# Optimizing Antiemetic Strategies Across Phases of Chemotherapy-Induced Nausea and Vomiting: Real-World Evidence in Breast Cancer

**Authors:** Akif Doğan, Hande Nur Erölmez, Goncagül Akdağ, Sedat Yıldırım, Özlem Nuray Sever

PMC · DOI: 10.3390/curroncol33020078 · 2026-01-28

## TL;DR

This study finds that different anti-nausea drugs work best at different times after chemotherapy, which could help improve patient comfort during breast cancer treatment.

## Contribution

The study provides real-world evidence of phase-specific antiemetic effectiveness in a homogeneous breast cancer patient cohort.

## Key findings

- Fosaprepitant was more effective in controlling acute-phase nausea and vomiting.
- Aprepitant provided better protection in the delayed and overall phases of chemotherapy-induced nausea and vomiting.

## Abstract

Nausea and vomiting caused by chemotherapy are among the most troublesome side effects for cancer patients and can significantly reduce quality of life and willingness to continue treatment. Several medications are used to prevent these symptoms, but their effectiveness may vary depending on the timing after chemotherapy. In this study, we compared two commonly used anti-nausea drugs in women with breast cancer receiving intensive chemotherapy. We found that one drug was more effective in preventing nausea and vomiting shortly after chemotherapy, while the other provided better protection several days later. These findings suggest that choosing anti-nausea treatment according to the timing of symptoms may improve patient comfort and treatment experience in routine clinical practice.

Background: Chemotherapy-induced nausea and vomiting (CINV) remains one of the significant challenges in oncology despite guideline-based prophylaxis, particularly in patients receiving highly emetogenic chemotherapy (HEC). While neurokinin-1 (NK-1) receptor antagonists are established as a key component of standard antiemetic regimens, evidence of their phase-specific effectiveness in real-world, homogeneous patient populations remains limited. This study aimed to determine which antiemetic regimen provides optimal control in each CINV phase to support a tailored prophylactic approach. Methods: This single-center, retrospective, real-world study included 260 female patients with stage II–III breast cancer receiving anthracycline–cyclophosphamide-based HEC. All patients had similar demographic and clinical characteristics, forming a relatively homogeneous cohort. Each received a triple antiemetic regimen consisting of a 5-HT3 receptor antagonist, dexamethasone, and an NK-1 receptor antagonist (either a single-dose intravenous fosaprepitant or a 3-day oral aprepitant). Complete response (no vomiting and no rescue therapy) and no-vomiting rates were assessed in the acute (0–24 h), delayed (24–120 h), and overall (0–120 h) phases. Results: In this relatively homogeneous cohort of high-risk patients, fosaprepitant-based prophylaxis achieved better symptom control during the acute phase, whereas aprepitant-based regimens were more effective in the delayed and overall phases. These findings suggest phase-specific variations in antiemetic effectiveness that reflect pharmacokinetic and administration-route differences rather than population heterogeneity. Conclusions: This real-world analysis demonstrates that antiemetic effectiveness varies by CINV phase, even within a relatively homogeneous, high-risk patient cohort. The results highlight the importance of phase-tailored prophylactic strategies to optimize symptom control and improve patient quality of life in highly emetogenic chemotherapy settings.

## Linked entities

- **Chemicals:** dexamethasone (PubChem CID 5743), fosaprepitant (PubChem CID 135413538), aprepitant (PubChem CID 135413536)
- **Diseases:** breast cancer (MONDO:0004989)

## Full-text entities

- **Genes:** TAC1 (tachykinin precursor 1) [NCBI Gene 6863] {aka Hs.2563, NK2, NKNA, NPK, TAC2}, TACR1 (tachykinin receptor 1) [NCBI Gene 6869] {aka NK1R, NKIR, SPR, TAC1R}, MAT1A (methionine adenosyltransferase 1A) [NCBI Gene 4143] {aka MAT, MATA1, SAMS, SAMS1}, CSF3 (colony stimulating factor 3) [NCBI Gene 1440] {aka C17orf33, CSF3OS, GCSF}, NR4A1 (nuclear receptor subfamily 4 group A member 1) [NCBI Gene 3164] {aka GFRP1, HMR, N10, NAK-1, NGFIB, NP10}, ERBB2 (erb-b2 receptor tyrosine kinase 2) [NCBI Gene 2064] {aka CD340, HER-2, HER-2/neu, HER2, MLN 19, MLN-19}
- **Diseases:** stage III disease (MESH:D007676), Hyperemesis Gravidarum (MESH:D006939), toxicity (MESH:D064420), Lobular Carcinoma (MESH:D018275), Breast Cancer (MESH:D001943), Ductal Carcinoma (MESH:D044584), CINV (MESH:D020250), cognitive impairment (MESH:D003072), injury to (MESH:D014947), Cancer (MESH:D009369), motion sickness (MESH:D009041), Nausea (MESH:D009325), HEC (MESH:D000084202), Anti (MESH:D006679), NV (MESH:D014839)
- **Chemicals:** AC (-), olanzapine (MESH:D000077152), Doxorubicin (MESH:D004317), palonosetron (MESH:D000077924), Fosaprepitant (MESH:C579707), dexamethasone (MESH:D003907), ddAC (MESH:C053645), OP (MESH:C572232), AP (MESH:D000667), DP (MESH:D004176), alcohol (MESH:D000438), serotonin (MESH:D012701), ondansetron (MESH:D017294), Anthracycline (MESH:D018943), Aprepitant (MESH:D000077608), Cyclophosphamide (MESH:D003520)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12939676/full.md

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Source: https://tomesphere.com/paper/PMC12939676