Latest / The BioHub - by Avetix / Episode 231 - Stacy Blain - CEO & Founder of Concarlo Therapeutics

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Episode 231 - Stacy Blain - CEO & Founder of Concarlo Therapeutics · The BioHub - by Avetix

0:06
So welcome back to another episode of the Bio Hub the of
0:08
ethics podcast. Today, we're delighted to
0:10
welcome on Stacey Blaine, who's the founder and CEO of Concalo
0:14
Therapeutics. Stacey is a cancer biologist and
0:17
entrepreneur who spent decades studying the mechanisms behind
0:20
cancer growth and treatment resistance with a particular
0:23
focus on cell cycle biology and the P27 pathway.
0:28
For the past several years, Stacey's been leading Concalo
0:30
Therapeutics, who have precision medicine oncology company
0:34
focused on diagnosing and treating cancer with an
0:37
innovative approach to targeting a unique cellular pathway.
0:41
In today's discussion, we'll talk through Stacey's journey
0:43
through the field, including her transition from scientist to
0:46
CEO, the next inflection points for Concala Therapeutics and the
0:51
biotech CEO sisterhood. So Stacey, look, it's a pleasure
0:55
to have you on. How are you?
0:57
I'm great, thank you for having me.
0:59
It's a beautiful day here in New York and happy to chat about all
1:04
things cancer cell cycle and Con Carlo.
1:07
Yeah, amazing. Look, it's a pleasure to to have
1:10
you on. So let let's just start off with
1:12
a little bit about your journey through the field and and how
1:14
you ultimately ended up as as CEO of Con Carlo Therapeutics.
1:18
So can you just talk us through your journey through the field
1:21
from your academic years to I guess to, to where you are now?
1:25
Yes, so I am, I think I always assumed I would be an academic
1:30
for life. That was just sort of part of my
1:32
vision. I had done my PhD in molecular
1:36
cellular biology and I was finishing, I was starting my
1:39
postdoc at Memorial Sun Kettering Cancer Center.
1:42
And when I showed up, they had just discovered this brand new
1:45
protein called P27. And they essentially handed me
1:48
the project. And we knew from the get go that
1:52
P 27 was going to be a really potentially in interesting
1:57
therapeutic because it was pulled out via its interaction
2:00
with CDK 24 and six, which were these kinases that drive all
2:05
cancer growth. And everyone wanted to drug.
2:08
This was, you know, 1995 and everyone wanted to drug as a 246
2:13
and no one can do it. And so this was another way we
2:16
thought, oh, we can go after drugging really important
2:19
markets. And then I went and I was a
2:21
professor at one of the state universities of New York for two
2:25
decades and ran a research group and taught medical school and
2:30
sat on a lot of committees and just, you know, was really
2:33
assuming that would be my path for life.
2:36
Very hardcore studying how does P27 interact and inhibit these
2:41
really important kinases? But then figured that out, you
2:44
know, and figured out how P27 was actually the on off switch.
2:48
And then that led to the idea, well, wow, we could actually
2:50
make a drug and use this as a therapeutic.
2:54
So we patented a bunch of technology and for a variety of
2:58
reasons, then we started we spun out that technology and started
3:01
con Carlo and you know, real. I realized that all of my focus
3:06
was really trying to understand how our drugs worked and how P27
3:12
interacted with the drugs and how we could make the drugs
3:15
better. And so then that sort of was one
3:17
of the reasons that I eventually left academia to move to
3:21
entrepreneurship full time and lead Con Carlo in its efforts to
3:25
move this brand new therapeutic approach into the clinic.
3:29
So I guess I could say I was a reluctant entrepreneur, but I
3:35
was an entrepreneur. I, I, I followed the science and
3:38
the science led me to make a discovery, which led me to start
3:42
the company, which led me to to the next thing.
3:45
And I also believe personally, it's really important to have a
3:51
vertical learning curve. And so, you know, as I was sort
3:53
of reaching, reaching the peak of academic, you know, mastery,
3:57
so to speak, it was good to throw myself into a whole new
4:00
environment and have to learn, you know, everything about being
4:02
ACEO. And, and I personally enjoy that
4:05
challenge of, you know, always being a little destabilized and
4:09
having to learn new things. So that's how I ended up where I
4:12
am today. And you know, it was, if you
4:14
look back, it probably was a very linear path, right?
4:17
I was studying approach that led to a therapeutic and let's make
4:20
the drug, but it it was not. There was no forethought on my
4:24
my part to end up here. Nice, amazing.
4:28
And just just talk us through, So you've obviously founded
4:31
Conchal Therapeutics, you've been in the CEO position for the
4:34
past past few years. Just talk us through like what
4:38
was the original unmet clinical needs you were trying to solve
4:40
when you were thinking about setting the company up?
4:42
Like what was the particular gap in in medicine, I guess that you
4:46
were looking to try and address? So everyone wanted to drug these
4:50
three proteins, CDK 2, CDK 4, CDK 6 and people had tried and
4:56
no one could really do it. And so remember this is also
4:58
before Ibrance or palbociclib. They didn't come on the the
5:02
scene until 1015, 2017 when they were first approved.
5:07
So no one could make small molecule inhibitors that were
5:10
specific. They had a lot of off target
5:13
effects. They caused a lot of toxicity.
5:16
There were a lot of attempts and so no one could do that.
5:18
So we figured that P27 is the endogenous, the normal master
5:23
regulator of these three proteins.
5:25
That's its job to turn CDK 24 and six on and off.
5:29
So we figured another way to turn these kinases off, which
5:33
everyone in the field wanted to do was to go after the
5:35
regulator. And the regulator is actually
5:38
part of these complexes. So we, we talk all the time
5:41
about CDK 4, CDK 2, CDK 6, Ibrance is the CDK 4 inhibitor.
5:45
Well, there's, it's actually a complex in the cell.
5:48
It's P27 cyclin DC DK4. So you know, it's P 27.
5:52
It's frequently forgotten, but it's really essential because it
5:55
is the, the way the cell turns these complexes on or off.
5:59
So it made a lot of sense for us that if we could figure out how
6:02
P27 acted like the on off switch, we could throw a monkey
6:08
and, you know, throw a wrench into that system and and get P27
6:12
to turn the kinases off. So that was the original
6:14
hypothesis. And then when we figured out how
6:18
that switch worked, which was due to a phosphorylation event,
6:21
right? So we like to describe P 27 as a
6:23
door. So the door is either closed,
6:26
the kinases are off or the door is open and the kinases are on.
6:29
And this open and closed closing of the door has to do with a
6:33
phosphorylation event. When P27 is phosphorylated it
6:36
the doors open and when it's not, not the doors closed.
6:39
So when we figured out that we said, well, what if we block the
6:41
phosphorylation and then that led to you know, where we are
6:44
today. We first had a peptide approach
6:48
and, and sort of and showed that we could turn off these kinases
6:51
in, you know, a variety of half dozen animal models and, and
6:55
lots of different cell cultures. So we really validated the
6:57
approach and then we used that to find oral small molecule
7:02
inhibitors. But it was, you know, even at
7:04
the get go, once we knew P 27 was interacting, we're all like,
7:08
how does it do this? How does it turn these kinases
7:11
on and off? And if we could figure that out,
7:13
then that would be a a therapeutic in, so to speak.
7:16
Yeah, just going into your background, so you started your
7:19
career for us as an academic scientist to CEO which is quite
7:23
a significant shift. I think when you normally look
7:25
at the phenotype of a biotech CEO, they might come from like
7:29
an operating or commercial or business development background.
7:32
You see less CSO people that make it to CEO.
7:36
What what were some of the hardest adjustments for you that
7:38
you had to make in stepping into that role?
7:41
You know, CSO is is full of a world of hypothesis driven
7:44
research, but how did did you manage, you know, going into
7:48
more of an operating role where you had to think about capital
7:51
raising and just generally running the company versus being
7:54
in the lab? Well, I think one thing that is
7:57
a misconception is that, you know, that scientists can't make
8:01
good CE. I think that we actually make
8:04
great CE OS because of a couple different things.
8:07
The first is that we're really, really good problem solvers.
8:10
That's essentially what, you know, an academic is we look at
8:14
problems, we create hypotheses, we execute on them, and if we're
8:17
right, great, and if we're wrong, new hypothesis.
8:20
So we're great at troubleshooting.
8:22
And that is definitely a skill that I think you need as a good
8:26
CEO. There's constant change.
8:28
There's constant, you know, change in the environment,
8:31
change in the, in a landscape, change different data.
8:34
So I think that skill is something that I carry through
8:38
and I, I feel is essential as ACEO.
8:41
The other thing is that when you, you know, I ran a research
8:44
lab and so I was responsible for hiring people and firing people
8:48
and I was responsible for raising all the money that I
8:51
used to do my research. So I wasn't out there talking to
8:54
VCs, but I was writing grants to the NIH or private foundations
8:59
and I had to raise every dollar that we used to pay personnel
9:04
and, you know, buy supplies and do all of our work.
9:07
And so in that sense, it's very similar.
9:10
And the other thing is, you know, I was in the classroom for
9:13
almost 20 years teaching. I wrote and, and taught the
9:17
cancer block for our medical school.
9:19
And So what you're doing as a a teacher is a professor is you're
9:23
selling a story information to medical students and, you know,
9:29
medical students, I taught first year medical students,
9:32
essentially, they're just really, really smart lay people.
9:35
And they also think that they, you have to convince them that
9:38
they need to know the information that you're teaching
9:41
them. So you have to do a really good
9:43
job to meet them where they are. And, you know, one of the things
9:48
that I did in my teaching block was really try to always relate
9:53
these very complex situations back to, you know, things that
9:57
they were familiar with, whether those were analogies or pop
10:00
culture or movies, and so that they would have that aha moment.
10:05
And so that's another skill that I think you need as ACEO, right?
10:08
You're constantly selling your science, you're selling your
10:12
ideas, you're selling your vision.
10:14
And I have been doing that for 20 years, right?
10:17
Both in the classroom and then in grant writing.
10:19
Like, why is this important? You know, when you're writing a
10:22
grant, you're trying to convince this cadre of viewers that your
10:26
vision can and change something about human health.
10:31
And so those are skills that are really appropriate.
10:34
I will say when I made the leap over what, even before I made
10:38
the leap, when I started the company, you know, I didn't know
10:41
anything about business, right? That just wasn't in my
10:43
Roadhouse. I didn't know what a cap table
10:45
was. I didn't know what a convertible
10:46
note was. I didn't know what an
10:48
addressable market was. But I'm a really fast learner,
10:51
right? You know, I'd had 30 years, so
10:54
to speak, of being a scientist and having to look at a problem,
10:58
figure out where do I get the information I need to learn
11:01
about this problem and solve the problem.
11:03
And so, you know, that stuff was, you know, I just dug in and
11:08
I learned it. I also reached out and had great
11:11
mentors. I was involved in a couple
11:14
accelerators or, you know, I was in the springboard program.
11:18
I was in creative Destruction Lab, you know, and those were
11:22
really great opportunities to interface and learn about, you
11:28
know, all the things business that I didn't know and, you
11:32
know, so that I could build that tool set.
11:34
And I think it was the ability to learn really quickly and
11:38
recognize that I don't know something I got to figure out
11:40
how to to learn about that. And I continue to use that
11:43
today, right, You know, and I think that anyone that isn't
11:46
constantly learning is sort of, you know, short shifting
11:50
themselves, right. There's always something to
11:52
learn, something to think about. So it was, it didn't feel that
11:56
unnatural a transition to me. And then, you know, I did rely
12:01
heavily on, on mentors and, you know, educational opportunities.
12:05
Yeah, amazing. So that just took us through
12:09
your lead program, which is designed to treat, designed to
12:12
target specific vulnerabilities in resisting cancer cells.
12:18
What's the underlying mechanism you're trying to exploit and
12:20
what makes this approach different from first or second
12:23
generation CDK or cell cycle therapies that came before it?
12:27
Just just talk us through that. Yeah.
12:29
So you know, Pablo Ciclip came to market in 2017 and that's a C
12:33
DK46 inhibitor. So if you think about these
12:36
three kinases, it hits two of them and they're really sort of
12:40
the the first drivers, They work sort of an order like CDK 46
12:43
first, then CDK 2. And so those are really
12:45
transformative drugs. They've changed the, the, the
12:48
course of treatment for women with ER positive breast cancer
12:53
and, you know, really revolutionized the field.
12:56
The, the fact, however, is that essentially almost 100% of the
13:01
women that take these drugs will become resistant to them with
13:04
time. And the metastatic, you know,
13:08
the overall survival rate, the median right now for metastatic
13:11
breast cancer hasn't changed as much as we would like it to.
13:15
It's still under 30%. So that means 70% of the
13:18
patients that take these drugs are going to have a difficult
13:22
time making a five year mark. So we know the the drugs work
13:26
well, but we know everyone becomes resistant to them.
13:28
So why do patients become resistant to the drugs?
13:31
Because that third right right there first to CDK 46 and CDK 46
13:38
have a sibling CDK 2 and CDK 2 with time can compensate for the
13:43
loss of CDK 46 and do CDK 46's job.
13:47
So it took some time for everyone to realize that in the
13:51
field and real, you know, that there's a whole host of
13:53
mutations that these patients who become resistant have, but
13:57
all of those resistant mutations turn on CDK 2.
14:01
So then that leads to a really simple obvious solution, right?
14:04
We have to hit CDK 46 and we have to hit CDK 2.
14:08
The problem with hitting CDK 2 is that it is very similar.
14:13
And in fact, the catalytic pocket is identical to an
14:16
essential kinase called CDK one. And the CDK kinome or the the
14:22
world of CDK's is quite big. They're almost 20 of them.
14:25
And so think about we want to hit these three siblings, but
14:28
the siblings have a lot of cousins.
14:31
And if we hit the cousins, then we're going to have a lot of
14:33
toxicity. So most of our attempts to hit
14:37
the siblings are not specific enough and they hit the cousins
14:40
and we have too much toxicity. And so that's what's really has
14:43
plagued and continues to plague this field.
14:46
We now have newer generation CDK 2 inhibitors that are sort of
14:51
moving their way through phase one or you know moving
14:54
clinically. But those are tricky programs
14:56
because they to get the specificity for CDK 2 and to
15:02
ignore the rest of the CDK kinome has been really difficult
15:05
to achieve. And so even you know last week
15:08
or two weeks ago B1 which had licensed CDK 2 inhibitor from
15:13
Ensign for $1.3 billion, maybe three years ago they just
15:18
discontinued that program. Just, you know that that
15:22
therapeutic window is very hard with that to get enough activity
15:27
and specificity to ignore or the rest of the cousins.
15:31
So you know the what are their approaches Currently people are
15:34
saying we need to hit these three kinases, we need to hit
15:37
the three siblings. So a lot of times they're trying
15:39
to combine, you know, ACDK 1 drug against CDK 46 or against
15:44
CDK four and then one drug against CDK two.
15:46
That is tricky because the toxicities associated with
15:50
hitting those kinases due to those off target effects are
15:53
different. So will we be able to achieve
15:59
effective therapy that doesn't a lot of toxicity?
16:02
So our approach is fundamentally different because P 27 is
16:07
different. P27 doesn't interact with the
16:11
rest of the CDK kinome. It interacts very specifically
16:14
with CDK 4, CDK 6 and CDK 2. So we've let nature be selected
16:19
for us and we don't have to worry about all that off target
16:23
toxicity. We're not interacting with CDK
16:25
one because P 27 is not present in the same time in the cell
16:30
cycle. It really interacts with just
16:32
these three kinases. So what I like about their
16:33
approach is, you know, nature's really smart and we're doing
16:38
what nature does. Nature normally regulates CDK
16:41
246 via this protein, P 27. Let's just do what nature does.
16:45
Let's not try to outsmart that. And that's what makes our
16:49
approach fundamentally different is that we're using the natural
16:53
inhibitor that has already been selected for these three
16:55
kinases. You have a small molecule
16:57
inhibitor. So it's it's an oral approach
17:00
and it acts like a molecular glue.
17:02
So it essentially, and that's a very popular term right now.
17:06
There's a lot of very popular drugs, you know, the new Ras
17:09
inhibitor from Revolution Medicine that is really just
17:14
killing it in pancreatic cancer, just doing so well is a
17:17
molecular glue. And So what this does is we glue
17:20
sort of P27 into that inhibitory form.
17:25
So we can't do the door open and door closed.
17:27
It sort of gets locked down. We glue it into that form and
17:31
and that seems to be a very effective way to deal with this.
17:35
So fundamentally, just in summary, fundamentally different
17:38
because we're letting nature choose, be specific for us, for
17:43
the three targets that we want to hit.
17:45
And we really do feel that you need to hit CDK 24 and six.
17:49
A lot of people now think, well, you should ignore CDK 6 because
17:53
you might have some toxicity in your myeloid lineages, so in
17:56
your immune cells. The problem with that is that we
18:00
know that if you don't hit CDK 46, you're going to get
18:02
resistance by CDK 6 being turned on.
18:05
So while you know Pfizer has a new CDK 4 specific inhibitor,
18:10
you know, I predict that the resistance you're going to see
18:13
to that inhibitor is now super activation of CDK 6.
18:17
So we do feel that you hit need to hit all three and nature
18:21
again sort of solve this problem for us because in myeloid
18:24
lineages it's really D3, so a slightly different complex and
18:28
P27 doesn't really like that complex in the myeloid lineages.
18:31
So again, we are just following what nature has done and doing
18:36
that. And I think that is sort of our
18:38
advantage, you know, hypothesis driven, let's just do, let's
18:41
just follow that paradigm. Yeah, super exciting.
18:45
And as you look across like the broader oncology ecosystems
18:49
today, how do you see Concola's positioning within there?
18:52
There's obviously multiple companies working in CDK
18:55
biology. So yeah.
18:57
What, what do you believe is the I know you mentioned a little
19:00
bit about what makes your approach different, but you
19:03
know, where do you see the the company fitted into the future
19:06
treatment landscape in in this area?
19:09
Yeah, I mean, people are still doubling down on small
19:12
molecules, CDK inhibitors, right.
19:14
So CDK 2, CDK 4, CDK 46. People are are, you know, really
19:19
interested in the degradation. So the PROTAC method, let's just
19:22
degrade and let's just get rid of CDK 2 or let's just get rid
19:25
of CDK 4. You know, the problem with that
19:28
approach is that these are targets that form complexes and
19:34
they like to be in complexes. And if you remove 1 member of
19:37
the complex, the complex is going to rejigger and find other
19:39
things to bind with and, and I think you're going to see a lot
19:43
of compensation and resistance that way.
19:45
So we see you know our first sort of tumor type that on which
19:50
we're interested is this drug resistance, so the IBRANCE or
19:54
abemaciclib or vercinio resistant metastatic breast
19:58
cancer. So patients that have been on
19:59
one first line therapy. And they're a real consensus
20:03
besides maybe changing the endocrine modulator.
20:06
How do we treat those patients? And some are treated with PI3
20:08
kinase inhibitors and some are treated with you know different
20:13
types of inhibitors. But we think that we are a can
20:16
slot in there as a viable approach for second line drug
20:20
resistant patients. We also think in the ovarian
20:23
cancer space where there are not really a lot of good targeted
20:28
therapies, particularly for women that are not eligible for
20:32
PARP inhibitors, most of ovarian cancer patients are just treated
20:35
with chemo and debulking. And so we think that is a tumor
20:39
type that's driven really strongly by the CDK 2 and then
20:42
ultimately can compensate for CDK 4.
20:44
So that is a really good tumor type.
20:45
So those are our two sort of initial entries into the field.
20:50
But we do believe that that, you know, targeting P27 could work
20:55
across numerous tumor types. And so eventually, you know,
21:00
trying to expand into different tumor types where we see this
21:03
sort of, you know, the siblings are working together is, you
21:07
know, our approach. And so obviously anyone who
21:09
enters the second line eventually wants to move into
21:11
first line and you know, that would be somewhere down the
21:14
line. But we are our initial goal is
21:17
just to try to establish ourselves as a a bona fide
21:21
second line therapy for these metastatic breast cancer
21:24
patients and then also a therapy post chemo for the platinum
21:28
resistant ovarians. Yeah, super exciting.
21:31
And just like as you look ahead over the next 12 to 24 months or
21:35
so, just talk us through what you think the major inflection
21:38
points that you guys are focused on, whether that's from a
21:41
scientific validation or preclinical milestones or
21:44
anything on the funding or corporate side.
21:48
Just talk us through what success may happen over the next
21:51
12 to 24 months and what would success look like for you
21:55
personally over the next few years with Konkala as well?
21:59
Yeah. So you know, I mean it's it has
22:01
been 25 was really, really tough and and still remains difficult
22:06
to fund first in class targets and it remains difficult to fund
22:11
early stage research, right. So a lot of people are
22:14
interested in funding you know stuff that is near phase one
22:19
ready or even has phase one data.
22:21
And so it is very difficult to phase funds for the stage where
22:27
we at. But one our, our biggest
22:31
milestone is we want to declare our developmental candidate and
22:35
we're pretty close to that. We we believe and that would get
22:41
us set up to do all of our Ind enabling work and then hopefully
22:45
enter the clinic sometime in 2028.
22:48
And so that is an aggressive timeline, but we think we can
22:51
meet that. And you know, we we're having
22:53
some good success, you know, in the fundraising.
22:55
So that is really our plan is to, you know, continue
23:00
optimizing the drug that we have now, improving some of its ADNEY
23:04
parameters. And you know, making what we
23:07
have is sort of, you know, a really great inhibitor right now
23:10
and make it into a really great drug that has all of these other
23:13
parameters that you need to, to have an effect effective
23:16
therapeutic and then roll into the Ind enabling work.
23:19
And then, you know, build out our our clinical trial sites and
23:22
actually start dosing patients. So that's our plan.
23:25
And of course that's all predicated on raising the money
23:29
to do all of that. And so we spend, I spend a lot
23:32
of my time talking to you know, potential investors in VCs.
23:36
I also talked to a lot of pharma partners who are either have
23:39
breast cancer franchises or are interested in the CDK space.
23:43
And you know, how could we fit into their franchises either now
23:47
or down the line. And I think that is, you know,
23:51
learning from them and then also telling our telling them about
23:54
our approach is something, you know, that's really interesting.
23:56
So where do I see us? What would, you know, a success
24:00
look like for us? I think we either raise all the
24:02
money and we run the phase one either by ourselves or in
24:06
partnership with a farmer partner that is interested in
24:09
this space. And you know, I think that I
24:12
would like to see this P27 asset go all the way through that
24:17
until it gets to a, a part where a point where it's really stable
24:20
and can either be picked up by someone else or we move it
24:23
forward into the phase two and, and move it towards, you know,
24:26
finally it's clinical approval. But we also have the, the, we
24:32
have a molecular glue as I said. So it's gluing the tail of P27
24:35
into this complex and we think that this is an approach that
24:40
can be used for several other big undrugged targets.
24:46
And so why do I say that? So P 27 is an intrinsically
24:50
disordered protein. So what that means is it has no
24:53
structure on its own. It's like a big floppy piece of
24:55
spaghetti in the cell. And it only forms structure when
24:58
it binds to like the cyclin CDKS.
25:01
And then it it will have structure and then the tail will
25:03
have unstructured and structure and unstructured.
25:06
And so there's a lot of really big targets like P53, like Nick,
25:10
these big things that we've known about as really hardcore
25:15
highly valuable targets for over 50 years, but we still don't
25:19
have effective drugs against them in oncology.
25:22
Most of the therapies that we've made which are amazing are
25:26
either small molecule kinase inhibitors that fit into little
25:28
pockets and cells or are antibodies that recognize things
25:32
on the cell surface. We haven't been successful at
25:35
drugging floppy intrinsically disordered protein.
25:38
So the platform that we use to come up with our small molecule
25:41
P 27 molecular glue, we think we can now parlay it to go after,
25:46
you know, targets like P53 like Mick.
25:49
And that would be for me, the next step, you know, sort of
25:53
trying to parlay all our expertise to develop these
25:58
programs to go after these big things that everyone knows we
26:02
should be drugging, but we've sort of cast aside because
26:05
they're difficult. And so, you know, I guess I like
26:09
difficult things. I told you at the onset, I like
26:10
to be in that destabilised state and and trying to really go
26:15
after these big transformative targets.
26:17
I think it's the next step for Con Carlo.
26:20
Yeah, sounds super excited. And just I guess on a separate
26:24
points, you've, you've obviously been in a career and in a field
26:27
that's historically been dominated by male leadership,
26:30
particularly at the CEO and and founder level.
26:34
Just talk us through from your experience, have you personally
26:37
seen the evolution of women's roles in biotech over the course
26:39
of your career from from academia to through to company
26:43
building? Just talk us through how you've
26:45
seen the the evolution of that. Yeah, you, you see me smiling
26:49
because I could talk a lot, a lot about this for a long time.
26:52
But look, academia is very male dominated.
26:55
And in fact, during my time in academia, that was, you know, it
27:00
was there was a huge boys club and it was very difficult to,
27:05
you know, I felt like I was constantly trying to work around
27:07
the obstacles that were put in my path and not necessarily in
27:10
my male counterparts path. And so, you know, I guess when
27:15
I'd hoped, I hoped that when I moved to the biotech, it would
27:21
be different. But the the fact is, you know,
27:24
the statistics suggest that it's not right if only 2% of women
27:29
LED companies are actually raising venture capital, that's
27:33
actually not random. That almost has to be on purpose
27:36
in the sense that, you know, 2% is a really low number.
27:39
That's that's sort of outside the bell curve where you should
27:43
be. And so is that because women LED
27:45
companies are working on things that are less interesting to
27:49
venture capital, right? We work on, we work on breast
27:53
cancer, ovarian cancer or Women's Health related issues.
27:56
Or are women still viewed as potentially difficult and less
28:02
trustworthy or not as secure? You know, but the fact is, I
28:06
think it still exists in biotech.
28:08
And so when I moved to biotech, I said, look, I have to meet a
28:12
whole new cadre of people. And this time around, I'm going
28:17
to really seek out women in this space and I'm going to try to
28:22
use that network and use those mentors.
28:25
How did they deal with, you know, it's sort of the boys
28:28
club. And so, for example, I joined
28:31
Springboard, which is a women's boot camp for women, CE OS or
28:38
SEA sweeters. And you know, you're learning
28:41
from other women and that was really important and forming
28:45
those connections. And you've already alluded to
28:48
the Biotech CEO Sisterhood, which is a organization of about
28:53
300 female CE OS. And that has been really
28:59
important to me to have that resource.
29:02
There's a very active Slack channel for the sisterhood and,
29:06
and you can ask questions and you can and get responses
29:10
without any sort of, you know, embarrassment or criticism.
29:14
I just went on the biotech CEO sisterhood retreat.
29:18
We were in Mexico, and that was an amazing experience.
29:21
For one, there wasn't a problem that I've encountered that
29:24
someone at the table hadn't already encountered, and so
29:27
that's incredibly refreshing. And then 2.
29:31
The sheer generosity and openness and willingness to help
29:36
a fellow sister or, you know, talk to talk to a fellow sister
29:41
is mind blowing and and such a refreshing difference from what
29:47
I had experienced before. So I think that there still are
29:52
problems for women CE OS I think the numbers just just say that
29:56
there's just no other way around it.
29:58
But I think organizations are trying to help women find, you
30:05
know, their, their place and their people so that we can be
30:08
successful. I'd like to envision a world
30:10
where it doesn't really matter, right, That the work speaks for
30:13
itself. But I think that we're not there
30:15
yet, and we still have a long way to go.
30:19
And I think organizations like the Sisterhood are are helping
30:22
us as women CEOs during that journey.
30:26
Yeah, we, we've had the pleasure of having a lot of people, lot
30:29
of members from the biotech CEO sisterhood on, on the podcast.
30:33
So I've got to know a little bit about the community, how much
30:36
it's grown over the past past few years.
30:38
I go to JPM every year, so I see the pink on the Tuesday at JPM
30:42
in in San Francisco. So I've, I've just seen the
30:45
yeah, the build up in, in, in momentum in that group
30:48
particularly. So it seems like, yeah, it's,
30:51
it's a, a super impressive group put together by some, some
30:55
amazing people as well. It's also very, you know, it's
30:59
very forward thinking. Like for example, we just had a
31:03
three hour educational system on Claude and how to really make
31:08
Claude work for us as biotech CE OS.
31:13
And it was an amazing experience, right?
31:17
We could have all done it individually, but there was
31:19
something about the communal nature where there were I think
31:22
100 people on Zoom and we're all learning, you know, working on
31:25
our own claws and asking questions.
31:27
And, you know, people were asking questions that I didn't
31:30
even know I really had, but as soon as I heard the question, I
31:32
was like, yeah, I need to know that too.
31:34
So I think that there's a huge opportunity, there's strength in
31:38
numbers. And you know, I think this the
31:40
biotech CEO sisterhood is, is digging into that they're like,
31:44
what do we need? What kind of services, what kind
31:47
of events, what kind of programming, what kind of AI
31:52
events would we would help us do our jobs better?
31:56
And you know, can we form our own club and learn how to do
31:59
these things and help each other along the way.
32:01
And so it is really comforting and supportive.
32:07
And again, as that's like the willingness and the openness for
32:10
all of these sisters to, you know, answer questions and, and
32:15
talk to people and, you know, educate each other.
32:17
It's, it's really, really refreshing and impressive.
32:21
So I, I urge any biotech CEO, female women out and women out
32:27
there, they should, you know, join the sisterhood.
32:30
And it's, it's just a great, it's been a great experience.
32:33
Yeah. And I know there's also now like
32:36
biotech CSCSO sisterhood, biotech CMO sisterhood, CFO
32:41
sisterhood, so on and so forth. So, yeah, it's not just a
32:44
community for CEOs, people at the top, but also people that,
32:47
you know, rising through the ranks in biotech.
32:49
There's there's all of these different communities that seem
32:52
to be appearing as well, which is again is great.
32:55
Yeah, I mean, look, you know, unconscious bias exists and we
33:01
have to work against that. But you can either just put your
33:06
head down as a female leader or a female, you know, CSO or CDMO
33:14
and say, OK, I'm just going to put my head down.
33:16
Work is going to speak for itself.
33:18
The fact is that is very difficult, right?
33:21
I, I call that the if, when scenario, right?
33:24
We say to ourselves as women, if I win the grant or when I win
33:30
the teaching prize or when my students graduate with honors,
33:34
then I'm going to be in the club.
33:36
The fact is we're not going to be in that club, right?
33:39
It's very difficult to break into that old, old boys club.
33:42
So we should make our own club and we should be supporting each
33:47
other as women and we should help each other as women.
33:52
You know, remember that it's, you know, it's not OK just to
33:56
put your head down and be, you know, suffer microaggressions
34:00
and macro aggressions. Like we need to work around
34:03
those that we can be successful. I think women, you know, I have
34:08
children and I never talked about my children at work for
34:13
probably 20 years because it just wasn't an environment where
34:17
I could do that. But I think being a mother, I'm
34:22
super efficient, right? Because I had two full time jobs
34:25
for 20 years when my kids were little.
34:27
I had worked all day and then I got home and I had a much harder
34:30
job because no one really listened to me, right?
34:32
And so I think that we as women tend to fall sometimes into the
34:37
trap of, OK, let me just, you know, let me just put my head
34:40
down and work through it. And so I do think organizations
34:42
like, you know, all the, the C, the biotech sisterhood programs
34:47
are really important to help women be successful at all these
34:51
different roles. And so I'm a huge fan and
34:53
believer in all of that. Yeah, for sure.
34:57
And look, this is a question that we would always finish with
34:59
on the on the podcast as well. But if you were to sit down and
35:03
have dinner with any free people from past or present, who would
35:07
you pick and why? It it doesn't necessarily need
35:09
to be people from biotech, although it could be if you
35:12
like. But yeah, free people you'd like
35:14
to sit down and and have a dinner with.
35:17
Yeah, so you told me this question ahead of time, so I had
35:19
a little bit of time to think about it.
35:21
And so I thought that I would love to sit down with like
35:24
Jennifer Dwadna or, you know, Carolyn Berzoli, you know, that
35:31
those people who are hardcore scientists.
35:34
And so like Jennifer Dwadna, she is a hardcore scientist and she
35:38
took risks because she followed interesting questions and
35:42
discovered CRISPR, right? And so I, I love that because
35:46
that's the beauty of science, just sort of taking you, you
35:49
know, we got it as scientists follow where the science takes
35:52
us. So I love that.
35:54
I'd also like to have, what is it Albert Borla from Pfizer,
35:58
because he is kind of rare in the sense that he is, you know,
36:02
an MD. He is a scientist that now has
36:05
achieved the highest level of, you know, he's leading Pfizer,
36:10
this global institution. And so how does science, his
36:14
science thinking influence his now hardcore operator role,
36:18
right? And as opposed to many people
36:20
who are just always operators, he really, I think came in that
36:23
way. And then finally, I'd love one
36:25
to sit down with either like Bob Langer or from I think it's MIT
36:32
who is, you know, a scientist but has spun out, you know, I
36:36
don't know, 50, a hundred, a lot of companies, George
36:41
Yancopoulos, who was, you know, CSO of Regeneron, you know, or
36:47
Greg Virgins, right? So these are hardcore scientists
36:51
who've been able to translate their science multiple times,
36:56
numerous times into successful products, successful companies,
37:01
and it really changed the the face of human health by stuff
37:06
that came out of their brains. And so I think that would be
37:09
really an interesting conversation.
37:13
But I think you see the the theme, which is, you know,
37:16
scientists who have thought really deeply about problems and
37:20
tested hypotheses and were able to then translate them into
37:25
really successful therapeutics, which have had huge impacts on
37:28
human health. So I think that would be a
37:30
really fun, interesting dinner. I would be humbled to be in the
37:35
audience of those three people or four people.
37:38
And, you know, again, as I said, I like to I, I and have no
37:43
problem not, you know, being, you know, the least smart person
37:47
in the room because I love to be in the presence of greatness.
37:51
So I think that would be really fun to, you know, just bask in
37:55
the, the brilliance and the glory of those three people and,
37:58
and learn and, and challenge myself.
38:00
So that's that would be a fun dinner.
38:02
Maybe you can make that happen. Yeah, yeah.
38:05
Look, 3 great answers there. And look, thanks so much for
38:09
coming on and and helping us out with this.
38:11
It sounds super exciting what you guys are building at Con
38:13
Carlo. So I'm looking forward to
38:16
keeping an eye out for the next inflection points.
38:19
And yeah, look, Stacey, it was a pleasure.
38:20
Thanks again for for coming on and helping us out with this.
38:23
Yeah, thanks so much. And you know, as a scientist, I
38:27
I love talking science. So it's that opportunity.