Optimizing Oral Targeted Therapies for HR+/HER2- Breast Cancer

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[00:00:00] Hello, and welcome to the Decera Clinical Education's Oncology Podcast. I'm your host, Sharif Morsalin. Today's podcast features Daniella Roman of Allegheny Health Network and Jordan Hill of the West Virginia University Cancer Institute. They will discuss optimal pharmacist care of patients with hormone receptor-positive, HER2-negative breast cancer receiving oral-targeted therapies.

For more information on our presenters, along with a link to the full educational program, please visit the show notes for this episode. Now, let's get started and hear what the experts have to say.

We're gonna be talking about advances in oral targeted therapies for hormone receptor-positive, HER2-negative breast cancer, best practices for oncology pharmacists. Targeted therapies have become such an important part of breast cancer treatment now both in the early stage setting as well as the metastatic setting, as single agents, as combination [00:01:00] therapy.

So a lot of really new, exciting data to discuss today. Give us an overview of the use of targeted therapies in the early stage setting. This is a really exciting area. We've seen a lot of targeted therapies being incorporated in our early-stage breast cancer patients, specifically those with high risk for recurrence to try to decrease that risk.

And so we're starting to see therapies that historically were thought about in the metastatic setting, such as CDK 4/6 inhibitors, as well as, uh, for patients that have, uh, BRCA1 or BRCA2 mutations. Um, we now have olaparib as a PARP inhibitor in this setting. And so I think it's, uh, a really exciting time to start to see these oral targeted therapies being incorporated not just in the metastatic setting but also in early stage.

The talk about high risk and how to determine whether a patient is high risk gets a little bit complicated with different trial inclusion criteria. But could you give us [00:02:00] just a, a few points about those high risk factors that you're looking at to determine whether a patient might be a candidate for some of these targeted therapies?

Yeah. As you mentioned, uh, the definition of high risk from trial to trial isn't always the same. But in general, things that are included as part of m-most inclusion criterias for these early stage trials are gonna be larger tumor size, um, node positivity, higher grade or higher proliferation rate, like Ki-67.

Um, other things that aren't always included but we do think about when we're looking at someone's clinical risk is, lower ER, PR levels can sometimes impact, uh, how we feel like that cancer is going to behave. BRCA mutations, that's an important consideration to think about for these patients, too.

Could you give us just a very high-level overview of some of the key trials, uh, that we should be aware of in this early stage setting? We can start with looking at our [00:03:00] CDK four/six inhibitors since those are going to be the ones that we most commonly see. And so, in this space, we're going to be mostly looking at MONARCH-E and NATALEE, um, which looked at abemaciclib for two years, um, and then ribociclib for three years in those high-risk patient populations.

And so for MONARCH-E, um, that included, uh, node-positive patients, either with four or more nodes or one to three nodes with an additional high-risk feature. And then for NATALEE, node-positive patients, , they didn't have to have that extra high-risk feature. Um, and even some node negatives, um, if they had additional high-risk features, um, even a stage two, like a T two N zero could be included.

Um, both of those have shown significant improvements in invasive disease-free survival with the addition of that, two to three years of CDK four/six inhibitor with endocrine therapy in the adjuvant setting. And then more recently with MONARCH-E, we [00:04:00] are even seeing an overall survival benefit with the addition of abemaciclib.

And so, um, potentially with a little bit longer follow-up from NATALEE, we'll see that overall survival benefit starting to show up there. It's a little bit too early to be able to say one way or the other. Um, but what we can definitely see is that consistent benefit in IDFS that with each subsequent year of follow-up, um, the magnitude does continue to increase in both studies.

So, that is very promising for the added benefit of these agents. We know we're adding side effects when we add these being able to see that benefit continue to improve, um, really makes it feel like that is, worth the added side effects. It does make it a little bit complicated in the sense that we do have two agents approved, um, with a lot of overlapping criteria.

So we do have several patients that are gonna be candidates for either of those. Knowing that we h- already have the overall survival benefit with abemaciclib in high-risk [00:05:00] patients, so those like four or more node patients, that tends to be where I lean towards. Whereas, um, our kind of like high risk but not as high risk patients , maybe that's where I'm seeing ribociclib being used more.

And then of course, there's several patients that qualify for ribociclib that don't necessarily qualify for abemaciclib. , How are you seeing that being decided in your practice? I have a similar thought process here. I think with, with knowing we have that overall survival benefit with MONARCH E, I think when we are able to use abemaciclib for those node-positive patients, then that is the agent that I'm leaning towards.

And it is two years versus three years, so that is a little bit easier from a, a kind of discussion with the patient standpoint. But for those patients that don't qualify f- um, based on the MONARCH E criteria, because we know NATALEE was inclusive of also node-negative patients with high-risk features.

So I think in this setting where, you know, a patient doesn't meet the MONARCH E criteria, then using ribociclib for three years is a [00:06:00] very reasonable option. Yeah, I agree. And I think occasionally we'll have some other factors concomitant comorbidities that may drive us one way or the other.

So it is really nice to have both, um, effective options available to us. I think an additional, Patient population that becomes challenging to decide what to do with is if they also have a BRCA mutation . Um, although less frequently do you have patients that, uh, qualify for all three agents, but it does happen sometimes, so that becomes pretty tricky.

Often in my practice, I'm seeing, uh, the olaparib be prioritized for a BRCA-mutated patient. But I am pretty frequently also seeing after that one year of olaparib as studied in the Olympia trial, then doing an additional, uh, CDK 4/6 inhibitor, which I know is very aggressive, but a lot of times these patients are very young and do have an aggressive disease biology.

So we are sometimes wanting to be [00:07:00] pretty aggressive in their management as well. Is that similar to what you're seeing? Do you tend to prioritize only one instead of se- sequencing them? It's highly dependent on the patient and their motivation for the therapy. So I would say when faced with, you know, patients that are candidates for both, think prioritizing using a PARP inhibitor for the BRCA mutation I kind of pri- I prioritize that, as you said as well.

I try to get that in first. You know, that's a year of treatment. And then for a patient that, you know, wants to continue on with a, the targeted therapy options and they're candidates for CDK 4/6 inhibitor, um, those trials did include patients that were a year out from their, um, initial treatment.

So I think it's very reasonable to consider that, although you... we don't have that clear clinical trial evidence to guide that decision-making. So it's, it becomes a little challenging thinking through how complex it looks in the adjuvant [00:08:00] setting and some of the decisions that we're making for these patients transitions well into thinking about the even added level of complexity that we're starting to see in the metastatic setting.

So these oral-targeted therapies that we've been talking about so far in the early stage setting are all commonly used in the metastatic setting as well, except with, uh, several additional targeted therapies in that setting. Um, and so I think that complexity just continues to increase as we think through what treatment choices and treatment decisions look like in the metastatic setting for a patient that's hormone positive, HER2 negative.

In the early stage setting, there is some biomarker decisions to be, um, made with our BRCA mutations, um, but not necessarily needed for our CDK4/6 inhibitors. Whereas when you start thinking about the metastatic setting, biomarkers really become essential, even starting potentially in the first line setting.

So thinking through our kind of [00:09:00] newly, um, approved, avolisib based on the ANOVA one twenty trial. Those patients were patients that received a biomarker, um, directed therapy in the first line setting. Now, of course, it's not all patients.

They had to have that PIK3CA mutation, and they also had to have an early recurrence. So, um, developing metastatic disease either while on meta-- uh, on adjuvant endocrine therapy or within twelve months of completing their adjuvant endocrine therapy. So it is more narrow of a patient population.

It's not all first-line patients, but starting to see these targeted therapies and biomarker-driven, um, treatment decisions even in the first line is really exciting. Um, the addition of anivolisa to palbociclib and fulvestrant showed a pretty significant and impressive, um, improvement in progression-free survival and more than doubling, and then a, uh, seven-month improvement in overall survival, which was statistically significant.

So I think [00:10:00] in a population that's typically associated, um, with a poor prognosis, given that rapid progression, this is a really exciting development that we've had recently. It is, you know, because of that narrow population, um, not something that we're using on a daily basis, but I'm curious if that, uh, is something that you are starting to see and incorporate what biomarker testing looks like for you.

Yeah, I think you bring up a really good point that the majority of patients are not going to fall into this categor-category. It, it really is that narrow patient population that has that endocrine-resistant disease and has that PIK3CA mutation.

So it's something that we're using, but I would say infrequently just based on the fact that, seeing those concurrently is not all that common. We're very used to getting that biomarker testing and using that to decide that second line metastatic treatment.

Um, but now recognizing that biomarker testing really is needed earlier on in therapy to make the most appropriate decision, knowing that there's an overall survival [00:11:00] benefit here we really should be testing for the PIK3CA mutation first line metastatic disease for those potentially eligible patients.

Yeah, I agree. And I think it's an additional layer of complexity and something we have to think about a little bit sooner than we would have, like you mentioned. Sort of what we are used to thinking about is that second line setting and thinking about what biomarkers are important in our second line setting.

And so historically, we've thought more about our PI3K/AKT inhibitors in that second line setting, thinking about capivasertib from CAPITOLO-two-nine-one, alpelisib from SOLAR-one. And so if someone doesn't kind of meet the criteria for early recurrence and they didn't receive that biomarker testing in the first line, um, it's really essential to ensure they're getting it, uh, uh, during progression to know what the best therapy is moving into the second line.

And so, for me, I think, um, knowing that there is a [00:12:00] progression-free survival advantage with capivasertib in combination with fulvestrant as well as alpelisib in combination with fulvestrant as compared to that single agent endocrine therapy. Um, and neither of them at this point have an overall survival advantage.

I tend to pick a more based off of side effect profile, is that what you're seeing as well in that both of these agents have, um, progression-free survival without overall survival, so just leaning more towards tolerability and picking between the agents?

For me, when I'm thinking about, you know, agents within a class you're first looking for any efficacy signals that might differentiate them, and we're not seeing that here. So I do think it really comes down to tolerability. And capivasertib is a tolerable agent, so that is... has become the one that we reach for in a patient that has a mutation in the PI3K/A-AKT/mTOR pathway.

And the fact that we have, expanded use here where it's not just those PIK3CA mutations, but also able to use it in [00:13:00] PTEN, um, and AKT alterations I definitely agree. I think even with the PIK3CA being the most common, we do often have patients with one of those other mutations that allows that biomarker-driven therapy.

So, um, I think that's an added benefit in addition to the tolerability. So that's a great point. Some kind of additional things to think about in the second-line setting are ESR1 mutations and our oral SERDs. That class is growing . We're getting more and more agents that fall into that class.

Um, so far we have elacestrant, emlinestrant, and then the PROTAC vepdegestrant. And they all have some overlapping indications in that they are all approved as a single agent for patients that do have ESR1 mutations, all showing improvements in progression-free survival as compared to standard endocrine therapy.

From the [00:14:00] EMBER-3 study, the emlinestrant does have that additional arm where it was given in combination with abemaciclib. So it is the only one that has that published data available for being used in combination with a CDK 4/6 inhibitor as opposed to a single agent. Even though it's not approved in that setting, it is an option in the NCCN guidelines.

And so it is an interesting, uh, way to think through these agents in the sense that for someone that has an ESR1 mutation, you have all three options. Uh, whereas for someone that maybe doesn't have that ESR1 mutation, um, then you're starting to think about Does that patient seem like somebody that would be a reasonable candidate for the combination of emlinestrant with abemaciclib since that arm of EMBER-3 did show improvement in progression-free survival regardless of ESR1 mutation?

This isn't a combination I've used all that much. Most [00:15:00] of the time I'm thinking about these agents in our ESR1-mutated patient populations and using them in a, as a single agent in people that got a long time out of their first-line CDK 4/6 inhibitor. But I'm curious what you're seeing in your clinic.

Do you see more of, uh, one agent over the other, mostly single agent? I- In patients that have an ESR1 mutation I, I tend to see the single agent used just, uh, really from a tolerability standpoint. But I, I think in the patients that a- are not candidates for single agent, so they do not have an ESR1 mutation I have seen the combination used in that setting.

It does add toxicity, so it, it is something to consider. But I echo your comments. I tend to think about it in those patients that have had a longer duration of response to their first-line therapy. Kind of also just giving us confidence with having, benefit, uh, with the combination as well Yeah,

it's an ever-growing area, even though we only have, um, published data [00:16:00] for one combination right now. With the number of ongoing trials looking at these oral SERDs in combination with other targeted therapies, I think that space is probably only gonna continue to grow. Similar to how we were talking about when patients qualify for more than one thing in the adjuvant setting that often happens in the metastatic setting too, where we have patients that have co-mutations in, um, PIK3CA as well as ESR1.

Um, I s- I tend to have a, a similar thought process here in that for patients that have both mutations, um, looking at comorbidities and then also looking at how long they were on their first-line therapy to pick between, um, whether I'm gonna go an ESR1 pathway and pick an oral SERD versus if I'm gonna go PIK3CA pathway and pick a PI3K/AKT pathway inhibitor.

For patients that have other comorbidities, maybe not as good a performance status, were on their first-line for a long time, I'm probably leaning more towards the oral [00:17:00] SERD thought process, whereas someone that I think can do well with the combination targeted therapy and endocrine therapy as opposed to just the single agent endocrine therapy, maybe I'm leaning more towards PI3K and AKT pathway inhibitor

Has that been what your experience has looked like? Yeah. I, I think about it in a very similar way. I think no patient-specific factors are driving me in one direction or the other I am tending to use something that is targeting that PI3K pathway. But I think there, there are a lot of patient-specific factors that you mentioned that would influence the decision-making.

Um, and so certainly a patient that is a little bit more frail and a patient that had a long duration of response to that first-line CDK 4/6 endocrine therapy those are potentially, great candidates for the oral SERD. We know those agents are very well-tolerated where when you're using something that's targeting that PI3K pathway you're probably going to get more toxicity Absolutely.

I think that brings us [00:18:00] nicely into talking a little bit more about the specifics of these agents, um, what their side effect profiles look like, and what role our pharmacist can have in monitoring and managing the side effects that we commonly see from each of these classes. So we can start, um, by looking at some of the key differences in CDK4/6 inhibitors, uh, that are essential to recognize when treating patients with these agents.

Um, so what are some of those key differences that you think about when selecting, monitoring patients receiving CDK4/6 inhibitors?

As we look at the CDK four six inhibitor class, I mean, there are some differences potentially in efficacy profile that we've seen in the trial, but we really are tending to look at the adverse effect profile as we make decisions about agents to choose here. So I think a really important thing to remember with this drug class is neutropenia is a major toxicity that we can see across the board with all three of these agents.

And so [00:19:00] monitoring, um, CBC with differential is very important as you start therapy. It is an earlier toxicity that we tend to see, so especially in those first couple of months, uh, very close monitoring, and then potentially being able to space out those moni- the monitoring for stable patients. I think the other things to highlight here is the diarrhea risk with abemaciclib.

Again, an early toxicity that we can see, but we wanna make sure patients are prepared for that, um, and have a plan for antidiarrheal therapy and making sure that they know dietary, uh, modifications and increase in hydration if it happens. Potentially some hepatotoxicity that we can see with abemaciclib and ribociclib.

I think the last thing I'll highlight here is the potential for QTc prolongation with ribociclib. Uh, so a toxicity particular to that agent that we would wanna monitor for, um, having an ECG at baseline and then about two weeks into treatment.

I did wanna highlight, uh, abemaciclib-induced diarrhea here. Um, and I think one of [00:20:00] the important kind of advances that we've seen recently is the TRADE trial, which is really, uh, I think has, has influenced practice and knowing that this is a, an early toxicity, that can be a reason that we see discontinuations from therapy.

This was a really interesting trial of a dose escalation of abemaciclib over that first month. So starting at fifty milligrams twice a day for two weeks, escalating that up as tolerated, um, over a four-week period to get to full dose. Jordan, is this something that you've implemented in your practice?

So we have. I, I won't necessarily say we do it on every single patient. Um, it is more of a consideration of, um, if we think the patient is gonna be more likely to experience diarrhea, even though we know it's very likely in almost all patients. So sometimes we do the full dose escalation, starting at the fifty, going to a hundred, and then a hundred and fifty.

But if we really have a lot of confidence that the patient will do fairly well, sometimes we only [00:21:00] do that middle and upper step, and we'll start at a hundred and then go to a hundred and fifty, and I've really had a lot of success with that too. And I agree with you, this has been a really nice addition to how we're able to start patients slowly on therapy and hopefully prevent them from discontinuing Yeah, I think, um, there's ways that you can kind of w- work with this data

I think the challenge is sometimes the multiple prescriptions that we may need to send out- Exactly ... early on. So any way to get around that in, uh, patients you think will do well is, is sometimes a little bit easier. Uh, one, I think really important point here is sometimes we have some concerns in modifying the dose.

We know that's a fairly common thing that we need to do with the CDK 4/6 inhibitor class is, you know, potential dose holds or dose reductions for some of these toxicities. And sometimes we have some concern from patients or maybe other members of the healthcare team that we're going to impact the efficacy with the dose [00:22:00] reduction.

So I think one important thing to highlight with our healthcare provider teams as well as the patients is the fact that we have some really good data that gives us confidence that reducing the dose does not appear to reduce the efficacy. So both sub- subgroups from MONARCH-E as well as NATALEE trials, um, have shown us that the invasive disease-free survival rates for those that had dose reductions versus those that didn't really are very similar.

So I think, um, that gives us a lot of confidence in that data. Anything, Jordan, in, in your practice? Is that conversations you've had with patients? Absolutely. I think not only from the physician perspective of concerns about dose reductions, it's a very, uh, significant concern for our patients. And so I think, um, to your point, being able to share that data, um, and give them the confidence that a dose reduction isn't gonna impact efficacy, and the most important thing is, um, being able to maintain therapy has really provided, um, a lot of [00:23:00] confidence in them feeling okay with that dose reduction that they really probably need.

Another drug class I'd like to highlight today is the the PI3K/AKT pathway inhibitor. So this is one that we've mentioned as being, you know, having some relevant toxicities for discussion here. So agents within this class being apelasib, capivasertib and evolocib. From a toxicity standpoint, I think the absolute number one thing to remember with this drug class is hyperglycemia is a risk here.

It tends to be something we see earlier in therapy. So median onset being usually within a one to two weeks of starting treatment. And therefore, you know, having baseline measures of fasting blood glucose and hemoglobin A1C, um, and then very kind of strict checking of glycemic control over the first month or so, uh, is very important to help identify this as an early toxicity.

Couple other things I think important to mention is diarrhea is a class effect here as well. Um, we tend to see this a little bit more with [00:24:00] capivasertib but can see it across the board. And then rash is another one that we can see a- as a class effect. Uh, apelasib tends to be a little bit greater incidence here.

And then stomatitis is something, uh, with evolocib, uh, to mention this toxicity that we can see early on. Uh, I do wanna, uh, quickly bring up with the hyperglycemia management, um, there is some data supporting use of prophylactic metformin with apelasib. Jordan, I'm curious, is this something you're doing in practice, and have you extrapolated this to any of the other agents within this class?

We have. So as you mentioned, we are, you know, often selecting based off of tolerability, and we know that, um, capivasertib, while it does have that higher risk of diarrhea, is a lot less likely to cause hyperglycemia. So we are preferentially using it, so it does kind of require some extrapolation, uh, for that prophylactic metformin.

But I do have patients that are pretty high risk, so maybe they have pre-diabetes as well as a [00:25:00] high BMI. And so we have... If they have kind of several hyperglycemia risk factors, um, extrapolated that data from Metallica and alpelisib to a patient that's getting ready to start on capivasertib. I've also escalated a patient's anti-hyperglycemic regimen if they already have well-controlled diabetes.

So if they're, you know, well-controlled and on a single agent, but I know I'm getting ready to start one of these agents, I've also escalated and added that second agent prior to starting, just kind of knowing they're probably at an especially high risk of hyperglycemia. Yeah. I totally agree. I think M-Metallica trial that looked at that prophylactic metformin was in patients receiving alpelisib, so I think that that's one...

I'm using a lot less of that these days, but if I do, I think that that is a patient population that regardless of risk factors, I'm probably going to institute a prophylactic metformin. But with capivasertib having that lower risk, I do think, uh, it's a great idea to be able to [00:26:00] stratify patients based on risk and, and maybe just doing that for the high-risk patients because metformin, we know adds risk of diarrhea.

Um, and that we know that that's something we can see with the, the drug class itself. So I think that's a great point in trying to really select the right patients to receive that. You had previously mentioned PARP inhibitors as a class that we're now using early stage and in the metastatic disease.

In terms of this drug class, I would say overall fairly well-tolerated, but I think the myelosuppression is still a, a toxicity that's important to pick out as a class effect here. Particular anemia, uh, does tend to be problematic and, problematic toxicity and a potential, uh, reason for holding or dose reductions.

I think the other big thing here to, uh, mention is nausea with olaparib. Jordan, anything that you're doing for these patients, are you using upfront prophylactic antiemetics, or are you starting with a PRN antiemetic? Most often I am starting with a PRN. I know [00:27:00] technically they would qualify based off of their emetogenic potential for scheduled.

Uh, but I do find some patients do okay with just PRN. So usually I tell them start with PRN, but if you're noticing that you are using it regularly, then we of course need to escalate that to just a scheduled, um, antiemetic prior to each dose of olaparib. I do tend to have them reevaluate after the first month to see if they do still need that scheduled antiemetic.

Um, is that something you're seeing where patients are able to go back to using it PRN after that initial month of scheduled if they are somebody that needs it scheduled? That's a great point. I have not actually noticed that trend in practice, but I think it's, uh, a great one to pick up on because, you know, this can be an early toxicity.

And we can see sometimes toxicities with our antiemetic class, constipation being a big one with our our... particularly ondansetron. So I think that's a great point and something I'll be looking at. I think another uh, counseling point here [00:28:00] is potentially administering that olaparib with food might- may help to decrease the nausea risk.

So I think using your antiemetics as necessary and then kind of administration timing and, um, and how they administer that with food may also be helpful. And then finally, the, the last class I'd like to touch on from a toxicity standpoint is the oral SERD class. We previously talked about this being, y- as a class generally being well-tolerated.

Um, but a couple things that I think of from a toxicity standpoint is fatigue. We see that across the board with, um, all three of our agents, our elacestrant, imlunestrant, and vepdegestrant. And then nausea's an- another one to pick up with this drug class as well. So I think tends to be a little bit less than what we see with, like, what we just mentioned with olaparib but can be a bothersome toxicity that certainly making sure at least having a PR and antiemetic, um, to start out with these agents I think is an important piece that we- a supportive care piece that we can help to improve [00:29:00] tolerance.

Um, Jordan, any thoughts you have on kind of the adverse effect profile of this class? I think similarly to what we discussed with olaparib and the non-pharmacologic things, thinking through that here some agents have to be taken without food, so you don't have the ability to take them with food. But specifically with elacestrant, um, they do recommend taking that with food to kind of minimize that nausea, and it is the one that's most likely to cause nausea.

So I do try to incorporate that counseling point for my patients to try to help minimize it, um, as much as we can. Yeah, I think, um, the... You bring up that important point. So imlunestrant is kind of the one to pick out here as administer on an empty stomach. So yeah, that, that trick isn't something that we can use with this particular agent.

But I think the last little bit here I wanted to wrap up is just the fact that sometimes persistence on these therapies can be very difficult. We've talked about the fact that these are often longer term therapies, um, and therapies that are associated with some [00:30:00] toxicity. So I think just a lot is needed here on our end as part of the healthcare team to try to, um, you know, address any potential barriers to care.

I think one of the things that I've found very helpful in my practice is just having an established workflow for regular communication with these patients. We're talking about oral therapies that they're administering a home setting. They may not be seeing... We might not be seeing them in person as much as we would with, um, infusional therapies.

So I think just having some sort of framework set up, whether that's, um, supported heavily by pharmacists or nursing providers or kind of a combination of that. I think having, um, that regular follow-up, especially early on in therapy, because a lot of these toxicities we are seeing early with our oral therapies is really an important, uh, piece to help patients persist on therapy.

Jordan, anything you're doing in, in your practice to help with this? I think that's a really good point. I think frequent check-ins, uh, especially [00:31:00] early, I- are really important to ensure adherence. The other, uh, kind of Tip that I think often helps my patients is knowing what we can do when these side effects happen.

That way, if they start happening, they don't just automatically discontinue um, and think, "No, I... You know, this isn't something I can deal with for two years, three years, or longer," if they're, uh, in the metastatic setting. So ensuring that they know these are the steps for at what point we'll hold and at what point we may consider dose reduction, making sure they know that dose reductions are equally effective.

Providing all of that upfront so that they know there are things that can be done if and when these side effects do occur. Yeah, patient education is so key in all of this, and really making sure that that education is happening before the patient is starting these agents to help set expectations and have patients hopefully be [00:32:00] comfortable, uh, with what to watch for and how to react to any side effects that are happening.

In addition to just, you know, the complexities of how to take the medication and how to store it, and all of those pieces that we can be helping patients, um, you know, feel more comfortable as they're starting treatment, I think is so important. Um, so Jordan, thank you so much for joining me today. I always learn so much from you in our conversations.

Thank you, Daniela and Jordan, for an informative discussion and for sharing your expertise with us. And many thanks to you, our listeners, for joining us today. Be sure to check back for more episodes on important oncology topics.