Triple-negative breast cancer accounts for a minority of breast cancer diagnoses but a disproportionate share of early deaths, and the absence of oestrogen, progesterone and HER2 receptors removes the three targets on which the rest of the discipline is built. Cytotoxic chemotherapy therefore remains the backbone of treatment, and its ceiling is set less by tumour resistance than by what the patient can tolerate. Nanoscale carriers were proposed as the escape from that constraint, on the argument that leaky tumour vasculature would concentrate a circulating particle where free drug could not go. Two decades of work have complicated that argument considerably. This review synthesises the preclinical and clinical evidence for lipid, polymeric, inorganic and cell-derived carriers in triple-negative disease, the ligand and stimulus-responsive strategies developed to compensate for the loss of hormone-receptor targeting, and the record of what has actually reached patients. The pattern that emerges from the clinical data is consistent and is not the one the preclinical literature predicts: every nanoformulation that has succeeded in breast cancer did so by reshaping pharmacokinetics, solubilisation or toxicity rather than by concentrating drug in tumour tissue, and the formulations designed explicitly for tumour targeting have failed in randomised comparison. The review argues that the productive future for nanomedicine in this disease lies in three directions that do not depend on passive accumulation: carriage of cargo that cannot otherwise be administered, particularly nucleic acids and immunomodulators; exploitation of the active transport and dose-threshold behaviour that governs particle entry into tumours; and prospective stratification of patients by measured particle deposition rather than by tumour histology alone.