Dr. Brian Durie:
Okay, Saad. I think we've covered some of the questions that were
listed there. I think it's time to take a look at all of these exciting new immune therapies and
how do we handle relapse in the first instance, and then how do we integrate into that some of the
therapies that we've used for relapse versus these new exciting cellular and antibody therapies.
Please welcome Dr. Saad Usmani, who is now the chief, I was going to say the head, but you're
the chief of the myeloma
service at Memorial Sloan Kettering in New York, having moved from Charlotte
from the Levine Cancer Center there. Welcome. Dr. Saad Usmani:
Thank you so much, Brian, and it's a pleasure to be on this panel with you and with Rafat. I
look forward to meeting in person probably next month for the summit. I'm going to try to cover
the relapsed myeloma landscape and try to build on what both of you have talked about, and then we
would love to have a question and answer session and address other q
uestions and concerns that
patients may have. These are my disclosures. I'll try to start off by sharing
that journey to that first relapse. I think for the most part, regardless of whether
patients are transplant eligible or ineligible, if we look at the landscape of myeloma treatment
internationally, patients are receiving more three-drug and four-drug combinations today based
on all the data that has been shared. And very rarely now do we use two-drug combinations,
but I wanted to share
the data there just to give an idea of all the different treatments
that patients receive. And then as patients get into maintenance, typically it's with one or
two drugs at the moment as a standard of care. The expected median PFS or progression
free survival, the period in which the patients remain in a good response after initial
treatment until the myeloma starts acting up, those average months of median PFS that I've
shared on the slide reflect the disease biology, whether patients ha
ve high risk or standard
risk disease. As you can see, we have patients who have different treatments and different
disease biologies. When they're relapsing, there are many different considerations
that we have for them in deciding treatment. The way that we think about this is
there are patient specific factors, which include their age, other
comorbidities, performance status. Then we also pay attention to how the
disease is relapsing. Are there any high risk features to the disease? Are
there
myeloma cells circulating in the bloodstream, which is a little atypical and perhaps tells
us about the myeloma getting aggressive? Or is the myeloma now spreading to lymph nodes
or soft tissue or other organs outside of the bone marrow? That's called extramedullary
disease. And then we also pay attention to what were the previous treatments received,
what kind of side effects patients had. I think one of the patients in the question
mentioned the risk of second primary malignancy,
which happens in a very small proportion of
patients, but it's something that we do pay attention to as we're thinking about the next
treatments in myeloma patients. All of these things are taking into consideration. The good
news is that for our early relapse patients, we have many options. We have many
three-drug and two-drug options with lenalidomide-based combinations,
carfilzomib-based combinations, pomalidomide-based combinations. And then
there are other treatments like selinexor be
ing approved with one of the proteasome
inhibitors, bortezomib, dexamethasone. And then for translocation, 11;14 patients,
there's a drug venetoclax that is quite active. For certain patients, we can actually get it
approved through their insurances and use it to good effect. I wanted to mention all of these
options to give an idea of measured hope to our patients that we have so many options.
I still remember a time, and I'm sure Dr. Durie has actually been such an integral
part of this t
herapeutic landscape journey, that we did not have many options. We only
talked about one or two drugs even when I was in my training trying to become a
myeloma physician and researcher. We have come a long way, and there are so many
other options that we have for our patients. As we think about all of those factors when
patients are relapsing for the first time, we want to see if they have been on lenalidomide
and are progressing on it, because the treatment options for those patients are
going to be
different than patients who are not refractory to lenalidomide. And then for patients who relapse
after that second line of treatment, we try to use options that have been not used before or try
patients on clinical trials, and then autologous stem cell transplant for young patients who
either did not receive a transplant as part of their initial therapy, or they actually had
a very good response to that initial transplant. That's something that we do consider
for for patients.
But what about later? This is where there is so much excitement
about the promise of T-cell redirection. What does T-cell redirection mean? T-cells are a
very important part of our immune system. There is a strategy called CAR T-cell therapy where we
can take a patient's T-cell, teach that T-cell through introducing an engineered protein
moiety to help recognize the cancer cells. In this case, there is a protein called BCMA on
the surface of myeloma cells that these T-cells are taught to r
ecognize, and then they're grown ex
vivo or outside the patient after the collection. And then once they've expanded, when we
have enough quantity, we give patients a lymphodepleting chemotherapy and then
infuse those T-cells. These T-cells then go identify myeloma cells and take them
out, and they also expand. That's one way of using patients' T-cells. We now have
two CAR T-cell therapies that are actually approved for advanced myeloma patients.
Then the other technology is what we call b
ispecific antibodies or bispecific T-cell
engager. The difference between those two is the peptide structure essentially,
but they're doing the same thing. One part of that structure can recognize a
specific surface protein on the myeloma cell, and the other part recognizes CD3 on T-cells.
It brings patients' T-cells to the cancer cell and helps skill the cancer cell. If we look
at our T-cells, and I promise I'm not going to be taking a quiz from you guys on this, you
don't have to remembe
r all this data, but the only part I've highlighted is how impressive the
responses we've seen with CAR T-cell therapies. If we look at the previous drug approvals we've
had in myeloma with pomalidomide, daratumumab, carfilzomib, all those drugs, the overall response
rate was between 25-30% of overall response rate. Here, for very advanced patients who've seen
five or six or more prior lines of treatment, we are seeing responses well over
65-70%. In case of Cilta-Cel, which is an FDA approv
ed BCMA CAR T-cell therapy, in
that single arm trial, the overall response rate rate was 98%. Almost every patient responded.
Very remarkable results with CAR T-cell therapies have been seen, and we have two approved products
that we utilize for our patients. We are starting to now move those treatments into earlier lines.
Here is an example of Ide-Cel, which is a BCMA directed CAR T-cell therapy. In fact, it was
the first one that was approved by the FDA. This is data that was presented at
ASH where we
looked at patients who have early relapse after autologous stem cell transplant and what happens
to these patients if we give them treatment. This was a group of patients who did not have a good
response to their initial treatment. In fact, only 24% of these patients had a complete
response. When they got this CAR T-cell therapy, the overall response rate is 84%. But look at that
complete response rate, 46%, even better than the first line treatment is what they got. Similar
results have been seen with the Cilta-Cel as well. But the bottom line is for our difficult to
treat functional high-risk patients who are relapsing early, these CAR T-cell therapies
are showing very good promise. We're looking forward to having these therapies available
for our patients in the future in earlier lines of treatment. It's not that BCMA is the only
target. We have another new target called GPRC5D. Again, my previous colleague, Eric Smith,
who is now in Boston, he actually as a
fellow identify GPRC5D as a target in myeloma
and started to develop a homegrown CAR T-cell therapy. And that GPRC5D directed CAR T was
then licensed to BMS for further development. This is the early data that was shared
at ASH with some of that experience, heavily pretreated patients with high proportion
of patients with high risk cytogenetics, as well as extramedullary disease. And then 40% of
these patients actually had a prior BCMA directed CAR T-cell therapy and additional 15% had BCM
A
directed other treatments. With this patient population, you can see that very high response
rates were seen with this particular CAR T-cell therapy. If patients did not receive a BCMA
directed treatment, 100% response rate. Even in those who had prior BCMA, 78% response rates were
seen and very high rates of complete responses. Even though the numbers are small, this is
a very important slide demonstrating to you the wonders that these immunotherapies can
do for our patients. We are rea
lly looking forward to further developing this specific GPRC
directed CAR T-cell therapy for our patients. If we look at the safety profile... It's not
just important to take a note of the activity, but we also want to see if we can manage
the side effects of these therapies. What was important to see that unlike some of the
CAR T-cell therapies that our lymphoma colleagues use, the neurologic side effects appear to
be lower than that patient population for our myeloma CAR T, whether it's B
CMA directed
treatments or GPRC5D directed treatments. I think one thing that we all are concerned about
and have to keep an eye on is the infection risk for patients as these therapies are utilized more
in clinical trials. The other important group that I talked about is bispecific antibodies. This
slide actually shows you the why there are so many different ones. Depending on the structure, these
are bispecific antibodies or T-cell engagers, can take different parts of the immunoglobulin
structure, put them together, and that creates different kind of half lives for these
antibodies and different kind of targets that they can bind to. They can bind to the same
target, but different parts of that same target. That's why you're going to see a lot of
these different bispecific antibodies. They're going to vary in the kind of
characteristics they have. Teclistamab, I appreciate Dr. Durie actually giving me a
shout-out for helping with this first FDA approval and a lot of hard
work and contributions from our
patients, caregivers, as well as the study team. But there are many other bispecific antibodies
that are coming down the pike. Teclistamab was our first one, first BCMA directed bispecific, but
we also have elranatamab, which is knocking at the door for an FDA approval. We have the ABBV-383,
which used to be called the Teneobio 383B. We have Alnuctamab. We have the Regeneron,
bispecific which is now called Linvoseltamab. We are going to have many different bi
specifics.
The good news is each of them are very active, but they're probably going to have different
schedules because of half lives. We'll have to figure out how best to use them in the
clinic. And then for academic centers, the use may be a little different because we have
access to a more dedicated inpatient service that can care for these patients. Whereas for
our community colleagues, the challenges might be a little different. We have a lot
of work to do on working out the logistic
s. Elranatamab, very similar to teclistamab, the
overall response rate for a relapse refractory myeloma patient population, patients who've seen
five different lines of treatment, again, response rate is very impressive at 61%, very similar to
what we saw with teclistamab at 63%. The good news about if you look at this progression-free
survival curve, there are patients who have stability of response. There is durability
of response with these bispecific antibodies. However, the important r
isk that we
need to consider is the infection risk, and that's what you see in this right table here. The way that the original bispecifics have been
studied in clinical trials is to continue giving them on a weekly or every other week basis
depending on their structure and their PKP, pharmacokinetics and pharmacodynamics, their
half lives. But we are now learning that we can give it less frequently to patients or
give it for fixed duration of treatment. That infection piece is something th
at we as
researchers are looking at right now to help make it a better option for our patients
long-term. All of us have those anecdotal patients who've been on these therapies
now for many years on clinical trials. Alnuctamab is another bispecific antibody. It's showing, again, very similar kind of
response rates and the same signal that we see with infections is being seen with this particular
antibody as well. I think it has to do with the BCMA bispecific portion of it. Again, overall
r
esponse rate, very similar, in the 60s percent. Overall response rate of 65% being seen with this
particular bispecific antibody as well. Instead of just going on and on about the BCMA ones, I
wanted to talk about Talquetamab, and I'm sorry, my slide because of the I guess MacBook versus
other, the formatting changed a little bit. Talquetamab isn't showing up the way it should, but the development of this particular
specific was led by my colleague Dr. Ajai Chari, who's actually moving to th
e West Coast, Dr.
Durie, to be closer to you in San Francisco. Dr. Brian Durie:
That's right. San Francisco. Dr. Saad Usmani:
Yes. This bispecific showed very high response rate in the 70% range and two different
doses were studied, the 0.4 milligram per kilogram being given weekly and the 0.8 milligram per
kilogram being given every other week. It looks like the durability of response may be better for
the Q2 dosing. The data looks promising. I think this is being examined by the FDA right
now, so we'll get a better idea of the approval timelines I guess later in
the summer. Even in patients who have had prior CAR Ts or prior bispecific therapy,
we are seeing response rates of 62.7%. It's important to see that this is an important
question that I think many doctors and researchers are asking how best to pick one treatment versus
the other. Can we sequence treatment? What we're finding with these different treatments is that
patients do respond to other therapies in terms of
sequencing. The response may not be as robust
or good, but patients do respond to treatment. I think that's another message that you can go
from one treatment to the other immunotherapy treatment. And then with GPRC5D, we just learned
about this new bispecific called forimtamig. Forimtamig actually has two different epitopes or
parts of the GPRC5D structure that it binds to. Initially, it was looked at as an IV formulation
and now there's a subcutaneous formulation. The interesting thing ab
out this one is the
dosing is every three weeks. It's not on a weekly basis like talquetamab. You can
give it less frequently. The data were early, but response rate is, again, in a very
similar kind of range. You can take one structure and show the same kind of responses
in highly relapsed refractory myeloma patients. The safety profile, any cytokine release
syndrome side effect that patients get, it's quite manageable, grade one or two for the most
part. Very few patients get high grade
symptoms. Just to give you an idea, I think we had Anne
wonderfully talk about what cytokine release syndrome is, but grade one cytokine release
syndrome is just having a fever and taking Tylenol. I think understanding these grading is
important for patients as well, but it's very, very manageable. There are also efforts to improve
cytokine release syndrome. There is a medicine called tocilizumab that we typically give to
patients when cytokine release syndrome happens. But in this study, D
r. Trudel, a wonderful
colleague from Princess Margaret Hospital in Toronto, Canada, she did a study where
she compared giving cevostamab, which is a bispecific that targets a different surface
protein called FCHR5. They did a study where a group of patients did not get any preemptive
tocilizumab, another group got tocilizumab to prevent CRS, and they saw quite a bit
of reduction in the overall percentage of CRS between one arm versus the other.
Just telling us that there are going to be s
trategies that we can use to reduce the
cytokine release syndrome for our patients. And then now I want to talk a little
bit beyond the CAR Ts and bispecifics. What we used to call immunomodulatory drugs, there is a newer class of drugs that belongs to
that same family, but they're called CELMoDs, because they modulate the immune system. There are
two different agents, iberdomide and mezigdomide, that have different ways in which they can
affect the proteosome machinery in trying to kill my
eloma cells. One of them is more
active or hypothetically more active and more proliferative kind of myelomas, and the other drug
is more immunomodulatory or cellular modulatory in nature. These agents bind to a protein called
cereblon, and that reduces the likelihood of degradation of certain proteins within
the cell that can lead to this modulation. With iberdomide, this particular CELMoD was
studied in an open label dose escalation and expansion study on its own and then
in combination
with other therapies. My colleague Dr. Sagar Lonial from
Emory is leading this study. What Dr. Lonial has shown is that iberdomide was
active on its own in about 30% of the patients. But in combination with daratumumab and
with bortezomib, along with dexamethasone, it appears to have a very similar safety
profile to what we have seen with lenalidomide or pomalidomide. Very similar safety has
been observed. And then the overall response rates even in patients who have had these
therapies be
fore appears to be quite high. Very promising results even in patients who
have seen therapy drugs in that same class, even in patients who were daratumumab
or bortezomib refractory getting this combination, they appear to respond.
That gives us that there is this new class of these oral therapies coming that
will actually be more effective for our myeloma patients. And then same is true for
Mezigdomide. This is a little bit different than iberdomide in terms of how quickly it can
act on p
roliferating myeloma cells. This may be an important CELMoD for our high-risk patients
and patients with extramedullary disease. Dr. Paul Richardson had presented these early data
showing an overall response rate of about 50%, or rather, sorry, 40% in all the patients, but
50% in patients with prior anti-BCMA treatments. Now Mezigdomide is being combined with bispecifics and other proteosome inhibitors. We are going
to hopefully see more data with this particular CELMoD later this year at AS
H. And lastly here, I
do want to mention this, another very interesting mechanism of faction being called immuno
cytokine. This is Modakafusp alfa, which is a CD38 targeted treatment, but it delivers
interferon alpha 2B to CD38 positive cells. CD38 is the same target that daratumumab and
isatuximab utilize to help kill myeloma cells for our patients. Very interesting
data in this particular study. You can see that this study had one part
where there was a dose escalation to figure out what
's the right dose for patients, and then
there was an expansion of two different doses, and this therapy is given either every three
weeks or every four weeks. But if you look at the patient population enrolled on each of
these on the study, vast majority of patients, 85%, 85 out of 100 patients, had prior anti-C38
antibody and they had become refractory to it. Despite that fact, what we see in patients
here is a response rate of 43%. If we look at patients who were either daratumumab or is
atuximab
refractory, we are seeing a response rate of 39%. Despite the fact that the patients had seen CD38
treatments, the response rates were quite high. In prior patients who had BCMA exposure, overall
response rate was 27%. In those who did not have BCMA exposure, it was 60%. The important thing
about the response is it's durable. The median duration of response was over a year, 12.5 months.
All of these therapies are very exciting and there are a lot of possibilities for us to use each
of
these therapies in earlier lines of treatment. This is what we are doing for the CAR T-cell
therapies and the bispecifics, but the CELMoDs and Modakafusp won't be far behind as well. We
just have to come up with a good rational way and figure out which patients would benefit from which
therapies. The key message is of measured hope that there is a better future ahead for all our
patients, and we are all in this together marching towards that goal. In the end, I would like to
acknowledg
e the myeloma service team at MSK, as well as our transplant cell therapy team.
Thank you so much for this opportunity, Dr. Durie. Dr. Brian Durie:
Well, thank you. Thank you so much, Saad, for that comprehensive overview of these
exciting therapies, the immune therapies and then also these more targeted therapies that you just
discussed at the end. While you've been talking, a lot of interest, a lot questions coming
in. I don't know how many we can handle, but I think that one key question
is related to the sequencing. There's so many exciting things. I
think that one important question comes in from Jack Aiello, for example.
If a patient has relapsed on a BCMA CAR T, would you consider a BCMA bispecific, or would you
move over to a different target? We already have some data that relate to that. Maybe you could
comment on that first, relapse for BCMA CAR T. Dr. Saad Usmani:
Yes, we have some real world data, Jack. By the way Jack,
it's good to know that you are here on this
platform. We have data from the CAR
T Consortium that was actually presented at ASH looking at the real world experience of
patients receiving Ide-Cel and then what happened to their outcomes and what subsequent treatments
they received. What we find is yes, you can use other bispecific therapies, but the duration of
previous exposure has to be more than six months. That's not just from the CAR T Consortium data,
but also from the Mount Sinai experience. There are a few other examples of e
xperiences. If
someone had a BCMA CAR and they got more than six months of response and the CAR T-cells are
gone, if the myeloma starts coming back, the BCMA on those myeloma cells doesn't go away and one
can utilize a BCMA directed specific. However, if they did not respond and they're progressing,
then it's better to use a different target. Use a GPRC5D in that case. That's how
we're thinking about it right now, but I think we'll have more data
later this year because one of my fellows i
s actually looking at this
and also looking at immune profiling to figure out if we can tease out who would
benefit from one strategy versus the other. Dr. Brian Durie:
Right, right. As I think actually Jack knows, we do have this immune
therapy registry or database starting. I think, Saad, you're participating in that where
we're trying to have real world data so we can try to answer all these questions.
Can you go from CAR T to a bispecific, from a bispecific to a CAR T? And then what
ha
ppens if you switch from one target to another? But I think that what was exciting to me was
to see the very strong data with the GPRC5D, both the bispecific, the talquetamab, as well as
the early data with the CAR T with this target. Very exciting actually. Let's see. Let's go
through some of these other ones here, sorry. Can you try several bispecifics?
I think that's certainly true. Dr. Saad Usmani:
Yes, we can. In fact, we have anecdotal experience with someone
who did not respond to on
e bispecific antibody because the target was different
responding to another bispecific antibody. I think just as Dr. Durie said, all of us are
trying to put our cumulative experience into this big International Myeloma Working Group database
database, and it's led by our colleagues, doctors Tom Martin and Elen. We'll get to understand
this better, how do we sequence these treatments? Dr. Brian Durie:
Right, exactly. There's a sensitive point here. A patient with kidney failure, are they eli
gible
for bispecific antibody trials or treatment? Is there an exclusion by renal status? I'd imagine if
you have renal failure, that's a problem, right? Dr. Saad Usmani:
Yeah. For clinical trial purposes, because these were early
phase clinical trials, I think there was a cutoff for estimated GFR of 30 or more. But
in the real world experience, we are treating patients who have lower EGFRs because we need
to provide these treatments for our patients. Dr. Brian Durie:
Absolutely. Dr. Saad U
smani:
That will be another benefit of the cumulative wisdom that we collect under the International Myeloma Working
Group umbrella in our immune database. Dr. Brian Durie:
Right, right. We'll see how that all works out.
Yes, yes, yes. Out of nowhere, STAR-LLD lenalidomide patch, do we have experience
with that? I don't. I don't know that anyone's used that particular patch. Anne, did you
know about the STAR-LLD lenalidomide patch? Anne:
No, I have not heard of it. Dr. Brian Durie:
I've actu
ally heard of it, but I haven't seen use of it. Yes, yes. Well, I think that we've given a lot of insight to
patients that these are so striking new therapies, so many of them with promising, promising results.
62% response seems to be a magic number. Many of these bispecifics have a 62% response rate. I
don't know what that means, but maybe in closing we could have some comments from each of you.
Maybe Rafat, of all of these exciting therapies, what are your top one, two, three that you thi
nk
are really going to have an impact moving forward? You're muted. You're muted. You need to unmute. Dr. Rafat Abonour:
You heard how complicated the field is. It's really not an easy answer.
I've been doing myeloma for a long time, and I remember the early days of testing
lenalidomide and bortezomib and the responses we got. And then we get the carfilzomib,
and then we get the anti-CD38 antibodies. We studied those in relapse patients and
very difficult patients. What I have not seen is t
he responses we've seen using bispecific
T-cell engager in patient with advanced myeloma. I mean, when you look at patients who have no
count, have a plasmacytomas growing everywhere and basically you almost were able
to get them on clinical trials, almost met the criteria for clinical trials and
you put them on this bispecific T-cell engager, and then in six weeks, they're back on
the motorcycle. It's just unbelievable. Dr. Brian Durie:
Right, right. It is remarkable. Dr. Rafat Abonour:
I
think the bispecific T-cell engager is just opening the door for understanding
something really important, because we have the myeloma cells in the body and we have the T-cells
in the body. Why you just need to bring them close to each other and that's what you get the
benefit. Is it really that simple? I don't think so. Basically what I tell the patient is that
when we give you the bispecific T-cell engager, it's like when you're having a bad infection,
the T-cells get activated. They get
angry. They produce cytokines. Some of these cytokines
are good, they're destroying the myeloma cells, but there's some of the cytokine causing
the fever, the tachycardia, hypoxemia. I think the science is going to be amazing when
we discover how these T-cells are now recognizing the myeloma. What is the antigen? Is it really
the BCMA antigen or some of these other antigens that we don't know? I'm really excited about
bispecific. I think the way that we use them now, even in advanced diseas
e, the ability
to manage the side effect is incredible and I think that's really where we're going to
build the future of myeloma therapy around that. Dr. Brian Durie:
Fantastic. Anne, I'd be interested in your comments in
terms of patients that you've seen. We haven't really talked about this. For
the BCMA bispecific like the teclistamab, there are concerns as patients stay on
the therapy about the infections. However, with the talquetamab, this seems to be less of
a problem. Do you have
any comments about that? Anne:
I do a lot of inpatient myeloma work and I agree that the bispecific teclistamab, we've
had quite a few admissions since the beginning of the year, and we've seen some nice responses
from a myeloma perspective. But unfortunately, some patients have had to discontinue therapy.
We've had some very challenging infections. As Dr. Usmani mentioned during his presentation,
the infections are quite problematic at times. We've had some fungal infections and some issues
where patients had to discontinue therapy. Great drugs for myeloma, but again,
they come with some issues that are quite challenging. Again, from a myeloma
perspective, some very good outcomes. Dr. Brian Durie:
I think just my 10 cents before I go back to you, Saad, for some final
comments, but I mean, with that in mind, for me, the CAR T approach, the one and done, you have a
decisive therapy with the CAR T that is working, that is more attractive in my mind.
If we can come up with a sec
ond generation or a third generation CAR T, maybe
incorporating both BCMA and GPRC5D, whatever, maybe for me, if those could be made accessible,
the problem is access, that would be a way to go. What do you think, Saad, in the balance
between the bispecifics and the CAR T? Dr. Saad Usmani:
I think there is clearly merit in the CAR T technology potentially having... If
we can overcome the cost accessibility globally and reliability of how quickly we can
produce it and get it to our patients,
I think that approach of giving it and patients
recovering from it and then not being on anything is very attractive. But we have our work cut
out. The other piece of this is I think we are probably going to have patients who are
not going to be eligible for CARs because of age or comorbidities and other issues where
I think the bispecifics may come into play. But these are good problems to have with those
responses and figuring things out. I do feel that CARs will win for majority of pati
ents, but
then we will always have room with bispecifics. I think to Anne's point, we are learning to limit
the duration of treatment with bispecifics. I want to share one anecdote, because it's one
of my patients who was on the MajesTEC-1 trial who came off of treatment because of
recurrent URIs with funky infections like NSAID after eight cycles of treatment,
and then stayed in an MRD negative state without any treatment for almost three years,
just like they would with CAR T-cell therap
y. They had never been off of any treatment. This
was their 16th line of treatment and they had been always on something continuously.
I'm just sharing that for some patients, even the bispecific use for a short duration would
be able to give you the same outcome as CARs. Dr. Brian Durie:
Right, right. I think that this is a key point. As I know you're aware,
Saad, I think that some studies with that, limiting the duration will be quite key moving
forward to get the efficacy and try to limi
t what can be pretty challenging toxicities with those
infections. I think that we've had a lot of really excellent presentations and discussions. I'd like
to thank all of you for participating, take time out of your really, really busy schedules. Anne,
Rafat, and Saad, really, really appreciate it. You can have some late dinner now. I'm not
sure how you're going to handle that, but...
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