Latest / The BioHub - by Avetix / Episode 94 - Cameron Turtle - CEO of Spyre Therapeutics

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Episode 94 - Cameron Turtle - CEO of Spyre Therapeutics · The BioHub - by Avetix

• 0:05
  Welcome back to another episode of the Biohub podcast.
• 0:07
  Today, we're joined by Cameron Turtle of Spio Therapeutics, and
• 0:11
  we're live in London from Jeffries.
• 0:14
  Welcome to London. Yeah, Thanks for having me.
• 0:16
  Yeah, awesome. How have you found things so
• 0:17
  far? It's great.
• 0:19
  I I normally live in Seattle and so the weather in London is not
• 0:21
  all that different, so it's good to be here.
• 0:23
  Yeah, perfect much. It's getting a little bit
• 0:25
  colder. It is.
• 0:26
  Yeah, it is. Yeah.
• 0:28
  Nice. No rain yet.
• 0:29
  Yeah. And you've been here since the
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  weekend and. Yeah, the weekend we were here
• 0:33
  for an investigator meeting recently with some of our
• 0:35
  European investigators. So it's the first time I've done
• 0:38
  this conference not overly jet lagged, which is great.
• 0:41
  Always bonus. Yes, yeah, exactly.
• 0:43
  Nice. Awesome.
• 0:44
  Well, let's get into it I guess. Yeah, we always sort of start
• 0:48
  off with a little bit of background on on yourself rather
• 0:50
  than just just fire, evidently. So, yeah.
• 0:53
  Can you walk us through your sort of journey in biotech?
• 0:56
  Yeah, sure. So training originally as a
• 0:58
  scientist actually did my my PhD over here in Oxford of
• 1:03
  cardiovascular medicine genetics and the inherited
• 1:06
  cardiomyopathies as as my PhD. And then I've been in the US
• 1:09
  doing US biotech ever since. So it's been a little over a
• 1:12
  decade now initially consulting, then I spent five years at a, at
• 1:16
  a company that was very small when I joined and not so small
• 1:19
  anymore called Bridge Biopharma. And then, you know, right about
• 1:24
  3 years ago, I had the opportunity, I kind of got a
• 1:25
  call to, to look at this company Spire to potentially come be the
• 1:29
  first employee and, and CEO here and thought it was a great idea
• 1:33
  when it was pitched to me. And so I came over and doing
• 1:35
  that for the last three years or so.
• 1:36
  Yeah, nice. And walk us through a little bit
• 1:39
  about the origins of Spire, because it's a pretty, yeah,
• 1:42
  interesting story. Yeah, yeah.
• 1:45
  I mean, though I was the first employee, I don't really take
• 1:47
  credit as a founder here. A lot of the initial ideas are
• 1:50
  not not exactly mine. I think it's actually pretty a
• 1:53
  clever approach that this investor group called called
• 1:55
  Fairmount had, which is kind of looking at the the broad
• 1:58
  therapeutic landscape and seeing quite a few biologic therapies,
• 2:02
  notably antibodies that kind of they've proven that they work on
• 2:06
  a particular target in terms of great safety and efficacy, but
• 2:09
  oftentimes left quite a bit to be desired in terms of the
• 2:12
  product profile. And this was in a range of
• 2:14
  different therapeutic areas. And, and I think using what we
• 2:18
  know about antibody engineering today, there's a lot of ways to
• 2:21
  improve the properties of the antibody, notably mechanisms
• 2:24
  that are pretty well proven to meaningfully extend the half
• 2:27
  life of an antibody without affecting its immunogenicity,
• 2:30
  its potency, its selectivity. So just really a better antibody
• 2:33
  frankly. And then simultaneously can also
• 2:36
  improve formulations and other things along the way.
• 2:38
  So it gives an opportunity to make, I think, at a relatively
• 2:42
  low biologic risk, a meaningfully better product
• 2:45
  against a proven target. So they've been doing this for a
• 2:48
  few years and they saw this opportunity in inflammatory
• 2:51
  bowel disease where exactly what I just described was the case.
• 2:55
  There was a bunch of these biologics that had been
• 2:56
  developed, leading products in the space, kind of mega
• 3:00
  blockbuster products in terms of sales.
• 3:03
  And they're being delivered, you know, every two weeks
• 3:05
  subcutaneously, which we know we can do a lot better than that.
• 3:09
  And it's also the case that sometimes with these extensions
• 3:12
  of half life, you can also improve more than just the
• 3:15
  convenience of these antibodies and how they're dosed.
• 3:17
  You can also, you know, you can get more drug on board at
• 3:20
  through levels without having to give as much at the Max levels
• 3:24
  of the drugs. You can sometimes get kind of an
• 3:26
  improvement in safety or efficacy as well with this
• 3:29
  approach. So they've been doing this in a
• 3:31
  bunch of areas. They thought IBD was was ripe
• 3:34
  for this opportunity and spent a couple years making new
• 3:38
  antibodies against what I, I still think actually are the
• 3:40
  best targets in the space. So it's A4 beta 7, which is the
• 3:43
  same target as a drug from Takeda called Entyvio.
• 3:47
  The second one is a against a target called TL1A.
• 3:49
  There's no commercial products there yet, but I think it's one
• 3:52
  of the most exciting targets in in, in I and I actually more
• 3:56
  broadly. And then lastly, a target called
• 3:58
  Illinois 23, same target as Skyrizi and Tremfya.
• 4:02
  And so we made what I think are better versions of each of these
• 4:05
  and we'll get into a bit more detail.
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  But they pitched me on that and I said, look, this is this is a
• 4:08
  high probability way of making a great product.
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  And so joined you almost three years ago and built the company
• 4:14
  from there. So what when you got the call
• 4:17
  like, how did they pitch it to you?
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  Was it about the modifications and?
• 4:21
  Yeah, that was that was really the start, which was kind of
• 4:23
  kind of largely what I mentioned there, which is let's take what
• 4:26
  are currently the best biologics in the space, make them
• 4:29
  meaningfully more convenient, right.
• 4:31
  So we can take things that are now we've we've shown phase one
• 4:33
  data for each of our antibodies now.
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  So in humans, we've shown that for each of these antibodies,
• 4:38
  they have more than three times the half life of the first
• 4:40
  generation molecules. And we have higher concentration
• 4:43
  formulations and kind of show that we can you know, hit these
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  targets as well or better than the first generation ones with
• 4:49
  much longer dosing. And so we think we're we're
• 4:52
  going to be dosing in our face while we are dosing in our phase
• 4:55
  two trial that have started either twice a year or four
• 4:58
  times a year in the maintenance setting.
• 4:59
  So just a dramatic improvement in convenience and not just
• 5:04
  convenience almost certainly improves adherence as well.
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  As in if you miss by a week or two when you're taking something
• 5:09
  quarterly doesn't make a huge difference.
• 5:13
  And, and even more so when you're dosing twice a year.
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  Whereas you know, when you're, when you're thinking about your
• 5:17
  disease, you have to take something every week.
• 5:19
  You always have a shot in your fridge.
• 5:21
  You don't forget that you have the disease.
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  You're thinking about it every day, especially in IBD, these
• 5:26
  patients are diagnosed median age is in college age years.
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  So you're talking about college age kids and median means half
• 5:33
  are younger, right? So you're talking about kids,
• 5:35
  college students who are having these biologics all the time in
• 5:39
  their fridge. They always have to be thinking
• 5:40
  about it when they're traveling. They always have to be worrying
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  about it as well. I think this approach removes
• 5:46
  that. It means you can take it, you
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  know, on the road, you can plan around it much more easily when
• 5:50
  you have this, this infrequent dose.
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  So much more convenient for sure.
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  Yeah, and the, and the other pitch was, hey, maybe it's not
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  just more convenient too. You can sometimes learn from how
• 5:59
  these drugs were made and against each of the targets
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  we're looking at what we see in kind of sometimes you don't see
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  it until the late trials, the phase three or even in the real
• 6:08
  world that maybe the first generation product wasn't
• 6:11
  actually the right amount of drug that that they delivered.
• 6:13
  We're all making these decisions with incomplete information
• 6:16
  during the drug development process.
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  And so it actually looks like we might be able to get better
• 6:20
  efficacy in some cases too by having more drug on board either
• 6:24
  in the induction phase or in the maintenance phase of treatment.
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  And so we're aiming for each of these monotherapy products to
• 6:30
  be, you know, at least as good efficacy as what's on the market
• 6:33
  today and meaningfully more convenient.
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  And I think that's that's a step forward that we see is kind of
• 6:38
  as as important to patients and physicians.
• 6:40
  And when we spoke beforehand like it's quite a simple
• 6:44
  modification really, right? Yeah.
• 6:46
  It's a 3 amino acid substitution.
• 6:48
  It's a relatively small change to the antibody that leads to
• 6:51
  this meaningful impact. And I think we and others have
• 6:54
  shown it doesn't typically impact the other aspects of the
• 6:57
  antibody either, the potency, the selectivity, which
• 6:59
  translates to the safety and efficacy of the antibody as
• 7:02
  well. So I think it's a relatively
• 7:04
  simple approach, relatively low biologic risk with a pretty high
• 7:08
  probability of delivering a superior product.
• 7:10
  Yeah, for sure. I mean, normally when you think
• 7:12
  of it, I mean simple terms, I'm not a scientist, but when you
• 7:15
  think of putting a higher dose in, you worry about right side
• 7:19
  effects, toxicity, whatever. Like, did the changes reduce
• 7:24
  that risk? Yeah.
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  So, so two things that I think are important is that one, we
• 7:28
  can get better coverage of these targets without actually giving
• 7:32
  more drug. In many cases, we can deliver
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  less drug and still get better coverage.
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  And, and what you care about in many cases is what we call the
• 7:38
  peak to through ratio, meaning how much drugs you have to give
• 7:41
  at maximum concentrations to achieve your target level of
• 7:44
  coverage at through concentrations.
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  And because we have these long acting antibodies, you can
• 7:49
  actually give quite a bit less at Max and have the half life
• 7:53
  kind of lead lead to higher through levels as well.
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  So that's why I think the key advantage is you actually don't
• 7:58
  have to more antibody to get the same coverage level.
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  And then importantly, we're picking targets in in IBD and
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  elsewhere that really do not come with meaningful safety
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  risks. So they're they're kind of are
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  not kind of compared to other targets in inflammatory bowel
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  disease. The ones we've picked are the
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  ones that do not have black box warnings for serious infections,
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  malignancies and other things. And that really would be a
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  limitation. You may not want a long acting
• 8:23
  drug if you have serious safety concerns, but that's part of the
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  reason why we picked those. It was that, you know, you can
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  have long acting versions and not have much to worry about,
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  yeah. And that through level is super
• 8:34
  important in a chronic condition.
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  That's, so that's, I mean in again, we get to learn from what
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  the first generation products did here.
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  And for each of them they've shown especially the ones that
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  have really large data sets like Entyvio, they see a pretty
• 8:48
  strong correlation between efficacy and the through levels
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  of the drug. Meaning, you know, the more the
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  higher your through levels are, the better the drug seems to
• 8:55
  work. And so that's a major advantage
• 8:57
  for a product like ours where we can get those through levels up
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  without having to get a lot more drug.
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  Yeah. Sure.
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  And those switches, those modifications are one part of
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  your approach. You also, you're running the
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  monetary trials, right, But you're also looking at
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  combinations as well, which in the face of it makes a lot of
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  sense in. So inflammation is a pretty
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  complex process with lots of different factors involved.
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  You want to walk us through what you're doing with those trials
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  as well? To be honest, that's what got me
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  excited about this, this opportunity to lead the company
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  here. Inflammatory bowel disease is a
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  really challenging disease to manage.
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  You know, we've been working on advanced therapies for IBD for
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  three decades plus. There's now meaningful progress,
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  a half dozen different approved classes.
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  And yet the physicians still refer to what they call the
• 9:44
  therapeutic ceiling, which means that you kind of across all of
• 9:47
  these classes, you really cannot get above about a 25% clinical
• 9:51
  remission rate. So only one in four patients
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  treated with all these different drugs gets into remission.
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  And those patients, they lose it over time too.
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  So you lose response, you lose remission.
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  And So what patients and physicians do is they often
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  cycle through many different drugs, rarely getting into
• 10:06
  complete remission. And then the consequences of
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  these diseases, diseases are, are pretty drastic.
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  You can have surgeries, hospitalizations, major quality
• 10:13
  of life impacts. And So what was done in the real
• 10:16
  world was that physicians kind of had the these patients that
• 10:19
  they really could not manage with any of the products that
• 10:21
  they had available, even if they started to have many.
• 10:24
  And so this what they started to do was testing multiple of them
• 10:27
  in the same time. And, and sometimes because these
• 10:29
  drugs can be expensive, as you know, kind of sometimes play
• 10:32
  games where they get one drug prescribed for their IVD and try
• 10:35
  and get another drug prescribed for psoriasis that they might
• 10:38
  have or something other condition to try and get
• 10:40
  multiple drugs on board. And, you know, dozens of
• 10:43
  publications now of physicians all over the world testing these
• 10:46
  combos and seeing that patients that are, you know, not
• 10:49
  responding to anything that are starting to respond when they
• 10:52
  can hit the disease with multiple pathways at the same
• 10:54
  time. And as you pointed out, it makes
• 10:57
  sense in a disease that's not driven by 1 pathway.
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  There's multiple things driving this disease.
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  The idea that blocking any one thing would be a silver bullet,
• 11:04
  it's probably a bit fanciful. So, so, so now and then, right
• 11:08
  as we were launching Spire, one of the first randomized trial
• 11:11
  came out in IBD. So J&J ran a trial, randomized
• 11:15
  combo trial where they tested their two drugs.
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  They have an IL 23 inhibitor and a TNF inhibitor.
• 11:21
  They each got about a 25% remission rate like everything
• 11:23
  else does. And then they tried the
• 11:26
  combination, the 2 of them and they got a 47% clinical
• 11:28
  remission rate, almost 1 + 1 was two really kind of, I think gave
• 11:33
  this field this hope that it might be possible to get
• 11:36
  meaningfully better efficacy by blocking multiple pathways.
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  And so when we saw that they said this is it, this, this is
• 11:43
  what we have to go after. Once you see that level of
• 11:45
  efficacy, there's there's no going back.
• 11:47
  It's almost double right? It's almost double.
• 11:50
  And again, this disease is incredibly challenging to
• 11:52
  manage. It's incredibly costly to
• 11:54
  manage. The consequences of the disease
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  are incredibly both damaging to the patients and, and their
• 11:59
  lives and their caregivers and really expensive from a, from a
• 12:02
  health system perspective to hospitalizations and surgeries
• 12:05
  are really costly. So, so this is kind of an
• 12:08
  opportunity to, you know, meaningfully, you know, get
• 12:11
  patients into remission faster to keep them in remission
• 12:14
  hopefully longer and then avoid those consequences that
• 12:17
  meaningfully impact their life and cost them in the system a
• 12:20
  huge amount of money. And I think combination therapy
• 12:23
  is quite likely to be that next step, as I would say most of the
• 12:26
  experts in the field believe that this is kind of likely to
• 12:28
  be the future. Yeah, nice.
• 12:30
  And where are you at the things at the moment?
• 12:32
  You've obviously mentioned you're at the investigators
• 12:35
  meeting and whatnot. Yeah, walk us through.
• 12:38
  Yeah. So, so to make a combination it,
• 12:41
  we think it's a pretty interesting and exciting
• 12:43
  development path. And we what's unique about Spire
• 12:46
  is despite kind of the huge players that are in IBD,
• 12:50
  relatively few actually own all of the best mechanisms in the
• 12:53
  space. Each of them owns one or two
• 12:55
  good things and then they're trying to kind of figure out how
• 12:57
  to do combos with what else they have.
• 13:00
  I I think we were unique in that we were planning to do this from
• 13:03
  the outset. And I think we were the only
• 13:06
  ones that I think own the three best mechanisms in the space
• 13:09
  with the three that I mentioned. And we own them all on this long
• 13:13
  acting basis, right? We made these these long acting
• 13:16
  antibodies and we spent a ton of time over the last few years
• 13:19
  ensuring that they were that we Co formulate them together so we
• 13:22
  can put them into a single shot, a single injection, which is not
• 13:26
  trivial and and not, not certain to do.
• 13:28
  And also doing kind of combination talks of each of our
• 13:31
  combinations and proving that they weren't just, you know,
• 13:33
  we've seen no talks with any of our individual molecules and
• 13:36
  we've seen no adverse effects even of our combinations dose
• 13:40
  together as well in a chronic setting.
• 13:42
  And So what that lets us do is run what I think is one of the
• 13:45
  more ambitious and exciting trials in the space.
• 13:47
  It's called a platform trial. I think it's, you know, the
• 13:50
  first large platform trial in ulcerative colitis where we're
• 13:53
  testing 6 different interventions in a single study.
• 13:56
  So this is, you know, 1 placebo, each of those 3 monotherapies,
• 13:59
  kind of long acting versions of what we think are the best 3
• 14:02
  targets. And then the three combinations,
• 14:04
  basically A+, BA plus C and B + C.
• 14:07
  And we're testing them all in one big study.
• 14:09
  This is kind of the only way to do this in a robust, rigorous,
• 14:11
  scientific way to see what works best and do the combinations add
• 14:16
  substantial value over their individual components.
• 14:19
  It's a huge initiative. Trial it is, I think it is, I
• 14:22
  think it's a very exciting trial.
• 14:24
  I think the physicians in this space are interested in seeing
• 14:26
  these mechanisms just by themselves compared to each
• 14:29
  other. And the idea that we can test
• 14:31
  long acting combinations of what we believe are the best
• 14:34
  mechanisms in this space is, you know, just potentially not, not
• 14:38
  an incremental improvement for this field, but a step change
• 14:41
  we're going from hopefully meaningful improvements in
• 14:43
  efficacy and at the same time meaningful improvements in
• 14:46
  convenience in one trial. Yeah, be a big step forward for
• 14:49
  sure. Yeah, I think it's exciting.
• 14:51
  So it's a big trial. So we're kind of kicking this
• 14:53
  off now. It'll be a big global study kind
• 14:55
  of 30 odd countries participating, a few 100 sites
• 14:58
  participating in the trial. We've been you know started
• 15:01
  about six months ago and we'll actually start to read out data
• 15:03
  from this trial next year, which is so we're going to start
• 15:06
  reading out the monotherapies first and then we'll follow up
• 15:08
  with the full combinations against the monotherapies.
• 15:11
  And I think, I think it's an incredibly exciting time.
• 15:15
  Not too far away either. No, I mean, no, you know when
• 15:18
  we, when we started this trial, we thought it would be
• 15:20
  attractive to physicians and patients because you know the,
• 15:24
  the efficiency of this design because we only have one placebo
• 15:27
  arm and six active arms. Most pay, I mean it's about a
• 15:30
  one in six odds of getting a placebo in this trial.
• 15:33
  And three of the six active arms are what physicians believe are
• 15:36
  likely to be the future of this space.
• 15:38
  And these combination therapies and all of them are more
• 15:41
  convenient than anything on the market, right.
• 15:43
  So, so it's, it's kind of a lot of reasons to be excited, a lot
• 15:46
  of reasons to participate in the trial and I think we're seeing
• 15:48
  that so far in in the early launch of the study.
• 15:51
  Yeah, the reason I mentioned it's not too far away is because
• 15:53
  speed's been a bit of a theme for you over the past, well,
• 15:57
  decade, I guess. Yeah, that's right.
• 15:58
  In your career, obviously you mentioned bridge bio when you
• 16:01
  when you first spoke. And yeah, I guess you've taken
• 16:04
  some learnings from what those guys were able to achieve.
• 16:06
  Right. Yeah, I mean, Bridge was a
• 16:09
  great, I mean, I joined when it was kind of A2 room office place
• 16:12
  and and, and you know, the company is now now doing
• 16:15
  incredibly well and got to work with exceptionally talented,
• 16:18
  hard working folks and saw, you know, a huge number of
• 16:22
  successes, plenty of challenges too along the way and growing
• 16:24
  kind of a small company from the outset.
• 16:27
  I do think one of the learnings that was very obvious now
• 16:30
  looking back all along the way, we were told, you know, it's
• 16:34
  going to be really challenging to compete against the larger
• 16:36
  players in this space. And in particular, one of the
• 16:38
  lead programs and still probably the most important product there
• 16:41
  is in a space called TTR cardiomyopathy.
• 16:44
  And you're competing there against, you know, Pfizer and
• 16:47
  some of the other largest biopharma companies in the space
• 16:50
  that, you know, we're both multiple years ahead of us and
• 16:53
  far better resourced in terms of kind of existing infrastructure
• 16:56
  to do these trials. And there was a perception that,
• 16:59
  you know, how can this upstart small company compete in that
• 17:02
  space? And, you know, I think, I think
• 17:07
  to be honest, yes. And I think kind of proved that,
• 17:10
  you know, a small group of folks that are really dedicated and
• 17:12
  focused on a singular mission and, you know, care deeply about
• 17:17
  it. I mean, in that trial, I went
• 17:19
  and visited dozens of the sites to go, you know, shake the hands
• 17:22
  of the investigators, convinced here's why I'm excited about
• 17:24
  this drug. Here's how it can help your
• 17:25
  patients. That is, is something that you
• 17:30
  that you may not see from the larger organizations.
• 17:32
  And I think it, I think it matters.
• 17:33
  I think it pays off in the long run.
• 17:35
  And I think it, it, it led to some of the successes at Bridge
• 17:38
  Bio. There was, you know, enrolling
• 17:40
  that phase three trial there was not trivial.
• 17:42
  It was during COVID Pfizer drug was launching.
• 17:44
  There was all sorts of challenges, but being fast,
• 17:47
  focused and, and caring a lot mattered.
• 17:49
  And frankly, I take a lot of those learnings into right,
• 17:52
  we're playing in inflammatory bowel disease.
• 17:54
  It's a $30 billion commercial market globally.
• 17:58
  It's J&J, Abby Takeda, some of the biggest players in this
• 18:01
  space that we're competing against.
• 18:03
  And, and, you know, it's again, kind of a small company with
• 18:06
  what I think is an exciting, ambitious approach.
• 18:09
  And I, I think, you know, being as quick as possible is, is
• 18:12
  critical to kind of, you know, beating, being more agile is one
• 18:15
  of the few advantages we have. Obviously, you all in then on
• 18:20
  that program and you're all in here, right.
• 18:22
  So I think, yeah, those big pharma businesses are naturally
• 18:26
  more spread out, right? They're focused.
• 18:27
  So, yeah, yeah, you go into the trial sites and shaking hands of
• 18:32
  the investigators, that's not something that's necessarily
• 18:34
  going to happen in those big businesses, right?
• 18:36
  Yeah. And I actually think it may be
• 18:38
  more obvious. We've talked a lot about our
• 18:39
  inflammatory bowel disease approach.
• 18:41
  We're actually running a trial in rheumatology as well.
• 18:43
  And I think it's, I think that might even be a more obvious
• 18:46
  case where we started working on this TL1A antibody a few years
• 18:50
  after the first ones were developed.
• 18:51
  Again, we saw these these first generation TL1A's that were made
• 18:54
  by a few very successful companies, but saw that, you
• 18:57
  know, these antibodies were maybe not the best you could
• 18:59
  make. And so we started making what we
• 19:00
  thought could be a better one. And and then we're saying, OK,
• 19:03
  IBD, we're we're quite sure it's going to work in IBD.
• 19:06
  That's where the data was, was very strong.
• 19:08
  But this target might work in a bunch of other indications as
• 19:10
  well, including in these rheumatic diseases, RAPSAX BA
• 19:15
  that are about the same size as IBD.
• 19:18
  And the evidence is quite good too.
• 19:20
  And we thought, look, this, this product could be great there as
• 19:22
  well in terms of the evidence for it and said, you know, why
• 19:26
  should we, we should go after this too.
• 19:28
  Like this product could be a big opportunity there.
• 19:31
  And frankly, we were surprised to not see the first generation
• 19:33
  players beat us to it. They probably had a couple year
• 19:36
  head start again, had all the infrastructure that we didn't
• 19:38
  have to run trials in different therapeutic areas.
• 19:41
  And then, you know, we started our trial a few months ago and
• 19:44
  then within a few weeks thereafter see that those first
• 19:46
  generation players actually started trials after us in the
• 19:49
  space. So it's, you know, it, it, it
• 19:52
  seems unbelievable that you can kind of be an upstart and, and
• 19:55
  kind of compete against the biggest players.
• 19:56
  But I, I, I don't think that's the case.
• 19:59
  I think sometimes you know a a small dedicated group of folks
• 20:02
  can can matter a lot. Yeah, I guess you're proving it
• 20:05
  as well. So yeah.
• 20:06
  Yeah, we'll see. Drugs still have to work.
• 20:08
  But yeah, I know. But, but I think, you know, in
• 20:10
  terms of getting the trials off the ground, picking the right
• 20:12
  indications and and going quickly, I think we've we've
• 20:14
  shown that we can do that, yeah. No, Awesome.
• 20:16
  It's gonna be yeah, really cool to watch.
• 20:19
  Watch the progress from the thought.
• 20:20
  It's going to be, yeah, really exciting time.
• 20:22
  Yeah. So we have, yeah, we're going to
• 20:23
  have six phase two readouts next year, kind of three in the
• 20:26
  inflammatory bowel disease trial and three in this rheumatic
• 20:29
  disease trial and followed up with a combination.
• 20:32
  So I, I think it's gonna be exciting, you know, a few
• 20:35
  quarters ahead. Yeah.
• 20:36
  For sure. Awesome.
• 20:37
  Well, appreciate you coming on. I guess we'll finish with the
• 20:40
  standard biohopper question. I'm quite excited to get your
• 20:43
  take on this, actually. It could be an interesting
• 20:45
  answer. And that's.
• 20:46
  Yeah. If you were able to have dinner
• 20:48
  with one entrepreneur or scientist, past or present, who
• 20:51
  would it be? Yeah.
• 20:52
  And why? Yeah, so I, my undergrad was in
• 20:55
  bioengineering and so it kind of fused math, engineering and and
• 20:59
  biology. And my favorite series of
• 21:02
  lectures were in a Physiology class that I had that was
• 21:07
  talking about the experiments done actually here in Cambridge,
• 21:09
  I think by Hodgkin and Huxley. So they, what they did was they
• 21:13
  looked at kind of giant squid axons like, and it was because
• 21:17
  like this is back in the, you know, 30s, forties, 50s, that
• 21:19
  they were doing these experiments and you, the
• 21:22
  equipment could only look at something that large.
• 21:24
  You couldn't look at kind of microscopic things.
• 21:27
  And they took this really complicated system and, and
• 21:30
  showed basically how electrical signals are conducted in axons
• 21:35
  and muscles. And they, they went from this
• 21:38
  kind of quite brutish experimentation to beautiful
• 21:41
  maths. So they, they, they have kind of
• 21:43
  these series of differential equations that describe how
• 21:46
  electricity is conducted in axons.
• 21:49
  Beautiful. So, so I would, I would.
• 21:51
  And they were kind of gentlemen scientists as well.
• 21:53
  So they kind of did these experiments and then the war
• 21:55
  broke out. And so they were working, you
• 21:57
  know, kind of in the war effort as well.
• 21:58
  So, yeah. I mean, you know, I'm sure 60
• 22:01
  years later they would be surprised by a lot of things we
• 22:03
  have today. And I think that'd be a great
• 22:05
  dinner guest. Yeah.
• 22:06
  We'll let you off. That's two guys.
• 22:08
  Well, two guys, yeah, I'll pick one.
• 22:10
  Hodgkin. Yeah, could be.
• 22:12
  Either way, it would work, yeah. Thanks for coming on.
• 22:15
  Coming. Seriously, thanks for having me.