March 19, 2025 • 21 mins
This week on BioTech Nation, we explore what happens when your immune system overreacts. Professor Niels Riedemann, CEO of InflaRx, explains how the body’s defense system can sometimes cause more harm than good, leading to serious conditions like rheumatoid arthritis, severe COVID-19, and lung failure. Learn how InflaRx is developing treatments to calm the immune system and why their breakthrough drug is getting attention from U.S. health agencies.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Dr. Moira Gunn (00:11):
What if you contracted a serious virus or
bacteria? You want your immunesystem to respond. But what if
your immune system overreacts?Or what if the foreign invader
isn't an invader at all, butyour own healthy tissue? This
may sound somewhat familiar tosome of you, but what Inphlorex
(00:32):
is doing about it is definitelyoriginal.
Professor Niels Reidemann is thecofounder and CEO of InflaRx.
Professor Reidemann, welcome tothe program.
Prof. Dr. Niels Riedemann (00:43):
Thank you so much, Moira, for having
me.
Dr. Moira Gunn (00:45):
Now what is C5a and why does it need to be
inhibited?
Prof. Dr. Niels Riedemann: Thanks for this question. Love (00:51):
undefined
to answer it. So C5a is a smallprotein in your blood that gets
activated and this protein canreally boost inflammation to a
point where inflammation cancause harm to your own organs
and tissue. Now I should mentionthat C5a is part of our immune
(01:13):
response.
Dr. Moira Gunn (01:14):
Now, I had say rheumatoid arthritis, how does
C5a work into that? How exactlydoes it work? And why is it
really a challenge forrheumatoid arthritis?
Prof. Dr. Niels Riedemann (01:29):
So I think rheumatoid arthritis is an
interesting example and youprobably heard the term
autoimmune disease before,right? So this term implies that
kind of your immune systemreacts against yourself, right?
And we talked about the immunesystem and C. VaVe being part of
our immune system. And I want tointroduce you to the fact that I
(01:52):
mentioned it's a small proteinthat's activated.
It's part of several proteinsfloating in your blood, that can
get activated and these severalproteins altogether are called
the complement system. Now whatis the complement system? It's
actually a very central part ofthat immune response we're
talking about. That getsactivated in autoimmune diseases
(02:16):
and there is also evidence thatC5a is elevated in patients with
rheumatoid arthritis especiallywhen they have a flare. So I
want to explain that a bit morein detail.
So what do these proteinsfloating in our blood do? Why
the heck are they there? Right?What do they do there? Well, of
that as a broad sensor that isin your blood and in your
(02:40):
tissues to sense anything thatshouldn't be there and give that
signal to your cells, to yourimmune cells to tell them, hey,
there's something in our systemthat shouldn't be there.
Get active, get rid of it. Nowthese immune cells, you can
think of them a little bit likethey're having weapons to get
rid of anything that's in oursystem. And these weapons are a
(03:03):
bit like dirty bombs. They canget rid of that. But if they get
activated dramatically, they canunfortunately, these dirty bombs
can also start damage our owntissue.
And what does it mean whentissue is damaged? It means, for
example, organs stop functioningas well. So it gets very
dangerous. And, you know, if youthink of that example that you
(03:26):
gave for rheumatoid arthritis,we all know the problem happens
in our joints when you have thatdisease. So something activates
the immune system and maybe alsothe complement system pretty
surely in that joint.
So cells get active, they moveinto that joint and they start
inflammation, they release thesedirty weapons. Well, guess what
(03:48):
they do? They damage our owntissue, in this case, the
cartilage and the cells thatshould function in your joints.
So there you have it, you havean autoimmune disease and the
complement system is almostalways involved. And that's why
I think it's important to keepthat term in mind.
Dr. Moira Gunn (04:06):
So the C5a is great if it's going after a true
foreign invader, real intruder,you know, doing bad things to
you. Really go after it. But ifit happens to identify your own
system, then you want to inhibitit.
Prof. Dr. Niels Riedemann (04:24):
That is true. But also when it gets
over activated, our body has theability to produce a ton of this
little activation product C5aand when it's over produced,
that happens in life threateninginflammatory settings, then that
becomes a double edged sword.The original positive meaning of
(04:47):
starting an immune responseturns into something very
dangerous and in fact evendeadly. And so if it's too
strongly activated, you want toblock it. If it is activated
when it helps the system to actagainst your own tissue, like in
an autoimmune disease, want toblock it.
Dr. Moira Gunn (05:04):
Now, Inflorex already has a C5a inhibitor
that's been authorized by theFDA under emergency use
authorization, and it's forcritical COVID-nineteen. What is
critical COVID-nineteen and whatis your drug doing?
Prof. Dr. Niels Riedemann (05:22):
Yeah, I really appreciate that
question too, happy to give youa bit more color. And it's
interesting now we're five yearspast the pandemic start and we
all want to not ever hear ortalk about it again, but yet we
know it's kind of the pandemicis done, but that viruses may
not be done with us. And that'sthe trouble we're in. So, we all
(05:44):
know that we take vaccines tohopefully not get as sick.
That's what we do before we getsick.
When we get sick and the virusis in our system, when we have
these flu symptoms that many, ifnot most of us experience, there
are antivirals, they stop thevirus from replicating and
hopefully that helps you.However, unfortunately, with or
(06:05):
without these medicines, somepatients develop that what we
talked about that strong immuneresponse that is overboarding.
And then they get severely sick,they have trouble breathing,
they need oxygen support, theyneed a breathing mask and
eventually they need invasivemechanical ventilation when the
(06:25):
lungs are no longer able tosustain their function to give
oxygen in your blood. Andexactly for those patients that
get so severely sick that theyneed invasive mechanical
ventilation or even lung supporttherapy. For these patients, we
tested this anti C5a antibodythat you mentioned that blocks
(06:47):
C5a, and we got this emergencyuse authorization from the US
FDA.
Dr. Moira Gunn (06:54):
So if we need your drug, we're in trouble.
Prof. Dr. Niels Riedemann (06:55):
You could say that.
Dr. Moira Gunn (06:58):
But thank goodness it's there. Okay. So
now this same c five a inhibitoris in other trials. And one is
very interesting to me, and thisis broader than the critical
COVID, response. But in 2023,BARDA, which is the biomedical
(07:18):
advanced research arm of theoffice of strategic preparedness
and response, which is part ofthe US government, hosted a
pitch event just like they're inSilicon Valley or something.
They they had the judges. Thejudges included the CDC, the
FDA, NIH, and other federalgovernment agencies. And biotech
(07:39):
and pharma companies came with18 drug candidates, that were in
what we call the end of phasetwo. They were still not
approved yet, but they were, youknow, they had demonstrated,
some level of efficacy. Thesewere very creative and promising
drugs.
And so of the eighteen, threedrugs were selected to be
(08:02):
studied. One was from a companywe would all recognize,
Genentech, and one was yours,Inflorex. Now what was the
medical condition that you wereall talking about? Why was is
this condition so critical? Allof these agencies are interested
in it.
(08:22):
And while the trials are stillunderway for these three drugs,
how might your C5a inhibitordrug work to treat it?
Prof. Dr. Niels Riedemann (08:30):
So the condition that is tested
there is really a very criticalcondition and there are no
treatments yet authorized forthis broader condition. And that
condition has to do with lungfailure and it's referred to as
ARDS or ARDS. That stands foracute respiratory distress
syndrome. And that means whenboth of your lungs, the left and
(08:53):
the right lung are so severelycompromised, that you're in
trouble, you need oxygensupport, you have trouble
breathing, etc. Similar to whatwe just discussed in COVID.
Now, it is recognized that thiscondition is caused by the
immune response we talked about.And it's also recognized that it
(09:14):
can result from different, Iwould call it, insults. It could
come from viruses like COVID orlike influenza, like avian flu,
but it could also come frombacterial infections in the
lung. It can even come fromchemical, injuries when you
inhale smoke or when you ingestsome chemicals. So this immune
(09:36):
reaction to this type ofinvasion either by
microorganisms or by othercausing damages, that immune
response causes this lungfailure.
And since there are notreatments, and the government
recognizes the importance. Also,when you think about pandemic
(09:57):
preparedness, just think aboutit. There was a drug that you
could pull off the shelfavailable if a new virus hits
and you could at least hopefullygive it to the most severely
sick to bring down mortality,ideally, and win time until
appropriate vaccines orappropriate antivirals. You
know, I'm just giving theseexamples from COVID because we
(10:19):
all still remember them or untilappropriate, you know,
antibiotics would be developedfor, you know, let's say a
bacterium for which antibioticsdon't work anymore. So such an
approach would to society.
So that's why the US governmentresearches these approaches.
Now, how does C5a fit in or mayfit in? Well, first of all, I
(10:40):
should say we still need to testit. We cannot just automatically
assume that it will work. But wetalked about earlier here today
about the important function ofthat little protein and the
complement system.
Remember, that sensor in oursystem that can get over
activated. So I think throughCOVID, we were able to show that
(11:02):
when it was given to these veryseverely sick patients that it
did lower the all causemortality in these patients. So
there is a hope that thisfunction is similarly important
in the broader ARDS setting.Now, as just as a side note, we
are not approved in The US withthe drug. We have, as you said,
(11:22):
an emergency use authorization.
We just recently, two monthsago, got an exceptional
circumstance approval in Europe.And that approval was for that
COVID part that can causemoderate to severe ARDS. So it's
different label than the use ofthe emergency use authorization
(11:43):
in The US, but there is thisrecognition of the causing ARDS,
in this case from COVID. Now
Dr. Moira Gunn (11:52):
one more quick question about this same drug,
different trial, and at least onthe surface, a very different
condition. It's called pyodermagangrenosum, and I'm sure I
mispronounced it, it soundsterrible. What is this disease
and how might this same drug,Inflorexis drug, apply?
Prof. Dr. Niels Riedemann (12:14):
Yes, so indeed it's a disease that's
not just difficult to speak,pyoderma gangrenosum, it's also
really a horrible skin disease.These patients suffer from large
ulcers that don't heal despiteof all sorts of treatment
including wound care and youknow off label trying and error
(12:35):
of different therapies. Well infact there's no drugs available
or approved in The US or inEurope for this condition. It's
a rare but really horrible skindisease. In some cases it can
even lead to amputation of legsand arms when these ulcers don't
heal and get larger and larger.
And I should mention thesepatients suffer a lot. The
(12:58):
patient advocacy group leaderonce told me that this is not
just like a wound. Just, shesaid, imagine you feel skinned
alive all day long. This is whatthis disease is. So horrible
condition.
And your second part of thequestion was how may that
mechanism that we talked aboutfit in? And so this is also a
(13:21):
condition where we believe thatit's kind of in the broader
autoimmune, auto inflammatorycondition. So again, the immune
response is recognized to play arole. Even though this condition
is not fully understood, thisdisease, these immune cells,
which I mentioned that can getactivated by the complement
system are abundantly presentand seem to cause these ulcers
(13:44):
or at least disturb them fromhealing. So we did initial
studies that showed somepromising results and we are
currently running a larger, moreinternational, different
countries, but with focus on TheUS phase three study.
So ultimately, our idea is thatone day we hopefully get an
approval and show that the drugis truly efficacious, but, it
(14:09):
still needs to be tested. Butagain, remember the immune
response we talked about, sothat may be applicable in
different diseases. I shouldprobably also go one step
further and say these cells,these immune cells that get
activated by C5a, they arecovered with the signal sensor
called C5a receptor. This iswhat gets them activated when
(14:32):
C5a binds to them. They havethat on their cell surface.
And particularly those that arefound in this disease are part
of the white blood cells, theycan cause damage. So there is a
link to damage in this case inthe skin, in this case very
locally, but you know with avery bad outcome for the
patient. So we have the hope toshow through this study that
(14:55):
there is an effect also benefitfor patients to heal these
ulcers.
Dr. Moira Gunn (15:00):
Now, you have other formulations, other
trials, but I wanna talk aboutthis. You and your cofounder,
doctor Renfeng Guo, werepostdocs, both MD postdocs
working in the same lab at theUniversity of Michigan. You came
from this tiny town in Germany.He came from a tiny town in
(15:21):
China. And yet, in addition toplaying table tennis and all the
kinds of things that thatgraduate students do, you
discovered that you were aterrific lab team, and you also
made a scientific discovery.
What were you working on? Whatdid you discover, and how did it
lead to today?
Prof. Dr. Niels Riedemann (15:41):
Yeah. Absolutely. Renfeng and I met as
postdocs in that discovered thatwe were working well and we were
part of a broader discovery teamin that lab of Doctor. Peter
Ward, a famous complementscientist, and we were part of
the team that researched exactlythe role of this protein C5a and
(16:03):
especially the receptor Imentioned on these immune cells.
Ren Feng and I discovered therole of this receptor
particularly in differentconditions in preclinical
science where it leads to damagein the lung, in the organs, in
the different tissues.
And we get so intrigued aboutthe broad potential
(16:25):
applicability of the mechanismfor so many different disease
settings that I think it was onenight past midnight, and I guess
I can say it today, I think wehad a beer in the lab today that
wouldn't be appropriate anymore,but back in the day you could do
that. We had a beer and we wereoftentimes working late and we
(16:45):
started talking about, wow, thisis so important. You know, we
should really think about makingthe drug addressing this. Now
you mentioned by now we have twodrug candidates. The one drug is
the antibody that blocks C5a andthe other one is the new
formulation that will be an oraltablet, a chemical inhibitor
that blocks the receptor wetalked about.
So the same pathway withdifferent mechanisms addressed.
(17:08):
And so we were part of thatdiscovery and yeah, here we are
many, many years later, a bitmore gray hair, at least on my
side, Renfeng looks reallystellar with no gray hair. But
but, yeah, we we we founded thecompany. Renfeng is in The US.
He's the chief scientificofficer of the company, and I'm
in Germany, but, you know, wehave this company together.
(17:31):
We oftentimes meet in The US,sometimes even in Germany. So it
goes a long way. And, yeah, itwas really nice times, by the
way. We we both are big fans ofAnn Arbor, and I'm so happy that
he's still there. He moved backfrom Germany to Ann Arbor, so
that gives me a perfect reasonto go back.
By the way, go blue. I shouldnot say that, but
Dr. Moira Gunn (17:52):
I do. K. Go Boilermakers. I have to put that
in. I'm so sorry.
So who was the better tabletennis player then, and who's
the better table tennis playernow?
Prof. Dr. Niels Riedemann (18:06):
I think, Ren Feng wins that game.
I have to say, yeah, he'sprobably the better table tennis
player. So
Dr. Moira Gunn (18:14):
but,
Prof. Dr. Niels Riedemann (18:14):
but that's not to say we had a lot
of fun, and I I think yeah. Wewe also do cook together. That's
sometimes very interesting. Youknow? Me, German background,
him, Chinese background.
You can imagine we're doingfusion fusion kitchen cooking.
But we have that theory that ifyou're a good scientist, you
must be also a good chef. I wecan't prove that, though.
Dr. Moira Gunn (18:36):
There you go. Well, I could just just see you
going back and forth. Pong.Pong. Pong.
Pong. And by the way and you'retalking science. And, hey. You
know, we could use it for this.So you must have a a lot of
conversations about besides whatyou're doing now, where this
both now the inhibitor as wellas something that blocks the
(18:57):
receptor that which receives iton those immune cells of the
C5a.
You must have some idea whereelse it can be used.
Prof. Dr. Niels Riedemann (19:05):
Yeah, actually I mentioned in the lab
we got very intrigued about thebroad applicability in these
different disease settings.Should caveat that any of that
still needs to be tested andproven in adequate clinical
studies. But we made public thatwe are very interested in other
diseases. We have a key focusright now as I mentioned in the
(19:27):
immunodermatological, so skindiseases, bad skin diseases,
inflammatory skin diseases. Wetalked about PAUDAMA.
We have two others where we'restarting with a small inhibitor,
the receptor inhibitor right nowtrials, phase two trials. We
have that focus, of the company,but we, have clear interest to
take this mechanism to broaderdisease settings and including
(19:52):
chronic renal diseases, kidneydiseases, including some
peripheral neurological diseasesand others. So if you think
about the broader autoimmunekind of disease space Now, now
you may say, you know, well,these guys are dreaming too
much, right? But there'sevidence that this exists. They
(20:13):
call this pipeline in a drugthat means you have one drug
that may be applicable forvarious different immune
diseases.
And, if you're unfortunate tohave an immune disease that
needs treatment with biologicaltreatments like antibodies,
there are some that are approvedup to 10 different indications
and more. So this happensbecause we talked about that
(20:34):
certain pathways and we believethe complement C5a, C5a receptor
pathways, one of those may beimportant for various different
disease settings. And there'sevidence for some of that.
There's also, you know, lots ofclinical studies, but we are
here to prove it and we stillneed to.
Dr. Moira Gunn (20:54):
Well, Professor Riedemann, thank you so much for
joining me. I hope you comeback, see us again.
Prof. Dr. Niels Riedemann (20:59):
Thank you so much for having us.
Really a big pleasure, Moira,and yeah, always happy to talk
to you. Thank you.
Dr. Moira Gunn (21:06):
Professor Niels Riedemann is the cofounder and
CEO of InflaRx. More informationis available on the web at
inflarx.com. That's inflarx.com.Inflarx Com.
What if you contracted a serious virus or
bacteria? You want your immunesystem to respond. But what if
your immune system overreacts?Or what if the foreign invader
isn't an invader at all, butyour own healthy tissue? This
may sound somewhat familiar tosome of you, but what Inphlorex
(00:32):
is doing about it is definitelyoriginal.
Professor Niels Reidemann is thecofounder and CEO of InflaRx.
Professor Reidemann, welcome tothe program.
Prof. Dr. Niels Riedemann (00:43):
Thank you so much, Moira, for having
me.
Dr. Moira Gunn (00:45):
Now what is C5a and why does it need to be
inhibited?
Prof. Dr. Niels Riedemann: Thanks for this question. Love (00:51):
undefined
to answer it. So C5a is a smallprotein in your blood that gets
activated and this protein canreally boost inflammation to a
point where inflammation cancause harm to your own organs
and tissue. Now I should mentionthat C5a is part of our immune
(01:13):
response.
Dr. Moira Gunn (01:14):
Now, I had say rheumatoid arthritis, how does
C5a work into that? How exactlydoes it work? And why is it
really a challenge forrheumatoid arthritis?
Prof. Dr. Niels Riedemann (01:29):
So I think rheumatoid arthritis is an
interesting example and youprobably heard the term
autoimmune disease before,right? So this term implies that
kind of your immune systemreacts against yourself, right?
And we talked about the immunesystem and C. VaVe being part of
our immune system. And I want tointroduce you to the fact that I
(01:52):
mentioned it's a small proteinthat's activated.
It's part of several proteinsfloating in your blood, that can
get activated and these severalproteins altogether are called
the complement system. Now whatis the complement system? It's
actually a very central part ofthat immune response we're
talking about. That getsactivated in autoimmune diseases
(02:16):
and there is also evidence thatC5a is elevated in patients with
rheumatoid arthritis especiallywhen they have a flare. So I
want to explain that a bit morein detail.
So what do these proteinsfloating in our blood do? Why
the heck are they there? Right?What do they do there? Well, of
that as a broad sensor that isin your blood and in your
(02:40):
tissues to sense anything thatshouldn't be there and give that
signal to your cells, to yourimmune cells to tell them, hey,
there's something in our systemthat shouldn't be there.
Get active, get rid of it. Nowthese immune cells, you can
think of them a little bit likethey're having weapons to get
rid of anything that's in oursystem. And these weapons are a
(03:03):
bit like dirty bombs. They canget rid of that. But if they get
activated dramatically, they canunfortunately, these dirty bombs
can also start damage our owntissue.
And what does it mean whentissue is damaged? It means, for
example, organs stop functioningas well. So it gets very
dangerous. And, you know, if youthink of that example that you
(03:26):
gave for rheumatoid arthritis,we all know the problem happens
in our joints when you have thatdisease. So something activates
the immune system and maybe alsothe complement system pretty
surely in that joint.
So cells get active, they moveinto that joint and they start
inflammation, they release thesedirty weapons. Well, guess what
(03:48):
they do? They damage our owntissue, in this case, the
cartilage and the cells thatshould function in your joints.
So there you have it, you havean autoimmune disease and the
complement system is almostalways involved. And that's why
I think it's important to keepthat term in mind.
Dr. Moira Gunn (04:06):
So the C5a is great if it's going after a true
foreign invader, real intruder,you know, doing bad things to
you. Really go after it. But ifit happens to identify your own
system, then you want to inhibitit.
Prof. Dr. Niels Riedemann (04:24):
That is true. But also when it gets
over activated, our body has theability to produce a ton of this
little activation product C5aand when it's over produced,
that happens in life threateninginflammatory settings, then that
becomes a double edged sword.The original positive meaning of
(04:47):
starting an immune responseturns into something very
dangerous and in fact evendeadly. And so if it's too
strongly activated, you want toblock it. If it is activated
when it helps the system to actagainst your own tissue, like in
an autoimmune disease, want toblock it.
Dr. Moira Gunn (05:04):
Now, Inflorex already has a C5a inhibitor
that's been authorized by theFDA under emergency use
authorization, and it's forcritical COVID-nineteen. What is
critical COVID-nineteen and whatis your drug doing?
Prof. Dr. Niels Riedemann (05:22):
Yeah, I really appreciate that
question too, happy to give youa bit more color. And it's
interesting now we're five yearspast the pandemic start and we
all want to not ever hear ortalk about it again, but yet we
know it's kind of the pandemicis done, but that viruses may
not be done with us. And that'sthe trouble we're in. So, we all
(05:44):
know that we take vaccines tohopefully not get as sick.
That's what we do before we getsick.
When we get sick and the virusis in our system, when we have
these flu symptoms that many, ifnot most of us experience, there
are antivirals, they stop thevirus from replicating and
hopefully that helps you.However, unfortunately, with or
(06:05):
without these medicines, somepatients develop that what we
talked about that strong immuneresponse that is overboarding.
And then they get severely sick,they have trouble breathing,
they need oxygen support, theyneed a breathing mask and
eventually they need invasivemechanical ventilation when the
(06:25):
lungs are no longer able tosustain their function to give
oxygen in your blood. Andexactly for those patients that
get so severely sick that theyneed invasive mechanical
ventilation or even lung supporttherapy. For these patients, we
tested this anti C5a antibodythat you mentioned that blocks
(06:47):
C5a, and we got this emergencyuse authorization from the US
FDA.
Dr. Moira Gunn (06:54):
So if we need your drug, we're in trouble.
Prof. Dr. Niels Riedemann (06:55):
You could say that.
Dr. Moira Gunn (06:58):
But thank goodness it's there. Okay. So
now this same c five a inhibitoris in other trials. And one is
very interesting to me, and thisis broader than the critical
COVID, response. But in 2023,BARDA, which is the biomedical
(07:18):
advanced research arm of theoffice of strategic preparedness
and response, which is part ofthe US government, hosted a
pitch event just like they're inSilicon Valley or something.
They they had the judges. Thejudges included the CDC, the
FDA, NIH, and other federalgovernment agencies. And biotech
(07:39):
and pharma companies came with18 drug candidates, that were in
what we call the end of phasetwo. They were still not
approved yet, but they were, youknow, they had demonstrated,
some level of efficacy. Thesewere very creative and promising
drugs.
And so of the eighteen, threedrugs were selected to be
(08:02):
studied. One was from a companywe would all recognize,
Genentech, and one was yours,Inflorex. Now what was the
medical condition that you wereall talking about? Why was is
this condition so critical? Allof these agencies are interested
in it.
(08:22):
And while the trials are stillunderway for these three drugs,
how might your C5a inhibitordrug work to treat it?
Prof. Dr. Niels Riedemann (08:30):
So the condition that is tested
there is really a very criticalcondition and there are no
treatments yet authorized forthis broader condition. And that
condition has to do with lungfailure and it's referred to as
ARDS or ARDS. That stands foracute respiratory distress
syndrome. And that means whenboth of your lungs, the left and
(08:53):
the right lung are so severelycompromised, that you're in
trouble, you need oxygensupport, you have trouble
breathing, etc. Similar to whatwe just discussed in COVID.
Now, it is recognized that thiscondition is caused by the
immune response we talked about.And it's also recognized that it
(09:14):
can result from different, Iwould call it, insults. It could
come from viruses like COVID orlike influenza, like avian flu,
but it could also come frombacterial infections in the
lung. It can even come fromchemical, injuries when you
inhale smoke or when you ingestsome chemicals. So this immune
(09:36):
reaction to this type ofinvasion either by
microorganisms or by othercausing damages, that immune
response causes this lungfailure.
And since there are notreatments, and the government
recognizes the importance. Also,when you think about pandemic
(09:57):
preparedness, just think aboutit. There was a drug that you
could pull off the shelfavailable if a new virus hits
and you could at least hopefullygive it to the most severely
sick to bring down mortality,ideally, and win time until
appropriate vaccines orappropriate antivirals. You
know, I'm just giving theseexamples from COVID because we
(10:19):
all still remember them or untilappropriate, you know,
antibiotics would be developedfor, you know, let's say a
bacterium for which antibioticsdon't work anymore. So such an
approach would to society.
So that's why the US governmentresearches these approaches.
Now, how does C5a fit in or mayfit in? Well, first of all, I
(10:40):
should say we still need to testit. We cannot just automatically
assume that it will work. But wetalked about earlier here today
about the important function ofthat little protein and the
complement system.
Remember, that sensor in oursystem that can get over
activated. So I think throughCOVID, we were able to show that
(11:02):
when it was given to these veryseverely sick patients that it
did lower the all causemortality in these patients. So
there is a hope that thisfunction is similarly important
in the broader ARDS setting.Now, as just as a side note, we
are not approved in The US withthe drug. We have, as you said,
(11:22):
an emergency use authorization.
We just recently, two monthsago, got an exceptional
circumstance approval in Europe.And that approval was for that
COVID part that can causemoderate to severe ARDS. So it's
different label than the use ofthe emergency use authorization
(11:43):
in The US, but there is thisrecognition of the causing ARDS,
in this case from COVID. Now
Dr. Moira Gunn (11:52):
one more quick question about this same drug,
different trial, and at least onthe surface, a very different
condition. It's called pyodermagangrenosum, and I'm sure I
mispronounced it, it soundsterrible. What is this disease
and how might this same drug,Inflorexis drug, apply?
Prof. Dr. Niels Riedemann (12:14):
Yes, so indeed it's a disease that's
not just difficult to speak,pyoderma gangrenosum, it's also
really a horrible skin disease.These patients suffer from large
ulcers that don't heal despiteof all sorts of treatment
including wound care and youknow off label trying and error
(12:35):
of different therapies. Well infact there's no drugs available
or approved in The US or inEurope for this condition. It's
a rare but really horrible skindisease. In some cases it can
even lead to amputation of legsand arms when these ulcers don't
heal and get larger and larger.
And I should mention thesepatients suffer a lot. The
(12:58):
patient advocacy group leaderonce told me that this is not
just like a wound. Just, shesaid, imagine you feel skinned
alive all day long. This is whatthis disease is. So horrible
condition.
And your second part of thequestion was how may that
mechanism that we talked aboutfit in? And so this is also a
(13:21):
condition where we believe thatit's kind of in the broader
autoimmune, auto inflammatorycondition. So again, the immune
response is recognized to play arole. Even though this condition
is not fully understood, thisdisease, these immune cells,
which I mentioned that can getactivated by the complement
system are abundantly presentand seem to cause these ulcers
(13:44):
or at least disturb them fromhealing. So we did initial
studies that showed somepromising results and we are
currently running a larger, moreinternational, different
countries, but with focus on TheUS phase three study.
So ultimately, our idea is thatone day we hopefully get an
approval and show that the drugis truly efficacious, but, it
(14:09):
still needs to be tested. Butagain, remember the immune
response we talked about, sothat may be applicable in
different diseases. I shouldprobably also go one step
further and say these cells,these immune cells that get
activated by C5a, they arecovered with the signal sensor
called C5a receptor. This iswhat gets them activated when
(14:32):
C5a binds to them. They havethat on their cell surface.
And particularly those that arefound in this disease are part
of the white blood cells, theycan cause damage. So there is a
link to damage in this case inthe skin, in this case very
locally, but you know with avery bad outcome for the
patient. So we have the hope toshow through this study that
(14:55):
there is an effect also benefitfor patients to heal these
ulcers.
Dr. Moira Gunn (15:00):
Now, you have other formulations, other
trials, but I wanna talk aboutthis. You and your cofounder,
doctor Renfeng Guo, werepostdocs, both MD postdocs
working in the same lab at theUniversity of Michigan. You came
from this tiny town in Germany.He came from a tiny town in
(15:21):
China. And yet, in addition toplaying table tennis and all the
kinds of things that thatgraduate students do, you
discovered that you were aterrific lab team, and you also
made a scientific discovery.
What were you working on? Whatdid you discover, and how did it
lead to today?
Prof. Dr. Niels Riedemann (15:41):
Yeah. Absolutely. Renfeng and I met as
postdocs in that discovered thatwe were working well and we were
part of a broader discovery teamin that lab of Doctor. Peter
Ward, a famous complementscientist, and we were part of
the team that researched exactlythe role of this protein C5a and
(16:03):
especially the receptor Imentioned on these immune cells.
Ren Feng and I discovered therole of this receptor
particularly in differentconditions in preclinical
science where it leads to damagein the lung, in the organs, in
the different tissues.
And we get so intrigued aboutthe broad potential
(16:25):
applicability of the mechanismfor so many different disease
settings that I think it was onenight past midnight, and I guess
I can say it today, I think wehad a beer in the lab today that
wouldn't be appropriate anymore,but back in the day you could do
that. We had a beer and we wereoftentimes working late and we
(16:45):
started talking about, wow, thisis so important. You know, we
should really think about makingthe drug addressing this. Now
you mentioned by now we have twodrug candidates. The one drug is
the antibody that blocks C5a andthe other one is the new
formulation that will be an oraltablet, a chemical inhibitor
that blocks the receptor wetalked about.
So the same pathway withdifferent mechanisms addressed.
(17:08):
And so we were part of thatdiscovery and yeah, here we are
many, many years later, a bitmore gray hair, at least on my
side, Renfeng looks reallystellar with no gray hair. But
but, yeah, we we we founded thecompany. Renfeng is in The US.
He's the chief scientificofficer of the company, and I'm
in Germany, but, you know, wehave this company together.
(17:31):
We oftentimes meet in The US,sometimes even in Germany. So it
goes a long way. And, yeah, itwas really nice times, by the
way. We we both are big fans ofAnn Arbor, and I'm so happy that
he's still there. He moved backfrom Germany to Ann Arbor, so
that gives me a perfect reasonto go back.
By the way, go blue. I shouldnot say that, but
Dr. Moira Gunn (17:52):
I do. K. Go Boilermakers. I have to put that
in. I'm so sorry.
So who was the better tabletennis player then, and who's
the better table tennis playernow?
Prof. Dr. Niels Riedemann (18:06):
I think, Ren Feng wins that game.
I have to say, yeah, he'sprobably the better table tennis
player. So
Dr. Moira Gunn (18:14):
but,
Prof. Dr. Niels Riedemann (18:14):
but that's not to say we had a lot
of fun, and I I think yeah. Wewe also do cook together. That's
sometimes very interesting. Youknow? Me, German background,
him, Chinese background.
You can imagine we're doingfusion fusion kitchen cooking.
But we have that theory that ifyou're a good scientist, you
must be also a good chef. I wecan't prove that, though.
Dr. Moira Gunn (18:36):
There you go. Well, I could just just see you
going back and forth. Pong.Pong. Pong.
Pong. And by the way and you'retalking science. And, hey. You
know, we could use it for this.So you must have a a lot of
conversations about besides whatyou're doing now, where this
both now the inhibitor as wellas something that blocks the
(18:57):
receptor that which receives iton those immune cells of the
C5a.
You must have some idea whereelse it can be used.
Prof. Dr. Niels Riedemann (19:05):
Yeah, actually I mentioned in the lab
we got very intrigued about thebroad applicability in these
different disease settings.Should caveat that any of that
still needs to be tested andproven in adequate clinical
studies. But we made public thatwe are very interested in other
diseases. We have a key focusright now as I mentioned in the
(19:27):
immunodermatological, so skindiseases, bad skin diseases,
inflammatory skin diseases. Wetalked about PAUDAMA.
We have two others where we'restarting with a small inhibitor,
the receptor inhibitor right nowtrials, phase two trials. We
have that focus, of the company,but we, have clear interest to
take this mechanism to broaderdisease settings and including
(19:52):
chronic renal diseases, kidneydiseases, including some
peripheral neurological diseasesand others. So if you think
about the broader autoimmunekind of disease space Now, now
you may say, you know, well,these guys are dreaming too
much, right? But there'sevidence that this exists. They
(20:13):
call this pipeline in a drugthat means you have one drug
that may be applicable forvarious different immune
diseases.
And, if you're unfortunate tohave an immune disease that
needs treatment with biologicaltreatments like antibodies,
there are some that are approvedup to 10 different indications
and more. So this happensbecause we talked about that
(20:34):
certain pathways and we believethe complement C5a, C5a receptor
pathways, one of those may beimportant for various different
disease settings. And there'sevidence for some of that.
There's also, you know, lots ofclinical studies, but we are
here to prove it and we stillneed to.
Dr. Moira Gunn (20:54):
Well, Professor Riedemann, thank you so much for
joining me. I hope you comeback, see us again.
Prof. Dr. Niels Riedemann (20:59):
Thank you so much for having us.
Really a big pleasure, Moira,and yeah, always happy to talk
to you. Thank you.
Dr. Moira Gunn (21:06):
Professor Niels Riedemann is the cofounder and
CEO of InflaRx. More informationis available on the web at
inflarx.com. That's inflarx.com.Inflarx Com.
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