Latest / The BioHub - by Avetix / Alex Blyth - CEO LifT Biosciences at BIO Boston 2025

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Alex Blyth - CEO LifT Biosciences at BIO Boston 2025 · The BioHub - by Avetix

• 0:04
  So here we are in Boston for bio.
• 0:06
  I'm with Alex Blythe, the CEO and founder of Lyft Biosciences.
• 0:10
  Just gives us a bit of context about who you are, Alex.
• 0:13
  Yeah, sure. So I'm the founder of Lyft and
• 0:17
  Lyft is a new to world technology and modality.
• 0:21
  Essentially, we use innate immune cells that we mass
• 0:26
  produce from stem cells, from people who have very good immune
• 0:31
  systems, and we use those to produce a special kind of white
• 0:35
  blood cell that restores innate immune function in patients, in
• 0:41
  particular cancer patients, and replaces their defective innate
• 0:46
  immune cells that are preventing cancer therapies working.
• 0:50
  Yeah, amazing. Just tell us a little bit about
• 0:54
  the journey of it. It's been a long road so far,
• 0:58
  right? But but really rewarding one at
• 1:00
  least, right? Yes, yes.
• 1:03
  So I originally came up with the idea behind Lyft some 10 years
• 1:09
  ago. I'd worked in the industry prior
• 1:13
  to that for about 15 years, bringing novel biopharma assets
• 1:18
  through to market, as you'd say, or through to patients.
• 1:22
  And often they would be targeted because what the industry likes
• 1:26
  to have is the idea that it works on the part of the body
• 1:29
  that you want to change without affecting the rest of the body.
• 1:35
  And that's because in the 1950s and through to about 1970s,
• 1:39
  there are a lot of dirty chemo drugs.
• 1:41
  And so that's been the direction of travel.
• 1:44
  And while that makes sense to a degree, in most areas of
• 1:48
  medicine where like a Swiss watch, you only want to mess
• 1:50
  with this bit and not the rest of it, unfortunately in cancer
• 1:54
  it makes less sense. And I experienced that first
• 1:57
  hand when my own mother got pancreatic cancer and she went
• 2:01
  on to cancer therapies that I'd been involved with, actually
• 2:04
  bringing them through to patients that were targeted.
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  And sadly, what I saw first hand was how the tumour adapts and
• 2:13
  the targeted therapy doesn't. And then you get something
• 2:17
  called tumour escape. And in reality, 90% of people
• 2:21
  who die from cancer die from tumor escape.
• 2:25
  In effect, you've got a lock and key mechanism.
• 2:29
  And when the only key you've got is one or two and there are
• 2:35
  1,000,000 different locks and they're all changing every
• 2:37
  couple of weeks, it's basically a, a failed attempt to try and
• 2:43
  control the tumor that that results.
• 2:46
  And that's why, sadly, you know, the vast majority of people who
• 2:50
  are no longer able to have surgery on their cancer because
• 2:53
  it's gone beyond that organ, particularly using to being
• 2:57
  metastatic throughout the body. You know, for those people, you
• 3:04
  know, sadly, you're going to have about 90% of people having
• 3:07
  a shorter life span than they would have thought.
• 3:10
  And a lot of them will not even live beyond 12 months.
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  And a lot of drugs have come through that are targeted drugs
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  and the industry is obsessed with them.
• 3:21
  And what they tend to measure is do we debulk the tumor?
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  Do we make it smaller? And do we actually then manage
• 3:29
  to get the tumor not growing for a a longer period of time?
• 3:34
  And they call this, you know, progression free survival, but
• 3:38
  it's no, with nothing like actual overall survival.
• 3:41
  All it's meaning is these primary tumor is shrunk down,
• 3:45
  but in 90% of cases they're going to die from a distant
• 3:48
  metastasy that doesn't relate to this primary tumor that's being
• 3:51
  hit with the target. And So what you see is a a very
• 3:55
  strange situation where we have new things like bispecifics
• 3:59
  coming out and a lot of money being thrown at them.
• 4:02
  And while the bispecifics made it better to reduce tumor size
• 4:05
  and improve progression free survival, and we've had people
• 4:10
  like Summit Therapeutics look like they had great data, when
• 4:13
  you actually look at overall survival, it doesn't change.
• 4:16
  And the reason it doesn't change is because it's tumour escape
• 4:20
  that is killing people. And just coming up with another
• 4:23
  way to use targets doesn't solve the problem of the patient's own
• 4:27
  immune system not being able to recognise a tumour.
• 4:30
  They can't recognise friend versus foe.
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  So once the tumour adapts around those targets, it just escapes,
• 4:37
  right? And no matter what they do with
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  different targeted agents, whether they put a, a payload on
• 4:44
  it and they call this a antibody drug conjugate, but it's like a
• 4:47
  little bomb on an antibody that goes into you.
• 4:51
  Or whether they're using a bispecific, which is 2
• 4:53
  antibodies, if you like. Together, all of these things
• 4:58
  are using the same targets that don't work.
• 5:00
  And it's like Einstein's very famous quote, you know,
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  repeating the same things and expecting different results is
• 5:07
  madness. And that's what they're doing.
• 5:10
  Yeah. And that's the sad thing I
• 5:12
  realized when I saw my mum die. And so I instead looked at,
• 5:17
  well, how is it that healthy people are destroying mutating
• 5:22
  cells in their body every day? Very successfully, in fact.
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  You know, today you will have, your body will have destroyed
• 5:29
  around 70 billion cells, which is about the same as A5
• 5:33
  centimetre cube, which is, you know, for a tumour, you could do
• 5:37
  that. You would be able to get rid of
• 5:38
  that. You're a healthy person.
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  So it seems crazy, but your immune system is very good at
• 5:43
  getting rid of your own cells. And that's all a tumour is
• 5:46
  actually. And so we we make it into
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  something else, like it's not your body, it's cancer.
• 5:51
  But no, it's your body and your body knows how to deal with
• 5:54
  that. So I looked at it was working
• 5:56
  for those people. So why don't we get that working
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  for patients? And So what in effect we do is
• 6:03
  we give patients the Super immune system that some people
• 6:07
  are privileged enough to have. Yeah, it's amazing.
• 6:10
  So where are you guys at with it now?
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  What's happening? Well, in order to go into
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  clinical trials with patients, you have to do a lot of
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  preclinical work to show that the the benefit is worth the
• 6:25
  risk to the patient. So you have to show that you are
• 6:29
  able to in models destroy tumors and do it in a Safeway.
• 6:35
  So for example, you know you're not harming mice and at the same
• 6:40
  time you're able to show in models could be a mouse model,
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  but can also be something called a tumoroid model, which is
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  little fragments of real human tumors that you're then showing
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  you can destroy in a three-dimensional way, or it can
• 6:55
  be a tumour chunk. So it's literally a chunk of the
• 6:58
  tumour, which is most realistic actually.
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  And you show how you essentially can destroy destroy that outside
• 7:05
  the body. And we've done a lot of those
• 7:07
  models to show it works very effectively at recruiting in the
• 7:10
  rest of the immune system to destroy these things.
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  But really a hindrance of all these models is you don't have
• 7:17
  the body's whole immune system there.
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  So the data is never going to be as good as it would be in a
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  person because the person has almost an infinite supply of
• 7:27
  white blood cells you can recruit and you've got your your
• 7:31
  lymphatic system and you've got your blood, which you are like
• 7:34
  the high speed transporters of these white blood cells, like
• 7:37
  having a little M25 in your body.
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  And you don't have that in these models.
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  And that's why drugs like Keytruda, which is a checkpoint
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  inhibitor that has revolutionised cancer care and
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  arguably is the most successful cancer drug in history, didn't
• 7:53
  actually do very well in preclinical models because it
• 7:57
  was showing that cells that are recruited, T cells have the
• 8:01
  breaks taken off and work well at killing.
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  But it didn't have a specific target type.
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  And so actually, it didn't look as good preclinically as it
• 8:11
  actually was in practice. But in the end it was, it was
• 8:15
  the best thing because it enabled your own immune system
• 8:18
  to destroy the tumors. But sadly, it only works in a
• 8:22
  small proportion of patients because if you have an
• 8:26
  ineffective innate immune system, it still won't work
• 8:30
  because the T cells need to be brought into the tumour.
• 8:34
  They need to be stimulated. And if the tumour adapts, you
• 8:38
  need something that's going to recognise the escape variants
• 8:40
  and kill it. Yeah.
• 8:41
  And that thing we're talking about is the innate immune
• 8:43
  system. And when that is not intact,
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  even if you've got a checkpoint inhibitor, it's not going to
• 8:48
  work. And that's now been shown in
• 8:50
  clinical papers that are published in Cell in Nature.
• 8:53
  Yeah. Amazing.
• 8:54
  So what's what's next then? Well, what's next is we've got
• 8:59
  our clinical trials starting in 15 months.
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  Amazing. So we've done our GMP good
• 9:05
  manufacturing practice. Essentially you, you can only
• 9:07
  put clean things into people's bodies.
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  And we're very excited to be doing that in Ireland.
• 9:13
  And the Irish government to their credit have given us a €13
• 9:18
  million grant to do that in, in Galway.
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  And that really speaks to their commitment towards ending cancer
• 9:27
  for their population. And I think it's something they
• 9:29
  should be very proud of. And, you know, we are delighted
• 9:34
  that we can be a part of that story.
• 9:36
  Yeah, that's incredible. Just looking at the industry as
• 9:40
  a whole at the moment, there's a general consensus there.
• 9:44
  It's not right. How?
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  How was it like being a smaller company with such big ambitions
• 9:50
  in in a space like this at the moment?
• 9:52
  Yeah, it's very hard. I mean, I feel like I've built
• 9:56
  an amazing speedboat that does all the things we wanted it to
• 10:00
  do. And I the data is better than I
• 10:01
  ever could have hoped for. You know, we can recruit in 1000
• 10:04
  T cells for one of our cells in the tumor.
• 10:06
  I never thought it would be that good.
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  And our cells live for a month there.
• 10:09
  You know, normally neutrals, like, live for a few days.
• 10:11
  So amazing data, but it's like coming out of the speedboat and
• 10:18
  the tide's gone out. Yeah.
• 10:19
  And it's just a desert. Yeah.
• 10:21
  So at the moment, trying to innovate when you're a
• 10:25
  preclinical oncology company with a cell therapy is
• 10:28
  incredibly difficult because the market has run away from
• 10:33
  biotech. Generally, then cell therapies
• 10:36
  like CAR T's didn't work very well in solid tumors, and they
• 10:39
  were too expensive to produce autologous.
• 10:41
  And although we're made from IPSCS and we're off the shelf,
• 10:44
  Yeah, there's an industry fear factor.
• 10:47
  So we've got it double, not just the biotech down, but we've on
• 10:51
  top of that, we've got the cell therapy down.
• 10:53
  And to be honest, oncology is down, yeah.
• 10:56
  And so it's a triple hit really. But we are unique in what we do
• 11:01
  and we've got extremely good results and the people who know.
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  So we have Nobel Prize winning supporters like Jim Allison and
• 11:13
  Pam Sharma who are joining us. You know, the people who are
• 11:16
  really smart and know their stuff.
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  They can see what we're doing makes sense.
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  And it's the missing piece of the jigsaw puzzle.
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  And it's because of those smart people who, you know, are not
• 11:28
  just following the trend. And they are people who can make
• 11:33
  their own minds up that we exist and we're able to keep moving
• 11:37
  forward. But they are a minority.
• 11:40
  I'm sorry to share. Yeah.
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  It's a shame, right? But also how do you deal with
• 11:45
  it? Like personally, your own
• 11:47
  mindset, It's. Yeah, it is hard.
• 11:52
  Yeah. When I started this, I thought,
• 11:56
  well, once I'd shown that these people in the population had
• 12:01
  superior neutrophils who were healthy versus cancer patients
• 12:05
  or people who had a family history of cancer, I thought,
• 12:07
  well, I'll just get those people, stem cells, boom, do
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  this in we go, project done three years and then somebody
• 12:15
  else will take this off me and off they'll go.
• 12:17
  And you know, charities don't do this sort of stuff.
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  They give money to universities. It's just wasted, doesn't go
• 12:23
  anywhere. They don't really do innovative
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  things like this. They just look for some academic
• 12:28
  to give the money to, and the academic's looking to publish
• 12:31
  his paper. Once he's published his paper,
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  he'll just move on to the next paper and the next.
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  No one ever gets around to actually doing these things.
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  And nor were they really working with that mission in in mind.
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  A lot of people were just doing things for their careers, I'm
• 12:46
  sorry to say. And not all, but many.
• 12:50
  Yeah. So I do find it personally very
• 12:52
  hard when you talk to people who've been affected by cancer
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  and they think if you've got something that could cure
• 12:57
  cancer, that everyone would be supporting you.
• 13:00
  And when I tell them it's just not like that, you know, people
• 13:03
  say they will cure cancer quietly if it helps their
• 13:08
  career. And if at any point 1 is at odds
• 13:10
  with the other, they will go with their career.
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  And that can just be not wanting to do something that looks
• 13:15
  risky, that looks like if it went wrong, they get Eggo on
• 13:18
  their face. And that's a career limiting
• 13:20
  step. So what they'll tend to do is do
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  the thing that's on the hyper train that everybody else would
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  do because it's more likely they can get support and momentum
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  from other people. And if it does go wrong, they
• 13:30
  can say, well, everyone else did it as well.
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  And unfortunately, that passive self-interest is totally
• 13:37
  demolishing progress in healthcare.
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  And it the result is that people are dying.
• 13:44
  You know, 10 million people die a year still of cancer.
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  And everyone doing the same thing that doesn't really work
• 13:51
  very well is not going to change that.
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  I've always said this like this industry is an interesting
• 13:58
  dynamic in the fact that every decision is a business decision.
• 14:03
  It's not always with patients in mind.
• 14:07
  So yeah. I agree.
• 14:08
  I'm sure like, yeah, let's finish it on on a positive note.
• 14:14
  You guys have come ahead a long way.
• 14:16
  We have it's. Been a great journey just so
• 14:19
  through like how grateful you are and in terms of what you
• 14:23
  achieved already. Yeah, I'm very grateful for the
• 14:25
  investors who've supported me and had the belief and were able
• 14:30
  to think for themselves. You know, that's been fantastic
• 14:34
  and my team have been fantastic in over delivering what I
• 14:38
  thought was ever possible. And you know if you follow the
• 14:43
  science you will get there eventually.
• 14:45
  I just wished that investors really did follow the science
• 14:48
  like they talked to most other investors.
• 14:52
  And I think as we make more and more progress and show this new
• 14:57
  way to help patients do better, the industry will be forced to
• 15:03
  adapt. It can't just continue to churn
• 15:05
  out more variations on using targets that don't really save
• 15:09
  people's lives. And so that's what I'm going to
• 15:12
  do. I'm going to force their hand to
• 15:14
  do the right thing, not because they're evil people, but because
• 15:19
  they're people doing what works already.
• 15:21
  And they just keep doing it and turning the handle.
• 15:23
  Yeah. And people don't understand
• 15:24
  that. They think it's some conspiracy,
• 15:26
  that, that that's not what's going on here.
• 15:27
  It's just people paying their mortgages, doing what works.
• 15:31
  And that isn't often a revolution.
• 15:33
  Yeah. Amazing to have you.
• 15:35
  On Thank you so much. Cheers.