Application of azetidine compound in preparation of medicine for preventing and treating triple-negative breast cancer

Abstract

The invention discloses application of an azetidine compound in preparation of a medicine for preventing and treating triple-negative breast cancer, and belongs to the technical field of biological medicine. By adopting an international common triple-negative breast cancer modeling method, the scheme shows that the compound can effectively inhibit the tumor growth state of nude mouse triple-negative breast cancer, inhibit STAT3 705 site tyrosine phosphorylation and induce tumor cells to generate G2-M phase arrest and apoptosis, and has remarkable prevention and treatment effects on triple-negative breast cancer; the compound is expected to become a novel medicine for treating triple-negative breast cancer.

Description

Technical Field

[0001] The present invention belongs to the technical field of biomedicine, and particularly relates to the application of azetidine compounds in the preparation of drugs for preventing and treating triple-negative breast cancer. Background Art

[0002] Globally, breast cancer accounts for approximately one-third of female cancers, and the mortality-to-incidence ratio is about 15%. In recent years, the incidence and mortality of female breast cancer have shown an upward trend. Statistical data in 2020 showed that its mortality rate ranked first among various malignant tumors in women. In 2022, approximately 280,000 new breast cancer patients were added abroad, of which 15% were triple-negative breast cancer. The probability of recurrence within 5 years for TNBC patients who have undergone surgery is approximately 30%-40%. In particular, patients with a low complete pathologic remission rate after neoadjuvant systemic therapy are more likely to relapse (about 50%). There are many factors affecting the incidence of breast cancer, such as non-modifiable risk factors like family inheritance and gene alterations (such as BRCA1 gene mutations, accounting for 11%-19% of TNBC), and early screening is recommended for all. The peak age of breast cancer incidence in Chinese nationals is about 45-54 years old. The Guidelines for the Diagnosis and Treatment of Breast Cancer of the Chinese Anti-Cancer Association (2024 Edition) recommend that the starting age for breast cancer screening in the general-risk population is 40 years old, and for high-risk populations, it is advanced to before 40 years old. Early detection, early diagnosis, and individualized treatment, regardless of the cause of breast cancer, are the keys to improving the prognosis and survival of breast cancer.

[0003] Currently, surgery and radiotherapy remain the primary choices for local treatment of triple-negative breast cancer patients. The surgical methods mainly include breast conserving surgery (BCS) and mastectomy (MRM). In the selection of surgical methods, the prognosis of breast conserving surgery is not necessarily worse than that of mastectomy, and at the same time, patients' acceptance of breast conserving surgery is also higher. The combination of surgery and radiotherapy also increases survival benefits. Although patients benefit more after surgery, there are still certain limitations. Since the disease course of TNBC patients is relatively advanced when they are diagnosed, most patients may not be able to meet the surgical indications, so it is particularly important to increase the surgical resection rate in the early stage.

[0004] For systemic treatment, there are various methods. 1. Chemotherapy. From the perspective of clinical treatment methods, chemotherapy is still the mainstay of current systemic treatment for TNBC. The drugs in common chemotherapy regimens are mostly anthracyclines, taxanes, platinum drugs, etc. According to the relative timing of chemotherapy and local treatment, it can be divided into neoadjuvant chemotherapy and adjuvant chemotherapy. 2. Immunotherapy. Immunotherapy can be divided into active immunotherapy and passive immunotherapy. Active immunization can be achieved through checkpoint blockade, tumor vaccines, cancer-testis antigens, etc. Atezolizumab, an immunotherapy drug that inhibits tumors based on the principle of immune checkpoint blockade through PD-1 / PD-L1, is the world's first immunotherapy drug for TNBC. Passive immunotherapy can be achieved through the principles of chimeric antigen receptor (CAR) T cell therapy and cytokine-induced killer (CIK) cell therapy. CAR-T therapy uses genetic engineering techniques to add a chimeric receptor to T cells that can recognize tumor cells and simultaneously activate T cells to kill tumor cells, turning T cells into CAR-T cells to target and kill tumor cells. 3. Targeted therapy. Currently, most TNBC targeted drugs have entered clinical trials, including poly ADP-ribose polymerase (PARP) inhibitors, epidermal growth factor receptor (EGFR) signaling pathway inhibitors, androgen receptor (AR) antagonists, PI3K-Akt-mTOR pathway inhibitors, anti-Trop2 antibody-drug conjugates (ADCs), etc. In recent years, the research focus of immune checkpoint inhibitors has been on PD-1 and PD-L1, and there has been some progress in the application research of related drugs in advanced TNBC. Bevacizumab is a representative preparation of VEGF inhibitors, and its therapeutic effect in breast cancer is somewhat controversial. The latest results of a phase 2 clinical study on the AR antagonist enzalutamide show that patients with AR-positive can benefit from enzalutamide. Trop-2 is a transmembrane protein found in human trophoblast cells that is involved in multiple intracellular signal transduction pathways and is a potential target. Currently, related drugs are in the clinical research stage. 4. Endocrine therapy. Due to the special nature of TNBC hormone receptor targets, the drugs commonly used in clinical breast cancer endocrine therapy cannot benefit TNBC patients, but 10%-40% of TNBC patients show positive AR. 5. Traditional Chinese medicine treatment.Triple-negative breast cancer (TNBC) is a type of breast cancer identified with the continuous development of modern molecular biology techniques. There is no specific corresponding traditional Chinese medicine (TCM) disease name, and it falls into the categories of "breast carcinoma" and "breast abscess with stony hardening" in TCM. Its formation is caused by deficiency of healthy qi, disharmony of the liver, spleen, and kidney functions, mutual binding of phlegm, toxin, and stasis, invasion of pathogenic factors, and stasis and obstruction of breast collaterals. In the treatment with TCM, on the one hand, it is used in combination with Western medicine to enhance efficacy and reduce toxicity, and improve the edema of the affected limb after surgery; reduce the toxic and side effects and increase the effective rate of treatment. On the other hand, when used alone in the preventive treatment stage without clinical symptoms, it can prolong the survival period of patients and reduce the recurrence and metastasis rate.

[0005] However, there are the following disadvantages in the above-mentioned systemic treatment process: Specifically, 1. Local treatment: Some studies have confirmed that the local recurrence rate and regional lymph node metastasis rate of triple-negative breast cancer patients after surgical treatment are slightly higher than those of non-triple-negative breast cancer. Although the impact of local recurrence on the prognosis of patients is not yet clear, patients may face reoperation due to recurrence. Therefore, it is recommended that triple-negative breast cancer patients routinely undergo axillary lymph node dissection and avoid sentinel lymph node biopsy. 2. Targeted therapy: Currently, the biological targeted therapy for triple-negative breast cancer is still in the clinical research stage. The main characteristic of triple-negative breast cancer is the lack of specific receptors available for targeted therapy, namely estrogen receptor, progesterone receptor, and HER2 protein. The absence of these indicators means that tumor cells may not have a response mechanism to specific drugs, so existing targeted drugs cannot be used for treatment. 3. Chemotherapy: Since triple-negative breast cancer cannot be treated with targeted therapy, the treatment options for patients are relatively limited. Currently, chemotherapy is the most common systemic treatment option for this type of breast cancer, but it has relatively large side effects and may cause a series of adverse reactions, such as nausea, vomiting, and myelosuppression. At the same time, the effect of chemotherapy may also be limited because of the lack of effective targets, and chemotherapy drugs may not be able to completely kill tumor cells. 4. Immunotherapy: Although some new immunotherapies (such as PD-1 / PD-L1 inhibitors) have shown certain efficacy in some triple-negative breast cancer patients, these drugs may also be accompanied by a series of adverse reactions. In addition, there are differences in the drug tolerance of different patients, and some patients may not be able to tolerate the side effects of chemotherapy or immunotherapy, resulting in treatment interruption or poor efficacy. 5. Limitations of treatment regimens: The treatment regimens for triple-negative breast cancer usually include conventional methods such as surgery, radiotherapy, and chemotherapy. However, the effects of these methods may be limited because of the lack of effective targets, making it difficult to precisely target tumor cells. In addition, the tumor heterogeneity of different patients may also lead to limitations in treatment regimens, making some patients insensitive to treatment or prone to recurrence. 6. Challenges of new treatment methods: Although the medical community is constantly researching and developing new treatment methods, such as cellular immunotherapy (such as NKT cell therapy), these methods are still in the clinical trial stage, and their efficacy and safety need to be further verified. At the same time, the cost of new treatment methods may also be relatively high, making it difficult for some patients to afford.

[0006] With a large number of clinical studies being conducted, considering drug adverse reactions and facilitating clinical application, the chemotherapy regimen based on anthracyclines or taxanes is used as the first-line treatment for TNBC. The taxane, anthracycline, and cyclophosphamide (TAC) is the preferred chemotherapy regimen, and it has been found that the sequential administration of anthracycline and cyclophosphamide (AC) followed by taxane (T) regimen (i.e., AC→T regimen) is superior to the synchronous TAC regimen. However, there are currently no recommended molecular targeted drugs for TNBC, and relevant clinical studies are still ongoing. Therefore, finding new targeted treatment regimens has become a research hotspot. Summary of the Invention

[0007] The object of the present invention is to provide the use of an azetidine compound in the preparation of a drug for preventing and treating triple-negative breast cancer. The azetidine compound belongs to a targeted inhibitor of Stat3, and this drug can effectively prevent the deterioration of TNBC by inhibiting the activity of the Stat3 target.

[0008] The present invention is achieved through the following technical solutions:

[0009] Use of an azetidine compound in the preparation of a drug for preventing and treating triple-negative breast cancer, the molecular formula of the azetidine compound: C 27 H 22 O4N5SF5, molecular weight: 607.56, and the structural formula is as follows:

[0010]

[0011] Preferably, the application of the drug in inhibiting the tumor volume of triple-negative breast cancer, inhibiting the growth of triple-negative breast cancer tumors, inducing apoptosis in triple-negative breast cancer cells, and inhibiting the proliferation of triple-negative breast cancer cells.

[0012] Preferably, the inhibition of the growth of triple-negative breast cancer tumors specifically includes: reducing the tumor weight of triple-negative breast cancer, inhibiting the growth of triple-negative breast cancer tumor tissues, and reducing the volume of triple-negative breast cancer tumor tissues.

[0013] Preferably, the induction of apoptosis in triple-negative breast cancer cells is achieved by inhibiting the phosphorylation of tyrosine at position 3705 of STAT3 or inhibiting the expression of Bcl-2.

[0014] Preferably, the inhibition of the proliferation of triple-negative breast cancer cells is achieved by inducing G2-M phase arrest in MDA-MB-231 cells by the azetidine compound.

[0015] A drug for preventing and treating triple-negative breast cancer, the main active ingredient of the drug is an azetidine compound.

[0016] Preferably, the drug further includes pharmaceutically acceptable excipients.

[0017] Preferably, the pharmaceutically acceptable excipients include any one or a combination of diluents, excipients, disintegrants, fillers, binders, lubricants, flavoring agents, surfactants, stabilizers, etc.

[0018] Compared with the prior art, the present invention has at least the following technical effects:

[0019] The present invention provides an application of an azetidine compound in the preparation of a drug for preventing and treating triple-negative breast cancer. By adopting the internationally common method for establishing a triple-negative breast cancer model, it is further verified that the compound can effectively inhibit the tumor growth state of triple-negative breast cancer in nude mice, inhibit the phosphorylation of tyrosine at position 705 of STAT3, induce G2-M phase arrest and apoptosis of tumor cells, and has a significant prevention and treatment effect on triple-negative breast cancer, and is expected to become a new drug for the research and development of treating triple-negative breast cancer. BRIEF DESCRIPTION OF THE DRAWINGS

[0020] Figure 1 It is a schematic diagram for comparing the tumor volumes of mice in each group in the influence of each group on the tumor volume of triple-negative breast cancer nude mice;

[0021] Figure 2 It is a schematic diagram for comparing the tumor weights of nude mice in each group in the influence of different administration groups on the tumor weight of triple-negative breast cancer nude mice;

[0022] Figure 3 It is a schematic diagram for comparing the tumor tissue volumes of nude mice in each group in the influence of different administration groups on the tumor growth of triple-negative breast cancer nude mice;

[0023] Figure 4 It is a schematic diagram for the influence of H333 on the expression of STAT3 upstream and downstream proteins in triple-negative breast cancer cells;

[0024] Figure 5 It is a schematic diagram for comparing the cell cycle distributions of the control group and different H333 administration groups;

[0025] Figure 6 It is a schematic diagram for the influence of different H333 administration groups on the apoptosis of triple-negative breast cancer cells. DETAILED DESCRIPTION OF THE INVENTION

[0026] The following will describe the implementation scheme of the present invention in detail with reference to the embodiments. However, those skilled in the art will understand that the following embodiments are only used to illustrate the present invention and should not be regarded as limiting the scope of the present invention. The specific conditions not specified in the embodiments are carried out according to the conventional conditions or the conditions recommended by the manufacturer. The reagents or instruments not specified by the manufacturer are all conventional products that can be obtained through commercial purchase.

[0027] The technical solution of a specific embodiment of the present invention is as follows:

[0028] Use of azetidine compounds in the preparation of drugs for preventing and treating triple-negative breast cancer. The molecular formula of the azetidine compounds is: C 27 H 22 O4N5SF5, molecular weight: 607.56, and the structural formula is as follows:

[0029]

[0030] The preparation method of the azetidine compounds is as follows:

[0031] Using compounds A and B as starting materials, compound C is prepared through a halogen substitution reaction, and compound D is obtained after removing the benzyloxycarbonyl group. Then, the azetidine compound (hereinafter referred to as H333) is prepared through a halogen substitution reaction. This compound is soluble in deionized water to complete the preparation.

[0032] A: C9H 12 NCl

[0033] B: C 22 H 27 O4N3Si

[0034] C: C 31 H 38 O4N4Si

[0035] D: C 23 H 32 O2N4Si

[0036] E: C 27 H 22 O4N5SF5

[0037] Reaction content of the molecular formula:

[0038]

[0039]

[0040] Experimental verification: Effects of H333 and different dosing groups on the efficacy of triple-negative breast cancer nude mice 1. Experimental materials

[0041] 1.1 Drugs

[0042] H333 was provided by the research group of Professor Xu Heng of the Department of Medicinal Chemistry, Institute of Materia Medica, Peking Union Medical College. The purity was determined by HPLC to be ≥98%. Paclitaxel was purchased from Shanghai Kanglang Biotechnology Co., Ltd.

[0043] 1.2 Cells

[0044] The human breast cancer cell line MDA-MB-231 was purchased from the Cell Center of the Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, and passaged and preserved in our laboratory. The cell culture conditions were all 37°C, 5% CO2, and saturated humidity. Balb / c nude mice were purchased from Beijing Spearf Bio-Technology Co., Ltd.

[0045] 2. Experimental methods

[0046] 2.1 Ectopic transplantation tumor nude mouse experiment for triple-negative breast cancer

[0047] Under sterile conditions, human breast cancer cells MDA-MB-231 were collected and the cell density was adjusted to 5×10 7 cells / mL with sterile normal saline. 0.2 mL was taken and inoculated subcutaneously into the axillary and dorsal regions of nude mice. When the tumor grew to a diameter of 1 cm, it was removed under sterile conditions and cut into tumor pieces of 1 mm×1 mm size, which were evenly inoculated subcutaneously into the axilla of nude mice. When the tumor volume was close to 200 - 400 mm 3 , the mice were grouped for drug administration and weighed, with 6 mice in each group.

[0048] Formal experimental grouping method:

[0049] The control group was gavaged with distilled water daily; the paclitaxel group was injected intraperitoneally at a dose of 10 mg / kg every two days.

[0050] Regarding H333, the following concentrations were set: the 10 mg / kg, 20 mg / kg, and 40 mg / kg drug administration groups were injected intraperitoneally, once every 2 days. The drug administration cycle was about 27 days.

[0051] Result evaluation:

[0052] The body weight was measured twice a week, and the length and width of the tumor were measured with a vernier caliper. The tumor volume was calculated according to the formula V = a×b 2 / 2, where a is the length of the tumor and b is the width of the tumor. The nude mice were sacrificed by cervical dislocation and photographed, then the tumor tissue blocks were removed and weighed. Finally, the tumor inhibition rate was calculated, and a part of the tumor tissue was immersed in 4% paraformaldehyde for fixation, and the other part was stored at -80°C.

[0053] 2.2 Detection of protein expression changes by Western Blot

[0054] Collect treated or untreated MDA-MB-231 cultured cells and prepare whole cell lysates using radioimmunoprecipitation assay (RIPA) buffer. Samples of equal amounts of total protein were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblot analysis. The primary antibodies used included anti-Stat3, EGFR, pY705-Stat3, Bcl-2, Bcl-xL, and β-actin. Cells were seeded in culture dishes at a density of 1.4×10 4 cells / cm². The next day, the cells were either untreated (DMSO control, 0.1%) or treated simultaneously with different concentrations of H333. After incubation for 12 h, the cells were harvested for whole cell lysate preparation and SDS-PAGE / immunoblot analysis.

[0055] 2.3 Flow cytometry analysis of cell cycle distribution

[0056] Digest MDA-MB-231 cells in the logarithmic growth phase into single cell suspensions and add 2 mL to 6-well plates at a density of 5×10 4 cells / mL. The next day, after treatment with different concentrations of H333 for 48 h, the cells in the 6-well plates were collected respectively, washed once with pre-cooled PBS, and the cell pellets were resuspended in 70% ethanol pre-cooled at -20°C. The cells were fixed overnight at -20°C. The next day, the cells were centrifuged at 4°C, 200×g for 5 min, the supernatant was discarded, washed twice with PBS, 5 μL of RNase A (1 mg / mL) was added, and the cells were treated at 37°C in the dark for 30 min to remove the influence of RNA; then 400 μL (150 pg / mL) of PI was added, and after staining in the dark for 20 min, the cells were detected by flow cytometry. The cell cycle was analyzed using Flow Draw 7.6 software.

[0057] 2.4 Flow cytometry detection of apoptosis

[0058] Digest MDA-MB-231 cells in the logarithmic growth phase into single cell suspensions and add 2 mL to 6-well plates at a density of 1×10 5 cells / mL. The next day, after treatment with different concentrations of H333 for 48 h, the cells in the 6-well plates were digested with 0.25% trypsin without EDTA, terminated with the supernatant medium, centrifuged at 4°C, 1000 rpm for 5 min to collect the cells, washed with pre-cooled PBS, centrifuged at 4°C, 1000 rpm for 5 min to collect the cell pellets, 100 μL of 1×Binding Buffer was added to suspend the cells, 5 μL of Annexin V-FITC was added and mixed well, and then incubated at room temperature in the dark for 15 min. 5 μL of PI was added for staining 10 min before detection, and 400 μL of 1×Binding Buffer was added for detection.

[0059] 3. Statistical analysis

[0060] The results are expressed as mean ± standard deviation. ANOVA was used to analyze the experimental data with SPSS statistical software, and P < 0.05 was considered statistically significant.

[0061] 4. Experimental result data:

[0062] Results of animal experiments:

[0063] 4.1 Effect of H333 on the tumor volume of triple-negative breast cancer nude mice

[0064] As Figure 1 shown, it is a schematic diagram comparing the tumor volumes of nude mice in different drug administration groups. Among them, compared with the control group, ***P < 0.001.

[0065] The results combined with Figure 1 showed that on the 27th day after modeling, the tumor volume of nude mice in the control group was 2317 ± 63 mm 3 , the tumor volume of nude mice in the H333 group was 621 ± 56 mm 3 , and the tumor volume of nude mice in the paclitaxel group was 978 ± 73 mm 3 .

[0066] The results indicated that H333 could significantly inhibit the decrease in the tumor volume of triple-negative breast cancer nude mice (P < 0.001), and with the extension of time, the effect was more obvious than that of the positive drug paclitaxel.

[0067] 4.2 Effect of H333 on the tumor weight of triple-negative breast cancer nude mice

[0068] As Figure 2 shown, it is a schematic diagram comparing the tumor weights of nude mice in different drug administration groups. Among them, compared with the control group, ***P < 0.001.

[0069] The results combined with Figure 2 showed that the tumor weight of nude mice in the control group was 2.45 ± 0.4 g, the tumor weight of nude mice in the H333 group was 0.24 ± 0.02 g, and the tumor weight of nude mice in the paclitaxel group was 0.38 ± 0.11 g.

[0070] Tumor weight is a gross index for the growth of triple-negative breast cancer.

[0071] The results showed that H333 could inhibit the growth of tumors in triple-negative breast cancer MDA-MB-231 nude mice (P < 0.001).

[0072] 4.3 Effect of H333 on the tumor growth of triple-negative breast cancer nude mice

[0073] As Figure 3 shown, it is a schematic diagram of tumors in the tissues of nude mice in different drug administration groups. There are five nude mice in each group.

[0074] The results combined withFigure 3 It can be seen that Control is the control group. The tumor tissues of the nude mice in this control group are relatively large, with a smooth and complete appearance, clear tissue structure, vascular tissue inside, and a relatively thick texture.

[0075] As Figure 3 The results shown in are the conclusions verified by using 20 mg / kg of H333, which proves that the dosage of 20 mg / kg is the most effective. The experimental verification of other concentrations of H333 has poor effects.

[0076] In the nude mice of the H333 20 mg / kg and paclitaxel groups, the volume of the tumor tissues can be seen to become smaller. Among them, the tissues of H333 20 mg / kg are significantly smaller than those of the paclitaxel group and the control group. The internal blood vessel growth is incomplete, and the growth of the tumor tissues is significantly inhibited.

[0077] Results of cell experiments:

[0078] 4.4 Effects of H333 on the expression of STAT3 upstream and downstream proteins in triple-negative breast cancer cells

[0079] As Figure 4 shown, it is a schematic diagram of the effects of H333 on the expression of STAT3 upstream and downstream proteins in triple-negative breast cancer cells.

[0080] Combined with the results Figure 4 It can be seen that the results of the expression of the STAT3 upstream protein EGFR by H333. With the increase in concentration, there is no obvious effect. It can be inferred that the action target of H333 is not upstream of STAT3.

[0081] At the same time, it was found that the phosphorylation of tyrosine at position 705 of STAT3 was inhibited in a concentration- and time-dependent manner, while the expression of the STAT3 protein itself was not affected.

[0082] It indicates that the inhibitory effect of H333 on STAT3 is mainly directed against the phosphorylation of tyrosine at position 705 of STAT3.

[0083] In addition, when the concentration of H333 is 10 μM, the expression of Bcl-2 is significantly inhibited, indicating that H333 can effectively induce apoptosis in triple-negative breast cancer cells.

[0084] 4.5 Effects of H333 on the cell cycle distribution of triple-negative breast cancer cells

[0085] As Figure 5 shown, it is a schematic diagram comparing the cell cycle distributions of the control group and the drug administration groups at different concentrations.

[0086] Combined with the results Figure 5It can be seen that, compared with the control group, the distribution of cells in the G2-M phase in the H333 administration group was significantly increased, resulting in the percentage of cell distribution in the G2-M phase increasing to 13.45±1.47, 15.23±2.19, and 17.85±1.35 respectively, and the increasing trend showed concentration dependence.

[0087] In addition, the cell distributions in the G0-G1 phase and S phase decreased with the increase in the administration concentration.

[0088] The results showed that H333 could effectively induce G2-M phase arrest in MDA-MB-231 cells, thereby inhibiting cell proliferation, and this was related to the inhibition of the expression of cyclins related to the G2-M phase by H333.

[0089] 4.6 Effect of H333 on apoptosis of triple-negative breast cancer cells

[0090] As Figure 6 shown, it is a schematic diagram of the effect of H333 on apoptosis of triple-negative breast cancer cells.

[0091] Combined with the results Figure 6 it can be known that after 48 hours of treatment with H333, in MDA-MB-231 cells, 0.5, 2, 0.5, and 5 μM of H333 could cause the apoptosis percentage to increase to 6.65±0.16, 12.59±1.29, and 31.57±2.13 respectively, suggesting that H333 could significantly induce apoptosis in breast cancer cells.

[0092] In summary, the above results showed that H333 could significantly inhibit the tumor weight and tumor volume growth of triple-negative breast cancer; inhibit the phosphorylation of tyrosine at position 3705 of STAT3, induce G2-M phase arrest in tumor cells, and cause cell apoptosis, thereby playing a therapeutic role in triple-negative breast cancer.

[0093] Finally, it should be noted that the above are only the preferred embodiments of the present invention and are not used to limit the protection scope of the present invention. Any modifications, equivalent replacements, improvements, etc. made within the spirit and principle of the present invention shall be included within the protection scope of the present invention.

Claims

1. The use of azetidine compounds in the preparation of drugs for the prevention and treatment of triple-negative breast cancer, characterized in that: The molecular formula of the azetidine compound is: 27 H 22 O4N5SF5, molecular weight: 607.56, structural formula is as follows:

2. An application according to claim 1, characterized in that: The drug is used in inhibiting triple-negative breast cancer tumor volume, inhibiting triple-negative breast cancer tumor growth, inducing triple-negative breast cancer cells to undergo apoptosis, and inhibiting triple-negative breast cancer cell proliferation.

3. An application according to claim 2, characterized in that: The inhibition of triple-negative breast cancer tumor growth specifically includes: reducing triple-negative breast cancer tumor weight, inhibiting triple-negative breast cancer tumor tissue growth, and reducing triple-negative breast cancer tumor tissue volume.

4. An application according to claim 2, characterized in that: The induction of apoptosis in triple-negative breast cancer cells is achieved by inhibiting tyrosine phosphorylation at position 705 of STAT3 or inhibiting the expression of Bcl-2.

5. The use according to claim 2, characterized in that: The inhibition of triple-negative breast cancer cell proliferation is achieved by inducing G2-M phase arrest of MDA-MB-231 cells by azetidine compounds.

6. A drug for preventing and treating triple-negative breast cancer, characterized in that: The main active ingredient of the drug is an azetidine compound.

7. A drug for preventing and treating triple-negative breast cancer according to claim 6, characterized in that: The drug also includes pharmaceutically acceptable excipients.

8. A drug for preventing and treating triple-negative breast cancer according to claim 7, characterized in that: The pharmaceutically acceptable excipients include any one or more combinations of diluents, excipients, disintegrants, fillers, binders, lubricants, flavoring agents, surfactants, and stabilizers.

Images