing science and
29:51
that those conversations, I think is super important because
29:56
I know by now that the the deals are best made by people who are
30:03
actual business professionals, right?
30:05
Because they pay attention to that level of comfort with the
30:13
overall story. But giving that scientific
30:18
perspective into this, right? I think it's, it's super
30:21
important because then we don't over promise and we keep things
30:27
bound to what we can actually show under any circumstances,
30:32
right? With any amount of funding.
30:35
Because some things we just wouldn't be able to do in, you
30:39
know, in a reasonable time frame or under reasonable budgets,
30:42
right? So that's, that's, that's one of
30:45
the roles, but also explaining how unique and differentiated
30:50
each approach might be is, is a phenomenal conversation to have.
30:57
So I, I really think that that's, that's also very
31:00
important contribution from the scientific perspective to those
31:02
conversations. Yeah, good.
31:05
And you've LED scientific teams in both large multinational
31:09
companies and nimble biotech start-ups.
31:13
What do you think the major differences are in terms of
31:15
leadership style and execution across the two different
31:19
environments? You know, this is always a super
31:23
interesting question and I don't know, there are humongous
31:30
differences really. So people interact with a
31:37
certain number of individuals regardless of the company's
31:42
size, right? So if you work in a super large
31:47
company, most of your interactions are internal or all
31:50
of them are. If you work in a very, very tiny
31:53
company, most of your interactions are external and
31:56
you work with CR OS or collaborators, etcetera, right?
32:03
But there are only so many interactions one can have in a
32:06
day. And that creates your network
32:08
and team and sort of processes you need to drive.
32:13
And those interactions, I don't think they change too, too much
32:18
based on where you are, right? There's a, a larger company, a
32:23
smaller company. I guess the only thing that
32:27
really changes is the number of approval levels, right?
32:32
So in a company the size of next point around 30 people, right?
32:38
It's all very clear, right? You can make decisions very fast
32:43
and you know that there is literally less than a handful of
32:46
people whom you can assemble within a couple days, right?
32:50
And the decision is made in the large organization that needs to
32:56
go through different levels, right?
32:58
And, and sort of to, to reach a decision, you need to go through
33:02
multiple different conversations and then bring a united front to
33:08
the final decision maker, right? But other than that, I don't
33:13
know if it really changes that much.
33:16
And I really enjoy staying involved in both scientific
33:20
detail and and in the sort of strategic level conversation
33:28
because I think that that that really creates that necessary
33:31
connection so that we stay real and true to what is possible.
33:37
Yeah, good. And last question and I know
33:40
wanted to give you a bit of a heads up on this, but if you
33:43
were to have dinner with three people past or present, who
33:47
would they be and why? They don't necessarily need to
33:49
be biotech innovators, although they can be if you like.
33:53
But yeah, three people for for dinner.
33:57
So thank you for asking this question.
33:58
Thank you for for warning me, right, because it's always a
34:02
super tricky thing to to come up with three names.
34:08
And first and foremost, that question really made me think
34:13
about people whom I can go out for dinner with in real life.
34:17
And I should really do that more, right?
34:21
So thank you for for that. I think that was a great sort of
34:28
call for action, right? But for the answer to your
34:33
question, I will stay hypothetical because
34:35
unfortunately I cannot meet any of those people anymore.
34:40
But the three names I want to bring to the conversation today
34:44
that are following. So one would be Maurice
34:47
Gladovska Curry, right, the famous radioactivity researcher
34:53
who had ginormous success in identifying our isotopes, right,
34:59
and sort of determining what the activity actually is.
35:06
But it would be just phenomenally interesting to ask
35:10
how she saw her life, right? Because what we know now, of
35:16
course, is always colored with a historical perspective and we
35:20
know how unique she was and what's the size of her
35:23
contribution. But how did she feel this
35:26
day-to-day? I think that would be just a
35:30
very, very, very exciting conversation with, with really
35:34
no end to it. So that's, that's, that's one,
35:39
right. The second conversation I would
35:41
love to have would be with Barbara Mcclintock.
35:45
So she is really a geneticist studying Maze mainly and she has
35:52
been a humongous innovator, right.
35:56
She actually found a way to visualize chromosomes and then
36:02
she was the discover of transposons among many other
36:05
things. She was also a person who looked
36:09
at what centrism and telomere are doing, so many things that
36:15
now really ended up in biology one O 1 books and from again
36:23
historical accounts. I never had a chance to hear her
36:28
talk or present. She was also just in love with
36:34
what she was doing and she could talk about how she sees those
36:39
genes jumping and how that really influences the genetic
36:44
material from one generation to the other and how one can
36:50
possibly change that path, right?
36:53
So to hear her passion about this, right?
36:56
And, and how she stayed focused on something that very few
37:01
people at that time believed is even possible, right?
37:07
Or many people believe that all her explanations were completely
37:11
wrong for for many years, right. So again, to hear that would be
37:17
would be phenomenal. And one more name, right,
37:20
Because you asked for three. So the last name would be
37:24
William Cawley, which I think brings us back to immunotherapy.
37:27
So he is believed to be the father of immunotherapy and over
37:32
150 a 160 years ago he was treating his patients with
37:38
bacterial extracts and about 10% of them or so went on to
37:44
completely resolve their tumors. Of course, the treatment he was
37:51
doing would have been absolutely impossible in today's world
37:54
because every bacterial extract preparation was different.
38:00
No one could control the dose, no one could control the side
38:03
effects. So it's not something that we
38:06
could do today, but this is certainly something that got
38:11
people thinking about immune system involvement and the fact
38:15
that causing inflammation can actually pretty much cure
38:20
tumors. Even though I know that in the
38:22
oncology field, no one likes to talk about cures because
38:26
unfortunately recurrence is a real thing.
38:29
But but in practical terms, right, this is this is
38:33
phenomenal tumor control and tumor undetected state.
38:37
So talking to someone like that right, with the knowledge of
38:42
today and hearing him explain how he was explaining the
38:47
effects, right would be just just amazing.
38:51
And I think connecting through history unfortunately is
38:56
impossible, but would be great for the development of the
39:01
field. Yeah, very good.
39:04
We'll look 3 terrific answers there.
39:07
And I think you've given a really unique perspective of of
39:10
your role, the immunotherapy space as well as next point, who
39:13
I'm really excited to follow as well.
39:15
So, yeah, thanks so much for helping us out with this.
39:19
It was a pleasure to have you on.
39:21
Thank you. Thank you.
39:22
I I really enjoyed the conversation.
39:25
Thank you for inviting me again and for all the questions.
39:29
It was a pleasure.