Objective — to evaluate the sensitivity of multiple primary bilateral synchronous breast cancer (BC) to neoadjuvant drug therapy. Subject and methods. The investigation enrolled 14 patients with multiple primary synchronous BC who received drug treatment at the first stage of combined treatment. Eleven patients underwent 6 to 8 cycles of neoadjuvant polychemotherapy (NAPCT); targeted therapy drugs were simultaneously added to taxane-containing regimens in 2 patients with HER2-positive tumors. Results. The mean age of the patients was 44.3±13.8 years, which was substantially younger than that of the total population of BC patients. The histological pattern of tumor nodules in both mammary glands was the same in 11 patients and the tumors in the mammary glands were different in 3 patients. Therapeutic pathomorphism (TP) was absent in 2 (8.3%) cases; it was poorly expressed (grade 1) in 4 (12.5%) cases, grades 2, 3, and 4 were seen in 7 (29.2%), 6 (16.7%), and 9 (33.3%), respectively. None of the 7 patients with the edematous-infiltrative form of BC achieved grade 4 TP despite its different biological types. The immunohistochemical study showed that edematous infiltrative BC was presented as a luminal type in 5 cases, as a triple-negative one in 1 case, and as a luminal type B, HER2-positive in 1 case. Nine of the 28 cases achieved complete TP in the primary tumor, but only one patient had it in both tumors with different biological types. Conclusion. In most cases, the reaction of synchronous tumors to NAPCT did not coincide in the same patient. A complete pathomorphism was most common in the triple negative type (33.3±16.6%), which corresponds to the current ideas on the behavior of this aggressive biological type of BC. The authors consider it necessary to further study the reaction of synchronous tumors to neoadjuvant therapy and to accumulate clinical materials for the reliable confirmation of the findings, which is important for the development of an adequate treatment policy and theoretical knowledge of the pathogenesis of drug sensitivity/resistance of breast tumors.