Spotlight on Immunotherapy at ASCO22


Jun 23, 2022

Dr. Diwakar Davar and Dr. Jason Luke, both of the University of
Pittsburgh’s Hillman Cancer Center, highlight key advances in early
phase therapeutics and immunotherapy that were featured at the 2022
ASCO Annual Meeting and also address toxicities, including immune
checkpoint inhibitor-associated myocarditis.



Dr. Diwakar
Hello, and
welcome to the
ASCO Daily
Podcast. My name is Dr.
Diwakar Davar, and I’m an assistant professor of Medical Oncology,
specializing in melanoma and phase 1 therapeutics at the University
of Pittsburgh’s Hillman Cancer Center. I am the guest host of
today’s podcast. My guest today is Dr. Jason Luke, a colleague and
the director of the Cancer Immunotherapeutics Center at the UPMC
Hillman Cancer Center here.

Today, we’ll be discussing advances
in early-phase therapeutics and immunotherapy that were featured at
the 2022 ASCO Annual Meeting. 

You’ll find our full disclosures in
the show notes, and the disclosures of all guests on the podcast
are available on our transcripts at 


Jason, thank you for coming on the
podcast today.

Dr. Jason
Thanks so much for
the invitation. It was a great ASCO, and I hope everyone had a good

Dr. Diwakar
So, onto our
abstracts. So, the first one that we’ll be discussing, and Jason as
you know we’ve done this before. We’ll be rapidly transitioning
between phase 1 therapeutics, melanoma, and advanced phase 2 and 3
trials, but you know this is something you do very well. So

, it’s a phase 1 trial of
TIM-3 inhibitor cobomilab immunotherapy and in combination with
PD-1 inhibitors nivolumab and dostarlimab. The AMBER Trial that was
presented recently, and in full disclosure, both you and I actually
are on this abstract. So, what do you think of this abstract? What
do you think of the data that is discussed, and how do we
contextualize this in relation to what needs to be done in this


Dr. Jason
So, I think this
is an exciting abstract because it brings forward what may be the
next high-priority immune checkpoint to try to target in clinical
oncology. To level-set, I think everybody listening will know about
PD-1 and CTLA-4 as immune checkpoints. In the last year, we’ve had
LAG-3 come forward as now a standard of care element of
armamentarium in melanoma, and we look forward to further studies
of LAG-3 and other tumor types as we think it should be a good
partner where PD-1 is otherwise

So here now, we hear about TIM-3,
which is another negative regulatory checkpoint on a number of
different immune subsets. And in this abstract, the antibody
targeting TIM-3 was cobolimab. So, TIM-3 is a very interesting
molecule. It has, what you might call, pleiotropic effects in the
immune system. So, while in the context of this abstract, it was
being targeted as another immune checkpoint on T cells, it’s
important to point out that TIM-3 has other regulatory roles in
other immune subsets such as myeloid cells and very particularly
dendritic cells, and that’s important because it might bring in
another element of the innate immune system to try to drive
anti-tumor responses. So, it’s an exciting target because it might
be able to expand the groups of patients who could benefit from
immune checkpoint blockade.

So, in this abstract, we see
initially the phase 1 data of combining cobolimab, anti-TIM-3 with
anti-PD-1 of a couple of different flavors. And what you could take
from this abstract is that in the phase 1 setting, the drug was
well-tolerated and combined well, and had pharmacokinetic
properties that would be consistent with what we’d expect for this
kind of a monoclonal antibody. I think we have to marry this
abstract, which is really the phase 1 data about safety in
pharmacokinetic (PK) to another abstract presented in the melanoma
session, which showed an expansion cohort of patients who got
cobolimab plus nivolumab or


And there we did see a 50% response
rate, albeit that there was heterogeneity of patients being
treatment naïve versus treatment-experienced. So, what I would say
to this on a high level is that I think these data are
preliminarily exciting, suggesting that further investigation into
TIM-3 may be valuable in terms of expanding the population of
patients initially in melanoma, but there will data coming soon in
lung cancer and in other tumor types with another novel checkpoint.
And I think if we think ahead into the future, the question is
probably going to end up being, which combinations of checkpoints
for which patients. That’s pretty exciting to think about. We’ve
seen a lot of data of PD-1 plus other molecules, and I think some
future biomarker stratification really will be necessary to know
which patient would benefit the most from which of these combos,
but for the time being, this is exciting data to see where the
field is going to go over the next couple of

Dr. Diwakar
Great. And I
guess, to your point, one important thing to highlight from the
abstract is your point about the role of the different
compartments. There was actually a very interesting dose-response
relationship with the highest dose of the drug not necessarily
being the most effective dose, suggesting that yes, as you
escalate, you may have different effects in different compartments,
and maybe therefore a broad selection of doses might be required to
ensure that you have optimal engagement of the optimal

So, the next abstract is
. This is the
tumor-agnostic efficacy and safety of erdafitinib. So, we now know
that FGFR pathway aberrations are found from 77% of all
malignancies, FGFR targets are now U.S. Food and Drug
Administration (FDA) approved in cholangiocarcinoma with
pemigatinib, infigratinib, and as well with erdafitinib metastatic
urothelial cancer. We know that these agents are not necessarily
effective tests in 1 tumor type because these alterations have
risen in multiple tumor types. So, the RAGNAR trial, looking at
this across multiple tumor types, what do you make of the interim
analysis result presented by Dr.


Dr. Jason
So, I’d say that
this is probably the future of targeted therapy. And so, I think
that where we have activity in 1 disease, it’s very likely we would
have activity in others. So, the author has described this as the
largest basket trial of a molecularly defined subset that’s been
pursued to date. There are upwards of more than 200 patients in the
study. I think it’s really important, as we think about the data,
to realize, though, that all
FGFR alterations are
not exactly the same thing. And so, in this study, they gave
erdafitinib to patients with solid tumors of any

altered status. And so that’s
2, 3,
4 mutations or gene fusions. And that’s a lot of heterogeneity
in there actually.

And in this study, there were
two-thirds fusions and one-third mutations, mostly in

and 3. That will become
relevant as we start to think about the results. On a high level, I
have to say that it is impressive in pan-cancer fashion, just
selecting by
alteration, there’s about a 30% response
rate observed. I think that no matter what, that’s going to be
valuable considering these were patients with refractory tumors
with 3 lines of prior therapy on median. I think what we need to
know more is the breakdown of which specific molecular alteration
in which tumor types drove most of the

So, for example, in bladder cancer
where erdafitinib is already approved, that’s almost entirely
fusion setting. So we know the drug is
effective there. And so I think there will be a further breakdown
of the data. As it matures more, you really start to tease out, is
it really the case that any
FGFR alteration can
be treated or there are some that really ought to be the high
priorities that we really ought to be going after. I think it would
be remiss not to also note, however, that while there’s excitement
about this sort of pan-cancer approach, the current generation
inhibitors are not exactly the easiest
drugs to take.

And so, the in-class,
hypophosphatemia and stomatitis really does lead to dose reductions
in a lot of the patients. And I think that that’s probably really
important to emphasize is that despite the pan-tumor activity,
there’s still a lot of potential in this field to refine further
because it’s almost certainly the case that if we had less
off-target toxicity, so to say, we could improve the efficacy
beyond that 30% that we saw here.

All the same, I think this is
exciting for the concept of a pan-cancer tumor agnostic sort of
approach, and we’ll really look forward to more data to come from
this study over the next, hopefully, few

Dr. Diwakar
And I guess 1
corollary to that is that we now need to start looking for

alterations in multiple tumor types. So,
tests, tests, tests. All right,
, phase 1a/1b dose
escalation and expansion study of the MDM2-p53 antagonist BI 907828
in patients with multiple solid tumors including advanced,
metastatic, liposarcoma. So, we’ve recently had data of the
previously undruggable
KRAS, and now we’ve
got previously undruggable p53, for which we now have targets. So,
Jason, what do you make of the p53 targeting approach, in this
case, using MDM2 and this particular drug from Boehringer

Dr. Jason
So, I think that
this is an exciting abstract exactly for the reason that you
mentioned, which is that p53 has been, and unfortunately, to some
degree, still remains, one of those holy grails but undruggable
targets in oncology. So MDM2, for those who are listening but might
not be aware, is a negative regulator of p53. So, the concept here
then is if you drug it, you might release p53 to reactivate
activity in that pathway, and then p53 being the guardian of the
genome, so to say, potentially leading to apoptosis of cancer

And so, this drug binds MDM2 and MDM2
can be amplified as a resistance mechanism in p53 and several tumor
types. And so here, they showed data for the early part of a
clinical trial investigating the small molecule, BI 907828, but
then they focus specifically in liposarcoma, which is a disease
known to be an MDM2 amplified. And so, the results were pretty
interesting. The toxicity of this kind of an approach, just to
note, is really in class. It leads to some gastrointestinal (GI)
toxicities as well as hematologic problems, and this goes again for
most regulators of the cell cycle will have these effects, whether
they’re CDK inhibitors or MDM2 or p53

But I think what was very
interesting, this is a disease liposarcoma where chemotherapy,
functionally speaking, has no role. We, unfortunately, give it to
some patients sometimes, but it has almost no activity, and they
observe that in poorly differentiated liposarcomas, the response
rate was about 12%, but the stable disease was quite durable. And
so, I think that really is potentially a big deal because this is
an orphan disease. It really lacks any other treatment. But as you
zoom out from that, if you start to think about targeting amplified
MDM2 in other settings, I think the activity that we see here is
intriguing, and potentially suggests that we may be coming to a
future where we’ll have multiple, sort of, orthogonal approaches
after reactivating p53. There were actually other abstracts at ASCO
Annual Meeting of other molecules that were less mature also along
this line.

See also  Mildred Stanmore | Pancreatic Cancer Stories

So, I think, very exciting to take
away from this, one, a potential treatment for liposarcoma for all
of those patients that anybody listening actually sees, but
secondarily this concept of targeting p53, which I think we’ll see
a lot more of over the next couple of

Dr. Diwakar
Excellent. Moving
on to the
, this is a phase 1,
two-part multicenter, first-in-human study of DS-6000a of an
antibody-drug conjugate comprising the anti-CDH6 IgG1 monoclonal
antibody that is attached to a topoisomerase I inhibitor payload
via a cleavable linker. And so basically, a way in which you can
give topoisomerase: (1) TOP1 inhibitor, (2) CDH6-expressing cells.
This was studied in advanced renal cell carcinoma (RCC) and
advanced ovarian cancer in this abstract presented by Dr. Hamilton.
Jason, what do you think of the results and what do you think of
this approach in general, this antibody-drug conjugate (ADC)
approach using novel targets as well as novel

Dr. Jason
I think this is
one of those that you can’t help but be pretty excited about, and I
think in the context of the data shown at the plenary session in
breast cancer for antibody-drug conjugates (
LBA3), I think this is
really where the field is going to start to go. So, you mentioned
that this is an antibody-drug conjugate that targets cadherin 6 or
CDH6, which people will remember from biochemistry class and
medical school, or something is a cell-cell adhesion molecule,
really a basement membrane protein. So, the concept of targeting it
really is just to go after a latch mechanism to get the molecule
into the tumor where you want. And CDH expression is very high in
renal cell carcinoma, upwards of 80% of samples, also high in
ovarian cancer, which is why they chose those 2 tumors to go

So, the ADCC, and you described its
structure just a little bit, but it’s essentially the same backbone
as trastuzumab deruxtecan, which we saw this outstanding activity
for HER2 and breast cancer on the plenary, with these 8
chemotherapies moieties attached to it, but here now, targeting it
instead to HER2, with this molecule now to CDH6. And I think,
again, you can’t help but be impressed. There were treatment
responses on almost every dose level of the dose escalation in this
study. There’s in fact only 1 patient whose tumor was not, at
least, stable disease or a PR, and I think that that just goes to
show the power of truly bringing the chemotherapy in a targeted
manner into the tumor microenvironment. Responses were
heterogeneous. They were not super deep responses per se, but the
stable disease was quite durable in the study, and the patients
were going out more than 7 months. And again, realizing this is at
the lower dose levels as we’re increasing the dose and move this in
their earlier lives of therapy is likely to be even more

They did show a waterfall plot of the
reduction in CA 125 for the patients with ovarian cancer that
really looked quite impressive. And given that that’s our clinical
biomarker that we commonly follow, it may actually even more
indicative of the benefit we would see as opposed to

Now, again, there is some toxicity.
It is a chemotherapy moiety that’s conjugated to the ADCs. So, the
most common toxicities were nausea, vomiting, and low platelet
counts, but these are kind of toxicities that we’re quite
accustomed to with chemotherapy. Just to summarize, I think there’s
a lot of promise for this kind of antibody-drug conjugate
targeting, and I think it can only be impressive that they had this
amount of activity in the dose escalation of the study. [I] very
much look forward to the expansion cohorts in renal and ovarian,
which we’ll presumably expect to see later this year, early in the
next year.

Dr. Diwakar
And as you
alluded to, this really was parallel that ASCO, by the standing
ovation given to Dr. Modi when she presented the DESTINY04 data of
trastuzumab deruxtecan in HER2-low breast cancer, basically now
redefining breast cancer from 4 camps, now we have to think of not
just HER2 amplified or HER2-high, but also HER2-low. So yes, really
have to now rethink how we classify these diseases (

So Abstract
, the efficacy of
anti-PD-1/PD-L1 immunotherapy in non–small cell lung cancer
dependent based on CD8 and PD-L1 status. So really Dr. Galon taking
us into what he has now described as the immunoscore—really a way
of characterizing tumors. A way of thinking about tumors that
you’ve also championed, Jason, in terms of this T cell-inflamed and
uninflamed hypothesis. So, tell us a little bit about how these
jives with your work and how you would think about lung cancer
patients responding and not responding to immune checkpoint
inhibitors (ICI) therapy in this

Dr. Jason
Yeah. I think the
focus quickly here on the immunoscore, so the people are aware of
that, I think is really important for diving into these specific
results. You have to realize our fundamental underlying predicate
for immune checkpoint blockade inhibitor response is that patients
have mounted an adaptive immune response. So, CD8 T-cells have gone
into the tumor where they elaborate chemokines and cytokines like
interferon gamma, which upregulates the expression of PD-L1 in the
tumor but also in the surrounding immune

So, you realize that even though
antibodies are targeting PD-1, it’s really that we’re targeting
that tumor microenvironment. So, the more robustly we can measure
that, and we understand it, the more likely we are to know whether
or not the patient is going to benefit. So, this is where the
immunoscore comes in. The immunoscore is actually a fairly simple
test. It’s one slide, immunohistochemistry slide where they can
stain jointly for CD8 and PD-L1 on the same slide. And that allows
them to do a number of different things beyond just testing the
total level of PD-L1. They can test the CD8 density, the PD-L1
expression, but then also the interaction between CD8 T-cells,
their distance from each other, from PD-L1 expressing cells, and so
on and so forth.

And so really [this] can give us a
much more robust analysis of what all is going on in the tumor
microenvironment again, off of a single slide. So here then, in
this abstract, for patients with non–small cell lung cancer
receiving anti-PD-1, they then compared the utility of only PD-L1
testing versus doing the immunoscore. And so, it was actually quite
a large set. They had about 250 patients in their analytical set
and then split about 150 or 180 or something into the training and
validation sets, and they compared the immunoscore against 2
different standard PD-L1 antibodies, the 22C3 as well as the SP263.
And what they saw was a high concordance for expression between
PD-L1 and the immunoscore.

That’s good, because, again, they’re
measuring PD-L1 in both of those. And so that was a good, sort of,
level set. The immunoscore, however, allows them to look to 7
different parameters, again, beyond just PD-L1, as I mentioned. So,
CD8 density, interaction, distance, and this kind of thing. Then in
these test and training cohorts, they were able to actually split
out patients who are PD-L1 positive into further groups, those that
were immunoscore low and that were high. And in so doing, they were
actually able to sort of dramatically predict the likely
progression-free survival on PD-1 checkpoint blockade in those
different non–small cell lung cancer

So why is this important? Selection
of patients by PD-1 has been very useful in the field of non–small
cell lung cancer, but it’s hardly a panacea. You’re not at all
assured your patient is going to do well just because they’re
PD-L1. And here comes a second assay that can be done in a standard
of care setting. So, the immunoscore is a test. You could just
order it, and that really does give you much more predictive power
about who’s likely to do well and who isn’t. And I think this test
and more broadly multi-spectral imaging is really going to become a
core component to how we risk stratify and predict outcomes to
checkpoint blockade and lung cancer, but broadly in other tumor
types over the next couple of years.

Dr. Diwakar
Okay. Now, moving
on from a biomarker for PD-L1 and PD-1 to a setting in which PD-1
was just recently U.S. Food and Drug Administration (FDA)-approved,
so I’ll give a brief background to the trial that you’ve actually
developed and led. And so, this is KEYNOTE-716, the abstract in
question is
LBA9500 (late-breaking
abstract) 9500, but this is the distant metastasis-free survival
(DMFS) data readout. The DMFS, distant metastasis-free survival
with pembrolizumab versus placebo in the adjuvant setting for
patients with stage IIB or IIC, that is high-risk node-negative
melanoma and the data from the phase 3 KEYNOTE-716

So, this data, at least the
recurrence-free survival (RFS) data was actually earlier published,
you had presented it earlier last year and also more recently this
year, but it was published recently in
Lancet. And we
know that 716 is a study in which, for the first time ever, we have
an immune checkpoint inhibitor PD-1 that was studied against
placebo with the high-risk node-negative setting in stage IIB and C
melanoma, demonstrated a significant RFS benefit in the setting
against placebo. And now we have the DMFS

Maybe you could tell us a little bit
about both the RFS and the DMFS data, and why this is such an
important advance for these patients.

Dr. Jason
Thanks. And I
agree this really is a sea change in how we thought about
stratification of patients with melanoma, but I think this broadly
has implications for other tumor types as well. So, in melanoma,
we’ve historically thought of its involvement of the lymph
nodes—stage III as being the high-risk disease, but we also, if you
look at the outcomes from the AJCC, we see the patients with stage
IIB and IIC, so deep primary lesions, actually have similar bad
outcomes as those patients with stage IIIA and IIIB. And so
anti-PD1 and adjuvant therapy and melanoma were originally proved
for stage III, but having understood that about 5 years ago
actually, started to think, well, why not also treat the patients
with stage II if they’re at similar

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And we pursued KEYNOTE-716 as you
mentioned, and it read out last year as a positive trial for
recurrence-free survival. And the abstract here then was to look at
the impact on distant metastasis-free survival. So, while the
regulatory consideration for approval, and it is approved and it’s
available for patients now, was based on relapse, what we really
want to be preventing is the development of metastatic disease
because presumably that would correlate with the eventual death of
the patient from cancer.

So, in the abstract here, we see the
first update for DMFS, which also was positive on its first
analysis, the hazard ratio at 0.64. And so, again, very similar to
the RFS benefit, showing about a 35-36% reduction in distant
metastasis-free survival. And this is a theme that we’ve seen
across adjuvant studies in melanoma, all the adjuvant studies in
fact, is that the RFS improvement, the relapse-free survival hazard
ratio mirrors very closely the distant metastasis-free survival
ratio. We saw that again here. I think it just emphasizes that
anti-PD-1 immunotherapy is highly effective in melanoma no matter
what stage it’s in, but rather related to the risk of death for

And so this really has a practice
changing in the field of melanoma oncology. Patients need to be
referred to medical oncology early for discussion around risk
stratification and consideration of adjuvant therapy—I think even
at the same time that they’re having resection of their primary
lesion, and it even calls into  question of whether or not we
should even fully be doing procedures like sentinel lymph node
biopsies any longer, considering we can make the decision to give
adjuvant therapy now based on the primary—albeit that’s a
controversial area of discussion.

And I would just love for this to
start to penetrate into other disease settings. We’ve seen more
recently, approval for neoadjuvant therapy in lung cancer and we
see in kidney cancer, bladder cancer. We see adjuvant therapy in—I
think we’re going to see immunotherapy starting to become an
important part of the armamentarium in these hard-to-treat cancers,
even at the time that perioperatively before or after

So definitely a major change in the
way we’re thinking about stratifying patients and emphasizes that
you need to get those patients with melanoma in to have that
discussion around adjuvant therapy probably at the time of the
primary lesion resection.

Dr. Diwakar
, single-cell profiling
of human heart and blood in patients with checkpoint
inhibitor-associated myocarditis. So, this is data from the NGH
Group, Dr. Villani and colleagues are presented by Dr. Blum. We
know that myocarditis is an uncommon but very serious

immune related adverse event (irAE), and
here in this particular dataset, this group which has done a lot of
underlying work to really uncover the role of certain key
phenotypes, cellular phenotypes, in the development of myocarditis
it’s presenting the data in the context of ICI-related myocarditis.
So, what do you think of this data, what do you think of the use of
checkpoint inhibitors are now, as you’ve said, migrated linear in
the lifecycle of the patient, what do we need to be thinking about
and how does this improve our understanding of both the use of the
drug and what we need to be worried

Dr. Jason
I think the
toxicities of immunotherapy, while, less frequent than, say,
chemotherapy, can actually be more disastrous. In the rare
patients, we have extreme immune-related adverse events, there is
an incidence of actually life-threatening and fatal events. And so,
myocarditis, associated with checkpoint blockade, is one of those
things that could be seen, and here at ASCO Annual Meeting, we saw
a couple of abstracts summarizing the experience from the National
Cancer Institute following myocarditis events, and then this
abstract in a translational level trying to better understand what
is actually going on in terms of the immune response in those
myocarditis cases.

And so, I thought this was actually a
very interesting abstract. There was only a small number of
patients. They had 13 samples from patients who had had
endomyocardial biopsies in the context of immune-related
myocarditis, and you might say, well, only 13 samples, but
fortunately, this is quite a rare event, less than 1% of patients
who get immune checkpoint inhibitors. And what they saw was
relatively unsurprising, which is that in patients who were having
myocarditis, they saw an increase in T cells and in K-cells, as
well as activated CD8 and CD4 T-cells.

I think what was very interesting was
when they started to dig into what were the phenotypes of the cells
and what were the pathways that were turned on. Again, it was not
especially surprising to see that they saw increased levels of
interferon signaling and immune-receptor signaling as well as
motility and adhesion, but this really, I think emphasizes that
there are potentially interventions beyond just the general
immune-suppression approaches that we give. They could be more
nuanced but perhaps more efficacious because sadly, patients do
pass away when they develop this. And in their cohort of 13
patients, 3 of those patients died. And specifically, in looking in
those 3 patients, they actually saw that all 3 patients had a
shared T cell cluster. And they can’t exactly say what it is
exactly yet, but I think it’s very interesting to see that because
it suggests that there’s probably something about the T cell
response in those patients that disproportionately triggered a
fatal event.

And if we can understand that better,
we then may be able to really tailor our interventions in a way
that is more useful. Because, frankly, the way these patients
usually present is they show up in the emergency room (ER), and
they’re seen by an ER doctor who thinks they’re having acute
coronary. They ship them off to the catheterization (cath) lab.
They open him up, and then they get in there, and there’s nothing
going on. There’s no plaque. And so now, all of a sudden, everyone
is quite confused. And so, if we had better ways to search for that
ahead of time to be aware of it, we might have better interventions
because usually what happens right at that moment is everybody gets
very confused and starts calling the oncologist, and we start
slapping on steroids and other immunomodulatory agents, but
sometimes it’s late.

So, I think this is a great abstract.
It’s really starting to preliminary give us an idea of what is the
actual biology that underpins these terrible events, and we can
hope that we can build off that over time hopefully to eventually
come up with better predictors and then obviously better
interventions to try to avoid these outcomes in a small but real
number of patients.

Dr. Diwakar
Excellent. One
other point is you and I are both involved in drug development, and
as we start thinking of side effects. Side effects are really on
the flip side of responses in drug development. So really 1 point
to make of this is that when people start developing side effects
rather than, as you say, putting your hands up in the air and
waving them around, 1 of the things that we should be doing in drug
development is possibly biopsying these patients because we could
get new PD insights into how these drugs work, why they work, and
particularly which sub-populations themselves they work on,
particularly in the early-drug development setting when you
oftentimes don’t have that many

With that, thank you, Jason, for
sharing your insights with us today.

Dr. Jason

Dr. Diwakar
And thank you to
our listeners for your time today. If you value the insights that
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podcasts. So, thank you for your attention, and we will sign

Honoraria: Merck, Tesaro, Array
BioPharma, Immunocore, Instil Bio, Vedanta

Consulting or Advisory Role: Instil
Bio, Vedanta Biosciences

Consulting or Advisory Role
(Immediate family member): Shionogi

Research Funding: Merck, Checkmate
Pharmaceuticals, CellSight Technologies, GSK, Merck, Arvus
Biosciences, Arcus Biosciences

Research Funding (Inst.): Zucero

Patents, Royalties, Other
Intellectual Property: Application No.: 63/124,231 Title:
of Pittsburgh–Of the Commonwealth System of Higher Education
Inventors: Diwakar Davar Filing Date: December 11, 2020 Country:
United States MCC Reference: 10504-059PV1 Your Reference: 05545;
and Application No.: 63/208,719 Enteric Microbiotype Signatures of
Immune-related Adverse Events and Response in Relation to Anti-PD-1

Stock and Other Ownership Interests:
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, Pyxis, Alphamab Oncology, Tempest Therapeutics, Kanaph
Therapeutics, Onc.AI, Arch Oncology, Stipe,

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Bristol-Myers Squibb, Merck, EMD Serono, Novartis, 7 Hills Pharma,
Janssen, Reflexion Medical, Tempest Therapeutics, Alphamab
Oncology, Spring Bank, Abbvie, Astellas Pharma, Bayer, Incyte,
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Therapeutics, Checkmate Pharmaceuticals, CStone Pharmaceuticals,
Nektar, Regeneron, Rubius, Tesaro, Xilio, Xencor, Alnylam, Crown
Bioscience, Flame Biosciences, Genentech, Kadmon, KSQ Therapeutics,
Immunocore, Inzen, Pfizer, Silicon Therapeutics, TRex Bio, Bright
Peak, Onc.AI, STipe, Codiak Biosciences, Day One Therapeutics,
Endeavor, Gilead Sciences, Hotspot Therapeutics, SERVIER,
STINGthera, Synthekine

Research Funding (Inst.):
, Bristol-Myers Squibb,
Incyte, Corvus Pharmaceuticals, Abbvie, Macrogenics, Xencor, Array
BioPharma, Agios, Astellas Pharma
, EMD Serono, Immatics, Kadmon, Moderna Therapeutics,
Nektar, Spring bank, Trishula, KAHR Medical, Fstar, Genmab, Ikena
Oncology, Numab, Replimmune, Rubius Therapeutics, Synlogic, Takeda,
Tizona Therapeutics, Inc., BioNTech AG, Scholar Rock, Next

Patents, Royalties, Other
Intellectual Property: Serial #15/612,657 (Cancer Immunotherapy),
and Serial #PCT/US18/36052 (Microbiome Biomarkers for
Anti-PD-1/PD-L1 Responsiveness: Diagnostic, Prognostic and
Therapeutic Uses Thereof)

Travel, Accommodations, Expenses:
Bristol-Myers Squibb, Array BioPharma, EMD Serono, Janssen, Merck,
Novartis, Reflexion Medical, Mersana, Pyxis,

Disclaimer: The
purpose of this podcast is to educate and to inform. This is not a
substitute for professional medical care and is not intended for
use in the diagnosis or treatment of individual

Guests on this podcast express their
own opinions, experience, and conclusions. Guest statements on the
podcast do not express the opinions of ASCO. The mention of any
product, service, organization, activity, or therapy should not be
construed as an ASCO endorsement.


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