Pharmaceutical composition for treating triple negative breast cancer

Abstract

The invention discloses a pharmaceutical composition for treating triple-negative breast cancer. Active ingredients of the pharmaceutical composition comprise actinomycin and adriamycin. The pharmaceutical composition is combined with a specific nucleic acid sequence in a targeted manner through the synergistic effect of actinomycin and adriamycin, the effect of treating or inhibiting triple-negative breast cancer is achieved on the basis of reducing the dosage of adriamycin, and the side effects of chemotherapeutic drugs can be effectively reduced.

Description

Pharmaceutical composition for treating triple-negative breast cancer Technical Field

[0001] The present invention relates to a pharmaceutical composition, and in particular to a pharmaceutical composition for treating triple-negative breast cancer. Background Art

[0002] The World Health Organization states that breast cancer is the most common cancer in women, with triple-negative breast cancer (TNBC) having the highest mortality rate. Triple-negative breast cancer, defined as cancers that are negative for three hormone receptors: estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth receptor type 2 (HER2), limits the treatment options available to patients. Furthermore, due to the high genetic variability of TNBC, patients face high recurrence rates and poor prognosis even after treatment. Therefore, the treatment of TNBC has always been a major clinical challenge.

[0003] Since triple-negative breast cancer patients lack the three receptors mentioned above, they cannot use hormone therapy and targeted therapy as treatment methods. They can only use chemotherapy as the main treatment method. However, in addition to side effects, chemotherapy drugs also have an upper limit for cumulative dosage. If the upper limit of the cumulative dosage is used, it is not recommended to continue using the drug, resulting in fewer treatment options for patients, such as cardiac toxicity and decreased immunity. For example, the most commonly used chemotherapy drug for triple-negative breast cancer in clinical practice: doxorubicin, has a lifetime cumulative dosage upper limit of 550mg / m 2 (body surface area), and the recommended dose of doxorubicin as a monotherapy for triple-negative breast cancer is 60-75 mg / m 2 , administered once every three weeks; the recommended dose for combined treatment with other chemotherapy drugs is 40-75 mg / m 2 , administered once every three to four weeks; therefore, there is a limit to the number of times a patient can receive doxorubicin treatment throughout their life. In addition to chemotherapy, immunotherapy is currently a new treatment option for triple-negative breast cancer. However, immunotherapy is not suitable for all triple-negative breast cancer patients and is expensive, making it not affordable for all patients.

[0004] Summary of the Invention

[0005] To address the above-mentioned problems, the present invention aims to provide a pharmaceutical composition for treating triple-negative breast cancer, which can reduce the dosage of conventional chemotherapy drugs in triple-negative breast cancer patients, thereby reducing drug side effects and improving prognosis.

[0006] Another object of the present invention is to provide a pharmaceutical composition for treating triple-negative breast cancer, which can delay the onset of disease caused by the accumulation of chemotherapy drugs in the body, thereby extending the time during which patients can use chemotherapy drugs.

[0007] To achieve the above objectives, the present invention provides a use of a chemotherapy drug for preparing a pharmaceutical composition for treating triple-negative breast cancer and its metastasis, wherein the chemotherapy drug comprises actinomycin D and doxorubicin. By administering the pharmaceutical composition containing an effective amount of actinomycin D and doxorubicin to a triple-negative breast cancer patient, the actinomycin D and doxorubicin can be incorporated into the GCCG sequence, enabling the pharmaceutical composition to bind to a nucleic acid molecule containing the GCCG sequence, thereby inhibiting the growth and metastasis of triple-negative breast cancer cells, thereby achieving the therapeutic effect of triple-negative breast cancer.

[0008] The pharmaceutical composition for treating triple-negative breast cancer is composed of actinomycin D and doxorubicin.

[0009] In one embodiment of the present invention, in the pharmaceutical composition, the effective amount refers to a dosage ratio of the actinomycin D to the doxorubicin of 1:100-1:600.

[0010] In another embodiment of the present invention, if the subject to be administered is a human, in the pharmaceutical composition, the effective amount preferably refers to a dosage ratio of the actinomycin D to the doxorubicin of 1:10-1:30, such as a dosage ratio of the actinomycin D to the doxorubicin of 1:25.

[0011] In another embodiment, the present invention discloses the use of a chemotherapy drug for preparing a nucleic acid intercalator, wherein the chemotherapy drug comprises actinomycin D and doxorubicin; the nucleic acid intercalator is configured to bind to a GCCG sequence in a nucleic acid molecule. Specifically, by administering an effective amount of the nucleic acid intercalator to a subject, the actinomycin D and doxorubicin are intercalated into the GCCG sequence, thereby binding the nucleic acid intercalator to the nucleic acid molecule containing the GCCG sequence to form a complex, thereby affecting the normal function of the nucleic acid molecule containing the GCCG sequence or the cell containing the nucleic acid molecule.

[0012] The dosage ratio of the actinomycin D to the doxorubicin is 1:100-1:600.

[0013] If the subject to be administered is a human, the dosage ratio of actinomycin D to the doxorubicin is preferably 1:10-1:30, such as 1:25.

[0014] The beneficial effects of the present invention are:

[0015] The present invention provides a pharmaceutical composition for treating triple-negative breast cancer. This pharmaceutical composition can reduce the dosage of existing chemotherapy drugs in triple-negative breast cancer patients, thereby reducing drug side effects and improving prognosis. It can also delay the onset of disease caused by the accumulation of chemotherapy drugs in the body, thereby extending the time during which patients can use chemotherapy drugs. Furthermore, in addition to inhibiting the growth of triple-negative breast cancer, it can also effectively inhibit the metastasis of triple-negative breast cancer cells to other organs. Specifically, the pharmaceutical composition provided by the present invention can be used to treat metastatic triple-negative breast cancer or advanced triple-negative breast cancer. BRIEF DESCRIPTION OF THE DRAWINGS

[0016] FIG1 is a schematic diagram of a complex formed by combining the pharmaceutical composition for treating triple-negative breast cancer disclosed in the present invention with the sequence: d(AGCCGT)2, wherein drug A is actinomycin and drug D is doxorubicin.

[0017] FIG2A shows the results of treating MDA-MB-231 cells with actinomycin and doxorubicin at different ratios, wherein A represents actinomycin and X represents doxorubicin.

[0018] FIG2B shows the results of treating 4T1 cells with actinomycin and doxorubicin at different ratios, wherein A represents actinomycin and X represents doxorubicin.

[0019] FIG2C shows the results of treating MCF-7 cells with actinomycin and doxorubicin at different ratios, wherein A represents actinomycin and X represents doxorubicin.

[0020] FIG3 shows the results of calculating and analyzing the CI index obtained by treating different cancer cells with different ratios of actinomycin and doxorubicin to obtain the cytotoxicity.

[0021] FIG4A shows the results of calculating the comprehensive synergistic score obtained by treating MDA-MB-231 cells with different ratios of actinomycin and doxorubicin, wherein A represents actinomycin and DOX represents doxorubicin.

[0022] FIG4B shows the results of calculating the comprehensive synergistic score obtained by treating 4T1 cells with actinomycin and doxorubicin at different ratios, wherein A represents actinomycin and DOX represents doxorubicin.

[0023] FIG4C shows the results of calculating the comprehensive synergistic score obtained by treating MCF-7 cells with different ratios of actinomycin and doxorubicin, wherein A represents actinomycin and DOX represents doxorubicin.

[0024] FIG5 shows the cell cycle distribution of MDA-MB-231 cells and 4T1 cells after treatment with different treatment regimens.

[0025] FIG6A shows the results of statistical analysis of the cell cycle distribution of MDA-MB-231 cells after treatment with different treatment regimens.

[0026] FIG6B is the result of statistical analysis of the cell cycle distribution of M4T1 cells after treatment with different treatment regimens.

[0027] FIG7 is a heat map of transcriptome changes in MDA-MB-231 cells after treatment with different treatment regimens.

[0028] FIG8A is a protein interaction network diagram of the combination therapy group relative to the control group.

[0029] FIG8B is a protein interaction network diagram of the combination therapy group relative to the doxorubicin treatment group.

[0030] FIG9 shows the results of thermal stability tests of SEQ ID No. 1 in combination with different drugs.

[0031] FIG10 is an analysis of the melting point changes of each treatment group.

[0032] FIG11 shows the CD spectra of actinomycin, doxorubicin, and actinomycin and doxorubicin after reacting with different sequences, respectively. A represents actinomycin, and X represents doxorubicin.

[0033] FIG12 shows the changes in tumor volume of mice in each group.

[0034] FIG13 shows the changes in the white blood cell count of mice in each group.

[0035] FIG14 shows the body weight changes of mice in each group.

[0036] Figure 15 shows the results of analyzing the tumor weight of each group of mice

[0037] FIG. 16 shows the results of analyzing the liver weight relative to body weight of mice in each group.

[0038] FIG. 17 shows the results of analyzing the heart weight relative to body weight of mice in each group.

[0039] FIG18 is an analysis of the amount of metastatic tumor in the lungs of mice in each group.

[0040] FIG19 is an analysis of the number of liver-metastatic tumors in each group of mice.

[0041] FIG20 shows the results of H&E staining of lung and liver sections of mice treated with different treatments. DETAILED DESCRIPTION

[0042] The present invention provides a pharmaceutical composition for treating triple-negative breast cancer, comprising actinomycin and doxorubicin. When an effective amount of the pharmaceutical composition for treating triple-negative breast cancer is administered to a breast cancer patient, the actinomycin and doxorubicin are embedded within the GCCG nucleic acid sequence, enabling the pharmaceutical composition to bind to the GCCG-containing nucleic acid sequence, thereby treating or inhibiting the growth and metastasis of triple-negative breast cancer and reducing drug side effects.

[0043] When actinomycin and doxorubicin are combined in a predetermined ratio, the two drugs can produce a synergistic effect. Actinomycin can cooperate with doxorubicin to embed into the GCCG position of the nucleic acid sequence, forming a complex with the nucleic acid sequence. In addition, actinomycin can enable doxorubicin to bind to the nucleic acid sequence GCCG in a targeted manner, thereby reducing the possibility of doxorubicin binding to non-target sequences, thereby effectively reducing the dosage of doxorubicin, thereby extending the time for patients to take the drug and reducing the incidence of side effects.

[0044] For breast cancer cells, particularly triple-negative breast cancer cells, the pharmaceutical composition disclosed herein can inhibit breast cancer cell growth when the dose or concentration ratio of actinomycin to doxorubicin is 1:100-1:600, such as 1:100, 1:200, 1:300, 1:400, 1:500, or 1:600. Specifically, when the actinomycin dose is 20 μg / kg, the doxorubicin concentration should be 2000-12000 μg / kg; and when the actinomycin concentration is 2 nM, the doxorubicin concentration should be 200 nM-1200 nM.

[0045] In one embodiment of the present invention, when the subject to be administered is a human, in the pharmaceutical composition, the effective amount refers to a ratio of the actinomycin D to the doxorubicin of 1:10-1:30, such as 1:15, 1:20, 1:22, etc., wherein the ratio of the actinomycin D to the doxorubicin is preferably 1:25.

[0046] As shown in FIG. 1 , the pharmaceutical composition for treating triple-negative breast cancer disclosed in the present invention can form a complex by binding actinomycin and doxorubicin to the sequence: d(AGCCGT)2, thereby disrupting the growth and metastasis of cancer cells, thereby achieving the efficacy of treating or ameliorating triple-negative breast cancer.

[0047] The disclosed pharmaceutical composition for treating triple-negative breast cancer utilizes the synergistic effect of actinomycin and doxorubicin to inhibit genes associated with the RAS pathway. This allows for the suppression of triple-negative breast cancer at a dose that is more than halved, thereby reducing drug side effects.

[0048] Since actinomycin and doxorubicin can be targeted and intercalated into GCCG sequences in nucleic acid molecules, another embodiment of the present invention discloses a nucleic acid intercalator, whose active ingredients include actinomycin D and doxorubicin for binding to GCCG sequences in nucleic acid molecules.

[0049] The term "triple-negative breast cancer (TNBC)" refers to a subtype of breast cancer that does not express estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), accounting for approximately 15% of all breast cancers. In the present invention, "triple-negative breast cancer" includes metastatic triple-negative breast cancer.

[0050] The term "pharmaceutical composition" refers to a composition containing at least two active ingredients that can be used to treat a disease or its related symptoms, and the active ingredients have a synergistic effect.

[0051] The term "treat" means to reverse, alleviate, inhibit the progression of the disorder or condition to which such term applies, one or more symptoms of such disorder or condition, or prevent the occurrence of the disorder or condition to which such term applies or its complications.

[0052] The term "effective amount" refers to that amount of the compound or its pharmaceutically acceptable salt being administered that is effective to alleviate one or more symptoms of the disease being treated, reduce the discomfort of one or more symptoms, or slow the progression of the disease.

[0053] Actinomycin D (ActD), also known as actinomycin, is a member of the actinomycin class of polypeptide antibiotics isolated from soil bacteria of the genus Streptomyces. It is used as a chemotherapy agent. Actinomycin inhibits RNA synthesis and blocks protein synthesis, and is primarily used to treat Wilms' tumor, testicular tumors, and rhabdomyomas.

[0054] The term "Doxorubicin (Dox)" has the following chemical formula (I), a molar mass of 543.52 g / mol, and a molecular formula of C 27 H 29 NO 11. Doxorubicin is a drug used to treat a variety of cancers. It belongs to the anthracycline antibiotic class. Its main mechanism of action is to inhibit the synthesis of DNA and RNA by binding to nuclear DNA, and at the same time interfere with the proliferation and division of cancer cells. Doxorubicin is usually part of the chemotherapy regimen in the clinical treatment of breast cancer. For example, doxorubicin is combined with cyclophosphamide to treat invasive breast cancer. However, when doxorubicin is used simultaneously with other chemotherapy drugs, it can cause different side effects, such as bone marrow suppression (impaired hematopoietic function), nausea, vomiting, hair loss, cardiotoxicity (myocardial damage), and liver toxicity. The most serious side effect of doxorubicin is dilated cardiomyopathy (abbreviated as cardiomyopathy), and the incidence of cardiomyopathy is positively correlated with the cumulative dose of doxorubicin. There is currently no effective treatment for cardiomyopathy in clinical practice. Therefore, for patients with triple-negative breast cancer, doxorubicin cannot be used as a long-term treatment.

[0055] The cells used in the following examples, such as the MDA-MB-231 (human triple-negative breast cancer) cell line, the 4T1 (mouse triple-negative breast cancer) cell line, and the MCF-7 (breast cancer) cell line, are readily available to those skilled in the art and therefore do not require storage. The 4T1 cell line is commonly used as a model for studying distant metastasis of breast cancer and for clinical drug screening.

[0056] The sequences used in the following examples: d(AGCCCT)2, d(AGCACGT)2, etc. are artificially synthesized sequences and are used to verify that the pharmaceutical composition disclosed in the present invention has the property of targeting the GCCG sequence, and are not used to limit the efficacy of the present invention.

[0057] The dosages used in the cell or animal experiments in the following examples are for illustration only and are not intended to limit the scope of the present invention.

[0058] Example 1: Synergistic cytotoxicity test

[0059] Table 1 below shows the half-inhibitory concentration (IC50) of each chemotherapy drug: actinomycin, doxorubicin, cisplatin, and 5FU for MDA-MB-231 cells, 4T1 cells, and MCF-7 cells.

[0060] Table 1: Half-inhibitory concentration of each chemotherapy drug for each cancer cell

[0061] Actinomycin and doxorubicin were used to treat MDA-MB-231 cells, 4T1 cells, and MCF-7 cells at varying ratios for 48 hours. The CI (CI index) was calculated based on cytotoxicity. The results are shown in Figures 2 and 3 and Table 2. A CI less than 0.9 indicates a synergistic effect between the drug combinations; a CI between 0.9 and 1.0 indicates additive effects. Figure 3 shows that the CIs for the cytotoxic effects of different ratios of actinomycin and doxorubicin on various breast cancer-related cells were all less than 0.9, indicating a synergistic effect between actinomycin and doxorubicin.

[0062] Table 2: CI index of each cell treatment group

[0063] SynergyFinder was used to calculate the combined reaction data of actinomycin and doxorubicin for interactive analysis and visualization. The results are shown in FIG4 . As shown in FIG4 , the comprehensive synergy score is greater than 10, indicating that the interaction between actinomycin and doxorubicin is synergistic in each breast cancer cell line.

[0064] Example 2: Cell test (1)

[0065] MDA-MB-231 cells and 4T1 cells were treated with actinomycin (0.25 nM), doxorubicin (5 nM), or a combination of actinomycin (0.25 nM) and doxorubicin (5 nM) for 24 hours. Nucleic acids were labeled with propidium iodide (PI) and cell cycle analysis was performed by flow cytometry. The results are shown in Figures 5 and 6.

[0066] The results in Figures 5 and 6 indicate that actinomycin can promote doxorubicin-induced arrest of triple-negative breast cancer cells at the G2 / M phase of the cell cycle. This indicates that the pharmaceutical composition disclosed in the present invention for treating triple-negative breast cancer can effectively inhibit the growth of triple-negative breast cancer, achieving therapeutic efficacy for triple-negative breast cancer.

[0067] Example 3: Cell test (II)

[0068] MDA-MB-231 cells were treated with actinomycin (2 nM), doxorubicin (600 nM), or a combination of actinomycin (2 nM) and doxorubicin (600 nM) for 24 hours. Transcriptome changes in each cell group were recorded, as shown in Figure 7. Furthermore, software analysis was used to generate a protein interaction network diagram for each cell group, as shown in Figure 8.

[0069] Example 4: GCCG sequence-specific binding assay

[0070] The sequence represented by SEQ ID No. 1 (at a concentration of 2 μM) was reacted with actinomycin, doxorubicin, and actinomycin and doxorubicin, respectively. For each single-drug treatment group, the sequence-to-drug ratio was 1:1, while the sequence-to-actinomycin and doxorubicin dosage ratios in the pharmaceutical composition disclosed herein were 1:1:1. The binding behavior of the drugs in each treatment group with each sequence and the changes in their melting points were analyzed, and the results are shown in Figures 9 and 10. The results in Figures 9 and 10 demonstrate that actinomycin and doxorubicin can form complexes with the sequence represented by SEQ ID No. 1.

[0071] Furthermore, the artificially synthesized sequences shown in Table 4 were reacted with different doses or ratios of actinomycin, doxorubicin, or actinomycin and doxorubicin, respectively. The CD spectra of each treatment group were analyzed, and the results are shown in Figure 11. The results in Figure 11 demonstrate that actinomycin can synergize with doxorubicin to bind to the GCCG nucleic acid sequence. This indicates that the pharmaceutical composition disclosed herein for treating triple-negative breast cancer is capable of targeted binding to the GCCG nucleic acid sequence, thereby maintaining efficacy in inhibiting or treating triple-negative breast cancer while reducing the dose of doxorubicin.

[0072] Table 4: List of artificially synthesized sequences

[0073] Example 5: Animal Experiment

[0074] An MDA-MB-231 breast cancer mouse model was established according to common knowledge in the art, and mice in each group were treated on days 0, 7, 14, 21, 28, 35, 42, and 49 of the experiment:

[0075] Group 1: no treatment was given;

[0076] Group 2: Administered actinomycin at a dose of 20 μg / kg (equivalent to a clinical dose of 15 μg / kg in humans);

[0077] Group 3: Adriamycin was administered at a dose of 0.5 mg / kg (equivalent to a clinical dose of 20 mg / m 2 );

[0078] Group 4: Actinomycin (20 μg / kg) and doxorubicin (0.5 mg / kg) were administered simultaneously;

[0079] Group 5: Actinomycin (10 μg / kg) and doxorubicin (0.25 mg / kg) were administered simultaneously, with the dose being 0.5 times that of Group 4.

[0080] During the experiment, the tumor volume, white blood cell count, and body weight of each group of mice were measured, and the results are shown in Figures 12 to 14. After the experiment, the tumor, liver, and heart weights of each group of mice were analyzed, and the results are shown in Figures 15 to 17.

[0081] As shown in Figures 12 to 17 , administration of the pharmaceutical composition disclosed herein for treating triple-negative breast cancer did not affect the subjects' body weight, liver weight, or heart weight, demonstrating the safety of the pharmaceutical composition disclosed herein. Furthermore, the pharmaceutical composition disclosed herein for treating triple-negative breast cancer effectively reduced the size and weight of the cancer at both a 1x dose and a 0.5x dose, demonstrating that the pharmaceutical composition disclosed herein can achieve a therapeutically effective dosage of actinomycin and doxorubicin by reducing the required dosage of both actinomycin and doxorubicin through the synergistic effect between actinomycin and doxorubicin.

[0082] As can be seen from the above description, since the pharmaceutical composition disclosed herein can reduce the dosage of actinomycin and doxorubicin by at least half, the pharmaceutical composition disclosed herein can effectively reduce the side effects caused by actinomycin and doxorubicin to an individual and prolong the period of drug administration in an individual, thereby achieving the effect of improving therapeutic efficacy and prognosis.

[0083] Example 6: Inhibition of cell migration test

[0084] A 4T1 breast cancer mouse model was established according to common knowledge in the art. The experimental period was 5 weeks, and each group of mice was treated on days 0, 7, 14, 21, 28, and 35 of the experiment according to the following conditions:

[0085] Group 1: no treatment was given;

[0086] Group 2: Administer cyclophosphamide at a dose of 5 mg / kg;

[0087] Group 3: Cyclophosphamide and doxorubicin were administered simultaneously, with a cyclophosphamide dose of 5 mg / kg and a doxorubicin dose of 0.5 mg / kg (equivalent to a human clinical dose of 20 mg / m 2 );

[0088] Group 4: Administered actinomycin at a dose of 20 μg / kg (equivalent to a clinical dose of 15 μg / kg in humans);

[0089] Group 5: administered with doxorubicin at a dose of 0.5 mg / kg;

[0090] Group 6: Actinomycin (20 μg / kg) and doxorubicin (0.5 mg / kg) were administered simultaneously;

[0091] Group 7: Actinomycin (10 μg / kg) and doxorubicin (0.25 mg / kg) were administered simultaneously, with the dose being 0.5 times that of Group 4.

[0092] After the experiment was completed, mice in each group were sacrificed and the number of breast cancer metastases in the lungs and livers of each group of mice was measured. The results are shown in Figures 18 and 20. Lung and liver sections of the mice were also taken and H&E stained. The results are shown in Figure 20.

[0093] As shown in Figures 18 to 20, the number of liver and lung tumors in Groups 2 and 3 mice decreased slightly compared to Group 1 mice, indicating that the treatment with cyclophosphamide alone or with doxorubicin was not significantly effective in treating breast cancer metastasis. The number of lung and liver tumors in Group 4 mice increased compared to Group 3, indicating that the effect of actinomycin alone on inhibiting breast cancer cell metastasis was not significant. The number of lung tumors in Group 5 mice was approximately the same as that in Group 3 mice, and the number of liver tumors was significantly less than that in Group 1. The results of the study on mice showed that doxorubicin alone only had a better effect on metastasis to certain organs, but overall, it was still unable to effectively inhibit breast cancer metastasis. The number of tumors in the liver and lungs of Group 6 mice decreased significantly, indicating that simultaneous administration of the pharmaceutical composition of the present invention can effectively treat metastatic breast cancer. Although Group 7 mice were also administered the composition of the present invention, the dosage was half that of Group 6, so the effect of inhibiting breast cancer cell metastasis to the liver and lungs was poorer than that of Group 6.

[0094] The results of this example demonstrate that the pharmaceutical composition disclosed herein can not only inhibit the growth of triple-negative breast cancer, but can also effectively inhibit the metastasis of triple-negative breast cancer cells to other organs. This means that the pharmaceutical composition disclosed herein can be used to treat metastatic triple-negative breast cancer or advanced triple-negative breast cancer.

Claims

1. Use of a chemotherapeutic drug for preparing a pharmaceutical composition for treating triple-negative breast cancer and its metastasis, It is characterized in that The chemotherapy drug includes Actinomycin D and Doxorubicin.

2. The use as claimed in claim 1, It is characterized in that The pharmaceutical composition consists of the actinomycin D and the adriamycin.

3. The use according to claim 1 or 2, It is characterized in that When the subject to be administered with the pharmaceutical composition is a human, the dosage ratio of the actinomycin D to the doxorubicin is 1:10-1:

30.

4. The use as claimed in claim 3, It is characterized in that When the subject to be administered with the pharmaceutical composition is a human, the dosage ratio of the actinomycin D to the doxorubicin is 1:

25.

5. The use according to claim 1 or 2, It is characterized in that The pharmaceutical composition is used to bind to the nucleic acid sequence GCCG in a targeted manner.

6. Use of a chemotherapeutic drug for preparing a nucleic acid intercalator, It is characterized in that The chemotherapy drug comprises actinomycin D and adriamycin; the nucleic acid intercalator is used for combining with the GCCG sequence in the nucleic acid molecule.

7. The use according to claim 6, It is characterized in that The nucleic acid intercalator consists of the actinomycin D and the doxorubicin.

8. The use according to claim 6 or 7, It is characterized in that When the subject to be administered with the nucleic acid intercalator is a human, the dosage ratio of the actinomycin D to the doxorubicin is 1:10-1:

30.

9. The use according to claim 8, It is characterized in that The dosage ratio of the actinomycin D to the doxorubicin is 1:25.

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