Metastatic breast cancer (mBC) remains incurable despite significant advances in systemic therapy, including the incorporation of antibody–drug conjugates (ADCs) into routine practice. ADCs such as trastuzumab deruxtecan (T-DXd; Enhertu®; Daiichi Sankyo and AstraZeneca) and sacituzumab govitecan (SG; Trodelvy®; Gilead Sciences) have demonstrated superior efficacy over chemotherapy in both HER2-low and triple-negative breast cancer (TNBC) [1][2][3][4][5] Both agents employ potent topoisomerase I inhibitor payloads—deruxtecan (DXd) for trastuzumab deruxtecan and SN-38 (7-ethyl-10-hydroxycamptothecin), an active metabolite of irinotecan, for sacituzumab govitecan—delivered via antibodies targeting distinct cell surface antigens (HER2 for T-DXd and Trop-2 for SG) [1][2][3][5][6][7]
Trastuzumab deruxtecan binds to HER2-expressing tumor cells, including those with low or heterogeneous HER2 expression, and is internalized and enzymatically cleaved, releasing its cytotoxic payload. This membrane-permeable payload can diffuse into neighboring tumor cells, producing a pronounced bystander effect that is particularly important in the context of low HER2 expression. [8]
In contrast, Trop-2—the target of sacituzumab govitecan—is highly expressed in the majority of TNBCs, and while sacituzumab govitecan also demonstrates a bystander effect, its clinical significance may differ due to the typically more homogeneous expression of the target [2][9].
Although their primary antitumor effect derives from the released cytotoxic payload, both ADCs possess high drug-to-antibody ratios (~8:1), are internalized and processed intracellularly, and can mediate antibody-dependent cellular cytotoxicity [5][9][10]. These advances, together with the introduction of PARP inhibitors and immunotherapy, have dramatically expanded and complicated treatment sequencing in advanced breast cancer.
Understanding mechanisms of resistance—ranging from antigen downregulation or alteration (impacting payload delivery) to payload-specific resistance via changes in signaling pathways or drug efflux—is increasingly critical for optimizing ADC use and sequencing in clinical practice [11][12]. However, there is a lack of evidence and established guidelines to inform the optimal sequencing of FDA-approved ADCs for individual patients. Hence, as the field rapidly advances with the development of new ADCs, a major unmet need has emerged: clinical trial data and algorithms are insufficient to guide subsequent therapy choices—such as switching from one ADC to another ADC with a different target or payload, using chemotherapy, or combining with immune checkpoint inhibitors—after resistance to an initial ADC. With cross-resistance between agents increasingly recognized in real-world settings [2][3], the need for precision tools to guide treatment selection and manage emerging toxicities is more pressing than ever. [12[13][14]
Sequencing and Cross-Resistance: Clinical Evidence
Although phase 3 randomized controlled trials have shown clear survival benefits for ADCs in advanced breast cancer compared to chemotherapy (pooled HR for OS: 0.66, 95% CI 0.50–0.87; HR for PFS: 0.45, 95% CI 0.33–0.63) [2], the majority of pivotal studies have excluded patients previously treated with another ADC. As a result, prospective sequencing data are lacking, and clinicians rely on real-world evidence to guide therapy after ADC progression. [15][16[17]
A recent multicenter retrospective cohort demonstrated that 53% of patients exhibited cross-resistance to a second ADC; real-world PFS was generally shorter with sequential ADC use, and PTEN loss was associated with resistance. Another single-center study of 82 patients receiving at least two sequential anti-HER2 ADCs found the T-DM1 → T-DXd sequence yielded the longest median total PFS (24.07 months), with the benefit primarily in HER2-positive disease. In contrast, HER2-low patients derived limited benefit from sequential ADCs, with PFS2 of only 3–4 months and objective responses <10%. These data highlight a ‘diminishing returns’ phenomenon and the urgent need for novel strategies to overcome resistance. However, the study authors conclude that further investigation is needed into the optimal ADC sequence and underscore the need for predictive biomarkers to optimize treatment selection for each patient with mBC. [15]
Digital Patient Organoid (DPO) Platform: Toward Precision Sequencing
Given the lack of validated tools to guide post-ADC therapy, a current investigational approach involves using digital patient organoid (DPO) models. In patients with mBC who have received or progressed on ADCs, the DPO platform was capable of deliniating between target- versus payload-based resistance, showing promise in predicting treatment responses and differentiating resistance mechanisms, providing a foundation for rational, individualized treatment selection in the post-ADC setting. This approach could help circumvent cross-resistance and optimize sequencing, although prospective validation is needed. [18][19]
Efficacy and Safety in Early and Locally Advanced Disease
A Meta-analysis of pooled data from nine randomized trials (n = 2,021; mean age 50.7±13.7) in early-stage HER2-positive breast cancer found that ADC-based neoadjuvant regimens without concurrent chemotherapy achieved similar pathologic complete response (pCR) rates comparable to those of standard chemotherapy, while substantially reducing grade ≥3 adverse events (OR 0.30, 95% CI 0.11–0.84) and without increasing treatment discontinuation (OR 1.10, 95% CI 0.39–3.12; I² = 85.8%), independent of platinum use.[20]
These findings suggest that ADCs may enable safe and effective chemotherapy de-escalation, although phase 3 trials with mature survival endpoints are required to confirm this.[20]
Combination Strategies and Innovative Agents
Outcomes from the FUTURE 2.0 trial (NCT05749588), a Phase 2, single-center platform study designed to evaluate the efficacy of precision, biomarker-driven therapies in patients with refractory, metastatic triple-negative breast cancer (TNBC), suggest that combining tizetatug rezetecan (SHR-A1921)—a Trop2-targeted ADC developed by Jiangsu Hengrui Pharma in collaboration with Suzhou Suncadia Biopharmaceuticals-with bevacizumab (Avastin®; Genentech/Roche) may further improve outcomes, especially in basal-like immune-suppressed TNBC, a disease associated with a poor prognosis. Rather than employing uniform chemotherapy, the FUTURE 2.0 trial assigns patients to targeted or immunotherapeutic regimens informed by molecular subtyping and genomic profiling of their tumors.
This adaptive platform enables the classification of TNBC into specific molecular subtypes, selection of therapies tailored to identified genetic vulnerabilities, and flexible incorporation of emerging targeted agents as new arms within the study. [21]
Tizetatug rezetecan plus bevacizumab achieved an ORR of 85.0% versus 40.0% for ADC monotherapy, and median PFS was doubled (9.2 vs 4.6 months; HR 0.47, P=0.001). These findings provide preliminary evidence for synergy between bevacizumab and ADCs—including tizetatug rezetecan—supporting a promising therapeutic strategy for basal-like, immune-suppressed TNBC. However, ongoing phase 3 trials will be essential to confirm the efficacy and safety of this combination approach.[21]
More innovation
Bispecific ADCs represent a promising frontier in targeted oncology, aiming to enhance antitumor efficacy and overcome some limitations of monospecific ADCs. One of these novel investigational agents, IBI3017, an innovative, first-in-class bispecific ADC developed by Innovent Biologics (Suzhou) Co., is designed to simultaneously target both Trop2 and B7H3—two tumor-associated antigens frequently co-expressed in a range of solid tumors, including breast cancer. [22]
By recognizing both antigens, IBI3017 is engineered to maximize tumor cell targeting while reducing off-tumor toxicity. The ADC is conjugated to a novel topoisomerase I inhibitor payload (NT1) with a high, homogeneous drug-to-antibody ratio (DAR 8). In preclinical studies, IBI3017 demonstrated robust antitumor activity in cell-derived xenograft (CDX) models with variable Trop2 and B7H3 expression, outperforming parental monospecific ADCs against either target alone. The bispecific design also confers an improved bystander killing effect and greater selectivity for tumors with dual antigen expression, potentially minimizing toxicity to normal tissues where only one antigen may be present. IBI3017’s promising safety profile and potent efficacy in preclinical models support its ongoing clinical development as a next-generation ADC with broad application potential across multiple solid tumor types.[22]
Safety Considerations and Management in Practice
Oral mucositis is a notable toxicity of ADCs, with significant long-term systemic complications. Oral mucositis is a debilitating adverse event that affects patients, impacts their nutritional intake, health-related Quality of Life (hrQoL), and treatment adherence, emphasizing the need for evidence-based nursing interventions.
In a large real-world cohort, oral mucositis was associated with increased risks of volume depletion, respiratory infections, circulatory diseases, and mortality, even after propensity score matching (PSM) [20]. These findings underscore the importance of proactive toxicity prevention and management strategies, including patient education, risk-stratified prevention, and dental integration. Study results presented at the 2025 ESMO Congress in Berlin, Germany (October 17 – 21, 2025), showed that implementing a standardized, multidisciplinary nursing pathway reduced the incidence and severity of oral mucositis, leading to better patient outcomes and uninterrupted cancer treatment. [23][24]
Immunotherapy and ADCs: Frontline Applications
Results from the global, open-label, randomized Phase 3 ASCENT-04/KEYNOTE-D19 trial (NCT05382286) demonstrated that sacituzumab govitecan plus pembrolizumab significantly improved progression-free survival (PFS) compared to pembrolizumab and chemotherapy in patients with inoperable (unresectable) locally advanced or metastatic triple-negative breast cancer (mTNBC) whose tumors express PD-L1 CPS ≥10 metastatic TNBC (median PFS: 11.2 vs 7.8 months; HR 0.65), with higher ORR (60% vs 53%) and more durable responses, supporting ADC-immunotherapy combinations as a first-line option.[25]
Oncotype DX recurrence score–guided versus clinician-guided treatment
In early-stage HR+/HER2- breast cancer, selection of adjuvant chemotherapy based on the 21-gene Recurrence Score (Oncotype DX RS) was associated with improved survival compared to decisions guided solely by clinician assessment, with particularly pronounced benefits observed in patients over 55 years of age and in Black patients. These findings indicate that reliance on clinicopathologic features alone may not accurately identify biologic risk, potentially resulting in unnecessary chemotherapy and associated toxicities for patients with low genomic risk.[26][27]
In contrast, RS-guided pathways utilize genomic profiling to better stratify risk, often superseding traditional clinical variables and reducing overtreatment. Clinician-guided approaches, which base chemotherapy recommendations exclusively on tumor size, grade, nodal status, and other clinical factors, frequently lead to overestimation of recurrence risk and unnecessary chemotherapy administration. Notably, the use of the Recurrence Score changes treatment recommendations in approximately 25% of cases, demonstrating its value in refining patient selection for chemotherapy. While traditional decision-making in breast oncology has relied on clinical and pathologic factors, these results underscore the importance of integrating genomic risk assessment to optimize adjuvant therapy and minimize overtreatment in this population.[26][27]
Discussion and Future Directions
Collectively, ADCs have established themselves as a more effective alternative to chemotherapy in pretreated HER2-low, TNBC, and HR+/HER2- MBC, conferring earlier and more sustained anti-tumor activity with manageable toxicity profiles [2,4,12]. However, cross-resistance, especially with sequential ADC use, remains a critical barrier, particularly in HER2-low disease. Platforms such as DPOs, rational combination strategies, and next-generation bispecific ADCs are promising avenues to address these challenges. Standardized sequencing trials, robust biomarker strategies, and real-world implementation studies are essential to fully realize the potential of ADCs and tailor therapy for individual patients.
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Clinical trials
DS-8201a in Pre-treated HER2 Breast Cancer That Cannot be Surgically Removed or Has Spread [DESTINY-Breast02] – ClinicalTrials.gov ID NCT03523585
Trastuzumab Deruxtecan (DS-8201a) Versus Investigator’s Choice for HER2-low Breast Cancer That Has Spread or Cannot be Surgically Removed [DESTINY-Breast04] – ClinicalTrials.gov ID NCT03734029
Trial of Sacituzumab Govitecan in Participants With Refractory/Relapsed Metastatic Triple-Negative Breast Cancer (TNBC) (ASCENT) – ClinicalTrials.gov ID NCT02574455
Study of Sacituzumab Govitecan-hziy and Pembrolizumab Versus Treatment of Physician’s Choice and Pembrolizumab in Patients With Previously Untreated, Locally Advanced Inoperable or Metastatic Triple-Negative Breast Cancer (ASCENT-04) – ClinicalTrials.gov ID NCT05382286
Study of Pembrolizumab (MK-3475) Plus Chemotherapy vs. Placebo Plus Chemotherapy for Previously Untreated Locally Recurrent Inoperable or Metastatic Triple Negative Breast Cancer (MK-3475-355/KEYNOTE-355) – ClinicalTrials.gov ID NCT02819518
FUSCC Refractory TNBC Platform Study (FUTURE2.0) – ClinicalTrials.gov ID NCT05749588
SHR-A1811 Plus Pertuzumab as Neoadjuvant Therapy for Early or Locally Advanced HR-Positive HER2-Positive Breast Cancer: A Prospective, Open-Label, Phase II Study – ClinicalTrials.gov ID NCT07307287
A Multicenter Phase III Clinical Study and Translational Research on Adaptive Neoadjuvant Therapy of De-escalation and Escalation for HER2-Positive Breast Cancer Based on Multi-Omics Response Evaluation Model – ClinicalTrials.gov ID NCT07239271
A Study of BL-M07D1 in Patients With a Variety of Solid Tumors Including Locally Advanced or Metastatic HER2-positive/Low-expressing Urinary and Gastrointestinal Tumors – ClinicalTrials.gov ID NCT06031584
Study of Olaparib Plus Pembrolizumab Versus Chemotherapy Plus Pembrolizumab After Induction With First-Line Chemotherapy Plus Pembrolizumab in Triple Negative Breast Cancer (TNBC) (MK-7339-009/KEYLYNK-009) – ClinicalTrials.gov ID NCT04191135
Highlights of Prescribing Information
Trastuzumab deruxtecan (T-DXd; Enhertu®; Daiichi Sankyo and AstraZeneca)[Prescribing Information]
Sacituzumab govitecan (SG; Trodelvy®; Gilead Sciences)[Prescribing Information]
Bevacizumab (Avastin®; Genentech/Roche)[Prescribing Information]
Reference
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Featured Image: General views at the American Society for Clinical Oncology (ASCO) annual meeting. Courtesy: © 2015 – 2026 ASCO/Max Gersh. Used with permission.
DOI
