Elderly patients with mantle cell lymphoma (MCL) achieved a high overall response rate (ORR) and durable survival after receiving ibrutinib (Imbruvica) and rituximab (Rituxan), according to data from a phase 2 ENRICH trials (NCT0180567) published in the 

The combination elicited an investigator-assessed best ORR of 96% among 48 patients, including a complete response (CR) rate of 71%, a partial response rate of 25%, and a stable disease rate of 4%. Within the intent-to-treat population (n = 50), the best ORR achieved with the doublet was 92%; this included a CR rate of 68%.

“Ibrutinib plus rituximab is an effective, easily administered, and chemotherapy-free option in elderly patients with nonblastoid MCL,” lead study author Preetesh Jain, MD, DM, PhD, of MD Anderson Cancer Center, and colleagues, wrote in the paper. “New onset atrial fibrillation was observed in 9 patients. We recommend that pretreatment assessment of cardiovascular risk factors is beneficial before ibrutinib/rituximab therapy.”

Patients older than 65 years with MCL treated with systemic chemotherapy tend to have inferior outcomes compared with younger patients with the disease. Standard treatment for elderly patients with MCL is rituximab-based chemoimmunotherapy followed by rituximab maintenance. However, a high incidence of grade 3 to 4 myelosuppression, hospitalization rates, infectious complications, and second cancers following this approach represent significant complications in this population.

The investigator-initiated, institutional review board–approved, open-label, single-institution, single-arm trial stemmed from a study originally designed to investigate the safety and efficacy of ibrutinib plus rituximab in relapsed or refractory MCL.

In 2015, another cohort was added to investigate the effects of ibrutinib and rituximab on elderly patients. The study enrolled 50 patients who were aged 56 years of age or older with previously untreated MCL. These patients had nonblastoid or pleomorphic histology, and/or a Ki-67% less than 50%, and an ECOG performance status of 2 or less. Notably, patients with a history of controlled atrial fibrillation were permitted.

Patients were administered oral ibrutinib 560 mg once daily in 28-day cycles with rituximab, which was given via an intravenous infusion at 375 mg/m2 once weekly for 4 weeks in the first cycle, followed by a dose on day 1 of every cycle starting in cycles 3 through 8. After cycle 8, rituximab was given on day 1 of every 2 months for up to 2 years. After 2 years, Ibrutinib was administered in continuous cycles until disease progression, toxicity, or other factors caused discontinuation.

The primary objective of the study was to estimate ORR, and key secondary objectives included progression-free survival (PFS) and overall survival (OS). Safety was also evaluated.

Participants were enrolled to the trial between October 2015 and November 2019. The median age of patients was 71 years (range, 69-76), and 71% were men. Bone marrow involvement was observed in 94% of patients, and gastrointestinal tract involvement was noted in 79% of evaluable patients. Additionally, 16% of patients had a high MCL international prognostic index (MIPI) risk score, and 28% had a high biologic MIPI score including Ki-67%. Furthermore, 3 of 18 patients had 

 aberrations detected in the bone marrow. Twenty-three percent of patients had a history of atrial fibrillation.

At a median follow-up of 45 months (range, 24-56), 45 patients were still alive and 5 had died. A total of 4 patients experienced disease progression; 2 of these patients transformed from classic to blastoid MCL and 1 patient transformed from classic to pleomorphic MCL.

Baseline PET scans were performed in 40 patients, and 35 were positive. Within that group, 26 patients were found to have achieved complete metabolic response (CMR) at best response (74%), 8 did not have a PET scan at best response, and 1 patient had residual disease. Of the 26 patients who experienced CMR, 81% (n = 21) were bone marrow negative for MCL and 1 patient had residual disease; 4 patients did not undergo bone marrow evaluation. The median number of ibrutinib and rituximab cycles to reach CR was 7 (range, 2-51).

Additionally, the median PFS and OS were not reached with the doublet. The 3-year PFS rate was 87% (95% CI, 0.73-0.94) and the 3-year OS rate was 94% (95% CI, 0.82-0.98).

Notably, those with a high Ki-67 were noted to have a trend of higher risk of disease progression and/or death vs those with a low Ki-67 (

= not significant). Moreover, those who experienced a CR as their best response to treatment were noted to have significantly longer PFS and OS vs those who did not. Those with high-risk simplified and modified MIPI score had a significantly higher risk of disease progression. OS was noted to be inferior in high-risk patients.

As of January 2021, 56% of the 50 patients discontinued ibrutinib/rituximab and left the study because of progressive disease (8%), toxicities (42%), or miscellaneous reasons (6%). Of the 21 patients who discontinued because of toxicity, 10 did so because of grade 3 atrial fibrillation. At the time of discontinuation, 16 of the 28 patients who discontinued were in CR. Of the 10 patients who experienced atrial fibrillation, 6 had new onset and 4 had a history.

Most adverse effects (AEs) reported with the combination were either grade 1 or 2 in severity. The most common grade 3 or 4 AEs included atrial fibrillation (22%), fatigue (18%), diarrhea (14%), and myalgias (14%). Grade 3 or 4 hematologic toxicities included anemia (4%), neutropenia (8%), and thrombocytopenia (4%).

A total of 4 patients experienced grade 3 or 4 bleeding while receiving ibrutinib; 3 of these patients were receiving aspirin and/or enoxaparin and 1 patient who had retinal bleeding had recently undergone glaucoma surgery and had a history of vitreous surgery. One patient experienced grade 3 hematuria and gram-negative urinary tract infection, although this resolved with the administration of antibiotics.

Thirty-four percent of the 50 patients developed atrial fibrillation, and 10 needed to discontinue ibrutinib because of a grade 3 effect. Nine of the 17 patients who developed this toxicity had no history, and 6 had baseline ECG abnormalities, including 1 with first-degree atrioventricular block, 1 with right bundle branch block, 3 with sinus bradycardia, and 1 with miscellaneous abnormalities.

“We recommend that pretreatment assessment of cardiovascular risk factors is beneficial before IR therapy,” study authors concluded. “Long-term follow-up and randomized studies with standard treatments are needed to further evaluate the efficacy, safety, and pattern of relapse with [ibrutinib and rituximab] combination.”

Jain P, Zhao S, Lee HJ, et al. Ibrutinib with rituximab in first-line treatment of older patients with mantle cell lymphoma. 

. Published online November 19, 2021. doi:10.1200/JCO.21.01797

This article was originally published on OncLive as “Ibrutinib/Rituximab Combo Represents Effective Chemo-Free Option for Elderly Patients with MCL”

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Ibrutinib plus rituximab is effective, easy to administer, and removes the need for chemotherapy in older patients, say experts. 

 Ibrutinib/Rituximab Combo May Be an Effective Chemo-Free Therapy for Older Patients With MCL

Patients with lower-risk myelodysplastic syndromes (MDS) appeared to benefit from receiving a fixed combination or oral decitabine and cedazuridine (Inqovi), according to results from the phase 3 ASCERTAIN trial. Findings on the combination’s efficacy and tolerability were recently presented during the 2021 American Hematology Society Annual Meeting & Exposition.

“Oral [hypomethylating agents] are a game changer for patients with MDS,” said study author James K. McCloskey, MD. “We’ve known this in high-risk disease, but this brings in an orphan patient population where we haven’t had other options previously. The oral nature of this drug is particularly important to consider when we’re talking about low-risk patients.”

®, McCloskey, chief, Leukemia Division, John Theurer Cancer Center, Hackensack Meridian Health, discussed the efficacy of oral decitabine plus cedazuridine, the combination’s potential role in lower-risk MDS, and what this could mean for the patient population.

®: What was the rationale for this study?

: Lower-risk MDS are diseases that we typically treat with a focus around a patient’s cytopenias and attempting to improve the quality of life. We understand these patients may live decades with their disease, but symptoms related to anemia and the impact of transfusion burden and iron overload can impact their outcome.

Unfortunately, outside of luspatercept-aamt [Reblozyl] for ring sideroblastic disease or lenalidomide for patients with 5q-minus associated MDS, we don’t have disease-modifying therapies that are helpful in low-risk disease. By contrast, the hypomethylating agents, including decitabine and azacitidine, are standard in higher-risk MDS where we know they improve overall survival, reduce transfusion requirements, and improve quality of life. [On] occasion, we might use these in low-risk patients, but we have not demonstrated that we improve their overall outcomes with the use of hypomethylating agents in low-risk MDS.

That brings us up to oral decitabine, which is an oral fixed dose of combination decitabine and a CDA inhibitor known as cedazuridine. This was FDA approved based on data from the ASCERTAIN trial, a randomized, crossover study that confirmed equivalent exposure to decitabine when we use this the oral fixed-dose combination compared with parenteral azacytidine. What we’re presenting ASH is an exploration of the patients on the ASCERTAIN trial who had lower-risk disease.

What were the methods that were utilized in the follow-up of this study?

The ASCERTAIN trial was a randomized, crossover study, where patients received 1 cycle of parenteral azacitidine. Then, during the remaining cycles of treatment, they were treated with oral combination therapy.

We obtained PK/PD data to confirm that there was equivalent exposure with the oral and parenteral forms. In this abstract, we're looking at those patients treated on the ASCERTAIN study who had low-risk disease.

Could you share the results that were presented at the meeting?

There were 133 patients in total treated on ASCERTAIN, and 69 patients had lower-risk MDS. The vast majority of those had an intermediate 1 disease, so 93% of these patients. When we look at their treatment, the median number of cycles was 9 but there were patients who received up to 28.

The most common toxicities were ones that might be predictable based on prior experience with hypomethylating agents in general and the previous published data with ASCERTAIN, [which] included cytopenias and infectious complications, including febrile neutropenia and pneumonia.

With that said, the overall response rate was 57%, and that included 23% of patients who achieved a complete response. What we got to see in this abstract was the rate of transfusion independence, which is important in low-risk patients. We saw 48% of those patients who were receiving red cell transfusions became transfusion independent and 67% of patients who were receiving platelet transfusions became platelet and transfusion independent. The trial also looked at median overall survival and leukemia-free survival, and the median survival endpoints for those patients had not been met at 32 months.

We talked about the treatment goal of...improving quality of life. These oral formulations may be an even bigger deal for low-risk patients who are often outside of our clinic, trying to live their life. By offering them an oral therapy, we are giving them the option to be treated at their home, reducing their visits with us, and hopefully, not only reducing infusion times for chemotherapy, but by offering them transfusion independence, they're going to reduce their time in our infusion chairs. That was one of the big points for me in this data…67% of patients coming off platelet transfusions and 48% off red cell transfusions.

This overall survival and leukemia free survival that exceeds 32 months is impressive. It is going to be interesting to see how this data matures [as we continue] to watch this patient population, and certainly, this gives us something to turn to for those patients that many of us might have been managing in clinic. They’re rare patients, but those patients who have isolated thrombocytopenia, more isolated anemia, this is reassuring data that allows us to apply the current FDA-approved label to those patients and offer them a new option.

Across the board there's a lot of excitement about the opportunity to use these oral [hypomethylating agents] as a backbone in combination trials, as well. Those are certainly ongoing, and there's a lot of exciting combinations that can be thought of. It gives us the opportunity in the future to be considering a completely oral regimen for our elderly, unfit patients.

This article was originally published on OncLive as “Oral Decitabine Plus Cedazuridine Combo Shows Promise in Lower-Risk MDS”

Oral decitabine, an oral fixed-dose of combination decitabine and CDA inhibitor cedazuridine, is an FDA-approved therapy for patients with lower-risk myelodysplastic syndromes.

Oral Decitabine and Cedazuridine Holds Potential to Reduce Clinic Visits, Infusion Time for Patients With Lower-Risk MDS

Aspacytarabine (BST-236), a novel antimetabolite, induced encouraging response rates in adult patients with newly diagnosed acute myeloid leukemia (AML) who are unfit for intensive therapy, according to data from a phase 2b trial (NCT03435848).

Findings presented during the 2021 ASH Annual Meeting showed that the agent produced a complete remission (CR) of 37% overall, 44% in patients with de novo AML (n = 39), 35% in those aged 75 years or older (n = 34), 32% in those with an ECOG performance status of 2 or higher (n = 25), 32% in those with an adverse European LeukemiaNet (ELN) score (n = 34), 27% in those who previously received hypomethylating agents (HMAs; n = 11), and 27% in those who had secondary AML (n = 26).

“These final CR data are extremely encouraging and strengthen our conviction in the potential of aspacytarabine as a potential standard-of-care treatment option for [patients with] AML,” Jessica Altman, MD, lead study investigator and professor of medicine in the Hematology Oncology Division of the Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center of Northwestern University, stated in a press release. “Notably, a CR rate of 37% was achieved in a challenging patient population, including [those] with secondary AML, prior HMA treatment, and older age.”

The novel proprietary antimetabolite is comprised of cytarabine that is covalently bound to asparagine, acting as a prodrug of cytarabine, which has served as a backbone of therapy in this disease for over 4 decades. Although strong efficacy can be achieved with cytarabine, the agent is also linked with severe bone marrow, gastrointestinal, and neurological adverse effects (AEs).

Aspacytarabine has been shown to have unique pharmacokinetics and metabolism which allows for high-dose treatment with less systemic exposure to free cytarabine as well as sparing normal tissues. For these reasons, investigators hypothesize that aspacytarabine may represent a superior option for AML and other malignancies.

For the phase 2 trial, investigators set out to examine the safety and efficacy of single-agent aspacytarabine as induction and consolidation treatment in patients with newly diagnosed AML who were not eligible to received standard induction chemotherapy. Those with secondary or therapy-related AML and those who previously received a HMA with or without venetoclax (Venclexta) for a preceding condition were permitted.

Study participants received aspacytarabine at 4.5 g/m2 per day, equimolar to 3 g/m2 per day of cytarabine. The agent was given via daily 1-hour infusions as part of 6-day courses for 1 to 2 induction courses and 1 to 3 consolidation courses.

The primary end point of the trial was CR, and key secondary end points included safety, overall survival (OS), duration of response (DOR), and minimal residual disease (MRD).

The median age of study participants (n = 65) was 75 years (range, 54-88), and 52% of patients were 75 years or older. Moreover, 62% of patients had an ECOG performance status of 0 or 1 and 38% had a status of 2 or 3. Additionally, 40% of patients had secondary AML, 29% of whom had disease secondary to myelodysplastic syndrome or chronic myelomonocytic leukemia and 11% of whom had disease secondary to therapy.

Seventeen percent of patients previously received an HMA. Moreover, 34% of patients had a bone marrow blast percentage of less than 30%, 25% had a percentage ranging from 30% to 50%, and 41% had a percentage of greater than 50%. Most patients (52%) had an adverse ELN risk score; 25% had an intermediate score, 14% had a favorable score, and 9% did not have this information available.

The data cutoff date for the analysis presented during the meeting was December 2021.

Additional findings from the trial revealed that CRs were reached after 1 to 2 courses of induction treatment, and 50% of those who achieved the CRs were MRD negative. The median DOR with the agent was 6.0 months (95% CI, 3.9–not reached).

Rapid complete hematological recovery was reported in all patients who achieved a complete bone marrow response, with a median time of 25 days (range, 11-39) for complete neutrophil recovery, and 26 days (range, 18-40) for complete platelet recovery.

Follow-up for the median DOR and OS is ongoing.

Regarding safety, the treatment-emergent AEs that were grade 3 or higher and were most frequently reported with the agent included febrile neutropenia (50%), thrombocytopenia (27%), anemia (21%), leukopenia (21%), hypokalemia (18%), sepsis (15%), neutropenia (14%), pneumonia (14%), hypophosphatemia (11%), and hypoxia (11%).

Related serious AEs included febrile neutropenia (9%), sepsis (6%), pneumonia (5%), thrombocytopenia (5%), and anemia (3%).

FDA granted a fast-track designation to aspacytarabine

 for use in patients with AML who are aged 75 years and older and who have comorbidities that preclude the utilization of intensive induction chemotherapy.

Biosight reports final primary endpoint data from phase 2b study of aspacytarabine (BST-236) for first-line acute myeloid leukemia therapy. News release. BioSight Ltd.; January 6, 2022. Accessed January 10, 2022.

Altman JK, Koprivnikar J, McCloskey JK, et al. Aspacytarabine (BST-236) as monotherapy is safe, well-tolerated and effective for the treatment of adults with newly diagnosed acute myeloid unfit for intensive therapy. Results of a phase 2 study. 

. 2021;138(suppl 1):1273. doi:10.1182/blood-2021-149361

Biosight granted US FDA fast track designation for BST-236 for the treatment of acute myeloid leukemia. News release. Biosight Ltd; August 4, 2020. Accessed January 10, 2022. 

This article was originally published on OncLive as “Aspacytarabine Shows Efficacy, Safety in Newly Diagnosed AML Unfit for Intensive Therapy”

Recently presented findings demonstrate that aspacytarabine may represent a viable treatment option for various subsets of patients with acute myeloid leukemia. 

Aspacytarabine May Be Viable Option for Patients with AML Who Are Unfit for Intensive Therapy

Patients with myelofibrosis and other myeloproliferative neoplasms (MPN) are often able to achieve improved survival outcomes and quality of life following treatment with ruxolitinib (Jakafi), a highly potent and selective JAK inhibitor, alone and in combination with other drugs. Despite this, treatment options designed to address disease progression itself are still lacking, explains Marina Kremyanskaya, MD, PhD.

These diseases are being attacked from all different angles possible,” Kremyanskaya said. “Hopefully, in the next few years, we will see some newer drugs that we can use and offer our patients that will have an impact on their disease course.”

, Kremyanskaya, an assistant professor of medicine, hematology, and medical oncology at Mount Sinai Hospital, discussed potential new combinations for treating patients with myelofibrosis and other MPNs, with a backbone of ruxolitinib.

In terms of disease modification, what is the current state of MPN treatment?

: MPNs are a group of heterogeneous disorders with variable disease scores and life expectancies. Although we talk about disease modifying agents, there is not really any medical therapy that is available that will offer patients a cure, except for stem cell transplantation. There are many agents that are in development that we are hoping will modify the disease course, but currently, there are no proven standard therapies that [can do that], as well as prevent disease progression, or offer patients a cure.

What add-on approaches with ruxolitinib are being explored to increase efficacy?

Ruxolitinib has been a standard-of-care treatment for patients with myelofibrosis, as well as patients [with] polycythemia vera, since its approval. Most patients [with myelofibrosis] get ruxolitinib soon after diagnosis, or at least when they become symptomatic and develop other disease characteristics that make it reasonable to start them on therapy. Many newer [treatment strategies] are using the approach of combining additional therapy with a JAK inhibitor, such as ruxolitinib, to achieve a more lasting and disease modifying effect. Ruxolitinib is a great drug for our patients. It offers improvement [in terms of] quality of life, many patients feel a lot better, and there are some benefits in survival. [However], it is not disease modifying, in the sense that it is not offering a cure and disease progression still happens.

There are many therapies that are looking at an additional effect, and the backbone of ruxolitinib is a very common in clinical trials [for this patient population] right now. One is a drug by Constellation [Pharmaceuticals], CPI-0610, which is a bromodomain inhibitor. In a phase 2 trial [NCT02158858], CPI-0610 was used as monotherapy for those patients who progressed on ruxolitinib, or who were intolerant of it, as well as in addition to ruxolitinib for patients who had suboptimal responses to it. [A third arm of the study assigned] JAK-naïve patients or those recently diagnosed who have not had experience with JAK inhibitors [to CPI-0610 plus ruxolitinib].

This drug has demonstrated some clinical activity in all 3 arms. There were splenic responses [reported], and there are patients who were transfusion dependent at baseline who have become transfusion independent on therapy. [Additionally,] there have been anemia responses in those patients who were not transfusion dependent. [We have also seen] improvement in symptom scores for patients in all the [different study arms]. Specifically, for those JAK-naïve patients who are receiving the combination therapy, the total spleen response seemed to be better than [that seen with] ruxolitinib alone. [This was also the case when] looking at other secondary end points, such as improvement in fibrosis, improvement in anemia, and all the other usual end points that we look at in myelofibrosis.

This phase 2 trial led to the opening of the phase 3 MANIFEST-2 trial [NCT04603495], where patients are going to be randomized to receive either ruxolitinib plus CPI-0610 or ruxolitinib plus placebo. This will give us much more information about the efficacy of these 2 drugs together as an upfront therapy.

Another combination [under investigation] is navitoclax [previously ABT-263] plus ruxolitinib. [The] phase 2 trial [will examined navitoclax] as monotherapy, and combination with ruxolitinib in those patients have already had suboptimal responses to ruxolitinib. Additionally, a phase 3 trial is opening where navitoclax will be used upfront in JAK inhibitor–naïve patients. An additional combination [includes] a drug from Insight Pharmaceuticals, which is a PI3K-delta inhibitor. [Similarly, there has been a] phase 2 trial with some clinical activity and promising results, and it is moving on to a phase 3 trial where it will be offered both upfront for JAK inhibitor–naïve patients, and as an add-on to those patients who are already on ruxolitinib and have had suboptimal responses. Ruxolitinib really is being used as the backbone for a lot of different combinations, so we will see it in combination with a lot of other drugs.

Are there any efforts being made with immunotherapy in this space?

Immunotherapy in myelofibrosis and other MPNs, in general, does not seem to be as advanced as in other fields, but this is a field that’s developing There are many treatment options that are being investigated and we will see them come up in early-phase clinical trials, either as single-agent or in combination with JAK inhibitors.

What are some of the next steps for this area? Are there any ongoing efforts that you're excited about?

These trials I mentioned [that are investigating combinations with ruxolitinib are all in phase 3 right now. [As these read out] we will have a better understanding of where all these drugs fit into [the treatment paradigm] of myelofibrosis. Currently, we still only have 2 JAK inhibitors that are approved, and once patients progress on the JAK inhibitors, there is not a lot that we can offer them outside of clinical trials. Because all these drugs are going into phase 3 right now, it will give us additional options for upfront therapy, where hopefully we can get deeper, more meaningful responses. Additionally, for those patients who already experienced JAK inhibitor therapy, these agents can be added on for a next line of therapy.

It will be exciting, and we will have choices. We will see where all these drugs fit with each other, and we will perhaps see a specific phenotype of patients with myelofibrosis who can go in one treatment direction vs another. In addition, there are other JAK inhibitors in development, and some of them are hopefully getting close to approval, such as pacritinib. This is an agent that can be used for patients with cytopenias, specifically thrombocytopenia, which is a difficult-to-treat population where there is a lot of unmet need. Hopefully, we will see improvement in survival in these patients. This will be another exciting area that can offer us more information.

What is the focus for treating patients who are resistant to ruxolitinib?

In practice for these patients, outside of clinical trials, there is nothing. We go back to older drugs that were used for myelofibrosis before. They may get a hypermethylated agent, depending on their disease, and they should go to transplant if that is an option for them.

An expert from Mount Sinai Hospital comments on potential new ruxolitinib combinations to treat patients with myelofibrosis and MPNs. 



Ruxolitinib Remains Backbone in Myelofibrosis and MPN Treatment 

Patients with relapsed/refractory multiple myeloma who received reduced doses of the triplet combination of selinexor (Xpovio), bortezomib (XVd), and dexamethasone (Velcade) achieved higher response rates and longer duration of responses, according to Sundar Jagannath,MBBS, professor of medicine and director of the Center of Excellence at Tisch Cancer Institute, Mount Sinai in New York, New York.

Specifically, in a post-hoc analysis of the phase 3 BOSTON Study (NCT03110562), which was recently presented at the 63rd American Society of Hematology Annual Meeting & Exposition, lower doses of selinexor (60 mg and 40 mg) were found to be more effective and tolerable compared with standard (100-mg) doses for this patient population.

Jagannath, who presented the data during the meeting, recently spoke with 

about nursing considerations and important patient education regarding selinexor. He highlighted the importance of medication adherence, nausea management, and proper hydration among patients about to receive this agent.

“This is an oral drug,” Jagannath said. “[Nurses] want to tell the patient to maintain a calendar—it is given only once a week [and] you have to ensure that they are taking the pill only once a week, [that] they are not by mistake, like a blood pressure medication, taking it every day... So, that's number 1.”

“We have to tell them, especially when [they are] starting on the medication, [that they are] going to take nausea medication, and dexamethasone because that alleviates the potential for nausea, [and] vomiting. Usually, we use ondansetron (Zofran)—it's available as an orderly dissolvable tablet. [It is important to] take it around the clock for 48 hours, not just 1 time before taking the pill; even if you don't feel sick, just take it for the first time around for 48 hours. If you tolerate it later on, after a month or so, [when] you are comfortable with the pill and [and] the side effect, you can always cut it down by not taking the nausea medication.’”

“You need to keep yourself well hydrated, especially in myeloma,” he continued. “If you're not able to keep yourself well hydrated because of the nausea, you [have] to give a call to the doctor's office, or go to the doctor to get some IV fluid and [receive] some nausea medication IV so that the nausea is medicated.”

He also advised that patients split their dose of dexamethasone across 2 days. “You can split and take it 2 days because dexamethasone with Zofran works synergistically in preventing the nausea. Even though you took all of this medication of selinexor in 1 day, taking the nausea medication with dexamethasone over 2 days also helps,” he said.

Selinexor is an oral selective inhibitor of XPO1-mediated nuclear export compound (SINE) which functions by enforcing nuclear retention, activating tumor suppress proteins, and inhibiting the translation of oncoproteins.

Clinical outcomes in patients (pts) with dose reduction of selinexor in combination with bortezomib, and dexamethasone (xvd) in previously treated multiple myeloma from the BOSTON study. Presented at: 2021 ASH Annual Meeting and Exposition; December 11-14, 2021; Atlanta, GA. Abstract 3793.

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An expert from the Tisch Cancer Institute highlights the importance of medication adherence, nausea management, and proper hydration for patients being treated with selinexor for relapsed or refractory multiple myeloma. 

Nursing Considerations for Using Selinexor in Multiple Myeloma 

Lisocabtagene maraleucel (liso-cel; Breyanzi) fostered a better quality of life (QoL) in patients with relapsed/refractory large B-cell lymphoma (LBCL) compared with current standard of care (SOC), according to data from a comparative analysis of the phase 3 TRANSFORM trial (NCT03575351) presented during the 2021 ASH Annual Meeting.

Using the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire – 30 items (EORTC QLQ-C30), a linear mixed model for repeated measures (MMRM) group analysis found that those in the liso-cel arm had more favorable overall least square (LS) mean changes from baseline to day 126 vs the SOC arm in most of the domains analyzed.

Evaluable patients who received the CAR T-cell therapy (n = 47) experienced a mean change in cognitive functioning of 2.21 (range, -1.48 to 5.90) vs -2.09 (range, -6.00 to 1.83) in those who received SOC (n = 43); this translated to a difference of 4.30 (range, -0.76 to 9.36) on day 126 from baseline.

Those in the liso-cel arm also experienced a mean change in fatigue of -1.95 (range, -7.40 to 3.51) compared with 3.75 (range, -2.17 to 9.68) in the SOC arm, equating to a difference of -5.70 (range, -13.24 to 1.84) on day 126 from baseline. In these domains, the liso-cel group improved, as the SOC group deteriorated.

Additionally, the liso-cel arm had a mean change in global health status/QoL (GH/QoL) of 3.08 (range, -1.83 to 7.99) from baseline to day 126; the SOC arm experienced a mean change of 0.04 (range, -5.24 to 5.31), resulting in a difference of 3.04 (range, -3.62 to 9.70) between the 2 arms.

The liso-cel group also experienced mean changes in physical functioning and pain of -2.75 (range, -6.76 to 1.25) and -11.14 (range, -16.37 to -5.92), respectively, compared with -2.17 (range, -6.64 to 2.30) and -15.56 (range, -21.25 to -9.88), respectively, for the SOC group. The differences between the 2 arms in physical functioning and pain were -0.58 (range, -6.17 to 5.01) and 4.42 (range, -2.72 to 11.56), respectively.

Individual-level analyses demonstrated that the proportion of patients with meaningful improvement was higher for GH/QoL, and deterioration was lower with liso-cel vs SOC from day 126 to month 6.

At the 6-month mark, 53% of patients in the liso-cel arm reported improvement in GH/QoL, compared with 14% of those in the SOC arm. Eighteen percent of patients in the liso-cel arm reported deterioration of GH/QoL at this time point vs 57% of those on the SOC arm. Furthermore, 47% of patients in the liso-cel group experienced improvement in fatigue at 6 months vs 29% of those in the SOC group. Eighteen percent of patients in the liso-cel arm experienced deterioration regarding fatigue at this time point vs 71% of those in the SOC arm.

“It is important to emphasize that higher scores on functionality domains and lower scores on symptom domains indicate a better QoL,” presenting study author Jeremy Abramson, MD, of Massachusetts General Hospital Cancer Center, said during the poster presentation of the data.

TRANSFORM enrolled patients between the ages of 18 and 75 years who had aggressive non-Hodgkin lymphoma and who were refractory or relapsed 12 months or less following first-line treatment containing an anthracycline and a CD20-targeted agent. To be eligible for enrollment, patients needed to have an ECOG performance status of 0 or 1, be eligible for hematopoietic stem cell transplantation and have a left ventricular ejection fraction of over 40%. Patients with secondary central nervous system lymphoma were permitted. There was no minimum lymphocyte count.

Participants were randomized 1:1 to receive either SOC comprised of 3 cycles of salvage chemotherapy and BEAM (carmustine, etoposide, cytarabine, and melphalan) plus autologous stem cell transplantation for responding patients, or liso-cel following lymphodepletion treatment. Crossover to the liso-cel arm was permitted for patients who failed SOC treatment. Patients received the CAR T-cell therapy at a dose of 100 x 106 CAR-positive T cells.

The primary end point of the trial was event-free survival (EFS), and key secondary end points comprised complete response (CR) rate, progression-free survival (PFS), and overall survival. Other end points of interest included duration of response, objective response rate, PFS on the next line of treatment, safety, and patient-reported outcomes (PROs).

In a prespecified interim analysis of data from TRANSFORM, liso-cel demonstrated highly statistically relevant and clinically meaningful improvement vs SOC regarding the primary end point of EFS, plus secondary end points of CR and PFS.2 In the analysis presented during the 2021 ASH Annual Meeting, Abramson reported findings pertaining to QoL.

Investigators evaluated QoL by leveraging the EORTC QLQ-C30 and FACT-LymS tools. The former evaluated cancer-associated symptoms and functioning and is comprised of 30 items that address 15 domains. Primary functional domains of interest that were evaluated in TRANSFORM were GH/QoL, physical functioning, and cognitive functioning. Primary symptom domains of interest were fatigue and pain. The FACT-LymS tool evaluated symptoms that were specific to lymphoma and was comprised of 15 items. With this assessment, higher scores are representative of better QoL.

To assess the between-treatment differences in overall LS mean change from baseline for each primary domain, a MMRM analysis was conducted, and this leveraged data collected up to day 126 for visits with a sample size per are of 10 or more. All analyses were prospectively defined, and the findings reported during the 2021 ASH Annual Meeting are descriptive.

To be eligible for PRO analyses, patients needed to complete a baseline assessment and at least 1 post-baseline assessment. Notably, a similar proportion of patients were included in the EORTC QLQ-C30 analyses sets for liso-cel (51%) and SOC (47%).

In the liso-cel group of 92 patients, 47 were evaluable for the EORTC QLQ-C30 analysis, and 45 were evaluable for the FACT LymS analysis. Notably, 45 patients were not included in the EORTC QLQ-C30 analysis because they did not complete a baseline assessment (n = 28), a post-baseline assessment (n = 1), or both (n = 16).

In the SOC group, 43 and 40 out of 92 patients were evaluable for the EORTC QLQ-C30 and FACT Lym-S analyses, respectively. Patients from this group were excluded from the EORTC QLQ-C30 analysis due to lack of baseline assessment (n = 20), lack of post-baseline assessment (n = 6), or lack of both (n = 23).

Additional data presented during the 2021 ASH Annual Meeting showed that with regard to the Functional Assessment of Cancer Therapy - Lymphoma Subscale (FACT-LymS), the difference in mean change between the 2 arms was -0.16 (range, -2.71 to 2.40). On the 126-day mark, the liso-cel group had a FACT-LymS mean change of 1.48 (range, -0.30 to 3.26), compared with 1.63 (range, -0.41 to 3.68) in the SOC group. Notably, for FACT-LymS, similar proportions of patients between the investigative and control arms experienced deterioration (24% and 29%, respectively) and improvement (47% and 43%) at month 6.

“Overall QoL was either improved or maintained from baseline in patients with relapsed/refractory LBCL who received liso-cel as second-line treatment,” Abramson concluded. “These results were achieved despite only responders to salvage chemotherapy remaining in the SOC arm past day 64. These findings corroborated with previously reported HRQoL associated with liso-cel treatment.”

Abramson J, Solomon S, Arnason J, et al. Improved quality of life (QOL) with lisocabtagene maraleucel (liso-cel), a CD19-directed chimeric antigen receptor (CAR) T cell therapy, compared with standard of care (SOC) as second-line (2L) treatment in patients (Pts) with relapsed or refractory (R/R) large B-cell lymphoma (LBCL): results from the phase 3 transform study. Presented at: 2021 ASH Annual Meeting; December 9-14, 2021; Atlanta, GA. Abstract 3845.

Bristol Myers Squibb announces positive topline results from phase 3 TRANSFORM trial evaluating Breyanzi (lisocabtagene maraleucel) versus chemotherapy followed by stem cell transplant in second-line relapsed or refractory large B-cell lymphoma. News release. Bristol Myers Squibb; June 10, 2021. Accessed December 14, 2021. 

A comparative analysis indicated that lisocabtagene maraleucel generated superior quality of life in patients with relapsed/refractory large B-cell lymphoma compared with the current standard of care. 

Liso-Cel Outperforms Standard Therapy in Improving QoL in Relapsed/Refractory LBCL

Although the majority of nurses and advanced practice providers (APPs) agreed that implicit bias is a problem which affects many health care professionals, most fail to acknowledge their own personal bias, according to a recent survey published in the 

, Kathy Burns, MS, APRN-CNS, AGCNS-BC, a benign hematology clinical nurse specialist at James Cancer Hospital, and study co-author, explains the importance of self-awareness and how oncology nurses can improve patient interactions by recognizing their own bias–particularly when prescribing medications for patients with substance abuse disorders.

“The number one thing is awareness, being aware of your own implicit bias, being aware of your personal triggers,” she said. “Reflecting on your own behavior and how others react to that behavior, reaching out to those you trust [to be] honest and help guide you.”

She acknowledged that with recent events in the pandemic, there is a plethora of resources available both within and outside of oncology institutions. She encouraged nurses and APPs to take advantage of these resources, to push themselves beyond their comfort zone, to interact with different people, and lastly, to seek ways to build their multicultural perspectives.

“In the last 12 months, the CDC has reported from March 2020 to March 2021, [over] 96,000 people died of an overdose

,” she added. “[Be] very mindful of what's going on in the world, how we react to that, and know that the needs of people are just going to shift and change.”

Burns K, McNally GA. Implicit bias training: improving outcomes for patients with cancer who have substance use disorders. 

. 2021;25(5):595-599. doi:10.1188/21.CJON.595-599

Provisional Monthly National and State-Level Drug Overdose Death Counts. CDC. November 7, 2021. Accessed Decembers 10, 2021. https://bit.ly/3rZb0SS

Kathy Burns, MS, APRN-CNS, AGCNS-BC, of the Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, comments on the importance of self-awareness as an oncology nurse when working to overcome one’s implicit bias.

Self-Awareness Is Critical in Treating Prescribing Patients With Cancer and Substance Abuse Disorders

Medical equality, equity, and disparity were the focus of this year’s Reuters Events Total Health USA, a well-known national medical conference I had the honor to attend.

Health care leaders came together to share insight and solutions to some of America’s broken health care systems. As an oncology nurse for more than 2 decades, I especially appreciated the concern about increased mortality rates among African Americans with multiple myeloma (MM).

Marc Harrison, MD, president & CEO of Intermountain Health Care, and Kathy Giusti, Founder & Chief Mission Officer of the Multiple Myeloma Research Foundation (MMRF), delivered an authentic presentation uncovering the negligence of this gap in care. Since both these powerhouse CEOs are MM survivors, the conversation became quite passionate. At one point, Giusti grinned at the moderator and said, “This is the joy when you have two patients doing a fireside chat who live with a death sentence.” Here, I will share the hope for improved health equity as seen through the eyes of these top executives.

Although both words sound similar, they are relatively different. Health care equality simply means that the opportunity for proper treatment exists, whereas health care equity involves tailormade plans designed specifically for an individual’s unique needs. Unfortunately, many believe that if there is equal opportunity for those diagnosed with cancer, there is also equity. Sadly, this is not the case. Dr. Harrison noted that it was difficult as an affluent, White male and CEO of a major health care system to get the care he needed when fighting MM. He acknowledged that accessing care is even harder for both people of color and financially disadvantaged individuals. Therefore, although a healthcare organization may offer lifesaving MM treatments, the capability (financial, social, economic) to implement those treatments is anything but “equal.”

Uncovering Why More African Americans Die From Myeloma Than Caucasians

Giusti described a pivotal moment in MM research with the launching of the CoMMpass Study (NCT01454297) over a decade ago.

 The significance of the study came from the large number of African American involvement. According to Giusti, the goal for any clinical trial is to have at least 20% Black participation to represent this population accurately. The CoMMpass trial had an unprecedented 17% African American participation rate.

However, this led to startling data revealing that Black patients with MM had a lower genomic risk profile than White patients—yet were dying at twice the rate. After much investigation, Giusti described, “Their access to triple and quadruple therapy or even a stem cell transplant was much lower, and as a result, it was the access to the most cutting-edge therapies that was the problem.” In fact, if Black patients received equal and equitable MM treatment, their outcomes would be as good or better as other ethnicities.

How to Improve Health Disparities in the African American Population

Firstly, Giusti believes that “the best equity officers are often CEOs who are truly passionate about the topic—and set a clear message to the company that health equity is a priority.” Secondly, she speaks about how crucial retrieving health data is. How can we understand MM and other diseases if the patients with these conditions are not in easily accessible databases?

She points out that if Black people with MM are not in registries, they will not have the opportunity to be located and guided to progressive clinical trials that improve survival. Harrison recognizes that Black patients with lower incomes are not seen in big, fancy academic centers. Instead, he suggests these companies are “taking care of as few poor people as possible,” leaving community-level health systems to care for the underprivileged. Both speakers fervently agreed that health care systems need to reveal where these patients are. It’s imperative that clinical research organizations (CROs), pharmaceutical companies, and NCORP share where these folks reside and are being treated.

Thirdly, once high-risk patient populations are identified, an infrastructure needs to be created to help alleviate the burden of getting patients into registries and clinical trials. Asking staff that is already overworked to review records and get these folks onboarded is burdensome. Giusti suggested creating a foundation at the community level armed with “coordinators, community liaisons, and navigators is crucial to successfully obtaining and distributing data.” Lastly, she believes patient education is critical. When equipped with the correct knowledge, patients are empowered to make well-informed health decisions.

During the fireside chat, Giusti’s laid-back presentation was nicely complimented by Harrison’s bulldog approach. Her professional activism, along with his demands for improvement, inspired many viewers to be change agents. In fact, after reminding the audience that one-third of Americans are rationing medications because they can’t afford them, Harrison directly addressed the pharmaceutical companies.

He challenged them to evaluate their overly priced products, stating, “It’s unfair for Americans to bear the disproportionate burden for the cost of these products when the rest of the world benefits. We have poor Americans achieving poor health outcomes because of how much healthcare costs, and that’s a tragedy in the richest country in the world, and it has to change.” In addition, Giusti believes that creating private/public partnerships between profit and nonprofit organizations could be essential to decreasing health disparities.

Oncology nurses are often the main point of contact for newly diagnosed cancer patients. We have the opportunity to ensure that each person starts their journey with equality and equity on their side. Since the first step in resolving medical disparities is acknowledging them, we must stay informed about how our patients are affected by these inadequacies. From there, we remain committed to reform by creating custom-made resources and providing innovative education to staff and patients. As Harrison proclaimed, “Poor patient outcomes based on someone’s demographics is intolerable.”

Harrison M, Giusti K. Fireside chat: Spotlight on improving equity and inclusion. Presented at: Total Health Reuters Events; September 2022; Chicago, IL.

The MMRF CoMMpass Study. Multiple Myeloma Research Foundation. Accessed December 17, 2021. https://bit.ly/3sgk2ey

Oncology nurses are often the main point of contact for newly diagnosed patients with cancer. We have the opportunity to ensure that each person starts their journey with equality and equity on their side. 

Top Executives Vow to Improve Health Disparities among Patients with Multiple Myeloma

Amphiregulin (AREG) may represent a useful longitudinal monitoring biomarker for patients with life-threatening acute graft-vs-host disease (GVHD), according to a sample of 2 prospective clinical trials that was presented at the 2021 ASH Annual Meeting. Specifically, patients with a high baseline of AREG are at an increased mortality risk and, therefore, should be monitored consistently during serial assessments.

Specifically, in a multivariate analysis for survival, day 28 responses (risk ratio [RR], 9.14; 

 <.0001) and baseline AREG (>212 pg/mL; RR, 2.72; 

 <.05) were the only factors found to be independently associated with survival.

When this was also evaluated in a multivariate analysis out of a University of Minnesota study, day 28 responses (risk ratio [RR], 4.94; 

 <.0001) and baseline AREG (>212 pg/mL; RR, 4.17; 

 = .03) were also the only factors found to be independently associated with survival.

“Patients with life-threatening acute GVHD often have severe symptoms related to organ and tissue damage, elevated blood biomarkers of acute GVHD, or both. Monitoring can be challenging due to unpredictable variations in symptoms that may not be related to acute GVHD severity or pathogenesis, including changes in nutrition and infections,” lead study author Shernan Holtan, MD, of University of Minnesota, said in a presentation of the findings.

Researchers evaluated AREG, ST2, and Reg3a as monitoring biomarkers in a University of Minnesota study, which treated patients with uhCG/EGF, they then compared those findings with an independent cohort of patients with steroid-refractory acute GVHD receiving second-line ruxolitinib in the REACH-1 trial (NCT02953678).

Samples were collected at baseline, day 7, 14, 28, and 56. The University of Minnesota study (hCG/EGF) enrolled a total of 51 patients. Amphiregulin was measured using an enzyme-linked immunosorbent assay, and ST2 and REG3a were measured via a multiplex Luminex-based assay. In this study, there was significant positive correlations between assay platforms. The median age for first-line, high-risk patients (n = 26) in this study was 61 years (range, 22-72), there were 19 males (73%), and the number of patients with GVHD grade II, IIII, and IV was 2 (8%), 21 (81%), and 3 (12%), respectively.

Among the second-line cohort (n = 26), the mean age was 62 years (range, 2-69), there were 20 males (77%), and the number of patients with GVHD grade II, IIII, and IV was 9 (35%), 8 (31%), and 9 (35%). Severity was mostly grade 3 or 4 in both these cohorts, according to Holton.

REACH-1 enrolled 60 patients and all 3 biomarkers were assessed using microfluidic immunoassay. Among REACH-1 participants, the mean age was 52 years (range, 18-73), 31 were male (52%), and the number of patients with acute GVHD grade II, IIII, and IV was 22 (36.7%), 24 (40.0%), and 14 (23.3%), respectively.

In REACH-1, biomarker levels were assessed at baseline, and it was revealed that patients with day 28 progressive disease (PD) had higher baseline levels of AREG compared with patients with a day 28 complete response (CR; 

 <.01). Similarly, ST2 levels were also higher for patients with day 28 PD vs CR (

<.01) or very good partial response (VGPR)/partial response (PR; 

 <.05). Baseline REG3a did not adhere to the pattern; levels of this biomarker were not significantly different between patients with day 28 CR, VPGR/PR, or PD.

In the University of Minnesota study, patients with a 28-day CR experienced a 3-fold decrease in AREG levels between baseline and day 56 (mean, 98 vs 32 pg/mL, 

= .006). However, among patients with a day 28 PR or no response (NR), AREG levels did not exhibit clinically meaningful change.

When this was evaluated in REACH-1, AREG levels decreased 2.8-fold from baseline to day 56 in patients with a day 28 CR (mean, 174.7 vs 63.6 pg/mL; 

 = .007). AREG levels also decreased 2.0-fold over time in patients with a day 28 PR (mean baseline 288 vs. 146.1 pg/mL at day 56; 

 = .017). AREG levels did not significantly change in those who had PD.

In the University of Minnesota study, patients with CR experienced a 1.4-fold decrease in ST2 over the course of 28 days (

 = .02), compared with patients with PR or NR. In contrast, in the same study period, REG3a did not exhibit any significant change in any of the response categories. This was similar in REACH-1 (ST2, 

In regard to biomarker cutoffs, AREG was linked to rapidly fatal courses. Generally, the levels of AREG were higher in patients enrolled in REACH-1 compared with those in the University of Minnesota study. This may reflect a difference in assay, severity of illness of both, according to the study authors.

In the University of Minnesota study, biomarkers cutoffs were linked to a rapidly fatal course. With an AREFG cutoff of 212 pg/mL, the median survival was not reached vs 62 days (

 = .006). With an ST2 cutoff of 292 ng/mL, the median survival was not reached vs 239 days (

 <.001), and with a REG3a cutoff of 13.5 ng/mL, the median survival was not reached vs 416 days (

In REACH-1, the AREG cutoff was found to be 336 pg/ml, and the median survival was not reached vs 74 days (

= .09), and the REG3a cutoff was 3.6 ng/ml (

“Based upon our current samples, there is not a close correlation between these biomarkers,” Holton said in a post-presentation discussion. “That's a good thing. This is the new and additional way to do monitoring.”

Holton concluded that amphiregulin is a useful longitudinal monitoring biomarker with patients who have life threatening acute graft-vs-host disease.

“We have also shown that patients with a high baseline amphiregulin are at high risk of early death,” she said. “They should be monitored on a consistent platform during serial assessments during their therapy.”

Pratta M, El Jurdi N, Rashidi A, et al. Validation of amphiregulin as a monitoring during treatment of life-threatening acute graft-versus-host disease: a secondary analysis of 2 prospective clinical trials. Presented at: 2021 ASH Annual Meeting and Exposition; December 11-14, 2021; Atlanta, GA. Abstract 259.

Patients with high levels of amphiregulin were at a higher risk of an early death in acute graft-versus-host-disease, according to a presentation at the 2021 ASH Annual Meeting.

Monitoring Amphiregulin May Be Warranted in Caring for Patients with Acute GVHD 

The triplet regimen of belantamab mafodotin-blmf (Blenrep) plus pomalidomide (Pomalyst) and dexamethasone (Pd) was revealed to have a manageable safety profile, which is consistent with the known individual safety profiles of belantamab mafodotin or Pd, in patients with relapsed/refractory multiple myeloma, according to updated findings from the ongoing, phase 1/2 Algonquin study (NCT03715478) that were presented during the 2021 ASH Annual Meeting.

The regimen was explored across 6 cohorts at different dosing schedules of belantamab mafodotin. Following a correlation with lower rates of blurred vision, neutropenia, and a superior progression-free survival (PFS), 2.5 mg/kw every 8 weeks was selected as the recommended phase 2 dose (RP2D) for this agent.

“Belantamab mafodotin in combination with pomalidomide and dexamethasone demonstrates a manageable safety profile that is consistent with the known safety profiles of belantamab mafodotin and pomalidomide, individually,” Suzanne Trudel, MD, of the Princess Margaret Cancer Centre, in a presentation of the findings. “Both those cohorts, [at a dose of] 1.92 mg/kg and 2.5 mg/kg every 4 weeks, demonstrated deep and durable responses, however, the 2.5-mg/kg dose cohort appears to have better efficacy with a [median] PFS of 25.3 months versus 16.2 months.

Belantamab mafodotin is a BCMA-targeting antibody-drug conjugate (ADC) that is currently approved for the treatment of patients with relapsed/refractory multiple myeloma who have received at least 4 prior therapies, including an anti-CD38 monoclonal antibody, a proteasome inhibitor, and an immunomodulatory agent.

As part of the ongoing phase 1/2 Algonquin study, 56 patients were enrolled in October 2021 to receive either 1.92 mg/kg or 2.5 mg/kg of belantamab mafodotin plus Pd. There were 6 cohorts in total: belantamab mafodotin at 1.92 mg/kg as a single dose every 4 weeks (cohort 1; n = 12), at 2.5as a single dose and a 2.5-mg/kg loading dose followed by 1.92 mg/kg every 4 weeks (cohort 1a; n = 12), at a split dose of 2.5 mg/kg (n = 8), at a split dose at 3.4 mg/kg every 4 weeks (cohort 2; n = 12), at a bi-monthly dose of 2.5 mg/kg every 8 weeks (cohort 3a; n = 12), and at a tri-monthly dose of 2.5 mg/kg (cohort 3b; n = 8).

Patients in all cohorts also received pomalidomide at 4 mg on days 1 to 21 and dexamethasone at 40mg weekly. Treatment continued until either disease progression or unacceptable toxicity.

In part 1 of the trial, the primary end points were maximum-tolerated dose (MTD) and/or highest dose with acceptable toxicity (RP2D), and objective response rate (ORR) was the primary end point in the part 2 portion. Secondary endpoints were defined as efficacy—progression-free survival (PFS), overall survival (OS), duration of response (DOR)—and safety, including ocular toxicities.

Among all participants, the median age was 64 years (range, 36-81) and the median prior lines of treatment was 2.5 (range, 1-5). All enrolled patents were exposed to a PI and lenalidomide, while 75.4% were PI/lenalidomide refractory and 48.2% were daratumumab/lenalidomide/PI refractory.

Belantamab mafodotin is an antibody-drug conjugate that functions by targeting BCMA and has demonstrated clinically meaningful activity in relapsed/refractory multiple myeloma.

Hematology