Application of liranaftate in preparation of anti-tumor metastasis drugs
Through the application of lirannaphthalate and its salts, combined with other anti-tumor components, drugs that can effectively inhibit tumor metastasis are prepared, which solves the shortcomings of tumor metastasis treatment in the prior art and provides an effective treatment option for malignant tumor metastasis , has significant inhibitory effect and good safety and economicality.
Patent Information
- Application Number
- CN202411274396.9
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2024-09-12
- Publication Date
- 2024-12-31
AI Technical Summary
Existing anti-tumor drugs mainly target primary tumors, and there is a lack of drugs that effectively inhibit tumor metastasis, resulting in more than 90% of patients with malignant tumors dying of tumor metastasis.
Liranalate or a pharmaceutically acceptable salt thereof is used to prepare anti-tumor and/or anti-tumor metastasis drugs, by inhibiting the metastasis, migration, adhesion and invasion of tumor cells, combined with other anti-tumor components such as paclitaxel and gemcitabine, Form a combination of drug with multiple dosage forms and routes of administration.
Lirannaphthalate significantly inhibits the metastasis and migration of tumor cells, enhances the inhibitory effect on distant metastases, and does not affect primary tumor treatment. It provides an effective treatment option for malignant tumor metastasis, which is safe and economical.
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Abstract
Description
Technical Field
[0001] The invention belongs to the technical field of biomedicine, and specifically relates to the application of liranabate in the preparation of anti-tumor metastasis drugs. Background Art
[0002] Malignant tumors are one of the most common causes of death worldwide. Although progress has been made in the treatment of malignant tumors in recent years, tumor metastasis is still the cause of death for more than 90% of cancer patients. In addition to infiltrating and growing at the primary site and affecting adjacent organs, malignant tumors can also break off from the primary tumor and invade lymphatic vessels, blood vessels, etc., spreading to other parts of the body to form distant metastatic lesions and metastatic tumors. This process is called tumor metastasis. Tumor metastasis involves a variety of complex mechanisms, such as epithelial-mesenchymal transition of tumor cells, occurrence of tumor stem cells, angiogenesis, resistance of tumor cells to anoikis, changes in cell adhesion molecules, etc. The basic manifestation of tumor metastasis is the enhancement of tumor cell adhesion, invasion and migration ability. Inhibiting the adhesion, invasion and migration of tumor cells can effectively inhibit tumor metastasis.
[0003] In recent years, the prevalence and mortality of malignant tumors have been increasing year by year. And because malignant tumors are prone to metastasis, clinical medication and surgical treatment are extremely difficult, so that more than 90% of malignant tumor patients die from tumor metastasis. At the same time, tumor metastasis can occur in the "early" state when the primary tumor is still very small. More and more evidence shows that when the primary tumor is still in a tiny state, tumor cells can already spread to distant sites. Therefore, inhibiting tumor metastasis has become a key link in the prevention and treatment of malignant tumors, and is also the focus of saving cancer patients.
[0004] However, although the FDA has approved more than 200 anti-tumor drugs of various types, most of them target primary tumors, directly kill primary tumor cells or inhibit the proliferation of primary tumors, and there is an urgent need for drugs that inhibit tumor metastasis. Therefore, for tumor treatment, providing a drug that can inhibit tumor metastasis has very important clinical practical significance.
[0005] In view of this, the present invention is proposed. Summary of the invention
[0006] The object of the present invention is to provide liranabate or a pharmaceutically acceptable salt thereof for use in preparing anti-tumor and / or anti-tumor metastasis drugs.
[0007] The technical solution adopted by the present invention is:
[0008] The first aspect of the present invention provides the use of liranabate or a pharmaceutically acceptable salt thereof in the preparation of an anti-tumor drug.
[0009] In some embodiments of the present invention, the tumor includes at least one of breast cancer, pancreatic cancer, lung cancer, melanoma, gastric cancer, malignant glioma, liver cancer, colorectal cancer, esophageal cancer, kidney cancer, prostate cancer, ovarian cancer, cervical cancer, thyroid cancer, and endometrial cancer.
[0010] The second aspect of the present invention provides the use of liranabate or a pharmaceutically acceptable salt thereof in the preparation of an anti-tumor metastasis drug.
[0011] In some embodiments of the present invention, the tumor includes at least one of breast cancer, pancreatic cancer, lung cancer, melanoma, gastric cancer, malignant glioma, liver cancer, colorectal cancer, esophageal cancer, kidney cancer, prostate cancer, ovarian cancer, cervical cancer, thyroid cancer, and endometrial cancer.
[0012] In some embodiments of the present invention, the metastasis includes lung metastasis, liver metastasis, lymph node metastasis, bone metastasis, and brain metastasis.
[0013] In some embodiments of the present invention, the lung metastasis includes lung cancer metastasis, breast cancer metastasis, liver cancer metastasis, colorectal cancer metastasis, pancreatic cancer metastasis, cervical cancer metastasis, thyroid cancer metastasis or melanoma metastasis.
[0014] The third aspect of the present invention provides the use of liranabate or a pharmaceutically acceptable salt thereof in the preparation of a medicament for inhibiting the metastasis and / or migration and / or adhesion and / or invasion of tumor cells.
[0015] Acceptable salts include acid addition salts and base addition salts.
[0016] In some embodiments of the present invention, the pharmaceutically acceptable salts include, but are not limited to, pharmaceutically acceptable acid addition salts, such as salts of inorganic acids such as hydrochloric acid, hydrobromic acid, phosphoric acid, metaphosphoric acid, nitric acid and sulfuric acid, and salts of organic acids such as acetic acid, benzenesulfonic acid, benzoic acid, citric acid, ethanesulfonic acid, fumaric acid, gluconic acid, glycolic acid, isethionic acid, lactic acid, lactobionic acid, maleic acid, malic acid, methanesulfonic acid, succinic acid, p-toluenesulfonic acid and tartaric acid; salts of pharmaceutically acceptable bases are ammonium salts, alkali metal salts (such as sodium salts and potassium salts) and alkaline earth metal salts (such as magnesium salts and calcium salts) and salts of tromethamine (2-amino-2-hydroxymethyl-1,3-propanediol), diethanolamine, lysine or ethylenediamine.
[0017] In some embodiments of the present invention, the medicament contains an effective dose of liranaftate or a pharmaceutically acceptable salt thereof.
[0018] In the present invention, the liranabactate or a pharmaceutically acceptable salt thereof significantly increases the metastasis and / or migration and / or adhesion and / or invasion of tumor cells at a concentration of 0 to 200 μM, wherein the concentration of liranabactate or a pharmaceutically acceptable salt thereof is not zero.
[0019] In some embodiments of the present invention, the effective dose is 5 to 150 mg / kg body weight.
[0020] In the present invention, the effective dose can be reasonably adjusted according to the actual situation and the judgment of the clinician. For different species, it can be reasonably adjusted based on the drug dose conversion formula or ratio between different species in the art.
[0021] In some embodiments of the present invention, the drug further comprises at least one other component having an anti-tumor effect.
[0022] In some embodiments of the present invention, the ingredients include paclitaxel and gemcitabine.
[0023] In some embodiments of the present invention, the drug further comprises a pharmaceutically acceptable excipient.
[0024] In some embodiments of the present invention, the pharmaceutically acceptable excipients include: at least one of a diluent, a binder, a wetting agent, a lubricant, a disintegrant, a solvent, an emulsifier, a solubilizer, a preservative, a pH regulator, an osmotic pressure regulator, a surfactant, a coating material, an antioxidant, an antibacterial agent or a buffer.
[0025] In some embodiments of the present invention, the dosage form of the drug includes at least one of a suspension, granules, capsules, powders, tablets, emulsions, solutions, pills, injections, oral preparations, suppositories, enemas, aerosols, patches or drops.
[0026] In some embodiments of the present invention, the administration route of the drug includes at least one of intravenous injection, intraperitoneal injection, intramuscular injection, subcutaneous injection, oral administration, sublingual administration, nasal administration, aerosol administration or transdermal administration.
[0027] The second aspect of the present invention provides a pharmaceutical composition, which comprises lanathate or a pharmaceutically acceptable salt thereof and an anti-tumor component; the anti-tumor component comprises paclitaxel and gemcitabine.
[0028] In some embodiments of the present invention, the molar ratio of lanaphthate or its pharmaceutically acceptable salt to the anti-tumor component is 0.1-400; for example, the molar ratio of lanaphthate or its pharmaceutically acceptable salt to the anti-tumor component is 1, 10, 40, 80, 100, 160, 200, 250, 300, 320, 350, etc.
[0029] The beneficial effects of the present invention are:
[0030] Liranabate has the effect of significantly inhibiting the adhesion, invasion and migration of tumor cells in vitro, and can significantly inhibit the spread and growth of metastatic tumors other than primary tumors in vivo. When liranabate is used in combination with anti-tumor drugs, it does not affect the therapeutic effect of anti-tumor drugs on primary tumors while exerting anti-tumor metastasis effects. Therefore, it can be used to prepare drugs for anti-tumor metastasis, especially it can be used in combination with chemotherapy, targeted drugs, etc. to "take a two-pronged approach" to prepare anti-tumor drug combination drugs that target both primary tumors and metastatic tumors. In addition, liranabate is a drug that has been used clinically for many years, with good safety and low price. As mentioned above, more than 90% of malignant tumor patients die from distant metastasis, and anti-tumor metastasis drugs are urgently needed clinically. In summary, the anti-tumor metastasis drugs prepared by liranabate can provide treatment options for a large number of malignant tumor patients, with high potential commercial value and attractive application prospects. BRIEF DESCRIPTION OF THE DRAWINGS
[0031] Figure 1 The inhibitory effect of liranablatate (LNT) on the metastasis biomarkers of breast cancer 4T1 cells in vitro (A), the inhibitory effect on the migration of breast cancer 4T1 cells in vitro (B), and the inhibitory effect on the adhesion of breast cancer HCC-1937 cells in vitro (C).
[0032] Figure 2 The inhibitory effects of liranabate (LNT) on the adhesion (A) and invasion (B) of lung cancer NCI-H1975 cells in vitro.
[0033] Figure 3 The inhibitory effect of liranablatate (LNT) on the adhesion of pancreatic cancer PANC-1 cells (A) and MIA PaCa-2 cells (B) in vitro.
[0034] Figure 4 The inhibitory effect of liranablatate (LNT) on the adhesion of melanoma A-375 cells in vitro.
[0035] Figure 5 The effect of lilanthate (LNT) combined with clinical anti-tumor drugs (paclitaxel (TAXOL), gemcitabine (Gemcitabine)) on the activity of malignant tumor cells from different organs. (A) Breast cancer HCC-1937 cells, (B) Lung cancer NCI-H1975 cells, (C) Pancreatic cancer Mia PaCa-2 cells, (D) Pancreatic cancer PANC-1 cells, (E) Melanoma A-375 cells. Compared with the Control group: ns no significant difference.
[0036] Figure 6Effects of liranabate (LNT) on experimental lung metastasis in a mouse model of syngeneic transplantation of breast cancer 4T1 cells. Tumor bioluminescence imaging (A), mouse body weight (B) and mouse survival rate (C). Compared with the model group: *P < 0.05, **P < 0.01.
[0037] Figure 7 Effects of liranablatate (LNT) on lung tumor metastasis in the experimental lung metastasis model of breast cancer 4T1 cell syngeneic transplantation mice. Bunn's staining (A) and statistical analysis results of lung metastatic tumors (C), H&E staining (B). DETAILED DESCRIPTION
[0038] The following will be combined with the embodiments to clearly and completely describe the concept of the present invention and the technical effects produced, so as to fully understand the purpose, characteristics and effects of the present invention. Obviously, the described embodiments are only part of the embodiments of the present invention, not all of them. Based on the embodiments of the present invention, other embodiments obtained by those skilled in the art without creative work are all within the scope of protection of the present invention.
[0039] Liranaftate (LNT) (CAS No. 88678-31-3) chemical structure (Formula 1) is a new antifungal drug that was first launched in Japan in August 2000. LNT is a squalene epoxidase inhibitor that inhibits the epoxidation of squalene in fungal cell membranes and inhibits the synthesis of ergosterol, a component of cell membranes, to exert antifungal effects.
[0040] Liranabate has good antifungal effects, has been used clinically for many years, has low toxicity to humans, is highly safe, and has good research and development value.
[0041]
[0042] Experimental Materials and Methods
[0043] 1. Cell level experiments:
[0044] Experimental Materials:
[0045] 1. Experimental cells
[0046] Tumor cell lines 4T1, HCC-1937, NCI-H1975, PANC-1, MIA PaCa-2 and A-375 cells were purchased from the American ATCC cell bank.
[0047] 2. Cell culture
[0048] Complete medium (RPMI-1640 medium containing 10% FBS and 1% double antibody) was used for routine cell culture of 4T1, HCC-1937, and NCI-H1975 cells. Complete medium (DMEM medium containing 10% FBS and 1% double antibody) was used for routine cell culture of PANC-1, MIA PaCa-2, and A-375 cells.
[0049] 3. Preparation of drug stock solution
[0050] Liranab ester (purchased from Maclean, purity> 99%) powder was weighed and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution with a concentration of 20 mM.
[0051] 2. Animal level experiments:
[0052] 1. Experimental materials and reagents
[0053] Liranabate, source as mentioned above. SPF Balb / c mice (6-8 weeks old, female) were purchased from Beijing Yaokang Biotechnology Co., Ltd. Paraformaldehyde, xylene, H&E staining solution set, and neutral gum were purchased from Beijing Solarbio Science & Technology Co., Ltd.
[0054] Experimental Example 1: Liranabate inhibits the expression of metastasis markers in breast cancer 4T1 cells
[0055] Test steps: 4T1 cells in logarithmic growth phase were cultured in 6-well plates, 5% CO2, and grown overnight at 37°C. Different concentrations of liranabactate (0 μM, 5 μM, 10 μM, 20 μM) were used in a culture medium containing 1% FBS. After 48 hours of treatment, the expression of tumor metastasis biomarkers was determined by conventional Western blotting.
[0056] Test results see Figure 1 A, shows the effects of different concentrations of liranablast on tumor metastasis markers in breast cancer 4T1 cells; the results indicate that liranablast inhibits the expression of N-cadherin, snail, and slug proteins in 4T1 cells in a concentration-dependent manner, and increases the expression of E-cadherin protein.
[0057] Experimental Example 2: Liranabate inhibits the migration of breast cancer 4T1 cells
[0058] 4T1 cells were seeded in 6-well plates and the cell density was adjusted to 2 × 10 cells per ml. 5When the cell density in the 6-well plate reached 90%, the cells were scratched with a pipette tip (10 μL), and different concentrations of liranabate (0 μM (i.e., Control, the same below), 5 μM, 10 μM, and 20 μM) were administered to the cells in a culture medium containing 1% FBS and cultured for 24 hours. The scratch conditions at 0 and 24 hours were recorded using a microscope.
[0059] Test results see Figure 1 B, shows the effect of different concentrations of liranabate on the migration of 4T1 cells. The results show that liranabate inhibits the migration of 4T1 cells in a concentration-dependent manner.
[0060] Experimental Example 3: Liranabate inhibits the adhesion of breast cancer HCC-1937 cells
[0061] Test steps:
[0062] Plate coating: Place fibronectin, matrigel and college I stored at -20℃ in a 37℃ water bath until completely dissolved, and prepare them into working solutions with a concentration of 10μg / mL using serum-free culture medium. Use 300uL / well of working solution to completely cover a 48-well plate, place at room temperature overnight, discard excess liquid and drain the plate.
[0063] HCC-1937 cells in logarithmic growth phase were cultured in 6-well plates, 5% CO2, and 37°C overnight. Different concentrations of liranabate (0 μM, 5 μM, 10 μM, and 20 μM) were used in a medium containing 1% FBS for 48 h, and then the cells were digested with trypsin and the cell number was adjusted to 2×10 5 The cells were cultured in a coated 48-well plate. After 2 hours, the cells were washed three times with PBS solution to remove the non-adherent cells. The cells were fixed in 4% PFA solution for 20 minutes and stained with crystal violet for about 15 minutes. The staining solution was then discarded and the cells were washed several times. After drying, the cells were observed under a microscope and multiple different fields of view were selected for photographic observation. The experiment was repeated three times.
[0064] Test results see Figure 1 C, shows the effect of different concentrations of liranabactate on the adhesion of HCC-1937 cells. The results show that liranabactate inhibits the adhesion of HCC-1937 cells in a concentration-dependent manner.
[0065] Experimental Example 4: Liranabate inhibits the adhesion of lung cancer NCI-H1975 cells
[0066] Test steps: Logarithmically growing NCI-H1975 cells were used for the experiment, and the steps were the same as those in Experimental Example 3.
[0067] Test results see Figure 2A, shows the effect of different concentrations of liranabactate on the adhesion of NCI-H1975 cells. The results show that liranabactate inhibits the adhesion of NCI-H1975 cells in a concentration-dependent manner.
[0068] Experimental Example 5: Liranabate inhibits the invasion of lung cancer NCI-H1975 cells
[0069] The Transwell chamber was coated with matrix gel in advance, and 200 μL of serum-free cell suspension was added to the upper chamber of the chamber, with a cell density of 1×10 cells per ml. 6 cells, add 600 μL culture medium (10% FBS) to the lower chamber, culture for 24 hours, discard the supernatant, wipe off the outer layer of cells in the chamber, fix with 4% methanol for 30 minutes. Dry, stain with 0.1% crystal violet for 10 minutes, and wash with PBS. After drying, observe under a microscope and select multiple different fields of view for observation. Repeat the experiment three times.
[0070] Test results see Figure 2 B, shows the effect of different concentrations of liranabate on the invasion of NCI-H1975 cells. The results show that liranabate inhibits the invasion of NCI-H1975 cells in a concentration-dependent manner.
[0071] Experimental Example 6: Liranabate inhibits the adhesion of pancreatic cancer PANC-1 and MIA PaCa-2 cells
[0072] Test steps: Logarithmically growing PANC-1 and MIA PaCa-2 cells were used for the experiment, and the steps were the same as those in Experimental Example 3.
[0073] Test results see Figure 3 , showing the effects of different concentrations of liranabate on the adhesion of PANC-1 and MIA PaCa-2 cells. The results show that liranabate inhibits the adhesion of PANC-1 (A) and MIA PaCa-2 (B) cells in a concentration-dependent manner.
[0074] Experimental Example 7: Liranabate inhibits the adhesion of melanoma A-375 cells
[0075] Test steps: A-375 cells in logarithmic growth were used for the experiment, and the steps were the same as those in Experimental Example 3.
[0076] Test results see Figure 4 , showing the effect of different concentrations of liranabate on the adhesion of A-375 cells. The results show that liranabate inhibits the adhesion of A-375 cells in a concentration-dependent manner.
[0077] Experimental Example 8: Effect of combined use of liranabactate and clinical anti-tumor drugs on tumor cell activity
[0078] HCC-1937, NCI-H1975 and A-375 cells in logarithmic growth phase were cultured in 96-well plates and grown overnight at 37° C. Liranabate and paclitaxel (TAXOL) were added to the culture medium containing 1% FBS for 24 hours, and the cell survival rate was determined by MTT method.
[0079] PANC-1 and MIA PaCa-2 cells in logarithmic growth phase were cultured in 96-well plates and grown overnight at 37° C. Liranabate and gemcitabine were added to the culture medium containing 1% FBS for 48 hours, and the cell survival rate was determined by MTT method.
[0080] Test results see Figure 5 When different concentrations of liranabate are used in combination with the clinical anti-tumor drugs paclitaxel (TAXOL) or gemcitabine (Gemcitabine), they will not affect the latter's killing effect on tumor cells.
[0081] Example 9 Effect of lanabetate on experimental lung metastasis in a mouse model of syngeneic transplantation of breast cancer 4T1 cells
[0082] 1. Establishment of 4T1 cell mouse breast cancer lung metastasis model
[0083] The artificial lung metastasis model of mouse malignant breast cancer 4T1 cells with luciference marker was selected for this example. After Balb / c mice (18 g ± 2 g) were adapted to the environment for one week, tumor inoculation experiments were performed. 4T1-LUC cells were digested with trypsin and the single cell suspension concentration was adjusted to 5×10 6 / mL, the cells were inoculated in a volume of 0.1 mL on the mammary pad of the second nipple on the right side of Balb / c mice, with an inoculum of 5×10 5 After 3 days, the in situ tumor formation of mice was observed, and mice without tumor formation were eliminated and divided into groups for drug administration.
[0084] 2. Experimental Grouping and Drug Administration
[0085] The successfully inoculated mice were randomly divided into the model group, LNT low-dose group (10 mg / kg), LNT medium-dose group (25 mg / kg), and LNT high-dose group (50 mg / kg), with 10 mice in each group. The specific dosage regimen was 0.2 mL / mouse / day for a total of 28 days, and the control group was given lysozyme saline. The weight of the mice and the size of the tumor were weighed and recorded every two days during the administration period.
[0086] 3. Bioluminescence imaging
[0087] The day after the end of the administration, mice were intraperitoneally injected (150 mg / kg) with 30 mg / mL D-luciferin (Biyuntian) in PBS. Bioluminescence was detected in automatic exposure mode. The bioluminescence signal was analyzed using Living Image 4.4 software (Perkin Elmer).
[0088] 4. Animal killing, sampling and sample processing
[0089] After the experiment, the mice were killed by cervical dislocation. The lung tissues of the mice were obtained after dissection and fixed and stained in Bunn's staining solution. The lung tissues were observed under a dissecting microscope and the number of metastatic nodules in the lungs was recorded. After taking pictures, the tissues were fixed in 4% PFA fixative.
[0090] 5. Histopathological examination
[0091] The lung tissues were fixed with 4% paraformaldehyde, embedded in paraffin, cut into 4 μm thick sections, stained with H&E, observed under a light microscope, photographed, and analyzed.
[0092] 6. Experimental results
[0093] 1) Liranabate significantly improved the survival rate of mice
[0094] To evaluate the effect of liranabate on lung metastasis of breast cancer in mice, a highly metastatic breast cancer model of Balb / c mice was established. Figure 6 A. From the bioimaging results, it can be seen that compared with the model group, the fluorescence value of mice in the liranabactate-treated group was significantly reduced. Figure 6 B shows the weight changes of mice after tumor inoculation and drug administration. There were no significant differences among the four groups. Figure 6 C is the survival rate of mice during the experiment;
[0095] The results showed that mice began to die on the 19th day after tumor inoculation, and the survival rate of mice in the model group was 70% by the end of the experiment. After treatment with different doses of liranabate, the survival rate of mice was significantly improved. Among them, the survival rate of mice in the medium and high dose groups was 90%, which was significantly different from that in the model group. Liranabate significantly increased the survival rate of tumor-bearing mice.
[0096] 2) Liranabate inhibits lung metastasis of breast cancer in mice
[0097] In order to more accurately evaluate the inhibitory effect of liranabate on lung metastasis of mouse breast cancer, the lungs of each group of mice were stained with Bouin's staining and H&E staining. Figure 7 shown.
[0098] Figure 7A and 7C show that the model group mice had obvious lung metastasis nodules in their lungs, while the number of lung metastasis nodules, nodule volume, and metastasis rate of mice given liranabate were significantly reduced. Figure 7 As shown in B, in addition to normal lung cells, there are a large number of cancer cells in the lungs of mice in the model group, and a large number of metastatic tumors are formed. There are only a small number of cancer cells and metastatic tumors in the lungs of mice in the low-dose and medium-dose liranabate groups. In particular, in the high-dose liranabate group, there are almost no obvious metastatic tumors visible to the naked eye, and only a small number of cancer cell metastases occur. The H&E results are consistent with the nodules visible to the naked eye in the aforementioned Bunn's staining results.
[0099] The above results indicate that liranabactate has a significant inhibitory effect on lung metastasis of breast cancer in mice.
[0100] The above specific implementations have been described in detail for the present invention, but the present invention is not limited to the above embodiments. Various changes can be made within the knowledge of ordinary technicians in the relevant technical field without departing from the purpose of the present invention. In addition, the embodiments of the present invention and the features in the embodiments can be combined with each other without conflict.
Claims
1. Use of liranabate or a pharmaceutically acceptable salt thereof in the preparation of an anti-tumor drug.
2. Use of liranabate or a pharmaceutically acceptable salt thereof in the preparation of an anti-tumor metastasis drug.
3. The use according to claim 1 or 2, characterized in that: The liranabate or a pharmaceutically acceptable salt thereof inhibits the metastasis and / or migration and / or adhesion and / or invasion of tumor cells.
4. The use according to claim 1 or 2, characterized in that: The tumor includes at least one of breast cancer, pancreatic cancer, lung cancer, melanoma, gastric cancer, malignant glioma, liver cancer, colorectal cancer, esophageal cancer, kidney cancer, prostate cancer, ovarian cancer, cervical cancer, thyroid cancer, and endometrial cancer.
5. The use according to claim 2, characterized in that: The metastasis includes at least one of lung metastasis, liver metastasis, lymph node metastasis, bone metastasis, and brain metastasis.
6. The use according to claim 1 or 2, characterized in that: The drug also includes at least one other component having anti-tumor effect.
7. The use according to claim 6, characterized in that: The ingredients include paclitaxel and gemcitabine.
8. The use according to claim 1 or 2, characterized in that: The drug also includes pharmaceutically acceptable excipients; Preferably, the pharmaceutically acceptable excipients include: at least one of a diluent, a binder, a wetting agent, a lubricant, a disintegrant, a solvent, an emulsifier, a cosolvent, a solubilizer, a preservative, a pH regulator, an osmotic pressure regulator, a surfactant, a coating material, an antioxidant, an antibacterial agent or a buffer; Preferably, the dosage form of the drug includes at least one of suspension, granules, capsules, powders, tablets, emulsions, solutions, pills, pellets, injections, oral preparations, suppositories, enemas, aerosols, patches or drops; Preferably, the administration route of the drug includes at least one of intravenous injection, intraperitoneal injection, intramuscular injection, subcutaneous injection, oral administration, sublingual administration, nasal administration, aerosol administration or transdermal administration.
9. A pharmaceutical composition comprising lanabetate or a pharmaceutically acceptable salt thereof and at least one other component having an anti-tumor effect; preferably, the at least one other component having an anti-tumor effect comprises paclitaxel and gemcitabine.
10. The pharmaceutical composition according to claim 9, characterized in that The molar ratio of the lanaphthate or its pharmaceutically acceptable salt to the anti-tumor component is 0.1-400.