The Evolving Role of Subcutaneous Therapies in EGFR+ NSCLC

During a recent Peer Exchange from TheAmerican Journal of Managed Care®, a panel of experts explored the treatment of patients with EGFR-positive (EGFR+) non–small cell lung cancer (NSCLC). They discussed the efficacy and safety data from recent studies and how these data are shaping EGFR+ NSCLC management in clinical practice. The panelists also addressed the increasing interest in the use of subcutaneous formulations of NSCLC treatments and how this mode of administration can advance patient care in EGFR+ NSCLC. The session was moderated by Jorge García, PharmD, MS, MHA, MBA, FACCC, FACHE, principal and founder of Patagonia Healthcare Solutions in Miami Lakes, Florida.

Treatment Landscape in EGFR+ NSCLC

Lung cancer is the leading cause of cancer-related deaths worldwide.¹ NSCLCs account for more than 80% of lung cancer cases,² and EGFR mutations are the most actionable biomarker in NSCLC.³ EGFR mutations occur in approximately 30% to 40% of Asian and 10% to 15% of White patients with NSCLC.⁴ The 2 most common mutations are EGFR L858R and deletion of exon 19, which account for 85% to 90% of all EGFR mutations.³ Rare mutations account for up to 15% of total EGFR mutations, including point mutations, deletions, and insertions in exons 18 to 25 of the gene, and are associated with poorer outcomes compared with the 2 most common mutations.^4,5

EGFR mutations have transformed the treatment landscape for advanced NSCLC.² Patients with EGFR mutations were historically treated with first- and second-generation tyrosine kinase inhibitors (TKIs) such as erlotinib, gefitinib, or afatinib, which are associated with a median progression-free survival (PFS) of 10 to 14 months.^6,7 However, most patients eventually developed resistance through secondary mutations, including the T790M point mutation, which is seen in more than half of patients.⁶ These mutations have led to the development of third-generation TKIs, including osimertinib.⁶ Osimertinib is an irreversible EGFR TKI that blocks both the common EGFR-activating mutations and the T790M point mutation.⁶ The phase 3 FLAURA trial (NCT02296125) compared osimertinib with first-generation EGFR TKIs in treatment-naive patients with advanced NSCLC and an EGFR mutation.⁶ Median PFS was superior with osimertinib (18.9 months vs 10.2 months with erlotinib and gefitinib).⁶ Based on these results, osimertinib was included as a first-line option in the National Comprehensive Cancer Network (NCCN) guidelines.²

Treatment with osimertinib, however, led to secondary resistance mutations, including EGFR C797S and MET amplification, and chemotherapy was added to the osimertinib regimen in order to improve patient outcomes.⁴ The randomized phase 3 FLAURA2 trial (NCT04035486) showed that first-line osimertinib plus pemetrexed and platinum-based chemotherapy resulted in improved median PFS vs osimertinib monotherapy (25.5 vs 16.7 months) in patients with EGFR-mutated advanced NSCLC.⁸ In an open-label extension of the phase 3 trial, the median overall survival (OS) was 47.5 months in the osimertinib plus platinum-pemetrexed chemotherapy group vs 37.6 months in the osimertinib monotherapy group.⁹

Newer therapies have been developed to help overcome osimertinib-based resistance. Amivantamab is an EGFR-MET bispecific antibody with immune cell–directing activity that is approved for the treatment of patients with EGFR exon 20 insertion mutations whose disease progressed on or after platinum-based chemotherapy.³ Amivantamab has shown activity against a wide range of activating and resistance mutations in EGFR-mutated NSCLC and in patients with MET exon 14 skipping mutations. Lazertinib, another third-generation TKI, was shown to be highly selective and central nervous system (CNS)–penetrant, demonstrating efficacy in activating EGFR mutations and T790M resistance.³

The combination of amivantamab and lazertinib was shown to improve PFS compared with chemotherapy in patients with EGFR-mutated advanced NSCLC whose disease had progressed during or after osimertinib therapy in the phase 3 MARIPOSA-2 trial (NCT04988295).³ In addition, the phase 3 MARIPOSA trial (NCT04487080) assessed the efficacy and safety of amivantamab-lazertinib vs osimertinib alone as first-line treatment in patients with EGFR-mutated advanced NSCLC.¹⁰ Patients in the amivantamab-lazertinib group showed a significantly longer median PFS than those in the osimertinib group (23.7 vs 16.6 months).¹⁰

First-, second-, and third-generation TKIs and treatment personalization have improved survival, and there is a growing preference for targeted regimens that require tissues to be preserved for molecular analysis.² People with uncommon EGFR mutations, including exon 21 L861Q, exon 18 G791X, and exon 20 S768I mutations, may respond to osimertinib and afatinib, and treatment should be considered on a mutation-specific basis.² Resistance mutations in EGFR exon 20 (other than T790M) are heterogeneous and may also respond to targeted therapy, including first- and third-generation TKIs.²

Despite these developments, tumor heterogeneity and resistance to EGFR TKIs resulting in MET amplifications and other mutations remain key barriers to long-term disease control in NSCLC. NCCN guidelines recommend that molecular testing be considered for all patients with metastatic NSCLC squamous cell carcinoma due to the potential for actionable biomarkers, and tissue biopsy should be considered at progression.² The identification of novel mutations that confer resistance to existing treatment can also lead to the development of novel targeted treatments.¹¹ Next-generation sequencing is widely used for detecting plasma circulating tumor DNA (ctDNA) for tumor rebiopsy and provides vital information for understanding specific resistance mechanisms in a clinical setting. This can help with decision-making and future treatment strategies.⁴

Stakeholder Insights

Identifying mutations such as exon 19 deletions, L858R substitutions, and rarer variants has enabled more precise, targeted therapy selection, said Fawzi F. Abu Rous, MD, a medical oncologist at Henry Ford Health in Detroit, Michigan. “In terms of first-line treatment for EGFR-mutated [NSCLC], now we have 3 first-line options: osimertinib, based on the FLAURA trial; chemo plus osimertinib, based on the FLAURA2 trial; and amivantamab plus lazertinib, based on the MARIPOSA trial,” he said.

Joshua K. Sabari, MD, a thoracic oncologist at NYU Langone Perlmutter Cancer Center in New York, New York, noted, “When you look at a novel combination of amivantamab, an EGFR and a MET bispecific antibody, in combination with lazertinib, a third-generation EGFR TKI, you also see a dramatic improvement in overall survival over osimertinib alone. The standard of care for me—and my practice—is combination strategies in all patients.”

Amanda Cass, PharmD, BCPS, BCOP, a clinical oncology pharmacist at Vanderbilt University Medical Center in Nashville, Tennessee, said, “Now that we have several different options to use in the first-line setting, we know that the resistance mechanisms are different for osimertinib than they are for amivantamab and lazertinib. We know that MET amplification is the most common resistance mechanism that we see with osimertinib. And other mutations in the RAS-RAF pathway are the most common with amivantamab and lazertinib. As we go forward, I think testing at the time of progression is going to be really important to help identify what those resistance mechanisms are and see whether we have another targetable therapy, or [whether] a broader therapy is going to be the best option in the second-line setting for these patients.”

Sabari agreed. “I think the resistance mechanisms are a big issue,” he said. “For me, rationally designing a therapy that can overcome the common resistance mechanisms that we see to third-generation EGFR inhibitors is going to be critical, such as C797S. You mentioned point mutations, Dr Cass, in EGFR, particularly the exon 20, but also MET amplification is really important.”

Cass said, “An unmet need that I see frequently is making sure that people are getting testing at the time of progression. We do have several options in guidelines that are not necessarily biomarker-directed in the second-line setting, such as using amivantamab plus chemo if osimertinib alone was used in the first-line setting. Or we have some new approvals of different antibody-drug conjugates that we can use in that setting. That being said, there are trials going on right now, such as the [phase 2] INSIGHT 2 trial [NCT03940703], which is looking at combination targeted therapy for patients who develop a MET amplification as a resistance mechanism.… [We need to ensure] that we have CNS-active therapies. We all know that brain [metastases] in these patients frequently occur, so we need to make sure, as we develop these new therapies, that we’re having that blood-brain barrier penetration, as well.”

Tammy McClellan, PharmD, a clinical oncology pharmacist at Riverside Healthcare in Chicago, Illinois, added, “Along with everything that’s been said, [we need to understand] the phenotypic structure of the tumor itself as we’re doing these tests, and the residual disease. And why is this tumor able to survive and procreate and kind of go into a senescence state? That is something else that we can pattern ourselves on and try to [find] the answers.”

Abu Rous said, “I think another area of unmet need is learning when to de-escalate. In the clinic, the recommended first line right now for metastatic EGFR [NSCLC] is combination therapy. Osimertinib as a single agent still has a place, but it’s not the most common scenario right now. But I think we still need to learn when to de-escalate after starting combination therapy, because as you all know and as we can all imagine, combination therapies come with better outcomes, but also a more adverse effect profile.… We need to learn about these de-escalation strategies, maybe using MRD [minimal residual disease testing] and other technologies that are coming up.”

Sabari asked, “What are some of those reasons to de-escalate? Say a patient is older, less fit, maybe has comorbidities, is oxygen dependent, for example, is in a wheelchair, or has difficulty getting to the cancer center. Most other patients, I would offer combination strategies. The question of when to use amivantamab and lazertinib over osimertinib and chemotherapy is a deep one. And I think it’s our job as clinicians to really have that discussion with every patient, to go through the risks and benefits of each therapy, but also to think about the biology of the disease and how we can overcome resistance mechanisms and allow patients to live well with good quality of life.”

He continued, “I think it’s important that we understand [which] patients need more aggressive therapy and [when] we can peel off some of the therapies. You mentioned MRD. We know that patients who are ctDNA negative [at the beginning] don’t seem to benefit as much from combination strategies. Maybe exon 19 deletion has better prognosis than L858R patients without CNS metastases, but we don’t have [those] data in the clinic to really make those decisions. I think those studies need to be done.”

Optimizing Treatment in EGFR+ NSCLC

FLAURA2 and MARIPOSA have demonstrated that intensified regimens with combination chemotherapy or amivantamab plus lazertinib result in PFS and OS benefits vs osimertinib monotherapy in patients with EGFR-mutant NSCLC.¹² However, these benefits come at the cost of increased toxicity, treatment burden, and health care resource utilization.¹² Both FLAURA2 and MARIPOSA demonstrated significantly higher toxicity with combination regimens, potentially affecting tolerability, treatment burden, and quality of life.¹² In FLAURA2, grade 3 or higher adverse events (AEs) occurred in 64% of patients treated with osimertinib plus chemotherapy, compared with 27% treated with osimertinib monotherapy.⁸ Discontinuation rates were markedly higher in the combination arm (43% vs 6%), with pemetrexed being the primary cause of treatment discontinuation.⁸ Similarly, in MARIPOSA, AEs of grade 3 or higher were observed in 75% of patients receiving amivantamab-lazertinib vs 43% receiving osimertinib alone. Venous thromboembolic adverse events were reported in 37% of the patients in the amivantamab-lazertinib group and in 9% of those in the osimertinib group, with pulmonary embolism and deep-vein thrombosis being the most common AEs.¹⁰

Prophylactic anticoagulation is now recommended during the first 4 months of treatment.¹⁰ Treatment discontinuation occurred in 35% of patients in the combination arm, compared with 14% in the control arm. AE management is particularly challenging in real-world settings, where frail and comorbid patients, often underrepresented in clinical trials, may be less able to tolerate intensified therapies.¹² The patients who would derive most clinical benefit from intensified regimens include clinically fit patients, who are carefully selected based on both clinical and molecular characteristics, while placing strong emphasis on quality of life and individual patient preferences.¹² As such, the future debate will not be whether to intensify, but how to personalize intensification.¹²

CNS progression is a leading cause of treatment failure in NSCLC. This emphasizes the value of agents with high CNS penetration and durable intracranial control, particularly newer TKIs capable of crossing the blood-brain barrier. Updated NCCN guidelines recommend CNS-active options for patients with brain metastases, as these agents may improve systemic and neurologic outcomes. This supports proactive CNS management as a key factor in treatment selection and patient survival. In FLAURA2 and MARIPOSA, approximately 40% of patients were affected by CNS metastases at baseline. In both studies, patients with CNS metastases experienced improved outcomes after receiving osimertinib plus platinum-pemetrexed or amivantamab plus lazertinib vs osimertinib alone. In FLAURA2, median PFS was 24.9 and 13.8 months in patients using osimertinib plus platinum-pemetrexed vs osimertinib alone, respectively.¹⁰ Although CNS-specific PFS data were immature, the combination arm showed a numerically longer median CNS PFS (30.2 vs 27.6 months), CNS overall response rate was 73%, and CR rate was 59% with combination therapy, compared with 69% and 43%, respectively, with monotherapy.¹³ In MARIPOSA, median intracranial PFS was 24.9 months with amivantamab plus lazertinib compared with 22.2 months with osimertinib.¹⁴

Bispecifics such as amivantamab, which targets both MET and EGFR, and recent regulatory approvals are changing the NSCLC treatment landscape.¹⁵ New approvals include sunvozertinib, which is approved in the second line for patients with metastatic NSCLC and an EGFR exon 20 insertion resistance mutation, after receiving chemotherapy or after receiving first-line treatment with chemotherapy plus amivantamab.^16,17 Accelerated approval was based on results from the phase 2 WU-KONG1B trial (NCT03974022), which evaluated the efficacy of sunvozertinib in 200-mg and 300-mg doses taken once per day. The trial showed an overall response rate (ORR) of 45.9% in the 200-mg group and 47.2% in the 300-mg group. Duration of response (DOR) was 11.1 and 13.8 months, with a 12-month OS rate of 62.1 and 73.7% with sunvozertinib in the 200-mg and 300-mg groups, respectively.¹⁶ Higher ORRs were observed in patients with baseline brain metastases (52.4% vs 28.6%) and previous amivantamab treatment (41.7% vs 25%) taking the 300-mg dose.¹⁶ New treatments and subcutaneous formulations are driving a shift toward more durable, mechanism-based, and patient-centered care strategies.¹⁵

Stakeholder Insights

“Amivantamab, when it first was approved, we were using it in the second line, and that was helpful because we got used to it and how to utilize it in the clinic,” Abu Rous said. “It comes with a lot of supportive medications to try to help with the [adverse] effect profile, such as infusion reactions, rash, and maybe the risk of VTE [venous thromboembolism] when we combine it with…lazertinib. So now, when we use it in the clinic or when we use it in our center, we follow the SKIPPirr protocol [NCT05663866], which uses dexamethasone and some other supportive medications to reduce the risk of infusion reactions.”

Sabari added, “I think in a patient with active CNS metastases, I would select amivantamab and lazertinib or osimertinib and chemotherapy. I would not treat with a third-generation EGFR TKI inhibitor alone. [A colleague of mine] looked at patients with leptomeningeal disease who received amivantamab and lazertinib, and we saw north of a 50% response rate in that patient population. I think it’s very stimulating, very exciting data that we need to further study in randomized trials.”

Cass added, “As we move forward and start using these combination therapies, what are the [AEs] we have to look at? When we’re looking at osimertinib plus chemotherapy, we’re seeing a little bit more myelosuppression, a little bit more GI [gastrointestinal] toxicity. When looking at amivantamab plus lazertinib, we’re seeing a different adverse effect profile. Those are going to be some of our dermatologic adverse events that I’ll talk about, and then the infusion-related reactions as well, and potentially increased risk of VTE when used in combination with lazertinib.… We do have different protocols that we can use that were not used in the trial that we can now use moving forward to help prevent some of these. So, the first one is going to be the COCOON regimen [NCT06120140], and that’s going to be for more of our dermatologic adverse events.”

She added that patients should have a good understanding of when to use supportive care. “[Putting] prompts in the EHR [electronic health record] to help physicians prompt patients for this decreased our rates of grade 2 dermatologic [AEs] to 42%, down from 75%.... When you combine amivantamab and lazertinib, you have an increased risk of VTE, particularly in the first 4 months. So, you can start these patients on VTE prophylaxis for those first 4 months…. It can be a backpack full of therapy for these patients.”

Sabari said, “Thirty percent to 40% of patients do not go on to receive second-line therapy. We need to use our best therapies first. And I think it’d be crazy...not to use amivantamab and lazertinib in the front line or osimertinib and chemotherapy in the front line, unless it was the patient’s preference to use single-agent osimertinib…. Then the question is: ‘What is the second best, or what is the next line of therapy that you utilize in your practice?’ And when someone asks [what the best therapy is], it’s always clinical trials. Because if you have a clinical trial option for a patient, you’re moving the needle forward for that patient, but also for the thousands and thousands of patients who will come after.”

Cass added, “Not only do we not know which patients are going to go on and receive second-line therapy, we don’t know what their mechanism of resistance is. Is it going to be small-cell transformation? It’s not really common, but I do see it. And I think this is just even a stronger point for using your best therapy up front.”

Abu Rous said, “This is a very important point when we’re talking about treatment sequencing. We always have to keep the resistance mechanisms in mind and try to sample and biopsy or send ctDNA whenever progression happens. Because small-cell transformation that can be detected via biopsy is not that common, but we see it in our clinic, and that’s a completely different disease or biology that needs to be addressed appropriately. Sometimes we see some of these very uncommon resistance mutations or even targetable mutations or alterations show up. We have some evidence from smaller studies about combining different TKIs in those patient populations and driving very good benefits.”

Subcutaneous Therapy Treatment Options in NSCLC: Key Considerations

The phase 3 PALOMA-3 trial (NCT05388669) assessed the noninferiority of pharmacokinetics, efficacy, and safety of subcutaneous vs intravenous (IV) formulations of amivantamab, combined with lazertinib in patients with EGFR-mutated advanced NSCLC who progressed after osimertinib and platinum-based chemotherapy.¹⁸ The study demonstrated noninferior pharmacokinetics and ORR of subcutaneous vs IV amivantamab-lazertinib, with numerically longer DOR and PFS.¹⁸ ORR was 30% in the subcutaneous group vs 33% in the IV group, median PFS was 6.1 vs 4.3 months, and median DOR was 11.2 months vs 8.3 months, respectively.¹⁸ OS was significantly longer in the subcutaneous group vs IV group (HR for death, 0.62; 95% CI, 0.42-0.92; nominal P = .02).¹⁸ When comparing the toxicity profiles, rates of infusion-related reactions (13% and 66%) and VTE (9% and 14%) were lower in the subcutaneous group than in the IV group, respectively.¹⁸

Subcutaneous amivantamab plus lazertinib enhanced patient convenience and reduced medical resource utilization compared with IV amivantamab plus lazertinib in the PALOMA-3 study. Significantly more patients reported the subcutaneous injection as convenient than those receiving IV infusion (85% vs 52% during cycle-1-day-1 [C1D1], and 85% vs 35% at end of treatment, respectively).¹⁸ Treatment administration times were significantly shorter for patients receiving subcutaneous injection than those in the IV infusion group, and more patients reported feeling unrestricted (C1D1, 66% vs 29%; cycle-3-day-1 [C3D1], 60% vs 42%, respectively), unbothered by administration (C1D1, 69% vs 30%; C3D1, 71% vs 45%), and reported gaining time for other activities (C1D1, 36% vs 7%; C3D1, 37% vs 6%).¹⁹

Additional studies of subcutaneous amivantamab treatment are under way. Initial experiences in the phase 2 PALOMA-2 bridging study (NCT05498428), which switched from IV to subcutaneous amivantamab monotherapy, indicated it is feasible and safe with a similar safety profile to the known subcutaneous amivantamab profile.²⁰ The phase 2b COPERNICUS open-label trial (NCT06667076) is investigating efficacy and safety of subcutaneous amivantamab plus lazertinib treatment with supportive care in first-line EGFR-mutated NSCLC.²¹ The study aims to prevent and proactively manage VTE and dermatologic AEs in a diverse, multinational, clinically representative population.²¹

Stakeholder Insights

“One of the things that these subcutaneous formulations can bring into play is streamlining pharmacy workflow,” Cass said. “Instead of a complex sterile compounding process, these subcutaneous formulations can just be drawn up in a syringe, potentially by the nurse themselves. And it also eliminates the potential for using closed-system transfer devices if needed.… Fewer people are going to have to be involved when compounding these, as well. In addition to shorter times preparing, we have to use less equipment, fewer IV lines, fewer IV pumps, and less chair time.”

McClellan added, “I would like to take the patient’s perspective. When we’re trying to administer these chemotherapy agents, some of them are considered vesicants, which can cause a lot of damage. That’s the reason why we do a lot of the ports.… We’re seeing with some of these subcutaneous injections, the reactions, the adverse reactions are lessened. We may have more of a volume over a shorter period of time, but the severe immediate reactions are lessened.”

She continued, “Historically, for IV formulations to saturate a receptor, you’d have to get more dose and more frequently than these depot subcutaneous formulations. Potentially, you could administer once every 4 weeks, which is not yet approved, but could be available for patients. So, when I ask my patients if they prefer an IV formulation over a subcutaneous formulation, hands down, patients say they prefer a subcutaneous formulation. Shorter administration time, shorter monitoring time…. It frees up the patient’s time, but it also frees up the chair in order for us to be able to treat other patients. And access is a huge issue in oncologic care in 2025.”

Abu Rous agreed, adding, “There is a huge value for subcutaneous formulation. I think about it from the patient’s perspective or from the institution’s perspective. When we think about the patient’s perspective, the 3 things that patients worry about or that we worry about are efficacy, tolerability, and quality of life.”

Sabari said, “It’s efficacy first and patient first. If the efficacy is inferior, I’m not going to utilize subcutaneous formulations over IV formulations. But as you mentioned, if they’re equivalent or maybe even better in the sense of toxicity profile or maybe even survival benefit, I think it’s a no-brainer. And it really does take a village to treat each patient on a day-to-day basis. You imagine a patient walks into a cancer center, there’s the greeter, there’s the intake team, there’s the [medical assistant] who rooms the patient, right? Then the doctor comes in, maybe the resident, the fellow. And then just before they go downstairs to get the infusion, probably another 10 people touch their case in the pharmacy. So, [what would be ideal is] if it could take less of a village to administer therapy at better cost and better efficiency to the practice, and at better tolerability to the patient. I think it makes a lot of sense to use these subcutaneous formulations.”

Regarding adoption of newer therapies, McClellan said, “We can switch in the middle of a therapy sometimes. It’s frowned upon, but [ask] the patient, ‘Do you have a preference?’ With all things considered, I think this is something that, honestly, we’ll move forward with.”

Cass agreed. “I would like to add along with the option for the patient and just choosing these agents, if this is appropriate for the patient, but even in the drug choice itself with the adverse events, all of this has to be taken into consideration and get back to the basics of whether these therapies are appropriate, and these methods of administration, as well,” she said.

“It’s our job as clinicians to educate patients at their level,” Sabari said. “I have patients who want to get back to their jobs and back to work. So, yes, from a convenience standpoint, I think patients will always select the shorter treatment. But [we should be] going through the data, educating them on the risks, the benefits first, starting with efficacy, and then also going through the adverse effect profile…. Subcutaneous may not be the best fit for every single patient, but if a drug is available and it has the same efficacy—if not better—if it has a better toxicity profile, and it also makes the practice more efficient, I think it’s the right therapy to choose.”

Abu Rous agreed. “I think we have to help our patients make an informed decision. And our job as providers is to provide them with this information and try to make it as easy as possible to understand and to digest,” he said. “When we’re talking about amivantamab, it’s definitely a lower toxicity profile. But there’s something interesting that might emerge in subcutaneous formulation, which is the local site injection reaction…. We have to be realistic and tell them that adverse effects can happen; however, it’s at a lower rate compared with IV formulations.”

In terms of pharmacy challenges and considerations, Cass said, “I think space, just the inventory alone, is a huge issue…. I’m pretty sure every single hospital struggles with space. And if you’re doubling the amount of inventory you have to keep for some of these products, that could take up a significant amount of room, especially if they have to be refrigerated or things like that.”

McClellan agreed that reimbursement is a big challenge that can affect uptake, adding, “I can also imagine that there might be some hesitancy in either switching or using subcutaneous formulation from our patients because they might think that this is less effective than the IV formulation…. We need to explain to them and educate them that the studies have shown that they’re either noninferior or maybe superior in some settings, in terms of efficacy.”

Cass said, “If patients are just getting their therapy in a fast track, are they no longer seeing the team? A lot of the visits have become uncoordinated, where you don’t need to see a provider, and you don’t have to have a contact point that day. We work toward the infusion chair; whenever that chair is available, that’s when the patient comes in…. Are we going to miss some of these adverse events? Could we have intervened differently? As we think about the administration of these therapies, we also have to build systems, call patients. Pharmacy techs are critical for connecting with patients if they’re not having all those touchpoints with the medical teams.”

Abu Rous said, “[In the PALOMA-2 trial,] most patients preferred the subcutaneous formulation over the [IV]. But I think this is something that we need to train and educate clinicians, nurses, pharmacists on how to do. I think we’re always very wary about changing any treatment unless there’s progression of disease or patients are not tolerating the therapy. Here, if there truly is equivalence, I feel like we should be able to transition if this is in the best interest of the patient.”

Sabari concluded, “We do need to keep the patient at the center of our discussion at all times. Remember what the goal is of these medicines. They’re to treat someone who has a malignancy, a cancer, to help improve their outcome without affecting their quality of life.” •

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