Racial differences in outcomes of patients with relapsed/refractory multiple myeloma treated with selinexor.

Authors

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Craig Cole

Michigan State University - Karmanos Cancer Institute, McLaren Greater Lansing, Michigan State University College of Human Medicine, East Lansing, MI

Craig Cole , Anne Maria Opalikhin , Matthew McCartney , Caroline Heideman , Swetha Pentapati , Ling Wang

Organizations

Michigan State University - Karmanos Cancer Institute, McLaren Greater Lansing, Michigan State University College of Human Medicine, East Lansing, MI, Michigan State University College of Human Medicine, Grand Rapids, MI, McLaren Greater Lansing, Michigan State University - College of Osteopathic Medicine, Lansing, MI, Division of Occupational and Environmental Medicine, College of Human Medicine, Michigan State University, East Lansing, MI

Research Funding

No funding received
None.

Background: Multiple Myeloma (MM) is the 2nd most common hematologic malignancy in the US, though survival in patients with MM has improved over the past decade. Survival improvements in African Americans (AAs) have been smaller, which may be due to disparity in access to therapies. There are also key differences in MM biology between races, including higher rates of IgA disease and genetics. Given underrepresentation of minorities in clinical trials, we analyzed whether outcomes were similar between AAs and other races in the phase 2 STORM trial (NCT02336815) of selinexor. Selinexor, an oral, first-in-class selective inhibitor of nuclear export via exportin 1, has proven efficacy for refractory MM. To our knowledge, this is the first race subgroup analysis of selinexor in any clinical trial. Methods: Pts from STORM who received study drug (N = 202) were included. Pts with heavily pretreated MM, including triple-class and penta- refractory MM refractory to the last line of therapy were given selinexor (80mg) + dexamethasone (20mg) twice weekly. We conducted a retrospective racial subgroup analysis. Cox proportional modeling was used to determine the hazard ratio (HR) for MM relapse between races controlling for covariates. Results: AAs represented 17% of pts (35 AAs, 148 White, 2 Asian, 11 other and 6 missing). AAs were younger compared to other races (median age 60.7 vs 65.3) with more females (74.3% vs 40.7%). Cytogenetic abnormalities and R-ISS staging were similar between races. AAs had a median progression free survival (PFS) of 6.5 mos (95% CI 4.7, NR) compared with 3.7 mos (95% CI 2.8, 4.6; p = 0.035) for other races. Overall response rate (ORR) was 25.7% (95% CI 12.5, 43.3) in AA pts vs 23.4% [17.2, 30.5] in other races), clinical benefit rate (37.1% [21.5, 55.1] vs 35.9% [28.7, 43.7]), median duration of response (5.6 mos [2.1, NR] vs 5.3 [3.6, NR]), median duration of treatment (9 wks [IQR 3-22 wks] vs 8 wks [4-16 wks]), and mean dose intensity (117.9 mg/wks [STD 35.1] vs 117.1 [34.7]) were similar between grps. Rates of Adverse Events (AEs) ≥ grade 3 (94.3% vs 95.8%), and AE-related dose reductions (45.7% vs 54.5%), discontinuations (22.9% vs 30.5%), and deaths (5.7% vs 10.8%) were also similar. The adjusted HR for MM relapse in AAs was 0.45 (95% CI 0.22, 0.92; p = 0.028) after controlling for gender, age and prior therapy. Conclusions: This subgroup analysis showed that compared with other races, AAs pts were younger and included a greater percentage of women. Although ORRs were similar, AAs had a longer PFS compared with other races after adjusting for covariates. Despite small sample size, the differences were statistically significant. It is unclear if the better PFS reflects a different biology, pharmacology of selinexor or both. Dose adjustments and tolerability were relatively comparable. These results could assist in the placement of selinexor in the treatment sequence of relapsed refractory MM for AAs.

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Abstract Details

Meeting

2023 ASCO Annual Meeting

Session Type

Publication Only

Session Title

Publication Only: Hematologic Malignancies—Plasma Cell Dyscrasia

Track

Hematologic Malignancies

Sub Track

Multiple Myeloma

Citation

J Clin Oncol 41, 2023 (suppl 16; abstr e20016)

DOI

10.1200/JCO.2023.41.16_suppl.e20016

Abstract #

e20016

Abstract Disclosures