Latest / The BioHub - by Avetix / Episode 127 - Ann Belien - Founder and CEO Rejuvenate Biomed

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Episode 127 - Ann Belien - Founder and CEO Rejuvenate Biomed · The BioHub - by Avetix

• 0:06
  So welcome back to the episode of the Bio Hub.
• 0:08
  Today we're delighted to be joined by Anne Bellion, founder
• 0:11
  and CEO of Rejuvenate BioMed, a clinical stage biotech advancing
• 0:15
  combination therapies for healthy ageing and age-related
• 0:18
  diseases. Anne brings more than 20 years
• 0:21
  of drug development experience, including scientific and
• 0:24
  leadership roles at J&J. And in 2017 she'd founded
• 0:28
  Rejuvenate BioMed to translate Cutting Edge ageing science into
• 0:32
  real preventative treatments. So join us today as we'll talk
• 0:36
  through the healthy ageing space, the encouraging recent
• 0:40
  data, as well as operating as a Belgium based biotech.
• 0:43
  So Anne, thanks so much for coming on.
• 0:45
  How are you I'm. Doing fine.
• 0:48
  Thank you so much and yourself. Yeah, good, good.
• 0:51
  Yeah, it's a pleasure to have you on.
• 0:54
  So look, let's just let's just dive into a little bit about
• 0:57
  your journey through the field. So you have a career spanning
• 0:59
  more than two decades across academia and industry, from your
• 1:03
  PhD in neuro oncology to senior strategy roles at J&J.
• 1:09
  Can you just give us a bit of a run through your journey and how
• 1:12
  you got to where you are today? Yeah, sure, absolutely.
• 1:15
  So indeed in I'm a scientist from background, did a PhD in
• 1:21
  Switzerland, moved to Belgium where one of my professors was
• 1:25
  working at J&J and he kind of convinced me to join pharma
• 1:31
  because he knew that I had a big law for translational science.
• 1:35
  So during my PhD, I looked at at glioblastoma, a cancer cell line
• 1:42
  or cancer that was migrating on white matter, where the rest of
• 1:45
  the group was actually looking at white matter in invasion.
• 1:48
  So I was doing the opposite from what the rest of the group was
• 1:51
  doing. And looking back to my career,
• 1:53
  that seems to be like the red line.
• 1:55
  I always seem to be looking at things just a little bit
• 1:58
  differently than others do, which makes it very interesting
• 2:01
  for me. So what I did is when I moved
• 2:05
  back to Belgium in 2000, I joined Johnson and Johnson as a
• 2:09
  scientist in the discovery setting, where I had the
• 2:13
  pleasure and an honor to be in a team where we identified first
• 2:17
  aid DAC inhibitors and set up also some animal models.
• 2:21
  And I was very curious on what's going to happen with this
• 2:24
  compound now when it leaves discovery because having an idea
• 2:28
  and a discovery in, in a preclinical settling doesn't
• 2:30
  mean that you have a medication for a person, right?
• 2:33
  So I was able to learn about the preclinical elements that come
• 2:38
  into play, talks, ultimate talks, all those elements and
• 2:41
  then also the CMC side. And then I also wanted to be to
• 2:47
  learn a little bit more about clinical and regulatory because
• 2:50
  I'm way too curious to have or to go for a status quo.
• 2:55
  And I was allowed in to do a rotation to the US where I
• 2:58
  learned about those elements in the drug development area, a
• 3:02
  little bit more on the late development side, both CNS and
• 3:06
  oncology. Then I moved back to Belgium and
• 3:09
  I joined another company of the Johnson and Johnson companies
• 3:13
  because as you know, they have multiple companies within the
• 3:15
  organization where I focus much more on early development.
• 3:20
  And that's where I started to look at what do we do in
• 3:24
  discovery, What do we do early development, what do we do late
• 3:26
  development and streamline those elements.
• 3:29
  And it is there that I then sort of become a move more into
• 3:33
  strategic roles, including being part of the integration of one
• 3:39
  of the companies that were acquired, but then also again
• 3:42
  corve outs of another part of that company.
• 3:45
  And then I ended up in the Netherlands in the Johnson
• 3:49
  Prevention Center where we're focusing on prevention of non
• 3:53
  communicable diseases. Yeah and you you've obviously
• 3:56
  spent a big bulk of your career in large farmer.
• 4:00
  What inspired you to take the leap and, and and find found
• 4:03
  Rejuvenate BioMed in 2017 and and how did you find that
• 4:07
  initially going from from big pharma to to building something
• 4:10
  out from scratch? Oh, I like that question a lot
• 4:14
  because it's a, it's, it's a very personal reason why I
• 4:19
  decided to set up Rejuvenate Biomat.
• 4:21
  So what I noticed was that my father was of course aging and
• 4:25
  he was suffering from multiple age-related diseases at the same
• 4:29
  time. And each time when we tried to
• 4:31
  treat one of them, another one would just pop up.
• 4:34
  Being the only one in the pharma area in my family, everybody was
• 4:38
  looking at me like what's happening here?
• 4:41
  So I started to dive into the biology of aging and started to
• 4:45
  understand about the hallmarks of aging where we see that a lot
• 4:48
  of different mechanisms are not functioning anymore very well.
• 4:52
  And the older people, so especially the repair
• 4:55
  mechanisms, these go from DNA repair to mitochondrial health,
• 5:00
  cell cell communication, inflammation.
• 5:03
  And I started to think about this a little bit differently
• 5:06
  because normally we focus on one specific target.
• 5:10
  And I thought, what if we can now have an impact on multiple
• 5:13
  hallmarks simultaneously and then also on a specific disease.
• 5:17
  So really taking into account the fact that the older body
• 5:20
  does not function anymore optimally like it does in the
• 5:24
  younger body. I looked into that when I was
• 5:28
  still at J&J and got the opportunity to do a scientific
• 5:33
  assessment. That won't seem to be positive.
• 5:35
  But again, having a scientific idea doesn't mean that you have
• 5:38
  a business opportunity. So I also went through a boot
• 5:42
  camp and we identified that this actually was a very interesting
• 5:46
  business opportunity. But I, of course, was working at
• 5:50
  J&J and I always say it was not a golden cage.
• 5:54
  It was a golden space where I could move around freely.
• 5:58
  So for me, it was a very difficult decision, but I really
• 6:02
  wanted to make a difference. And yeah, having of course, my,
• 6:07
  my father, which is my everything, I really wanted to
• 6:11
  make that difference. And I took all the courage that
• 6:15
  I could find. And I did make the step into or
• 6:20
  to set up a biotech company. Nice.
• 6:23
  I love it when there's a personal story behind it.
• 6:25
  So yeah. And was there a particular gap
• 6:29
  that you saw in the biotech landscape at the time, both
• 6:32
  scientifically or strategically, that convinced you that this was
• 6:36
  the right moment to build a an ageing focus company?
• 6:39
  What was the many of the companies doing?
• 6:41
  I guess what you guys are doing at that point in time when you
• 6:44
  decided to set the company up? Yeah.
• 6:46
  So there was still a quite large gap in the sense that there was
• 6:49
  a huge amount of very, very good basic signs that happened.
• 6:53
  Done in the biology of aging or the geoscience, depending on the
• 6:58
  nomenclature. But the translation into
• 7:02
  something that can be used in humans was not there yet.
• 7:06
  That was one element that was definitely missing at that
• 7:10
  moment in time. Like how do you translate this?
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  Because there is no condition called aging for which you have
• 7:16
  a regulatory trajectory. So how do you deal with these
• 7:19
  things? That was one element.
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  The other one was more from biological perspective.
• 7:27
  Like normally when a disease hits a body, there is a specific
• 7:32
  target that is being impacted and then you go in and you fix
• 7:35
  the targets. In this case, you don't have one
• 7:39
  target, you have multiple targets and you have multiple
• 7:42
  pathways. So it's even more complicated
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  than how we used to look at normal or established diseases.
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  Then the second thing was if you go into a new space, which aging
• 7:55
  of course is 1 important element is that to do no harm rule.
• 8:01
  You don't want to develop something that can harm the
• 8:04
  people, especially in a new space where nothing has been
• 8:08
  developed yet. You have to go in there very,
• 8:10
  very, very carefully. So we decided to work with
• 8:14
  products from which we have human safety data at hand and
• 8:18
  then use those to generate new combinations that can have an
• 8:22
  impact on multiple pathways simultaneously, but at least be
• 8:25
  sure that we have safety at hand.
• 8:28
  That were a couple of the of the things that were at that moment
• 8:31
  definitely missing. But as I mentioned also a lot of
• 8:35
  unbelievable good research already had been done, so it was
• 8:38
  a good moment to come in and start to translate and.
• 8:41
  When you look at like the space that you're in now and I, I
• 8:44
  never like to use the word competitors because I think
• 8:47
  ultimately you're doing it for the patients.
• 8:49
  But like who are the companies that I guess you're competing
• 8:53
  against or doing similar sort of stuff to you?
• 8:55
  Who else is sort of in that space?
• 8:57
  Yeah. So the the interesting part is
• 8:59
  indeed, as you mentioned, it's not like a very competitive
• 9:02
  space because we're all new to it, because it is a new field
• 9:05
  and everybody's trying to apply their own knowledge to move
• 9:10
  forward. I think one thing that we all do
• 9:12
  in common is we do of course recognise that aging today is
• 9:16
  not and and condition for which you have a regulatory
• 9:21
  trajectory. So all of us have that long term
• 9:24
  vision of healthy aging in the back of our minds.
• 9:27
  But they're also looking and how can we in the short run really
• 9:32
  help patients that suffer from a specific disease and then
• 9:36
  generate all the data that we need to broaden them later to
• 9:40
  show that there is a general health impact and healthy aging
• 9:45
  impact. So that's one of the things that
• 9:47
  we do in common. In Europe, we don't have a lot
• 9:49
  of companies focusing on this space at this moment in time.
• 9:54
  US is a little bit more active I would say.
• 9:58
  So I think none of us really still has that claim of we
• 10:02
  develop a compound to ensure health ageing, but we all became
• 10:06
  very realistic and define specific disease area where we
• 10:10
  will focus on. And just so obviously the the
• 10:13
  space is still emerging as a, as what's recognised as a
• 10:16
  therapeutic category. Can you or how would you explain
• 10:19
  your disease agnostic approach to people who are used to
• 10:22
  thinking in terms of like one disease 1 drug?
• 10:26
  The way I try to explain it to people is that you can.
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  So how we have been educated is of course to look at each organ
• 10:36
  separately, but not really looking too much about the cross
• 10:39
  talk between organs. Our whole health support system
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  is structured that way. You have a cardiologist, you
• 10:48
  have somebody focusing on renal diseases, somebody focusing on
• 10:53
  lung. So that's how we are structured
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  and that's how we are trained. So we are not used to look
• 10:59
  across organs. The way I explain why it is
• 11:02
  important to do that is by making a comparison with the
• 11:06
  mosaic of the world. If you look at the world and
• 11:09
  every country gets a specific color, you have a very beautiful
• 11:12
  mosaic. Now if you color that's those
• 11:16
  same countries with the language they are speaking, then you see
• 11:20
  that your mosaic becomes different and then you see that
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  similar languages are being spoken in different parts of the
• 11:26
  world. That's a little bit how you now
• 11:28
  can look at the organs. So the organs are the countries,
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  but for instance, mitochondrial health is important for every
• 11:35
  organ, cell cell communication is important for every organ.
• 11:39
  Inflammation is present everywhere.
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  So if you now tackle those languages and you start to learn
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  to speak the languages, you can reach so many more countries
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  being the organs compared to just focusing on one element
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  alone. That's probably the easiest way
• 11:56
  to explain it. Nice.
• 11:58
  And just to delve into the pipeline a little bit further.
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  So your lead program, RGX 01 targets sarcopenia, a condition
• 12:07
  with no approval therapies today.
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  Why did you choose to focus on muscle aging diseases first?
• 12:15
  So what we noticed as as you mentioned in the beginning, we
• 12:18
  are very disease agnostic. So we have a platform that helps
• 12:23
  us to identify compounds that can have an impact on multiple
• 12:27
  hallmarks simultaneously and then finds a way to link that
• 12:32
  specific combination to a specific disease.
• 12:35
  So the first exercise that we did when we looked at the
• 12:41
  hallmarks of aging, we saw that there was a combination product
• 12:45
  that potentially could have an impact on multiple hallmarks at
• 12:48
  the same time. To now address if there was an
• 12:51
  impact on health span, we looked and see elegance which are
• 12:55
  little worms and to see if indeed we had an improvement in
• 12:59
  health span with a combination product, we saw that we did have
• 13:03
  that and we noticed there an impact on the muscle.
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  So the muscle fiber structure was much more conserved after
• 13:10
  treatment with RGX one versus non.
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  That's kind of how we moved into that muscle field very quickly.
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  Based on the activities that we could extrapolate, we saw that
• 13:23
  sarcopenia actually is fitting this age-related disease
• 13:30
  necessity. So it does fall in the category
• 13:33
  that we want to move into. We also know that it's very
• 13:37
  complex and sarcopenia has also hallmarks as we call it.
• 13:43
  So that means that you have a disturbance of the neuromuscular
• 13:45
  junction. That's the cross talk between
• 13:47
  the neurons and our muscles. You have a problem with
• 13:50
  mitochondrial health, so energy goes down.
• 13:54
  You have a problem with inflammation.
• 13:56
  So that means that you have a chronic inflammation status
• 13:58
  which is disturbing normal cell cell communication.
• 14:01
  And you had multiple of these elements.
• 14:03
  So it resembled a lot what actually happens when you are
• 14:07
  aging. So having a disease that you now
• 14:10
  can have a trajectory for from a regulatory perspective and that
• 14:15
  you can bring to the market to a specific field helps us to study
• 14:21
  healthy ageing. So that's how we came to
• 14:23
  sarcopenia. So the data basically drove us
• 14:27
  in that direction. Indeed, sarcopenia is a quite
• 14:31
  new disease. So when I started in 2017 or 16
• 14:35
  to look at at the first steps, sarcopenia was not very well
• 14:40
  understood yet. In the meantime, we understand
• 14:43
  that way much more. It's much more recognized.
• 14:46
  We see it in a lot of different situations.
• 14:49
  We typically talk about chronic sarcopenia.
• 14:52
  When we talk about sarcopenia loss, loss of muscle
• 14:55
  performance, it's mainly performance in the old
• 14:59
  generation. But what we also see that it can
• 15:02
  be induced and it can be induced because of another disease.
• 15:06
  So we call it disease induced sarcopenia.
• 15:09
  For instance, people who are suffering from COPD, their
• 15:13
  muscle is not doing very well. But it can also be induced for
• 15:17
  other reasons like treatment induced sarcopenia in obesity.
• 15:21
  The GLP ones are doing a marvelous job in getting people
• 15:25
  away from the obesity and also helping them with their general
• 15:29
  health. Unfortunately, there's one
• 15:31
  element and that's the the strong loss of the muscle that
• 15:35
  is also being in used. There's another situation where
• 15:38
  you can make a difference and there are several of those as
• 15:41
  well. So that's why sarcopenia is
• 15:44
  actually a very interesting disease because it has a quick
• 15:47
  win in acute settings where you can study it fast and you can
• 15:52
  develop the compound fast and bring it forward.
• 15:55
  On the other side, you can translate it very well to
• 15:57
  chronic sarcopenia since it is so multi mechanistic, you learn
• 16:03
  about a lot about the different mechanisms and all these
• 16:06
  mechanisms are also important in aging.
• 16:09
  So you have like a super win win win relationship by developing
• 16:13
  the compound now for sarcopenia, but also having the aging in the
• 16:17
  back of your mind. And just onto the data that you
• 16:20
  just mentioned, then what, what did you learn from that study
• 16:23
  and how does it shape your confidence going into into phase
• 16:27
  two trials? Right.
• 16:29
  So the first study that we did, we call the phase one study
• 16:33
  because we do it in healthy volunteers.
• 16:35
  But actually you can also call the phase two study.
• 16:40
  In that study we had 42 healthy volunteers which had allowed us
• 16:47
  or the CRO of course to have a full lack cost for two weeks.
• 16:53
  By having a full lack cost for two weeks, you induce acute
• 16:56
  sarcopenia. That means that you can also
• 16:59
  treat it. So we provided in a double-blind
• 17:02
  placebo-controlled randomized study the products to these
• 17:07
  people during the casting, but also during the four weeks after
• 17:11
  the casting. And what we noticed is that the
• 17:13
  people that were on RGXO 1, we're now outperforming the
• 17:18
  people that were taking the placebo at the level of muscle
• 17:21
  strength. So the regain of the strength
• 17:24
  after having lost it because of the immobilization was improved
• 17:28
  and the people that took RJX, so on.
• 17:31
  And the other thing that we noticed were very complex
• 17:34
  elements like radar velocity development and so on.
• 17:37
  But what I basically mean is if I would push you, are you able
• 17:41
  to put your leg in front of you fast enough but also generate
• 17:44
  enough strength to not fall? These data were already
• 17:47
  generated in that phase one study where we saw a clear
• 17:50
  difference between the RGXO one treated group and the non
• 17:55
  treated group that were very important clinical outcome
• 17:58
  parameters, which also confirmed what we had seen preclinically
• 18:02
  because preclinically in C elegans but also in killifish
• 18:06
  and also in two animal models, 2 mice models we saw had seen
• 18:10
  those data. The other thing that was
• 18:13
  important to us coming from that trial were mechanistic insights.
• 18:18
  So we knew that the compounds had the potential to work on a
• 18:22
  lot of different hallmarks. And So what we did in this study
• 18:26
  is we had muscle biops and I called them these healthy
• 18:30
  volunteers, very brave because they also gave us muscle biops
• 18:34
  before the cost, after the cost, at the end of recovery, we could
• 18:38
  see that with the model we induced the problem which is
• 18:41
  going down of mitochondrial health, going up of fibrosis and
• 18:45
  going up of inflammation and RGX, one could actually reverse
• 18:50
  back that problem and bring back down the inflammation, down the
• 18:55
  fibrosis and back up the mitochondrial health.
• 18:58
  So it means more energy, less information and less disturbing
• 19:04
  material in the environment. These were the biggest elements
• 19:08
  that we learned from the phase one study, as we call it here in
• 19:12
  Europe, even though it's it's more like a Phase 2.
• 19:15
  So those data actually allowed us to start the phase two study,
• 19:19
  the COPD study. So that study is already
• 19:23
  ongoing. We are already very, very
• 19:25
  actively enrolling. And here we study in people that
• 19:29
  suffer from COPD, the muscle integrity and the muscle
• 19:33
  strength. Here we are treating for six
• 19:35
  months, so it's a quite long period.
• 19:38
  These people are also coming back in on a regular base
• 19:43
  because we ask them to come back in so we can do all the
• 19:45
  assessments. But they sometimes also come
• 19:48
  back in because of an exacerbation.
• 19:50
  And that means that they need some additional bed rest, which
• 19:53
  is again detrimental for the sarcopenia, and it's pushing
• 19:56
  them even more in that sarcopenia angle.
• 20:00
  So those phase one days are actually already provided us a
• 20:04
  chance to move into phase two in the COPD study.
• 20:10
  As mentioned before, there are other opportunities as well.
• 20:13
  And what we would like to do is to look at obesity in older
• 20:17
  people because you don't want them to push them into the
• 20:21
  sarcopenia status to see if we can protect their muscle there.
• 20:25
  But there are some other opportunities on top of that.
• 20:28
  So having a compound and can protect muscle strength loss is
• 20:35
  having a lot of different applications for which it can be
• 20:38
  used not only within aging but also outside of the aging
• 20:43
  environment. And and that's what we of course
• 20:46
  like we want to have a solution for as many people as possible
• 20:50
  throughout the world. What I have seen unfortunately
• 20:54
  from first line is that if your muscle is deteriorating, you
• 21:00
  start to move less and you become an isolation.
• 21:03
  And that's also what happened to my father.
• 21:05
  So at a certain moment he became very sarcopenic.
• 21:08
  And that means that you are also losing your mental stimulations
• 21:12
  because you're not being social anymore.
• 21:14
  So it's it's a horrible situation to me in.
• 21:17
  And like as you look forward to the next sort of 12 to 24
• 21:21
  months, what are the next sort of key major milestones that
• 21:24
  you're most looking forward to both from the lead program
• 21:27
  perspective, but also the more broader company?
• 21:29
  What are some of the major and key milestones that you're
• 21:32
  you're most excited about? So we have 3 pillars within the
• 21:36
  company. We have our platform, We have
• 21:39
  our preclinical assets, which are currently in preclinical
• 21:42
  development. And then we have, of course,
• 21:43
  RGXO one, as you pointed out. So for RGXO One, end of 2026, we
• 21:49
  will have the data of the COPD study.
• 21:52
  So that's going to be a major, major milestone.
• 21:55
  We wish to also start the GLP one study in combination with
• 22:00
  RTX one to protect the muscle in that setting.
• 22:04
  Then from our preclinical assets, we are just are
• 22:08
  declaring a new compound, a new combination to move forward and
• 22:14
  early next year we want to nominate an additional new
• 22:20
  combination. And another indication.
• 22:23
  Then from the platform perspective, we're using the
• 22:25
  platform now a lot in house and we just made a new version of
• 22:30
  our platform. What we would like to do in the
• 22:33
  next 12 to 24 months is to make it more commercially available
• 22:38
  via collaboration settings because we developed the system
• 22:42
  out of necessity, not because we are a software group, but out of
• 22:46
  necessity because we want to identify compounds, link them to
• 22:50
  ageing, but also link them to age-related diseases.
• 22:53
  And we want to do that in a combination.
• 22:56
  So that means that we can have now a modular system that we can
• 23:00
  use for a lot of different reasons.
• 23:02
  We can help people to actually prioritize their compounds by
• 23:08
  generating new omics data that we can pour into the system.
• 23:12
  We can help people to repurpose compounds.
• 23:15
  So there's a lot of different things that we can do with our
• 23:17
  platform. So that are the three things our
• 23:20
  platform get us ready for collaborations, new preclinical
• 23:24
  compounds and ARCH X1, the data available for Phase 2.
• 23:29
  So the, I mean, the company's based in Belgium, which I think
• 23:32
  is seen as an increasing increasingly vibrant place for
• 23:36
  biotech for sure. If you if you just looking at
• 23:39
  like the pros and cons of being based in Belgium, Yeah.
• 23:42
  What have the pros been in terms of like how the company's grown?
• 23:46
  I guess what's been some of the challenges of building a a
• 23:48
  biotech team in in Belgium as well?
• 23:51
  I'll, I'll start with the challenge.
• 23:52
  The challenge is, of course, talent.
• 23:54
  You need to bring in talent as much as you possibly can.
• 23:58
  That's why the location in Belgium was for us also very
• 24:01
  important. So we're close to the
• 24:03
  university, but we are also located at the border of the
• 24:07
  Netherlands and Germany. So we have that international
• 24:10
  angle here, very locally available.
• 24:13
  Then there's definitely a lot of pros.
• 24:17
  One is the fact that the Belgian government is very good in
• 24:20
  funding. So we have here a system which
• 24:22
  is called Flyo that's on the flavour site where we are
• 24:25
  located. And you can send in proposals
• 24:29
  and then there is a contribution from the government in the money
• 24:32
  that you need to execute the project.
• 24:34
  It's not only the money that is important, but they have experts
• 24:37
  in place, so they help you also or they challenge you on the
• 24:41
  project. So they basically make you
• 24:43
  smarter and make sure that the project is really very well
• 24:46
  oriented and also translatable. The other point is that from a
• 24:53
  research perspective, of course, there's a lot of IP protection,
• 24:58
  which is here just as well as anywhere else.
• 25:00
  But from a research perspective, there is a little bit more
• 25:03
  freedom if you want to compare things, not of course if you
• 25:06
  want to develop them, but from a comparison perspective, we have
• 25:09
  more scientific freedom than you would have in in other places as
• 25:14
  well. On top of that, there's some tax
• 25:17
  incentives. Government is very supportive of
• 25:20
  any scientific work that goes on over here and helps us with
• 25:25
  that. We of course are also very small
• 25:28
  country and we do have here like almost every big farmer is
• 25:31
  represented in Belgium. So we also do have a lot of
• 25:35
  knowledge. So the the level of drug
• 25:37
  development and experience is really, really high.
• 25:41
  So we can really benefit from that as well.
• 25:44
  And this is just a question that we've we've finished with on the
• 25:47
  Bio hub. If you were to have dinner with
• 25:50
  any free people, past or present, who would you go from?
• 25:54
  Why? It doesn't necessarily need to
• 25:57
  be people in biotech, although it can be if you like.
• 26:01
  But yeah, three people you'd like to have dinner with.
• 26:03
  So there are a couple that I do have already dinner with.
• 26:05
  So I there's for instance, Roswell Schaumbach is one of
• 26:09
  these people. So, but on my wish list of
• 26:11
  people that are not accessible anymore, hope you don't like
• 26:14
  that is two people. One is Marie Curie, or I should
• 26:23
  say, and I had to, I have to to see that I pronounced it
• 26:26
  correctly. Maria Sklodoska.
• 26:29
  That's her original name, but everybody knows her, of course,
• 26:32
  that's Marie Curie. She is, of course, a female,
• 26:38
  which 100 years ago, she's exactly 100 years older than I
• 26:42
  am. She's not here anymore, of
• 26:44
  course, but and I admire her a lot because she was working in a
• 26:49
  in a period in time where it was not so obvious for women to go
• 26:53
  into science. On top of that, she was driven
• 26:56
  and very passionate because of a personal experience that she had
• 27:00
  with her sister and her mother. So when I'm reading through her
• 27:04
  background, I can understand a lot of the decisions that she
• 27:09
  made in her life. But I would, I really would love
• 27:13
  to just have a conversation with her to talk about what she went
• 27:16
  through, how she did it, how she overcame the challenges because
• 27:21
  there are so many, right, and how she dealt with that.
• 27:24
  So that definitely would be a person that I would love to have
• 27:28
  dinner with. And of course, my favorite
• 27:31
  person, my father would be wonderful if I could have a
• 27:35
  dinner with him again. But unfortunately, he's also not
• 27:38
  amongst us anymore. So yeah.
• 27:40
  Well, three brilliant answers there and thank, thanks so much
• 27:44
  for coming on and helping us out with this.
• 27:46
  It sounds like what you're building at the moment is super
• 27:48
  exciting. The progress that you've made
• 27:51
  recently has been great and I look forward to seeing that the
• 27:53
  next steps for you guys, which sounds like you're doing a a
• 27:57
  great job. So yeah, thanks again for coming
• 27:59
  on and helping us out with this. It was a pleasure.
• 28:01
  And. Thank you so much for having me
• 28:03
  and giving me the opportunity to talk about something that I
• 28:05
  love, that I breathe, and that I'm so passionate about.
• 28:08
  So thank you so much.