Latest / The BioHub - by Avetix / Episode 137 - Steffen-Sebastian Bolz - Co-founder of Aphaia Pharma

Transcript

Episode 137 - Steffen-Sebastian Bolz - Co-founder of Aphaia Pharma · The BioHub - by Avetix

• 0:06
  So welcome back to another episode of the Bio Hub and
• 0:09
  Avetics podcast. Today I'm joined by Stefan
• 0:12
  Sebastian Vogbolts. He's a scientist, physician,
• 0:15
  entrepreneur and Co founder of A Fire farmer, a clinical stage
• 0:19
  biotech developing precision targeted drug formulations to
• 0:22
  treat and prevent metabolic disorders like obesity and pre
• 0:26
  diabetes. We'll be talking about the
• 0:29
  science behind affair, why they're not building with an
• 0:32
  exit in mind, and how staying lean and under the radar has
• 0:36
  helped them advance to phase two.
• 0:38
  It's an absolute pleasure to have you, Stefan, how are you?
• 0:41
  I'm very well. It's a pleasure to me, Max.
• 0:43
  Yes, it's a pleasure to have you.
• 0:45
  Honestly, I want to start a little bit about you and then
• 0:50
  also what's LED you to Co founder fire.
• 0:52
  So in that intro, I talked about you wearing many hats, you know,
• 0:56
  scientist, physician, entrepreneur.
• 1:00
  How? How did your journey then lead
• 1:02
  to to a fire? Well, you know, it's, it's a
• 1:07
  rather long, long journey. Therefore long story.
• 1:10
  I tried to keep it very short. I started medicine in Germany,
• 1:14
  the US and Canada. And when I came, I came back to
• 1:16
  Germany, I actually started a residency.
• 1:19
  And due to this residency, I got obviously exposed to certain
• 1:24
  certain disease patterns that I tried to understand.
• 1:28
  And what is special about the German system is the German met
• 1:32
  school systems that you want to get your doctoral degree, you
• 1:35
  actually have to perform a thesis.
• 1:36
  And the thesis worker was something, something between a
• 1:39
  master's and APHD in Canada, where I'm right now.
• 1:43
  So, and I had a sort of perspective on certain diseases.
• 1:46
  And then I thought, well, you know, the way we think about
• 1:49
  certainly the diseases is, is not really right.
• 1:52
  We, we could do better. So I thought I should go back to
• 1:56
  to basic science and fix a few of those misconceptions.
• 2:00
  And because I was young, I gave myself two years to do all this
• 2:04
  and it actually got massively long.
• 2:07
  I stated basic science and I have now for professor of the
• 2:11
  University of Toronto since 2006.
• 2:14
  Very happy there to have my group there and actually Co
• 2:18
  founded founded. I Co founded two companies and
• 2:20
  the 1 is a fire and I got into a fire because I helped a friend
• 2:24
  of mine here in Germany where I'm right now actually here in
• 2:28
  Germany to to raise funds for project.
• 2:32
  And this project was the idea to use the aerial brake, which is
• 2:37
  the idea the idea that the very distal part of the small
• 2:41
  intestine can actually regulate hunger and when you eat too much
• 2:44
  would actually reduce hunger and stop stop you stop eating.
• 2:48
  So this is where the easier brake idea comes from, to use
• 2:51
  this to actually treat diabetes. And so that was an interesting
• 2:56
  project and I helped him review it and fundraise it for it.
• 3:00
  And when we were ready and when we have the money, when we
• 3:02
  raised the money, the money, the team actually for lack of a
• 3:06
  better way of quitting this assembly.
• 3:08
  So we thought, OK, how can we do this now?
• 3:11
  And he decided to do it ourselves.
• 3:13
  And this is how I got into a fire.
• 3:15
  Very happy that this happened that way.
• 3:17
  It was completely serendipitous. And then we started working on
• 3:21
  this. So this is where I ask those
• 3:23
  hats I have this Professor Shiv I, I have those, those two
• 3:27
  companies that I that I helped to lead and yachts.
• 3:33
  It's an interesting, it's an interesting scenario.
• 3:35
  It's cross fertilizing in all on all levels, right?
• 3:37
  So This is why this is not really strictly separated.
• 3:40
  It's actually something that works very well, very well
• 3:43
  together. For people who don't know a fire
• 3:46
  as well, your your concept's pretty novel and I know you
• 3:49
  explained it a little bit there, but can you just go more into
• 3:52
  detail about a fire's approach and what makes it different from
• 3:56
  other strategies tackling obesity and metabolic dis
• 3:59
  disorders? Absolutely so and actually very
• 4:03
  pleasure to do this. So a Fire's approach is
• 4:06
  different from what we're currently experiencing, what
• 4:08
  we're reading about all over, all over the place.
• 4:11
  What's let's start with with what's being done currently.
• 4:14
  Currently, what's being done is that diabetes and in extension
• 4:19
  obesity is being treated by injecting homes, hormones that
• 4:23
  are known to regulate satiety, hunger and and homeostatic
• 4:28
  functions. And it's, it's well known that
• 4:32
  people with obesity, diabetes and and metabolic disease
• 4:36
  actually have a have reduced levels of those homes.
• 4:39
  And, and so the idea is to kind of replace them and, and
• 4:44
  actually yield those effects on blood sugar, on glucose
• 4:48
  metabolism and on on on weight, weight loss or weight control.
• 4:52
  What we thought. But and, and actually, I should
• 4:55
  say that in order to do this, they, those homes are are
• 4:58
  injected and very high levels. So it's a very high
• 5:01
  concentration. So it has to actually and they,
• 5:04
  they, they are not the natural hormones that can be modified.
• 5:07
  They are injected. They they remain within the
• 5:11
  system for a week and then you get the next shot as Aspen we
• 5:14
  about the Govia to Sepatide and what what they do is they
• 5:19
  replace a certain amount of those homes which are we do,
• 5:22
  which are lacking, which are reduced.
• 5:23
  So when with a fire, we actually thought, let's go back to the
• 5:27
  drawing board and think about what's really missing.
• 5:29
  Think, let's think about what the problem is.
• 5:32
  And the problem really is that when you look at the small
• 5:36
  intestine and how we regulate harness satiety and our
• 5:39
  homeostasis, which means the balance in our body.
• 5:43
  What's very important to know is that when you when you look at
• 5:46
  the stomach and then when you go from the stomach and do the
• 5:49
  small entire time, you have an upper part of the small
• 5:51
  intestine and a lower part of the small intestine.
• 5:53
  And these two parts are very differently equipped with, with
• 5:58
  with cells and molecular tools. The other part just absorb
• 6:02
  nutrients. Where's the lower census
• 6:05
  nutrients? And together it makes sense if
• 6:07
  there's an overflow of nutrients, food components from
• 6:11
  the other part to the lower part, the lower part can sense
• 6:14
  then and actually generate signals to stop eating, reduce
• 6:17
  the tidy and increase the tidy, reduce cyber and so on.
• 6:21
  And is the reason why this is working, why this is happening,
• 6:23
  is that within those in, in this distal part of the small
• 6:27
  intestine, there are specialized cells that actually have on the
• 6:31
  surface have, have proteins and transporters that can actually
• 6:35
  measure the, OR can sense the presence of food.
• 6:39
  And when this, when they do so, they generate signals which,
• 6:43
  which are, which are homes that'll be released into the
• 6:45
  bloodstream. And not just one or two as we
• 6:47
  inject them, but hundreds. And they can also excite nerve
• 6:52
  endings that project directly to the brain.
• 6:55
  So this is what this whole thing comes from, that the small
• 6:58
  intestine is hardwired to the brain because this is true.
• 7:01
  And so whatever happens in the small intestine is immediately
• 7:05
  forwarded to the brain. So the brain knows at any given
• 7:09
  point in time what happens where the small intestine.
• 7:13
  And that's the system that falls down with, with with my
• 7:16
  lifestyle. We're happy with the food we're
• 7:18
  eating, which is fats, which and proteins in, in, in fats and and
• 7:24
  not doesn't have enough fibers and carbohydrates.
• 7:27
  So which which creates a scenario where we eat food that
• 7:31
  that passes to the to the upper upper intestine very slowly.
• 7:36
  So we have to massive reduce speed of the, of the food
• 7:41
  passage of the, the, the food is, is very slow.
• 7:43
  And on top of everything, the food we're eating is highly
• 7:46
  refined. So it's not natural, highly,
• 7:49
  highly complex towel wires or whatever.
• 7:51
  No, it's actually sugar reformulated and different.
• 7:54
  You know what a mosque are, whatever you might put comes to
• 7:56
  mind, right? So it's, they're easy to absorb.
• 7:59
  That's the key point here. It's very easy to absorb.
• 8:02
  So you have this mix, this scenario where you have food
• 8:05
  traveling slower than usual and food that is very easy to
• 8:09
  absorb, that leads to, to, to, to a situation where you have
• 8:14
  massive absorption, slow passage, and only only very
• 8:19
  small amounts of food really going down to the small
• 8:21
  intestine where they could be sessed.
• 8:23
  And This is why the sole sentence sensing system falls
• 8:26
  dormant. And this is exactly what we
• 8:28
  started the thought, Princess, this is what I thought, you
• 8:31
  know, we we could actually repair this.
• 8:33
  The only thing in only quotes, the only thing we would need to
• 8:36
  achieve is to bring something down there, right?
• 8:39
  To bypass the food bowlers, to go down there and rain down
• 8:43
  nutrients on top of those cells to kind of put them on again,
• 8:47
  right? And to kind of re reinitiate all
• 8:50
  those, those signaling cascades and what we thought about what
• 8:53
  we should Gray down on those cells, we look at those cells
• 8:56
  and we kind of saw that when you look at what they, what they do
• 9:00
  best, right? They can, they can sense lipids,
• 9:03
  so fats, they can sense proteins, but what they sense
• 9:07
  best is glucose, remarkably enough, right?
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  And there's, there are many reasons for that.
• 9:12
  It makes different sense from an evolutionary perspective.
• 9:15
  So we actually took glucose, encapsulated it and and tried
• 9:21
  for four years to actually find a formulation that as we wanted
• 9:25
  it bypasses the the the fruit bottles and releases at a very
• 9:30
  distinct point in the small intestine.
• 9:32
  You mentioned the target release, that is the target
• 9:35
  release and similarly in all patients.
• 9:39
  So you and I have a different height, different age, different
• 9:44
  comorbidities and so on, right. This would, this would allow to
• 9:50
  predict that even though small intestines have different
• 9:52
  length, maturity and whatever. And yet what we found were
• 9:56
  leases at exactly the same time, at exactly the same part point
• 10:00
  in both of us. And that's the key that we
• 10:03
  achieve. So we and we could show that,
• 10:06
  and this is what we just recently published, we could
• 10:08
  show that we can really be, we are kind of wake up ourselves.
• 10:13
  But I use I, I, I used to use this Sleeping Beauty analogy
• 10:18
  where the cells are Sleeping Beauty falling dormant and we
• 10:20
  just deliver the prints to the doorstep that kisses the cells
• 10:25
  awake. And, and so this is, this is
• 10:27
  what we cheat. And we can show this because we
• 10:29
  can measure all those halls that'll be released by those
• 10:31
  cells at an extension of that. And as a duction from what we
• 10:35
  see that we can also assume that all these nerve findings are
• 10:39
  being stimulated. And we can see in our, in our
• 10:41
  phase two studies, the study that we did in, in pre diabetic
• 10:45
  patients, that we can improve the glucose tolerance.
• 10:48
  So it's working. And now we have an obesity study
• 10:51
  that we're currently analyzing what we see very encouraging,
• 10:54
  encouraging data. It's not fully analyzed that
• 10:57
  yet. So This is why I can't cannot
• 10:59
  talk about it. But I can give a little bit of a
• 11:01
  preview. We see those increase in hormone
• 11:04
  profiles, those many hormones that we release in, in our
• 11:07
  released in our in our test population of phase one studies,
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  we see this and those sick patients, obese patients with,
• 11:14
  with diabetes and NAF, LG or Nash or even medical syndrome.
• 11:18
  So they all react similarly to our treatment.
• 11:21
  And that's very encouraging because if the hormones are
• 11:23
  there, they do something. And so now we're optimizing this
• 11:26
  treatment and we're quite, we're quite positive or quite not.
• 11:33
  We're more than hopeful. We're almost sure that we will.
• 11:37
  Well that will see good, good data or weight loss as well,
• 11:40
  right. But as I said, this is going to
• 11:41
  be an analysis very, very encouraging data.
• 11:44
  But this we will pop, we will release the new data and the new
• 11:48
  code data in Q22020. Amazing.
• 11:52
  Yeah, I I think it's super impressive that you already have
• 11:54
  a league candidate in. Well.
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  Two phase two trials, right. Could you, could you talk
• 12:01
  specifically about those, those two candidates?
• 12:05
  You mean the two trials that we did?
• 12:07
  Yeah, exactly. Yeah.
• 12:09
  Yeah. So, so the first trial, the
• 12:11
  first trial when we what you have to do when you you want,
• 12:14
  when you want to do a trial, you have to talk to the e-mail here
• 12:17
  in Europe out to the FDA in the States or Health Canada as we're
• 12:20
  just for another trial. So you, you have to talk to the,
• 12:22
  to the authorities because for good reason, this is a higher
• 12:25
  highly regulated environment. So you have to go to them to
• 12:28
  explain to them what, what you want to do.
• 12:30
  And so we did this and, and with the FDA and, and the e-mail
• 12:34
  allowed us to do our phrase one status where we showed those
• 12:36
  nice horror profiles and stuff. We went back to the emir and
• 12:39
  said this all happened without any side effects, right?
• 12:43
  Because I mentioned briefly that the hormone treatments that we
• 12:46
  that we'll read about, like the Govi intercepati are than
• 12:50
  efficient and, and have a huge effect on weight loss and also
• 12:53
  cardio, cardio metabolic endpoints, which are so good,
• 12:56
  but they have massive side effects and, and they haven't
• 12:59
  changed. Despite many trials to or tries
• 13:02
  to change this, they haven't changed.
• 13:04
  So but we went back to the to the FDA and said, well, we'll
• 13:07
  see all those hormone profiles but have no side effects or the
• 13:10
  patients have no side effects. They were like, wait a minute.
• 13:12
  So this this is actually quite signing because you could use
• 13:15
  this in patient groups who are not Ledger for treatment with GF
• 13:19
  21 agonis like pre diabetic patients.
• 13:23
  And so as I used to say, when when the FDA tells you you could
• 13:26
  do this, then you better do right.
• 13:28
  So we we kind of that is, is how our first first phase two study
• 13:34
  was. It was kind of inspired and then
• 13:36
  initiated what we used what we had 30 patients with with with
• 13:41
  pre diabetes. Pre diabetes is not is the name
• 13:45
  suggests it's not diabetes yet, but depending on your on your
• 13:49
  sex, your your, your comorbidities, your age, you up
• 13:56
  to 70% progressed to the full diet full blown diabetes within
• 14:00
  a year. So kind of intercept thing with
• 14:02
  this would be a good thing to do.
• 14:04
  So this is what the FDA came from and said you know what,
• 14:07
  this might be something where you are side effect free
• 14:10
  treatment would be actually quite useful.
• 14:13
  And so we actually this is what we did and we could show that
• 14:16
  those those patients up to six weeks of treatments massive
• 14:19
  benefit and significantly benefited from our treatment,
• 14:22
  which actually means that we measured that were aura glucose
• 14:25
  tolerance. So how well do they handle
• 14:27
  glucose that he actually give them that they drink of how well
• 14:31
  do they handle this. And we actually we could show
• 14:34
  that this tolerance improved after six weeks of treatment.
• 14:39
  So this is the Aura glucose tolerance.
• 14:41
  It's very difficult to find comparatives because as I said
• 14:44
  before, those patients are normally not eligible for
• 14:47
  treatment with the GF 21 agonist except for one group that we
• 14:50
  found and those were women who actually were pre attempt and
• 14:55
  perhaps there's something yet that you try to try to avoid at
• 14:59
  all costs and in a pregnancy. So they actually got Luregatite,
• 15:03
  which is the GF 1 agonist. And we could compare the
• 15:06
  decrease in the increase in, in glucose tolerance that we saw in
• 15:10
  our study started with, with those disorder study.
• 15:14
  And we went during the same ball for they had 52 weeks of
• 15:17
  treatment. We had six weeks of treatment
• 15:18
  and we were quite proud to see this.
• 15:20
  And so this is, this is the moment where we said, OK, let's
• 15:23
  move on. And the second one was a study
• 15:26
  where we set our feeling. Now we go, now we go front and
• 15:30
  we, we look at obese patients with all comorbidities that they
• 15:35
  usually have diabetes and AFLD Nash, as I said before,
• 15:39
  metabolic signal or no comorbidities.
• 15:41
  And then we started treating them and we gave them this
• 15:44
  formulation and told them that they should take 30 minutes, 2
• 15:49
  hours, at least 30 minutes before the main meal, which they
• 15:53
  did. The the problem it was a little
• 15:55
  bit that everyone has his or her main meal at different times of
• 15:59
  the days, which actually instills some variability.
• 16:01
  And even over the week, patients change, right?
• 16:04
  If the good old someday rolls just still very popular, as we
• 16:06
  found out in the Diaries. So they're the, the main meal
• 16:09
  changes, right? Even it within one patient it
• 16:12
  changed. And so we thought I'd keep maybe
• 16:14
  that's not the right approach. And then we updated the protocol
• 16:17
  and actually did it twice per day application.
• 16:19
  So and we could, we could and this had also the background of
• 16:23
  our trust. But the application is not only
• 16:25
  to kind of, if I may use this again in quotes to rein the
• 16:29
  patients in into a certain time and to a very strict pattern,
• 16:32
  right, to reduce variability. It was also inspired by the by
• 16:36
  our knowledge that which is public knowledge, obviously,
• 16:38
  that, that all those hormones that we that we set our hope on
• 16:44
  to actually do the things we want them to do to to induce
• 16:47
  wake control would restore balance and all this kind of
• 16:51
  things that all those homes have a very profound circadian
• 16:54
  pattern. So their their release right
• 16:57
  changes over the course of the day.
• 17:00
  And so you can strategically place your treatments right in
• 17:03
  that cycle. And that's what we did.
• 17:04
  So and we're very, very, we're looking forward to analyzing to
• 17:10
  getting the full fully analyzed set of data.
• 17:13
  And we already what we've seen so far has already inspired the
• 17:17
  third phase two study, which we kind of eaten at a third one,
• 17:21
  which we're recruiting for right now, which is the one that will
• 17:24
  be finished. It's a half year study which
• 17:26
  will be finished by June next year.
• 17:28
  And then we'll take the whole thing, the whole obesity complex
• 17:32
  together. And I think we will be able to
• 17:34
  really present our study, study and story to be kind of leave
• 17:39
  from what you said from this idea to release those hormones
• 17:43
  to really show that they are beneficial and and the way how
• 17:46
  we got there. Yeah.
• 17:49
  I mean, I have to commend what you guys are doing to have three
• 17:53
  candidates potentially in Phase 2 is, is unbelievable for as a
• 17:57
  lean team. When you look at the future of a
• 18:00
  fire, what what do you believe will be the key factors that
• 18:04
  that determine your success? I think that the the key factors
• 18:09
  will be it it's, it's in the case of a fire, it's a very low
• 18:13
  request to you, it's low request for active pump view.
• 18:16
  But especially here, because let me start with with what my, what
• 18:21
  my favorite scenario would be. My favorite scenario would be
• 18:24
  that we find a strong that we find a strong partner, a partner
• 18:28
  that actually allows us to to move on because from we've done
• 18:32
  three phase two studies. And thank you for your
• 18:34
  compliment. We've done this with the very
• 18:37
  lean setup, I think quite successfully so, but now it gets
• 18:41
  expensive. Now we would need to go into
• 18:43
  phase three. I should say that our phase two
• 18:45
  study was constructed as a phase three study.
• 18:48
  So everyone who looks out of phase two data, we'll see.
• 18:51
  Well, it's not so different from what you do usually do in two,
• 18:54
  in a phase three, which we did. We took the risk because it
• 18:58
  mitigates the risk for Phase 2-3 studies for someone who acquires
• 19:01
  that. It's a massively reduced risk
• 19:04
  because when you look at at when you look at the data for
• 19:07
  tacipatide and the Govi out of the phase two studies where
• 19:11
  patients were were were coached, calorie restricted, had to do
• 19:15
  exercise and all these kind of things, you saw between 60 and
• 19:21
  20% weight loss. And now the real world face to
• 19:24
  face comparison between to separate out the Govi, it's much
• 19:27
  less weight loss, which is still fantastic because it's more than
• 19:30
  we ever had because it's the fruit.
• 19:31
  Those are the first drugs that really work.
• 19:33
  But it's, it's, it's definitely, it's definitely much less.
• 19:37
  So it, what I'm trying to say here is that when you go from
• 19:41
  phase two to real world, the, the lots, lots of surprises can
• 19:45
  happen. Not so much for a fire, because
• 19:47
  what we did in Phase 2 is very close to, to phase three because
• 19:52
  our constraints for the patients are minimal.
• 19:54
  You just tell them, take it and A and 48 AM, 4:00 PM, That's it.
• 20:00
  All right. They can do whatever they want
• 20:01
  otherwise. And, and so and they do, I
• 20:03
  guess, but this is, This is why what we have this, this
• 20:07
  mitigated risk. And so our Phase 2 is, I think
• 20:10
  is, is a good deal for everyone who's, who's going to do it
• 20:12
  because, because it's very foreseeable what's going to
• 20:15
  happen. But we have to find this, this
• 20:17
  company, we have to find those teams that actually buy into and
• 20:20
  that's the next thing. What we do is completely off
• 20:24
  mainstream. You could say we thought outside
• 20:27
  the box, which sounds better, but the truth of matter is it's
• 20:30
  completely out of mainstream. So what we had to do together
• 20:34
  with, with our, with the team and, and AC, we had to actually
• 20:39
  think about how can we promote this?
• 20:42
  How can we, how can we, how can we people listen to our idea?
• 20:47
  So I toured lots of conferences and and we do lots of interviews
• 20:51
  and I'm very grateful for this opportunity here with you.
• 20:54
  We just tell our story and people start to buy into.
• 20:58
  And this is this is the best feeling right now because people
• 21:01
  say, yeah, I get this. It's it could work and it and we
• 21:03
  can actually show you the dozen work.
• 21:05
  And so it's a very different it's a very different way to to
• 21:09
  to approach the problem. We it's it was on us to show
• 21:14
  that it works and we did. And now it's it's it's, yeah,
• 21:18
  it's actually, it's actually, it's left to those who move this
• 21:24
  further. I would like to stay involved,
• 21:26
  right, because we have designed this over the years.
• 21:29
  But who knows what's going to happen.
• 21:30
  I just want to see this treatment helping people.
• 21:33
  This is again where my Mt hat comes through.
• 21:36
  Hopefully it doesn't, it doesn't sound too realistic, but it's
• 21:39
  really because I think what I, what we should also the last
• 21:42
  point we should make it if you, if you look at the number that's
• 21:46
  currently being treated with, with TA-2 on agonists, it's 3 to
• 21:50
  6% of the eligible population. So it's, it's, we have 9090
• 21:57
  whatever 94 to 97% of patients left who are not being treated.
• 22:03
  This has to do with the pricing. This has to be with
• 22:06
  accessibility and the copies trying to fix that problem.
• 22:09
  But it will remain and even and, and when you would mostly when
• 22:13
  you read this numbers, you talked about the Yas and maybe
• 22:16
  in Europe, but we're not talking about the global situation.
• 22:20
  We have this, we have similar problems, mass problems in
• 22:22
  India. We have mass problems in, in,
• 22:25
  in, in China. We have it in the in, in Africa.
• 22:28
  And all those patients don't have access to treatments in
• 22:31
  China. It's changing of course with a
• 22:33
  very strong biotech, but it's, it's difficult in other places.
• 22:37
  So we want to just or what our fires, our fire formulation to
• 22:42
  two. It could actually it allows to
• 22:45
  scale and it it will shake, it will change.
• 22:49
  It will be a game changer, which when it comes to to
• 22:51
  accessibility, because it's sugar, right?
• 22:55
  And sugar and the only, the only thing that we need to strategic
• 22:59
  and where if there's one thing, we have another on this planet,
• 23:02
  it's super. And so we only need the
• 23:05
  formulation cause the, the polymer that would need to be
• 23:07
  distributed. But before we plan all this out
• 23:09
  and model because it's possible. So it's it's much easier to
• 23:13
  actually bring this to all corners of the world at some
• 23:16
  point and hopefully not distant future than the current
• 23:19
  medications, which is another, which is another opportunity and
• 23:22
  advantage I would say. Yeah, yeah.
• 23:26
  And you, you mentioned as well about like potentially
• 23:29
  collaborating or like collaborating with some kind of
• 23:32
  pharma company or research institution would, would make
• 23:34
  sense now like how do you guys approach that, that and
• 23:39
  strategize around that? So a fire farmer from it's all
• 23:44
  said has massively benefited from the fact that I'm from
• 23:49
  those multiple hats or many hats on were three actually, I'm
• 23:52
  worry and the fact that I'm deeply rooted and in an academic
• 23:57
  system and I'm a very convinced academic.
• 23:59
  I'm I'm proud to be part of faculty of the University of
• 24:03
  Toronto where where we have where you have everything you
• 24:06
  want and need to have. We'll talk about GFP one Ted
• 24:08
  Drucker is the Ted Drucker is is a very big name in in this
• 24:12
  field, right? He's he's in he's in our
• 24:15
  department and and lots of people work on GFP one in in
• 24:19
  Toronto. So This is why I have the
• 24:21
  perfect environment to go back to say this is guy.
• 24:23
  Do you think, guys, do you think it's possible to use sugar this
• 24:27
  way? And we got feedback.
• 24:28
  So it was very, very hurtful to have comics, well meaning
• 24:33
  comics. So you could actually discuss
• 24:34
  this with and we did and and then we decided, yeah, that's
• 24:38
  right. So this was a very important
• 24:40
  this academic routes of those academic routes were very
• 24:44
  important to re kind of kind of make a decision at some point.
• 24:47
  The other thing is that when it comes to collaboration with
• 24:51
  companies, the, the fact that we have this formulation is not
• 24:55
  because we invented it. It's because our partner in
• 24:57
  Puerto Rico actually a genius when it comes to formulating
• 25:03
  drugs and substances, just told us, you know, it's when we have,
• 25:08
  we've tried many things. So he looked at us and said,
• 25:10
  hey, this is not difficult, let's try.
• 25:12
  And he did it literally overnight completely.
• 25:15
  It's serendipity and and a blesser and he is our partner.
• 25:19
  He's our partner now. It has been our partner for many
• 25:21
  years now. We do this together and
• 25:24
  everything is built on his, his ability to formulate this and I
• 25:28
  this is all his thing. And so on our way forward, we
• 25:33
  talked to pretty much every, every company out there and tell
• 25:36
  the story and get their feedback, which is positive.
• 25:39
  But everyone obviously it's economically driven at that
• 25:43
  point, everyone waits for data. So we kind of give them more
• 25:46
  data, show them more data and build trust and, and, and
• 25:50
  confidence in what we do in those companies.
• 25:53
  And this hopefully culminates next, next summer when we
• 25:56
  actually have them find data set to say, take it and go it's or
• 26:01
  whatever. So this is made, this is, this
• 26:04
  is, this is how we build this. And it's all about
• 26:06
  communication. I think we communicate quite
• 26:08
  well and and frequently slow. I got to do a help from again
• 26:12
  from in this case MSC who is who has opened many doors for us to
• 26:17
  to actually talk to people and get get hurt.
• 26:21
  I think it is really cool the way you've done things you
• 26:24
  commend you to like how far you've got and what you what
• 26:27
  you're doing next as well. It's really exciting.
• 26:30
  So it's been awesome to to hear it first hand and get it out
• 26:34
  there to to people listen to the pod.
• 26:37
  So we, we come to the final question now, Stephen, which is
• 26:41
  a it's a question I ask every guest and it finished at the end
• 26:45
  of the podcast. So if you could have dinner with
• 26:47
  any scientist or innovator, past or present, who, who would it be
• 26:51
  and why? Well, there's without any
• 26:54
  hesitation, Leonardo da Vinci. I since, since I was a little
• 26:59
  kid, I, I, when I saw his paintings and when I saw what he
• 27:04
  tried to do and what he managed to do, which actually bridged
• 27:07
  from medicine to to painting or drawing through engineering.
• 27:12
  I mean, the first helicopter, the idea of the first helicopter
• 27:14
  came from Leonardo. He was such a genius that, that
• 27:19
  I would give a lot to really have time with him and, and just
• 27:23
  experience such such a person. I think that is the Renaissance
• 27:27
  man that he actually created himself.
• 27:29
  I mean, that is that was it. It's, it's unbelievable.
• 27:33
  He has he has pushed, he has pushed boundaries and an
• 27:39
  unprecedented manner. He has suffered because of that.
• 27:42
  He he did this against a lot of resistance.
• 27:46
  But we we still we're still benefiting from from his work.
• 27:50
  And I think this is This is why I would, I would really, as I
• 27:53
  said without any but a lot of preference above and shows
• 27:56
  above. Anyone else that would like to
• 27:58
  meet that? Yeah, thank you for that.
• 28:01
  It's such a cool answer. Yeah.
• 28:05
  Thank you so much for coming on, Stefan.
• 28:07
  It's been an absolute pleasure. Wish you guys the best with what
• 28:10
  you're doing next. Who knows?
• 28:12
  Follow up episode at some point. I will be there for you if you
• 28:17
  need it. I'll be there.
• 28:20
  Thank you so much. Please everyone like and
• 28:22
  subscribe to the Bio Hub and thanks again, Stefan.
• 28:26
  Thank you, Max.