Latest / The BioHub - by Avetix / Episode 230 - Nick Sireau - Chairman at Serenatis Bio

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Episode 230 - Nick Sireau - Chairman at Serenatis Bio · The BioHub - by Avetix

• 0:06
  Welcome back to the Bio Hub podcast by Avetix.
• 0:10
  Today I'm joined by Nick Saro, Executive Chairman and Co
• 0:15
  Founder of Saranatis Bio, a biotech that's developing novel
• 0:20
  treatments for obsessive compulsive disorder.
• 0:22
  Now Saranatis is building a pipeline around the underlying
• 0:26
  biology of OCD with its lead program approaching the clinic
• 0:29
  and additional assets in preclinical development.
• 0:32
  Today we'll discuss Nick's journey into biotech.
• 0:35
  My OCD remains so underserved, the science behind seranatis
• 0:39
  approach, and what the company hopes to achieve over the next
• 0:42
  few years. Nick, thanks for joining me
• 0:44
  today. Great.
• 0:46
  Pleased to be here. Thank you very much, Ben.
• 0:48
  No worries at all. I mean, your room into biotech
• 0:51
  was, was pretty personal. You know you first spent more
• 0:54
  than 20 years developing a treatment for your own
• 0:57
  children's rare disease and then founded Seranatis after your own
• 1:01
  experience with with OCD. How did that journey ultimately
• 1:06
  lead you into building this company?
• 1:07
  Yeah, Yeah. So you're exactly right.
• 1:09
  I mean, the journey started when two of my boys were born 25 and
• 1:14
  23 years ago with an ultra rare disease called alcatinuria AKU,
• 1:19
  also known as black bone disease, actually the first
• 1:21
  disease to be ever shown to be inherited.
• 1:23
  So, you know, quite an iconic disease.
• 1:25
  And so I then spent 20 years developing a drug.
• 1:29
  So set up a consortium, raised around €30 million in grants,
• 1:35
  worked very closely with a team at the, the LIP University and
• 1:39
  hospital. And we developed a drug through
• 1:40
  pre clinical phase two and phase three.
• 1:43
  And we got it approved by the European Medicines Agency five
• 1:46
  years ago. And then separately, our
• 1:48
  partners at the NIH got it approved by the FDA last year.
• 1:52
  So it's, it's an amazing drug. The boys are in their 20s now.
• 1:55
  They've been taking it for about 7 or 8 years.
• 1:57
  And for them, because they've taken it early enough, it's a
• 1:59
  functional cure, so they have zero symptoms of the illness.
• 2:02
  So it's gone way beyond anything I could have ever hoped for.
• 2:06
  It's just been an amazing journey.
• 2:08
  And, and so really then decided to work on another area of deep
• 2:12
  personal interest, which is obsessive compulsive disorder
• 2:14
  OCD, which is a mental illness that I've suffered from on and
• 2:19
  off the past 35 years that runs very deeply in my family.
• 2:23
  I have quite a number of family members affected and I've run a
• 2:26
  support group in Cambridge for just under a decade and I lost
• 2:29
  my best friend from my support group to suicide due to very,
• 2:33
  very severe, extreme OCD. It was, it was catastrophic.
• 2:37
  And so 10 years ago I set up whilst I was still working on
• 2:41
  our captain area, I set up in parallel a foundation called
• 2:44
  Orchard OCD that I'm still very involved with.
• 2:47
  Orchard is doing really well, did a big conference on OCD only
• 2:50
  this year, big international conference and is now part of a
• 2:53
  very large welcome trust grant to do a longitudinal study of
• 2:56
  OCD with a group at King's College and and Sweden and
• 3:00
  Brazil. And then a couple of years ago
• 3:03
  set up Serenatis Bio as a biotech, as a commercial biotech
• 3:07
  with my Co founder called David Kavalan.
• 3:10
  I've known him for about 15 years.
• 3:12
  He's a neuroscientist, he's a chemist.
• 3:14
  He did his PhD in Cambridge, then went off to the National
• 3:18
  Institute of Mental Health, worked at, you know, GSK Small
• 3:21
  Farm. He's an entrepreneur and
• 3:22
  everything. And we decided to set up
• 3:24
  Saranati's bio really, because when I looked at the landscape
• 3:29
  out there, there was next to nothing being done on a
• 3:35
  commercial drug development point of view in OCD.
• 3:37
  Yeah. And that is staggering.
• 3:39
  That is absolutely staggering. And it's scandalous actually, if
• 3:43
  you really think about it, because OCD is not what people
• 3:46
  think. It's not about lining up your
• 3:48
  pencils, it's not about colour coding your spreadsheets.
• 3:51
  It's a devastating disorder, OK. And I, I, I've actually recently
• 3:55
  launched a sub stack where I write different articles about
• 3:58
  it. And I, and one of them recently
• 3:59
  was about the incidence and prevalence of OCD.
• 4:02
  And it was really interesting because I went into the
• 4:04
  literature and found that until about until about 50 and years
• 4:08
  ago, until about half a century ago, people thought it was a
• 4:11
  borderline rare disorder. You know, estimates was about
• 4:14
  one in 2000, which is borderline rare disorder according to EMA.
• 4:18
  You know, now all the surveys show it's around 3% of the
• 4:22
  population, 3%. That's a quarter of a billion
• 4:25
  people. That's 1.5 million just in the
• 4:28
  Uka quarter of a billion worldwide.
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  So it's 10 times more prevalent than schizophrenia.
• 4:33
  You know, it's a huge problem. And people and I, I, people
• 4:36
  always ask me, well, why is that, you know, and why is not
• 4:39
  more being done? The reason for that is due to
• 4:42
  the very nature of OCD. You know, it's an incredibly
• 4:46
  shameful disorder and a very hidden, it's a silent epidemic.
• 4:51
  So for instance, my, my, my best friend who took his own life, he
• 4:54
  had false memory OCD and he would have false memories of
• 4:58
  horrific events, you know, was he a paedophile?
• 5:01
  Had he murdered somebody and all that?
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  These were false memories, but they were so vivid that he would
• 5:06
  obsess 24 hours a day, seven days a week, 52 weeks a year,
• 5:10
  for years and years about had he done these awful things, you
• 5:13
  know, and he would tell nobody, you know, you're not going to go
• 5:17
  to your GP and say, well, I might have a false memory of
• 5:20
  having murdered somebody or I, I, you're not, you're going to
• 5:23
  hide in shame. And in my support group, I had
• 5:26
  one mum who had suffered from OCD for 30 years, post Natal
• 5:30
  OCD. She had had post Natal OCD where
• 5:32
  she would have false images of harming her children, you know,
• 5:36
  which were just horrific. And we were the first people she
• 5:39
  ever told in 30 years. So you can see such a shameful
• 5:42
  disorder and it's only been in the past 1015 years that people
• 5:46
  have started to basically talk about it on social media,
• 5:49
  celebrities and everything. And there's been a lot of
• 5:52
  articles in the media recently all about how severe OCD is, and
• 5:56
  that's why diagnosis rates have gone up.
• 5:59
  So it's not become more prevalent.
• 6:00
  It's just that at last we're capturing just how prevalent it
• 6:05
  is, you know, and that's why big pharma has not caught onto it
• 6:07
  yet. You know, the reason is, is that
• 6:10
  big Pharma follows societal trends, you know, and so they
• 6:13
  are just some of them, like particularly one really big
• 6:16
  pharma company we're speaking to has now put OCD as a target
• 6:20
  indication because they've now realised just how prevalent it
• 6:23
  is, but also what a commercial opportunity it is, you know, and
• 6:26
  I believe others will start catching up.
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  So there's a huge unmet need and also a huge commercial
• 6:31
  opportunity. And you're still sort of less
• 6:34
  than two years into development. What what, what essentially was
• 6:38
  that founding thesis 2 years ago behind the company?
• 6:41
  And why did you really believe that OCD was an area where a
• 6:46
  focused biotech could genuinely change that treatment landscape?
• 6:51
  Yeah, I mean, these are really good questions, Ben.
• 6:52
  So why did what was the kind of thesis behind it?
• 6:55
  Well, I'm not going to claim that it's all ours.
• 6:58
  You know, we have free assets and the people always ask us
• 7:01
  why, why you work on three different drugs.
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  The reason that is very simple, you know, in psychiatry, you
• 7:07
  never get a drug that works for everybody.
• 7:09
  It just doesn't happen. You see that with SSRIs, with
• 7:11
  antipsychotics, everything you know, you never get one that
• 7:14
  works for everybody because these disorders are quite
• 7:17
  heterogeneous. Although I would argue that OCD
• 7:20
  is less heterogeneous than other disorders and that's really the
• 7:24
  beauty of studying OCD. It's a very well characterised
• 7:27
  circuit disorder. So it's the cortical cortical
• 7:32
  striatothalamo cortical loop going through the prefrontal
• 7:34
  cortex down to the base of ganglion back, a very well
• 7:37
  understood circuit where there are also several circuits kind
• 7:39
  of going on there and stuff. And of all the psychiatric
• 7:43
  disorders, OCD is the only one when neurosurgery really works
• 7:48
  where they target the anterior cingulates, which is the part of
• 7:50
  the brain that does error monitoring.
• 7:52
  You know, there's loads of different modalities that work
• 7:55
  in OCD. And also the genetics of OCD are
• 7:57
  increasingly wonderful. So it's a very well
• 7:59
  characterised disorder, you know, much more than depression,
• 8:02
  much more than bipolar and all that kind of stuff.
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  And the animal models are surprisingly good.
• 8:07
  You know, we've worked on three with three animal models, the
• 8:10
  mouse model, the SAP app 3, which is the most widely used,
• 8:12
  probably not the best, but you know, it's, it's quick and
• 8:14
  everything. A rat model, a checking model
• 8:17
  here in Cambridge where they use the same experimental paradigm
• 8:19
  in rats and humans and also a marmoset model here in
• 8:23
  Cambridge, you know, so it's very well characterised, very
• 8:25
  well understood. But also there's our, our kind
• 8:29
  of our, our chief scientific advisor is a scientist called
• 8:33
  Professor Trevor Robbins here at the University of Cambridge,
• 8:36
  Emeritus professor, now very big name in neuroscience, really
• 8:40
  good guy. I've known it for 10 years.
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  And when I lost my friend to suicide six years ago, I went to
• 8:46
  see Trevor and I said, look, what can we really do, you know,
• 8:48
  to make a big difference in OCD. And he was working on a big
• 8:52
  grant from the Welcome Trust and he'd taken 30 patients with OCD
• 8:56
  and he put them in a super high resolution 7 Tesla magnetic
• 9:01
  resonance spectroscopy scanner at Addenbrooke's Hospital.
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  So 7 Tesla is really high resolution.
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  And the reason he did that, there's only two in the in the
• 9:08
  UK. The reason he did that is he
• 9:09
  wanted to separate glutamate from glutamine, OK.
• 9:13
  And So what he detected in his patients with real statistical
• 9:17
  significance was an imbalance of the glutamate neurotransmitter
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  against the GABA one in two parts of the brain that drive
• 9:24
  OCD symptoms, the anterior cingulate, which monitors for
• 9:27
  error, which is the part of the brain that says what if?
• 9:29
  What if? What if the doors not locked?
• 9:31
  What if it's it's what if it's a real memory?
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  And the supplementary motor area, which is the part that
• 9:36
  drives the urges. And on top of that, he linked
• 9:39
  particularly the supplementary motor area to OCD symptom
• 9:43
  severity. OK.
• 9:45
  Right, OK. As measured by the clinical
• 9:48
  endpoint, the Gale Brown obsessive compulsive score that
• 9:50
  the FDA, the EMA, everybody insists on.
• 9:53
  So this was really ground breaking and it came out in
• 9:55
  Nature Communications. So he said the aim would be to
• 9:59
  restore this glutamate camera imbalance only in those parts of
• 10:03
  the brain where it's excessive and hence reduce OCD symptoms.
• 10:07
  So really, really good precision psychiatry.
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  And to do that, he said we should target a receptor called
• 10:14
  the mglu R2 receptor, the metabotropic glutamate receptor
• 10:18
  2. There's seven of them.
• 10:20
  Mglu R2 he he was telling us was the best one because it's pre
• 10:23
  synaptic and has the most influence on glutamate release.
• 10:28
  OK. And there are drugs that work in
• 10:30
  mglu R2. Just this morning I was speaking
• 10:31
  to the lead author of a study from 20 years ago of an MGLU R2
• 10:36
  in general anxiety disorder. You know where they where they
• 10:39
  really detected a real strong signal, OK, but they had to
• 10:43
  abort it for all kinds of reasons, you know, in early
• 10:46
  stage schizophrenia. So there is clinical evidence
• 10:48
  that these drugs can really work.
• 10:50
  So we started working on that and our lead asset is an Mblu R2
• 10:54
  positive allosteric modulator. So it kind of tickles the MBLU
• 10:57
  R2 receptor and resets glutamate levels where it's excessive in
• 11:01
  the brain, not everywhere. So really, really selected and
• 11:04
  that one is getting ready for a phase 1B study in humans with
• 11:08
  OCD. So that's really interesting.
• 11:11
  The second one is really comes out of what my Co founder has
• 11:14
  done. It's a really interesting drug.
• 11:16
  It reduces inflammation in the prefrontal cortex.
• 11:20
  And it's based on, you know, some some studies that show that
• 11:24
  in OCD there's a lot of inflammation.
• 11:26
  Prefrontal cortex. That's the second one.
• 11:28
  You know, that's a preclinical stage.
• 11:29
  And the third one is really interesting because it comes
• 11:33
  with a genetic biomarker, a saliva test.
• 11:36
  And so the third one comes out of work that I that we've done
• 11:39
  with the University of Chicago. So there's a psychiatrist there
• 11:43
  called Professor John Grant, who's a big name in OCD.
• 11:45
  He's been studying OCD for decades and he has been studying
• 11:48
  for a long time a very old drug called tolcapone.
• 11:51
  OK, tolcapone is used was one of the first drugs in Parkinson's
• 11:56
  used with L dopa. And tolcapone inhibits an enzyme
• 12:00
  called the COMT enzyme, which is all over the body, but in the
• 12:04
  prefrontal cortex, the COMT enzyme breaks down dopamine.
• 12:08
  So if you inhibit, dopamine levels go up.
• 12:12
  And as dopamine levels go up, gradually you get more
• 12:15
  flexibility in your thinking, more cognitive flexibility, and
• 12:18
  that allows you to detach from your obsessions.
• 12:21
  OK. And he showed that this worked
• 12:24
  really well in pathological gambling.
• 12:26
  And now he's done a study showing it's efficacy in OCD,
• 12:30
  you know, and that is really interesting become because it
• 12:33
  comes with a genetic biomarker, a snip that predicts how people
• 12:38
  respond to that. But it's got a huge problem.
• 12:40
  It's an old drug and it has an FDA black box warning.
• 12:43
  So it has liver toxicity. There were three deaths in the
• 12:46
  80s. So no one will prescribe it
• 12:48
  widely. So it's just it's kind of a
• 12:49
  proof of principle, you know, that he's done that.
• 12:52
  So what we have done at Serenatis OK is we have
• 12:55
  developed a completely novel CONT inhibitor, OK.
• 13:00
  We are really working at the moment on its brain penetrance
• 13:04
  and it does not have the liver toxicity.
• 13:06
  Basically. Oh wow.
• 13:08
  Yeah, yeah, yeah. So it's not it's, it's not
• 13:10
  Tolcapone, it's not based on Tolcapone.
• 13:12
  It's a completely novel one that we're working on that's a
• 13:15
  preclinical. So that was also really
• 13:17
  interesting. And you could ultimately combine
• 13:19
  them, even ultimately combine them, you know.
• 13:22
  So that's that's quite a long winded answer to your question,
• 13:24
  but that's kind of the thesis behind what we're doing.
• 13:26
  Yeah. I think we've sort of gone
• 13:27
  through a couple of the topics that we we, we wanted to cover
• 13:31
  as I think one that would be great just to go into a little
• 13:34
  bit more detail on is SB001 and the M blue R2 pathway to talk to
• 13:43
  us. Really, I know you touched on
• 13:45
  it, but it knew sort of in depth about that biologic rationale
• 13:48
  behind that. You know what really gives you
• 13:50
  that confidence that modulating this pathway could have a
• 13:54
  meaningful impact on compulsive behaviour?
• 13:59
  Absolutely. So really what what we are
• 14:01
  trying to target are those two areas, the anterior cingulate
• 14:04
  cortex and the supplementary motor area.
• 14:07
  Those are crucial, particularly the anterior cingulate.
• 14:10
  The anterior cingulate comes up in all the brain scans and it
• 14:14
  also comes up in the in, in, in the genetic studies.
• 14:18
  So last year there was a huge publication, I think it was in
• 14:22
  Nature Genetics, where a group led by a researcher called Strom
• 14:29
  basically amalgamated all these GEOS studies and found 30 genes,
• 14:34
  genome wide significance involved in OCD.
• 14:37
  OK. And a lot of them are in the
• 14:39
  anterior cingulate and on the glutamatergic neurons.
• 14:43
  Right. So that's the first thing.
• 14:46
  Second thing, when they do neurosurgery in OCD, they target
• 14:50
  the anterior cingulus and we had a presentation of that at the
• 14:52
  Orchard conference that we did in June where we had a top
• 14:55
  neurosurgeon from London, from Queen Square.
• 14:58
  He was talking about neurosurgery.
• 14:59
  They take out just one or two millimetres from the anterior
• 15:02
  cingulus. So we also know that is a key
• 15:04
  area. Also DTMS, transgraded magnetic
• 15:08
  stimulation also ends up targeting the anterior
• 15:11
  cingulates, you know, so that's also a, a, a, a thing that we
• 15:15
  know there, you know, so you get genetics, you get neurosurgery.
• 15:17
  The brain stimulation doesn't directly target the ACC, but
• 15:21
  targets the interior limit of the internal capsule, the
• 15:24
  anterior internal capsule, which links the ACC down to the
• 15:27
  striatum. So everything really goes to the
• 15:29
  anterior cingulates. And also with EG
• 15:32
  electroencephalography, OK, We know that there's a biomarker,
• 15:37
  OK, for the anterior cingular, it's called error related
• 15:41
  negativity. So this is a, a thing where it
• 15:44
  will spark when you make a mistake.
• 15:46
  So for instance, you might be typing and suddenly you type the
• 15:49
  wrong word, damn wrong word, your ERN will spike or you get
• 15:53
  something wrong. Someone asks you a question, you
• 15:54
  get it wrong. That's the ERN.
• 15:56
  In OCD, it is always spiking because people are always
• 15:59
  detecting an error. You know, because OCD is the,
• 16:03
  the, the French word la folli, the the folly of doubt and the
• 16:07
  ACC, the anterior singular is really the key area there.
• 16:11
  And there's too much glutamate against GABA.
• 16:13
  That's why it's over excited and noise firing.
• 16:15
  So what we believe is that if our M2R2 positive illustrate
• 16:20
  modulator OK can get to that area and we believe it can, you
• 16:24
  know, this brain scan showing that these drugs get there and
• 16:26
  everything. It will then reduce the
• 16:28
  glutamate when it's excessive and that will interrupt the
• 16:31
  whole circuit. Right, OK.
• 16:33
  So then the whole CST circuit starts to calm down because the
• 16:37
  ACC is no longer firing these questions, you know.
• 16:40
  What if I've committed this horrific thing?
• 16:43
  What if, you know these memories are true and I'm paedophile?
• 16:46
  What if the doors unlocked and someone will break in and kill
• 16:48
  my family? I better go and check it.
• 16:50
  Have I really checked it? What if it's not checked?
• 16:52
  Oh my God, I better take a photo of it.
• 16:54
  What if the photo is not real? I better go.
• 16:56
  You know you're interrupting the whole circuit.
• 16:58
  Basically that is the rationale behind it.
• 17:00
  So here in Cambridge, Professor Robinson, his group had been
• 17:04
  doing a study on marmosets. OK, so these are small monkeys,
• 17:07
  so, you know, pretty close to humans, you know, as a non human
• 17:10
  primate. And what they do is that they
• 17:13
  put these thing called dreads into the frontal lobes of the
• 17:17
  marmosets. And these dreads are inactive
• 17:19
  until you give it a special compound that activates them.
• 17:22
  And the dreads go from the frontal lobes to the anterior
• 17:25
  cingulate, basically. And when you give them that
• 17:28
  compound, they start to develop this very habitual compulsive
• 17:31
  behaviour, which is very similar to OCD style checking.
• 17:34
  OK. And they have this kind of
• 17:36
  experiment where they get them to, to, to check for something
• 17:39
  or to press something repeatedly.
• 17:40
  And, and so once they've talked, once they've activated this,
• 17:43
  that the, the, the monkeys develop this OCD like behaviour,
• 17:46
  you know, and when you give them an M blue R2 positive L estate
• 17:50
  modulator, it resets them to normal behaviour.
• 17:54
  Yeah, yeah, yeah. You know, so that is and that is
• 17:57
  the closest to humans. So we know that these drugs
• 17:59
  work. There's evidence that these
• 18:01
  drugs work in general anxiety disorder in humans.
• 18:03
  There's evidence that they work in early stage schizophrenia in
• 18:06
  humans. There's evidence that they work
• 18:08
  in an OSD model of marmosets. There's evidence that they work
• 18:11
  in OSD rat model and there's evidence that they work in an
• 18:14
  OCD mouse model. You know, So what we are doing
• 18:16
  now, once you know we've finished raising all around, is
• 18:20
  hopefully we will show that these work in humans with OCD.
• 18:24
  Yeah. And what walk us through a
• 18:26
  little bit about that phase one BI mean you're sort of
• 18:29
  potentially incorporating neuroimaging alongside early
• 18:32
  changes in symptoms. How how did you think about the
• 18:36
  design of that study? And when you come towards the
• 18:39
  end of it, what would you really constitute?
• 18:41
  A compelling proof of mechanism? Read out.
• 18:45
  Yeah, that's a really good question.
• 18:46
  So we spent a long time working on this study, you know, and we
• 18:50
  spoke to all the top Kols. So Professor Robbins, for
• 18:53
  instance, had been telling us for a while, we really need to
• 18:55
  do a mechanistic study to show that an MDR 2 palm, you know,
• 19:00
  restores or at least reduces the glutamate gabrin balance and
• 19:04
  hopefully shows something in symptoms.
• 19:06
  So we've been working on that for a while and all that.
• 19:08
  And then we we went out and spoke to the big pharma
• 19:10
  companies. We spoke to several of them, you
• 19:12
  know, the really big ones, those with a huge interest also in
• 19:15
  psychiatry and stuff. And, and several of them were
• 19:18
  really good and gave us a lot of time, you know, and went through
• 19:21
  our, our synopses and everything.
• 19:23
  And we ran the ideas past them. And they were like, look, we'd
• 19:26
  be really interested in the target engagement study like
• 19:29
  this, really interested, you know, because, because, because
• 19:32
  they're driven by the science. Fundamentally these big pharma
• 19:34
  companies, they're driven by the science, you know, so we ran the
• 19:37
  synopsis by them. And that's how eventually we
• 19:39
  came up with this with the, the kind of protocol that we've got
• 19:41
  now where we're going to be using 7 Tesla Mrs. target
• 19:45
  engagement to see whether the drug really does reduce the
• 19:49
  glutamate gabrin balance and then hopefully start to see a
• 19:52
  reduction in symptoms. You know, it's a phase 1B.
• 19:55
  So it's not looking for, you know, Q statistical significance
• 19:59
  in the kind of main symptoms and all that kind of stuff.
• 20:01
  You know, it is a phase 1B. It's not a phase two, it's not a
• 20:04
  phase three, you know, So you have to be realistic on that.
• 20:06
  But I mean, it's super exciting, super exciting because, yeah, I
• 20:11
  mean, you know, the, the, the, the, the level of science you
• 20:13
  can now get to with these 7 Teslas is absolutely
• 20:16
  extraordinary. And they're very rare.
• 20:18
  You know there aren't many around.
• 20:19
  You know the UK. Yeah.
• 20:20
  I, I guess then if, if we were to look forward the next, let's
• 20:26
  say sort of 18 months, what are the key milestones that you're
• 20:30
  hoping or expecting to hear across all three of the
• 20:33
  programmes that we've spoken about?
• 20:35
  And, and what, what do you really need to see to have a
• 20:38
  meaningful impact that could ultimately change the trajectory
• 20:42
  of the company? Yeah, absolutely.
• 20:45
  Well, so, so we're two years old.
• 20:47
  We did a pre seed round a year ago basically.
• 20:50
  So that was really good. And we've done a heck of a lot
• 20:52
  of stuff. We're pretty limited resources
• 20:55
  actually, you know, and, and, and now we've just launched a
• 20:58
  seed round and that seed round will basically finance the Phase
• 21:02
  1B and we'll also finance the preclinical development of the
• 21:05
  other two compounds. So if all goes well, I mean,
• 21:07
  it's drug development, isn't it? So it's not about its risks, you
• 21:10
  know, perfectly honest and blunt about this, you know, it's not
• 21:13
  about its risks. But if all goes well within the
• 21:16
  next 18 months to two years, we would hopefully have a good
• 21:19
  readout from the Phase 1B where we would show, you know, a
• 21:23
  reduction in the glutamate gabrin balance, some improvement
• 21:25
  in symptoms, you know, something on those lines.
• 21:27
  I can't really go too much into detail here for, you know, for
• 21:30
  kind of confidentiality reasons. And then the other two, we would
• 21:34
  like them to get to, you know, ready for Ind enabling studies
• 21:38
  basically and even into Ind enabling studies, that would be
• 21:41
  the end with the other two, you know.
• 21:42
  Yeah. Well, look, I mean, fingers
• 21:44
  crossed for you on this fundraise.
• 21:45
  It sounds as though it's going to be it's going to be funding
• 21:48
  some really instrumental work and you know, hopefully things
• 21:51
  that can be paradigm shifting for for such an important sort
• 21:55
  of treatment landscape. I guess just to sort of round
• 21:58
  things off here then, Nick, as we typically do on this podcast,
• 22:01
  if you were able to have any or if you were able to have dinner
• 22:04
  with any scientist or innovator either past or present, who
• 22:07
  would it be and why? Oh, gosh.
• 22:10
  William Harvey. William Harvey.
• 22:11
  So William Harvey, as most people know, was the kind of
• 22:15
  the, because the founder of modern medicine, you know, I
• 22:18
  think it was in the 16th or 17th century, he's the one who kind
• 22:21
  of discovered blood circulation. And the reason why is he has a
• 22:26
  very famous quote, you know, which actually, I can't remember
• 22:29
  word for word, but it was something along the lines of the
• 22:32
  study of rare maladies or whatever he called it helps us
• 22:35
  understand human biology, you know, and he was really
• 22:37
  advocating for the study of rare diseases to understand human
• 22:42
  biology. And that's true.
• 22:43
  Like studying my kids rare disease has helped us understand
• 22:46
  better osteoarthritis, which is a very common disorder, you
• 22:49
  know, But I would translate that to OCDOCD is not a rare disease,
• 22:54
  but it's a neglected disease. And at the Orchard OCD
• 22:59
  Scientific Conference last June, I asked Professor Trevor
• 23:03
  Robbins, why are you so interested in OCD
• 23:05
  scientifically? And he said because OCD is a
• 23:08
  gateway to understanding all psychiatric disorders and the
• 23:12
  human brain, you know, because it's such an iconic, such a well
• 23:16
  characterized disorder, the circuits have to do with fear,
• 23:19
  with reward, with error. These are really deep seated
• 23:23
  basic structures within the human brain, you know, and it's
• 23:27
  a gateway to understanding all of that.
• 23:28
  But I would actually argue it's a gateway to understanding
• 23:31
  modern society. You know, we live nowadays in an
• 23:34
  age of compulsivity, you know, all the online addictions, all
• 23:38
  the kind of phone addictions for social media addictions, all the
• 23:42
  kind of, you know, drug addictions, you know,
• 23:45
  pathological gambling, everything.
• 23:46
  These are all disorders of compulsivity.
• 23:48
  And there's more and more of it in our society.
• 23:51
  And what we are showing is that the study of OCD helps us
• 23:54
  understand compulsivity because it's the archetypal disorder of
• 23:58
  compulsivity. So it's got much wider
• 23:59
  ramifications that go way beyond OCD.
• 24:03
  Yeah, no, super exciting. And yeah, it's been a been a
• 24:06
  pleasure having you join me today, Nick.
• 24:07
  I really appreciate you taking the time.
• 24:09
  Thank you, Ben. Appreciate it.
• 24:11
  Thank you. And thanks for everyone for
• 24:13
  tuning in. Make sure you drop a like on the
• 24:15
  episode and and subscribe to the Biohub page.
• 24:18
  There will be plenty in the future, but for now that's all.
• 24:21
  Thanks and goodbye.