457P - Disparities in receipt of CDK4/6 inhibitors with endocrine therapy as therapy for hormone receptor-positive, HER2-negative metastatic breast cancer in the real-world setting

Background

This retrospective study, using real-world evidence (RWE), compared outcomes for patients receiving treatment for hormone receptor-positive (ER+), HER2-negative, metastatic breast cancer (MBC) with CDK4/6 inhibitors (CDK4/6i) in combination with endocrine therapy (ET) versus ET alone and explored disparities in use of CDK4/6i.

Methods

We used the nationwide electronic health record-derived Flatiron Health de-identified database to examine real-world impacts of CDK4/6i and ET. A total of 3,917 patients received CDK 4/6i+ET (n=2170) or ET alone (n=1747) in the first-line setting between February 2015, and November 2021. Characteristics of patients receiving CDK4/6i+ET versus ET alone were compared using statistical tests. Baseline characteristics were balanced using inverse probability weighting (IPW). Kaplan-Meier method and Cox proportional hazards were used to test the impact of CDK4/6 treatment on rwPFS and rwOS.

Results

Compared to patients receiving ET alone, those received CDK4/6i+ET were younger, more likely to have presented with de novo MBC (36% vs. 29%, p<0.001), had better performance status (50% vs. 40% patients with ECOG value 0, p=0.001), and more likely to have lower number of comorbidities (30% vs. 27% with at least 1 comorbidity, p=0.04). After IPW adjustment, CDK4/6i+ET treatment was associated with significantly longer median PFS compared to ET alone (27 vs 17 months; hazard ratio [HR]=0.61, p<0.001). Median OS was 52 months in the CDK4/6i+ET group and was 42 months with ET alone (HR=0.74, p<0.001).

Conclusions

RWE confirms the added PFS and OS benefit of adding CDK4/6i to endocrine therapy in patients with ER+, HER2-negative MBC. We found disparities in CDK4/6i use by age, stage at diagnosis, baseline Ecog value, and number of comorbidities. Future work is needed to improve access to this important class of drugs.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

This work/study was supported by American Cancer Society/Flatiron Health, grant number ”RWIA-21-123-01-RWIA”.

Disclosure

G. Kimmick: Financial Interests, Personal, Advisory Board: Eisai, Biotheranostics; Other, Personal, Advisory Board: Immunomedics, Seattle Genetics (dinner 4/6/19); Norvartis (dinner 10/17/19); Foundation Medicine (dinner 12/10/19); Other, Personal, Speaker, Consultant, Advisor: Genomic Health 2019; Agendia [MammaPrint] (dinner 2019); Other, Speaker’s Bureau: Eisai (2018); Resarch-To-Practice – Interview with Niel Love 11/19/2021; Financial Interests, Personal, Royalties: UpToDate, Springer; Financial Interests, Research Funding: Bionovo, PUMA, Roche; Financial Interests, Institutional, Funding: Abbott Laboratories, AbbVie, Abraxis BioScience, Alphavax, AstraZeneca, Bionovo, BiPar Sciences, Bristol Myers Squibb, Celldex Therapeutics, Celsion, EMD Serono, Exelixis, Genentech, GSK (CARG Trial), Incyte Corporation; Other, Research Grant: Novartis (CAREB 2019) Pfizer (BQual-D 2020-2021) + (Needs Assessment 2021); Other, Member: Editorial Boards JNCI – 2021, 2022 Journal of Geriatric Oncology Breast Cancer Research and Treatment - past. R. Anderson: Financial Interests, Personal, Stocks/Shares: Pfizer. All other authors have declared no conflicts of interest.