HR+, HER2- Metastatic Breast Cancer
ET Advancements
Scientific advancements in endocrine therapy (ET) seek to maximize antagonizing the estrogen receptor (ER) pathway in ER-positive (ER+), human epidermal growth factor receptor 2–negative (HER2-) advanced breast cancer.1-3
AIs block estrogen production by inhibiting aromatase. SERMs block ER transcription by competitively inhibiting the binding of estrogen to ER. SERDs block ER translocation to the nucleus, and upon binding to ER, results in degradation of the SERD-ER complex. PROTACs bind to both ER and the E3 ubiquitin ligase, resulting in ubiquitination and degradation. CERANs block both transcriptional activation domains of ER. SERCAs inhibit ER gene transcription by binding to the C530 cysteine residue on ER.3
- Sustained high, dose-dependent exposure supporting oral options1-3
- Potent and highly specific binding to both wildtype and mutated ER1,3
- Maintain activity in aromatase inhibitor (AI)-resistant and ESR1-mutant models1-3
- Selective estrogen receptor degraders (SERDs) and proteolysis targeting chimeras (PROTACs) have potent ER degradation and suppression of ER-dependent signaling1-3
As healthcare providers, it is important to stay updated on next-generation oral ETs and how they may be used as monotherapy or in combination with targeted therapies. For more information on advancements in novel ETs and ongoing clinical trials, please see additional resources below.
References
- Llyod MR, et al. Ther Adv Med Oncol. 2022;14:17588359221113694.
- Mittal A, et al. Cancers (Basel). 2023;15(7):2015.
- Patel R, et al. NPJ Breast Cancer. 2023;9(20). doi: 10.1038/s41523-023-00523-4
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