A matching-adjusted indirect comparison of the efficacy of elranatamab versus teclistamab in patients with triple-class exposed/refractory multiple myeloma

Abstract

For patients with triple-class exposed/refractory multiple myeloma (TCE/RMM), where effective treatments options are limited, B-cell maturation antigen and CD3-directed bispecific antibodies offer a promising new approach. Teclistamab gained conditional approval in Europe and accelerated Food and Drug Administration (FDA) approval based on the MajesTEC-1 trial (NCT03145181). Elranatamab, approved by the FDA demonstrated its safety and efficacy in the MagnetisMM-3 trial (NCT04649359). Given the absence of head-to-head trials, an unanchored matching-adjusted indirect comparison (MAIC) was conducted to assess their relative efficacy. Key baseline characteristics were adjusted to be comparable between the two trials. In the MAIC, elranatamab demonstrated significantly better objective response rate and progression-free survival (PFS) than teclistamab, and numerically better complete response, duration of response, and overall survival (OS). These results suggest that elranatamab is an efficacious option for treating patients with TCE/R MM.

Keywords:

• Elranatamab
• matching-adjusted indirect comparison
• multiple myeloma
• survival
• response rate
• teclistamab

Introduction

Multiple myeloma (MM) ranks as the second most prevalent hematologic malignancy worldwide, with an estimated global incidence of approximately 160,000 cases per year. Despite the availability of various treatments, MM remains incurable, with a 5-year survival rate of 52.3% [1]. Patients with MM often require multiple lines of sequential therapy, typically involving three main classes of therapy: proteasome inhibitors (PIs), immunomodulatory drugs (IMiDs), and anti-CD38 monoclonal antibodies [2–6]. Those who have been exposed to at least one PI, one IMiD, and one anti-CD38 monoclonal antibody are classified as having triple-class exposed/refractory (TCE/R) MM and commonly experience relapse or treatment refractoriness. Consequently, these heavily pretreated patients have a particularly poor prognosis [4,7,8].

In the real-world MAMMOTH (Monoclonal Antibodies in Multiple Myeloma: Outcomes after Therapy Failure) study conducted in the United States, which investigated the outcomes of patients with TCE/R MM, receiving physician’s choice of treatment, the median progression-free survival (PFS) was 2.8 months, and the median overall survival (OS) was 8.6 months [9,10]. Another real-world study, LocoMMotion, conducted predominantly in Europe, reported a median PFS of 4.6 months and a median OS of 12.4 months for patients with TCE MM [11].

B-cell maturation antigen (BCMA)- and CD3-directed bispecific antibodies constitute a novel approach to treating TCE/R MM. Teclistamab, a humanized IgG Fc BCMA-directed bispecific antibody, was granted a conditional marketing approval in Europe in August 2022 and accelerated approval by the US Food and Drug Administration (FDA) in October 2022 based on results from the phase 1/2 MajesTEC-1 trial (NCT03145181). Elranatamab, a humanized IgG2A BCMA-directed bispecific antibody was granted accelerated approval by the FDA in August 2023 [12]. It has shown promising safety and efficacy in the phase 2, open-label, multicenter MagnetisMM-3 trial (NCT04649359), which focused on patients diagnosed with TCE/R MM [13–16]. The MagnetisMM-3 trial consisted of two distinct cohorts: cohort A, comprising patients without prior BCMA-directed treatment, and cohort B, which included patients who had previously received BCMA-directed antibody drug conjugate or CAR-T cell therapies.

Despite several available treatments, there is no clear consensus regarding the standard of care therapy for patients with TCE/R MM. The current European Society for Medical Oncology (ESMO) guidelines recommend selinexor plus dexamethasone or belantamab mafodotin monotherapy as treatment options for TCR MM [2]. Other alternatives may include conventional chemotherapy, salvage autologous stem cell transplantation (ASCT), or BCMA-directed bispecific antibody treatment [4,5,17–19]. The National Comprehensive Cancer Network (NCCN) guidelines were recently updated to include BCMA chimeric antigen receptor (CAR) T-cell therapy and teclistamab-cqyv as recommended options for patients with TCE/R MM who have received at least four lines of therapy [5]. These treatments have not been studied in comparative randomized controlled trials and have only recently been implemented in clinical practice; therefore, evidence of comparative effectiveness is sparse.

The lack of direct comparative studies evaluating novel treatments presents a challenge in making informed decisions regarding value assessment and treatment selection. In the absence of randomized controlled trials comparing interventions directly, indirect treatment comparisons serve as a valuable method to gather evidence on the relative efficacy of different therapeutic approaches [20,21]. In this analysis, we employed matching-adjusted indirect treatment comparisons (MAIC) to evaluate the comparative effectiveness of elranatamab in relation to teclistamab [22,23].

Methods

Data sources

Studies of interest were identified via a targeted literature review conducted in March 2021 and updated in May 2022. For elranatamab, individual patient data (IPD) from MagnetisMM-3 (cohort A (BCMA-naïve); N = 123) were used. Published summary data from MajesTEC-1 (N = 165) reported in Sidana et al. were used for PFS and OS for teclistamab [24]. The baseline characteristics and response outcome data for the MajesTEC-1 study were obtained from Moreau et al. [25]. Length of follow-up was 14.7 months for MagnetisMM-3 and 14.1 months for Moreau et al. and ∼23 months for Sidana et al.

Endpoints

The comparative effectiveness of elranatamab versus teclistamab was determined for objective response rate (ORR), ≥complete response (CR) rate, duration of response (DoR), PFS, and OS. Overall, endpoint definitions were similar between MagnetisMM-3 and MajesTEC-1. ORR was defined as the percentage of patients with a partial response or better and ≥ CR was defined as patients with either a complete or stringent CR. DoR was defined as first documentation of overall response that is confirmed until earliest date of progressive disease per IMWG criteria. PFS was defined in both studies as time from the date of initial dose until progressive disease per IMWG criteria, or death due to any cause. Both studies defined OS as time from date of first dose until death (all-cause) or study completion, whichever occurred first.

Identification of prognostic variables and effect modifiers

Univariate Cox proportional hazard models were used to identify potential prognostic variables based on the MagentisMM-3 data for the time-to-event outcomes. As a single-arm trial, assessment of effect modifiers in MagnetisMM-3 was not feasible via clinical data alone [23]. Additional prognostic variables and effect modifiers were identified through a systematic literature review conducted in 2021 in relapsed or refractory MM, a review of the recent clinical trials in TCE/R MM, and a review of recently published indirect treatment comparisons in triple-class exposed/refractory multiple myeloma (TCE/RMM). They were subsequently confirmed through clinical expert opinion. Of note, the systematic literature review did not include response-related endpoints, and the published indirect treatment comparisons we identified generally did not distinguish between prognostic variables and effect modifiers for response outcomes and survival outcomes; therefore, the same list of prognostic variables and effect modifiers used for PFS was also employed for the MAICs for response outcomes.

Matching-adjusted indirect comparison

To adjust for cross-trial differences, patients from MagnetisMM-3 were reweighted to match the selected key baseline characteristics of patients who received teclistamab in MajeTEC-1 as reported by Moreau et al. [25]. Weights were determined using a propensity score-type logistic regression via the method of moments [22], based on age, median time since diagnosis, International Staging System (ISS) disease stage, high-risk cytogenetics as defined by the presence of one of t(4;14), t(14;16), or del17p, extramedullary disease, number of prior lines of therapy, Eastern Cooperative Oncology Group performance status (ECOG PS), penta-drug exposed and penta-drug refractory status. Sex was included in the analysis for OS. Effective sample size (ESS) was assessed after conducting the MAIC. The ESS is the number of independent non-weighted individuals that would be required to give an estimate with the same precision as the weighted sample estimate [26]. The ESS is one key statistic which shows the statistical power of the MAIC analysis. A small ESS is indicative of large differences in patient populations between the comparators.

In MagnetisMM-3, certain adjusted baseline characteristics contained missing values. To potentially enhance the ESS, a sensitivity analysis was conducted. This involved imputing the missing values for the adjusted baseline characteristics of elranatamab using a random sample of observations from MagnetisMM-3.

Unanchored MAIC analyses were conducted in R studio 12.0 (R version 4.2.2) following the code provided in the National Institute for Health and Care Excellence (NICE) Decision Support Unit (DSU) 18 by Phillippo et al. [26]. In the MAICs, adjusted ORR, ≥CR, DoR, OS, and PFS after 14.7 months of follow-up for elranatamab were compared with teclistamab. For binary endpoints such as ORR, the results are presented in the form of rate differences, indicating the difference between elranatamab and teclistamab (in this case, the between-group difference in proportions, i.e. in the ORR or ≥ CR rates), accompanied by odds ratios along with their corresponding 95% confidence intervals (CIs).

To assess time-to-event endpoints, Kaplan–Meier’s curves from MajesTEC-1 were digitized following the methodology outlined by Guyot et al. [22]. Subsequently, a weighted (based on the weights assigned for the adjustment of baseline characteristics) Cox proportional hazards model was employed to estimate each hazard ratio (HR) and its respective 95% CI. Conclusions regarding significantly better or worse outcomes were drawn based on whether the 95% CI excluded 1 (for odds ratio/HR) or 0 (for rate difference). Numeric conclusions are based on the HR/odds ratio value.

Results

Compatibility assessment

Patient baseline characteristics from MajesTEC-1 and unweighted baseline characteristics of cohort A of MagnestisMM-3 are presented in Table 1. Overall, the inclusion and exclusion criteria of the trials were similar; however, MajesTEC-1 excluded patients with ECOG PS >1 whereas MagnetisMM-3 allowed enrollment of patients with an ECOG PS of 2. As such, patients with ECOG PS = 2 in the MagnetisMM-3 trial were removed from the analysis (resulting N = 116). In the MajesTEC-1 trial, extramedullary disease was defined as the presence of one or more extramedullary soft-tissue lesion. This definition was slightly different from the definition in the MagnetisMM-3 trial where it was defined as the presence of any plasmacytoma (extramedullary and/or paramedullary) with a soft-tissue component. Therefore, a new variable for extramedullary plasmacytomas was created for elranatamab using the MagnetisMM-3 IPD. This variable more closely follows the definition of extramedullary disease in MajesTEC-1 and was used in this MAIC study.

Table 1. Patient demographics and baseline characteristics.

	MagnestisMM-3 (cohort A; n = 116)	Majestec-1 (n = 165)
Age, median, years	68	64
≥75 years	18%	15%
Sex, male	55%	58%
Median time since diagnosis, years	6.2	6.0
High-risk cytogenetics	27%	23%
ISS risk stage
Stage I	30%	52%
Stage II	37%	35%
Stage III	20%	12%
ECOG status
0	39%	33%
1	61%	67%
Extramedullary disease	28%	17%
Number of prior lines, median	5	5
>3 lines of therapy	79%	74%
Refractory/exposure status
Triple-class refractory^a	97%	78%
Penta-drug refractory	41%	30%
Penta-drug exposed	71%	70%

ECOG: Eastern Cooperative Oncology Group; ISS: International Staging System.

^aTriple-class refractory status was not possible to adjust for in the MAIC due to the small size of the resulting ESS.

Between the two trials, median age, proportion of male patients, median time since diagnosis, and proportion with high cytogenetic risk were similar. MagnetisMM-3 had a higher proportion of patients with ISS stage III and a lower proportion of patients who were ISS stage I compared with MajesTEC-1. In addition, there was a higher proportion of patients with extramedullary disease and TCR or penta-drug refractory status in MagnestisMM-3 versus MajesTEC-1. After adjustment in the MAIC, the key prognostic variables and effect modifiers (i.e. age, sex (for OS endpoint only) median time since diagnosis, ISS stage, high-risk cytogenetics, extramedullary disease, number of prior lines of therapy, ECOG performance status, and penta-drug exposed and penta-drug refractory status) were comparable between patients who received elranatamab and those who received teclistamab.

Response outcomes

The results of the naïve, base case MAIC adjusted, and sensitivity analysis of response rates for elranatamab versus teclistamab are presented in Table 2. For the ORR and DoR analysis, the post-matching ESS for elranatamab was 75 in the base case and 89 in the sensitivity analysis. In the base case analysis, elranatamab was associated with a significantly higher ORR of 75.3% versus 63.0% with teclistamab, yielding a rate difference of 12.30 (95% CI 0.70–23.90). The odds ratio was 1.79 (95% CI 1.01–3.19) in favor of elranatamab. The results of the sensitivity analyses for ORR were similar to the base case results, with a rate difference of 12.44 (95% CI 1.28–23.60) and an odds ratio of 1.80 (95% CI 1.04–3.14) in favor of elranatamab over teclistamab in MajesTEC-1.

Table 2. ORR and ≥ CR for elranatamab versus teclistamab (naïve, base case adjusted, and sensitivity analysis results).

Analysis	Elranatamab	Teclistamab	ESS (n)	Rate difference (95% CI)	Odds ratio (95% CI)
ORR
Naïve comparison	62.1%	63.0%	116	−0.96 (–12.46, 10.54)	0.96 (0.59, 1.57)
Base case	75.3%	63.0%	75	12.30 (0.70, 23.90)	1.79 (1.01, 3.19)
Sensitivity analysis	75.5%	63.0%	89	12.44 (1.28, 23.60)	1.80 (1.04, 3.14)
≥CR rate
Naïve comparison	36.2%	39.4%	116	−3.19 (–14.68, 8.31)	0.87 (0.53, 1.43)
Base case	43.0%	39.4%	75	3.63 (–9.08, 16.33)	1.16 (0.69, 1.96)
Sensitivity analysis	43.1%	39.4%	89	3.70 (–8.50, 15.89)	1.16 (0.70, 1.93)

CI: confidence interval; ESS: effective sample size; ORR: objective response rate; CR: complete response.

Bold values denote statistical significance. Response outcome data for elranatamab and teclistamab from MagnetisMM-3 and MajesTEC-1 are based on a similar length of follow-up (14.7 and 14.1 months, respectively). n represents the ESS. ESS is the number of independent, non-weighted individuals needed for an estimate with the same precision as the weighted sample estimate. The ESS increased in the sensitivity analysis compared to the base case, due to the imputation of the missing values.

For ≥ CR, the base case adjusted rate was 43.0% with elranatamab versus 39.4% with teclistamab, yielding a rate difference of 3.63 (95% CI −9.08 to 16.33). The result of the sensitivity analysis was similar. Median DoR was not estimable with elranatamab after 14.7 months in MagnestisMM-3 and was 21.6 months in MajesTEC-1. In the MAIC, patients treated with elranatamab had numerically better DoR in both the base case (HR 0.64; 95% CI 0.33–1.23) and the sensitivity analysis (HR 0.77; 95% CI 0.42–1.34) (Figure 1).

Figure 1. DoR results for elranatamab in cohort A of MagnetisMM-3 versus teclistamab in MajesTEC-1. While DoR is only captured among patients with a response, the MAIC weighs all patients (regardless of response). CI: confidence interval; DoR: duration of response; HR: hazard ratio; NE: not estimable.

Survival outcomes

The unweighted and MAIC-weighted Kaplan–Meier’s curves for PFS are presented in Figure 2. In MagnetisMM-3 cohort A, the median PFS with elranatamab at 15 months was not estimable, whereas the median PFS for teclistamab was 11.3 months in MajesTEC-1. For PFS, the post-matching ESS for elranatamab was 75 in the base case and 89 in the sensitivity analysis. In the MAIC, elranatamab was associated with significantly longer PFS than teclistamab (HR 0.59; 95% CI 0.39–0.89). Results of the sensitivity analysis were similar to the base case, in which elranatamab offered significantly better PFS than teclistamab.

Figure 2. PFS results for elranatamab in cohort A of MagnetisMM-3 vs. teclistamab in MajesTEC-1. CI: confidence interval; HR: hazard ratio; NE: not estimable; PFS: progression-free survival.

Median OS with elranatamab in MagnestisMM-3 cohort A was not estimable at 15 months. In MajesTEC-1, teclistamab treatment yielded a median OS of 21.9 months. In the MAIC for OS, the ESSs were 73 and 87 for the base case and scenario analyses, respectively. Elranatamab was associated with numerically longer OS than teclistamab, as evidenced by a weighted OS HR of 0.66 (95% CI 0.42–1.03) (Figure 3). The sensitivity analysis yielded results similar to the base case, with HRs in favor of elranatamab.

Figure 3. OS results for elranatamab in cohort A of MagnetisMM-3 versus teclistamab in MajesTEC-1. CI: confidence interval; HR: hazard ratio; NE: not estimable; OS: overall survival.

Discussion

In the complex and rapidly evolving therapeutic landscape of TCE/R MM, the availability of comparative evidence regarding the relative effectiveness of available treatment options is essential to healthcare decision-making. Although randomized controlled trials are regarded as the gold standard for establishing efficacy, conducting head-to-head trials is not always feasible. In such circumstances, leveraging indirect treatment comparisons is a key approach to gain valuable insights. However, to ensure the robustness of these comparisons, it is imperative to employ rigorous statistical methodologies that adequately address potential baseline differences in patient populations.

In the current analysis, we conducted unanchored MAICs to explore the relative effectiveness of elranatamab from cohort A of the MagnetisMM-3 trial versus teclistamab in MajesTEC-1, which constitutes the first MAIC comparing these two novel BCMA- and CD3-directed antibodies. The analyses adjusted for age, median time since diagnosis, ISS disease stage, high-risk cytogenetics, extramedullary disease, number of prior lines of therapy, ECOG PS, penta-drug exposed and penta-drug refractory status, and sex (for OS). Across base case and sensitivity analyses, adjusted ORRs were significantly higher with elranatamab than teclistamab (base case: odds ratio 1.79; 95% CI 1.01–3.19). There was a favorable trend for other response outcomes with elranatamab as well. The adjusted ≥ CR rate was numerically higher for elranatamab than teclistamab (43% vs. 39%), though the results were not statistically significant.

Additionally, elranatamab was associated with a higher likelihood of maintained response as evidenced by a weighted HR for DoR of 0.64 versus teclistamab (Table 3). In contrast to PFS and OS, response rates for elranatamab and teclistamab were based on similar follow-up times (∼14 months). Elranatamab was associated with longer survival than teclistamab, with HRs in favor of elranatamab for PFS (HR: 0.59 [95% CI 0.39–0.89]; p = .01 and OS (HR: 0.66 [95% CI 0.42–1.03]; p = .07). According to the NICE DSU 18 guidance, a key consideration for unanchored comparisons that is relevant to this analysis is the assumption of homogeneity of outcomes on treatment [26]. In the present analysis, we aimed to limit bias due to heterogeneity of effects by including prognostic variables/effect modifiers, as identified in an SLR, other trials, and other MAIC analyses to mitigate the risk of bias from not including a prognostic variable.

Table 3. DoR for elranatamab versus teclistamab (naïve, base case adjusted, and sensitivity analysis results).

Analysis	ESS (n)	HR (95% CI)	p value
Naïve comparison	116	0.78 (0.45, 1.36)	.38
Base case	75	0.64 (0.33, 1.23)	.18
Sensitivity analysis	89	0.77 (0.42, 1.39)	.38

CI: confidence interval; DoR: duration of response; ESS: effective sample size; HR: hazard ratio.

While DoR is only captured among patients with a response, the MAIC weighs all patients (regardless of response). n represents the ESS. ESS is the number of independent, non-weighted individuals needed for an estimate with the same precision as the weighted sample estimate. The ESS increased in the sensitivity analysis compared to the base case, due to the imputation of the missing values.

When considering the MAIC-adjusted outcomes with elranatamab in context of outcomes with other novel BMCA-directed therapies, there is a trend to support elranatamab as a treatment of choice in TCE/R MM. The adjusted ORR achieved with elranatamab (75%) compares favorably to teclistamab (63%) in this analysis, as well as when comparing side-by-side with ORR results with belantamab mafodotin observed in DREAMM-2 (31%) in patients with TCE/R MM [27]. While approved CAR-T therapies have demonstrated high ORRs ranging from 57% to 94% in trials [28,29], their utilization can be challenging as the modality requires time for manufacturing as well as access to specialized care centers. Such obstacle can contributes to non-negligible attrition rates of approximately 10–15% for patients with planned CAR-T treatment seen in trials [28–30]. Of note, in a recent Swiss study, the manufacturing success rate was 88% and the median time to ide-cel infusion following lymphapheresis was up to 11 weeks [31]. Therefore, the need for effective off-the-shelf treatment options for patients with TCE/R MM remains high.

BCMA-directed treatments offer improved response rates and survival in comparison to existing standard therapies. Therefore, the population of patients with TCE/R MM receiving BCMA-directed treatment is expected to increase. The MagnetisMM-3 study included BCMA-naïve (cohort A) and BMCA-exposed patients (cohort B). However, since patients who received prior BMCA-directed therapy were excluded from MajesTEC-1, the present study specifically examined cohort A within the MagnetisMM-3 trial. Future investigations encompassing the entire population of MagnetisMM-3 and comparing treatment outcomes with elranatamab both to conventional and emerging therapies hold promise in shedding light on the relative efficacy of BCMA-directed treatments as the number of patients receiving such interventions continues to grow.

The consistency of the results of the base case and sensitivity analyses observed with elranatamab in the MAIC across outcomes contribute to confidence in our results. Moreover, all MAIC results were also aligned with the naïve comparisons with the exception of OS (naïve HR 1.05 [0.74, 1.50]), in which the HR marginally favored teclistamab. While there are a few potential explanations for why the naïve comparison may have slightly favored teclistamab, the most clinically plausible is that MagnetisMM-3 had a substantially higher proportion of patients who were TCR or penta-drug refractory relative to MajesTEC-1 (TCR MM 97% vs. 78%; penta-drug refractory 41% vs. 30%, respectively). Both characteristics are strongly associated with poorer survival [9,11]. In the MAIC, the adjusted OS and DoR point estimates all favored elranatamab, which is in line with the significantly better ORR and PFS observed in the analysis. Though the CIs for DoR and OS included unity, there appears to be a favorable trend overall for improvements in response and survival with elranatamab.

In addition to the consistency, the strength of this analysis stems from the robust methods for the indirect comparison and approach undertaken to consider prognostic variables and effect modifiers for adjustment, which included a systematic literature review, an analysis of clinical trials, and clinical expert opinion. We also conducted a sensitivity analysis that employed imputation via a random sample of observations. This method has the benefit of preserving the data distribution, imputing only values observed within the dataset, and avoiding bias through the assumption of missing completely at random [32].

Our study did have a few limitations which should be noted. The main limitation relates to the inherent challenge of MAIC in that it is only possible to adjust baseline variables that are mutually reported between trials, and therefore it cannot address the potential unmeasurable differences between the trials. Nevertheless, we conducted an extensive systematic literature review of previous clinical trials and indirect treatment comparison study, with a specific focus on prognostic variables and effect modifiers. This review was further supplemented and validated through clinical expert opinion. Therefore, the thoroughness of the adjusted key differences between the two trial populations is assured, and any potential bias stemming from unmeasurable differences is considered limited.

Out of the identified prognostic variables and effect modifiers, only creatinine clearance was not included in the MAIC of elranatamab versus teclistamab because the variable was not reported in the MajesTEC-1 data. The bias due to the excluded variable is regarded as limited, as this variable was not considered to be a key prognostic variable or effect modifier, based on the statistical testing, the systematic review, and clinical opinion.

This study utilized the aggregated data of teclistamab published in MajesTEC-1 [25]. Further research might be needed when more data are available for teclistamab.

Both trials were conducted during periods of elevated rates of COVID-19 and observed COVID-19 related deaths which could impact efficacy endpoints. However, specifically for ORR and PFS, not all COVID-19 deaths would necessarily affect the results as response and PFS censoring events (e.g. progression) may have occurred prior to the death leaving the ORR and length of PFS unaffected.

Lastly, we were unable to adjust for the notable difference in proportion of patients with TCR MM in MagnetisMM-3 (97%) versus MajesTEC-1 (78%) due to the resulting reduction in ESS; however, this approach is likely conservative as patients with TCR MM tend to have poorer outcomes than those who are simply TCE.

Conclusions

In the present MAIC, elranatamab exhibited clinically and statistically significant improvements in ORR and PFS compared with teclistamab. Furthermore, in both the base case and sensitivity analysis, elranatamab demonstrated numerically better DoR and OS. These findings collectively indicate that elranatamab represents a promising and efficacious therapeutic choice for patients with TCE/R MM.

Ethics statement

This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors.

Acknowledgements

The authors would like to acknowledge Elizabeth Hubscher for her technical writing support. IM and YH are employees of the Cytel, Inc. which received funding from Pfizer in connection with the development of this manuscript.

Disclosure statement

IM and YH are employees of Cytel, which received funding from Pfizer to conduct this study. TWLB has received honoraria for consulting/advisory boards from AbbVie, Agilix, Agios/Servier, Astellas, AstraZeneca, Beigene, BlueNote, BMS/Celgene, CareVive, Flatiron, Genentech, GSK, Lilly, Meter Health, Novartis, and Pfizer; speaking related honoraria from AbbVie, Agios, Astellas, BMS/Celgene, and Incyte; equity interest in Dosentrx (stock options in a privately-held company); royalties from UpToDate; research funding from the AbbVie, American Cancer Society, AstraZeneca, BMS, Deverra Therapeutics, Duke University, GSK, Jazz Pharmaceuticals, the Leukemia and Lymphoma Society, the National Institute of Nursing Research/National Institutes of Health, and Seattle Genetics. JC, HC, GN, DA, AS, and PH are employees of Pfizer and equity holder in Pfizer.

Data availability statement

Upon request, and subject to review, Pfizer will provide the data that support the findings of this study. Subject to certain criteria, conditions, and exceptions, Pfizer may also provide access to the related individual de-identified participant data. See https://www.pfizer.com/science/clinical-trials/trial-data-and-results for more information.

Additional information

Funding

This study was sponsored by Pfizer.