Application of Talniflumate in preparation of medicine for preventing and / or treating nasopharynx cancer

Abstract

The invention discloses an application of Talniflumate in preparation of a medicine for preventing and / or treating nasopharyngeal carcinoma, and particularly, the Talniflumate inhibits expression of SFPQ protein and can be used for treating the nasopharyngeal carcinoma. The invention reveals that the Talniflumate can be used as a small-molecule inhibitor to directly target and combine with oncogenic protein SFPQ and promote the degradation of the oncogenic protein SFPQ for the first time. According to the application disclosed by the invention, the Taniflufen is used for inhibiting the growth of nasopharyngeal carcinoma for the first time, and the Taniflufen shows remarkable inhibition capability on proliferation and migration of nasopharyngeal carcinoma cells and tumor growth in in-vitro and in-vivo experiments. According to the invention, a small-molecule inhibitor of the SFPQ is found through a computer virtual screening mode for the first time, it is found and verified for the first time that when the tanniflufen-ethyl and the cis-platinum are combined for use, a remarkable synergistic anti-tumor effect can be generated instead of simple effect superposition, and the anti-tumor effect of a combined medication group is remarkably superior to that of any single drug.

Description

TECHNICAL FIELD

[0001] The present application relates to the technical field of antitumor drugs, in particular, the application of Talniflumate in the preparation of a drug for preventing and / or treating nasopharyngeal carcinoma. BACKGROUND

[0002] Cisplatin exerts its anticancer effect by causing DNA double-strand breaks, and cancer cells can repair the damage and escape death by activating DNA damage repair pathways, especially the non-homologous end joining pathway, thereby developing drug resistance.

[0003] Although targeting DNA repair pathways to sensitize chemotherapy is a well-known concept, developing specific small molecule inhibitors targeting key regulators of the NHEJ pathway is still an unmet need in clinical treatment. SFPQ protein is just such a highly potential target, which is a multifunctional nuclear protein. Recent studies have gradually revealed its key role in cancer: 1. General upregulation of SFPQ in tumors and pro-cancer function: Independent studies have confirmed that SFPQ is highly expressed in various human cancers (such as liver cancer, colorectal cancer, etc.) and is closely related to the occurrence and development of tumors. For example, a study published by Feng Xinhuas laboratory at Zhejiang University in December 2023 in Developmental Cell revealed that SFPQ can form biomolecular condensates through liquid-liquid separation, trapping the key tumor suppressor protein Smad4, thereby directly inhibiting the tumor suppressor function of the TGF-β signaling pathway. This mechanism provides new important evidence for the pro-cancer function of SFPQ.

[0004] 2. Key role of SFPQ in DNA repair and chemotherapy resistance: SFPQ has been reported to be involved in DNA damage response and associated with the NHEJ repair pathway. However, in the specific context of nasopharyngeal carcinoma, whether and how SFPQ mediates cisplatin resistance by regulating the NHEJ pathway remains unknown.

[0005] 3. Exploration of SFPQ as a therapeutic target: Although existing technologies have recognized that SFPQ is a carcinogenic protein and a potential therapeutic target, there is currently no reported SFPQ small molecule inhibitor that can be used to treat cancer. Existing intervention methods are mostly limited to basic research level such as gene knockdown. For example, some studies have shown that knocking out SFPQ in BRAF V600E mutant colorectal cancer cells can induce synthetic lethality, but this has not been translated into a clinically available drug treatment regimen.

[0006] Talniflumate is a known drug. Its disclosed uses include: as a calcium-activated chloride channel blocker to reduce mucin synthesis and release, and has been studied for diseases such as cystic fibrosis; as an anti-inflammatory and analgesic, it works by inhibiting cyclooxygenase; recent studies have reported that Talniflumate can induce apoptosis in breast cancer cells and shows a synergistic effect when used in combination with paclitaxel, the mechanism of which is speculated to be related to the inhibition of mucin synthase GCNT3, etc.

[0007] To date, no literature or patent has disclosed or suggested that talniflumate can inhibit the SFPQ protein, let alone its use in the treatment of nasopharyngeal carcinoma or in reversing cisplatin resistance. The known mechanisms of action of talniflumate (chloride channel blockade, anti-inflammation) are entirely different from the novel mechanism of inhibition of SFPQ and interference with DNA repair discovered in this invention.

[0008] The existing technology mainly has the following problems: 1. Drug development targeting SFPQ protein remains a blank: Although existing technologies have confirmed SFPQ as a potential anti-cancer target through basic research (such as gene knockdown), there is still a lack of small molecule compounds that can directly and specifically inhibit SFPQ protein function. Although previous studies have confirmed that the oncogenic protein SFPQ is a key factor regulating the NHEJ pathway and mediating cisplatin resistance, gene manipulation techniques cannot be translated into clinically usable drugs. This has meant that "targeting SFPQ" has long remained a theoretical concept and cannot be applied to actual treatment. Currently, there are no targeted drugs in clinical practice that can effectively inhibit the non-homologous end joining (NHEJ) DNA repair pathway to sensitize cisplatin.

[0009] 2. Limited Solutions for Reversing Cisplatin Resistance: Overcoming cisplatin resistance is an urgent need to improve the treatment efficacy for nasopharyngeal carcinoma patients. However, current methods for overcoming cisplatin resistance mostly focus on broad-spectrum DNA damage response inhibitors, which often have unclear targets, high toxicity, or poor efficacy. Existing technologies have failed to provide an effective solution for reversing cisplatin resistance in nasopharyngeal carcinoma by precisely inhibiting the specific pathway of "SFPQ-NHEJ DNA repair." Therefore, there is an urgent clinical need for novel sensitization strategies targeting key node proteins with clear mechanisms, as exemplified in this invention, and for developing new drugs or strategies that can synergize with cisplatin.

[0010] 3. There are limitations in our understanding of the uses of the known compound tanylfluoxetine.

[0011] The prior art's understanding of talniflumate is limited to its traditional uses as an anti-inflammatory drug or a chloride channel blocker. These known mechanisms completely fail to reveal its core value of being able to target SFPQ and interfere with the DNA repair pathway. Therefore, the prior art essentially masks and underestimates the great application potential of talniflumate in the treatment of malignant tumors (especially in overcoming chemotherapy resistance), resulting in a waste of resources where an "old drug" fails to be "repurposed".

[0012] In summary, there is an insurmountable gap between current theory and application. That is, although it is known that SFPQ is the key to drug resistance, there is no available drug; although it is known that talniflumate is a safe compound, its subversive new function of targeting SFPQ is unknown. The present invention is completed to fill this gap. Summary of the Invention

[0013] The object of the present invention is to provide the use of Talniflumate in the preparation of a drug for preventing and / or treating nasopharyngeal carcinoma to inhibit the growth of nasopharyngeal carcinoma and reverse cisplatin resistance.

[0014] To achieve the above object, the present invention provides the use of Talniflumate in the preparation of an SFPQ inhibitor. The Chinese name of Talniflumate is talniflumate (chemical name: 2-(3-trifluoromethylphenyl)aminonicotinate, CAS No.: 66898-62-2), and its molecular formula is C 21 H 13 F3N2O4, and its chemical structural formula is as follows: .

[0015] As one of the preferred technical solutions, the SFPQ inhibitor is used to inhibit the expression or function of the SFPQ protein; the SFPQ protein has the amino acid sequence shown in SEQ ID NO: 1, or a variant having at least 90%, 95%, 98% or 99% sequence identity with SEQ ID NO: 1 and retaining the same biological function.

[0016] The present invention provides the use of Talniflumate in the preparation of a drug for preventing and / or treating solid tumors with high SFPQ expression. The Chinese name of Talniflumate is talniflumate, and its molecular formula is C 21 H 13 F3N2O4, and its chemical structural formula is as follows: .

[0017] The present invention provides the use of Talniflumate in the preparation of a drug for preventing and / or treating nasopharyngeal carcinoma. The Chinese name of Talniflumate is talniflumate, and its molecular formula is C 21 H13 F3N2O4 has the following chemical structural formula: .

[0018] As one of the preferred technical solutions, the nasopharyngeal carcinoma is EBERs-positive nasopharyngeal carcinoma.

[0019] As one of the preferred technical solutions, the nasopharyngeal carcinoma is drug-resistant nasopharyngeal carcinoma.

[0020] As a further preferred technical solution, the nasopharyngeal carcinoma is cisplatin-resistant nasopharyngeal carcinoma.

[0021] The present invention also provides a composition of Talniflumate and cisplatin.

[0022] As one of the preferred technical solutions, the molar ratio of Talniflumate to cisplatin is 1:1.

[0023] The present invention also provides the use of a composition of Talniflumate and cisplatin in the preparation of a medicament for the prevention and / or treatment of nasopharyngeal carcinoma.

[0024] As one of the preferred technical solutions, the combination of Talniflumate and cisplatin is used in the preparation of drugs for the treatment of drug-resistant nasopharyngeal carcinoma.

[0025] As a further preferred technical solution, the drug-resistant nasopharyngeal carcinoma is cisplatin-resistant nasopharyngeal carcinoma.

[0026] The present invention has the following beneficial effects: This invention provides the use of Talniflumate in the preparation of medicaments for the prevention and / or treatment of nasopharyngeal carcinoma. Specifically, Talniflumate inhibits the expression of SFPQ protein and can be used to treat nasopharyngeal carcinoma.

[0027] Compared with the prior art, the core improvement of this invention lies in: 1. This invention achieves a breakthrough from target recognition to practical application: Existing technologies only point out that SFPQ is a "potential" therapeutic target, while this invention provides a small molecule entity (tanifluoxetine) for the first time to achieve effective pharmacological intervention on this target, transforming theoretical concepts into feasible treatment plans.

[0028] This invention reveals for the first time that talniflumate can act as a small molecule inhibitor, directly targeting and binding to the oncogenic protein SFPQ, and promoting its degradation.

[0029] 2. This invention represents a revolutionary discovery of the functions of known compounds: This invention completely breaks away from the traditional framework of tanylfluridine's "anti-inflammatory" and "chlorine channel blocking" effects, and for the first time reveals and verifies its novel identity as an "SFPQ protein inhibitor" and its anti-cancer function. This is a fundamental expansion and deepening of our understanding of existing compounds.

[0030] This invention marks the first time tanidazole has been used to inhibit the growth of nasopharyngeal carcinoma. Tanidazole demonstrated significant inhibitory effects on the proliferation, migration, and tumor growth of nasopharyngeal carcinoma cells in both in vitro and in vivo experiments. Tanidazole effectively degrades the SFPQ protein, thereby inhibiting the NHEJ DNA repair pathway and making tumor cells more sensitive to cisplatin-induced DNA damage. It successfully reversed cisplatin resistance in nasopharyngeal carcinoma in both in vitro and animal models.

[0031] 3. This invention provides a novel synergistic treatment approach: This invention not only provides a single new drug, but also constructs a novel combination therapy (tanifluoxetine + cisplatin) with synergistic effects, providing a specific and effective tool to overcome the clinically challenging problem of cisplatin resistance.

[0032] This invention is the first to discover a small molecule inhibitor of SFPQ through computer virtual screening. It is also the first to discover and verify that the combination of tanidazole and cisplatin can produce a significant synergistic anti-tumor effect (CI<1), rather than a simple additive effect. The tumor-suppressing effect of the combination drug group is significantly better than that of either drug alone, achieving a "1+1>2" therapeutic effect.

[0033] The mechanism of this invention is clear and highly targeted: all technical effects are achieved through the clear mechanism of direct targeting and degradation of SFPQ by tanylfluoxetine. The target is clear and the logical chain is complete, providing a solid basis for precision drug treatment.

[0034] In addition to the objectives, features, and advantages described above, the present invention has other objectives, features, and advantages. The invention will now be described in further detail with reference to the figures. Attached Figure Description

[0035] The accompanying drawings, which form part of this application, are used to provide a further understanding of the invention. The illustrative embodiments of the invention and their descriptions are used to explain the invention and do not constitute an undue limitation of the invention. In the drawings: Figure 1Taniflurane showed significant inhibitory effects on the proliferation, migration, and tumor growth of nasopharyngeal carcinoma cells in both in vitro and in vivo experiments. Among them, A shows that taniflurane, as an SFPQ inhibitor, effectively reduced SFPQ protein levels; B shows cell proliferation as detected by the CCK-8 assay; C shows cell proliferation as detected by the colony formation assay; D shows cell migration as detected by the Transwell cell migration assay; E shows cell migration as detected by the scratch healing assay; F shows the synergistic effect of taniflurane combined with cisplatin; and G shows that taniflurane inhibited nasopharyngeal carcinoma tumor growth in vivo and had a synergistic effect with cisplatin. Detailed Implementation

[0036] The embodiments of the present invention will be described in detail below with reference to the accompanying drawings. However, the present invention can be implemented in many different ways as defined and covered by the claims.

[0037] Example 1 Tanifluobate, as an SFPQ inhibitor, effectively reduces SFPQ protein levels. 1.1 Test objective: To verify that tanniflurane can downregulate the expression of SFPQ protein in nasopharyngeal carcinoma cells in a concentration-dependent manner.

[0038] 1.2 Test Method (Western Blot): Cell lines: HK-1 EBV and HONE1 EBV.

[0039] Preparation of stock solution: Dissolve tadalafil powder (TargetMol, T4503) in dimethyl sulfoxide (DMSO) to prepare a high-concentration stock solution (10 mg / ml) and store at -20°C. Before use, dilute with RPMI-1640 (Sango BBI, E600028-0500) complete medium containing 10% fetal bovine serum (FBS, Gibco) to ensure that the final DMSO concentration does not affect cell viability (typically below 0.1% (v / v)).

[0040] Cells were treated with different concentrations (0, 10, 20, 50 μM) of tanylfluoxetine for 24 hours.

[0041] Specific steps: Total protein was extracted from cells (using RIPA lysis buffer containing protease inhibitors).

[0042] Protein concentration was determined by the BCA method.

[0043] Take equal amounts of protein for SDS-PAGE electrophoresis.

[0044] Proteins are transferred to a PVDF membrane.

[0045] After blocking with TBST solution of 5% (w / v) skim milk for 1 hour, incubate with primary antibody at 4°C overnight.

[0046] Primary antibody used: Anti-SFPQ antibody (Santa Cruz, sc-374502).

[0047] Incubate with the corresponding HRP-labeled secondary antibody (ABclonal, AS003) at 37°C for 1 hour.

[0048] The signal was developed using the ECL chemiluminescence kit (BeyoECL Star, P0018AM) and detected using the chemiluminescence imaging system (SageCapture™ minute iChemi chemiluminescence imager).

[0049] 1.3 Evaluation Methods: Using β-Actin as an internal control, the gray values ​​of the SFPQ protein band were compared between the tansylate treatment groups and the DMSO control group at different concentrations. The degree of protein level reduction was semi-quantitatively analyzed using image analysis software (such as ImageJ).

[0050] 1.4 Experimental Results: Treatment with tannic acid ester significantly decreased the level of SFPQ protein in nasopharyngeal carcinoma cells in a concentration-dependent manner. Figure 1 (A) Example 2 Tanidazole effectively inhibits the activity, proliferation, and migration of nasopharyngeal carcinoma cells. EBV-positive nasopharyngeal carcinoma cell lines HK-1 EBV and HONE1 EBV were obtained from Professor Cao Shihua of the University of Hong Kong (PMID: 20091869).

[0051] CCK-8 assay for cell proliferation: Seed cells at an appropriate density (3000-5000 cells per well) in 96-well plates.

[0052] After the cells adhered, add gradient concentrations of tanylfluoxetine (0, 10, 20 μM) and incubate for 48-72 hours.

[0053] The cells were cultured at 37°C and 5% CO2 for 48 to 72 hours.

[0054] Add 100 μL of cell culture medium containing 10% CCK-8 reagent (supplier: APE×Bio) to each well.

[0055] After incubation for 1-4 hours, the absorbance at 450 nm was measured using an ELISA reader.

[0056] Results Calculation: The cell proliferation inhibition rate of the tannic acid ester treatment group compared with the solvent control group was determined by the absorbance value at 450 nm.Figure 1 (B) Clonal formation assay for cell proliferation: Cells were seeded at a low density (500-1000 cells) in 6-well plates.

[0057] Add tanylfluoxetine (20 μM) or DMSO, and change the solution every 3 days.

[0058] After culturing for 10-14 days, fix with 4% paraformaldehyde, stain with crystal violet, and count clones with more than 50 cells.

[0059] Results: Clonal counts were performed and statistical analysis was conducted (Image J software). Compared with the tanylfluoxetine treatment group, the number of colonies formed in the DMSO control group was significantly reduced (p<0.01). The results indicate that tanylfluoxetine can effectively inhibit the colony-forming ability of cells, thereby inhibiting tumor cell proliferation. Figure 1 (C) Transwell cell migration assay: Experimental methods: Nasopharyngeal carcinoma cells in the logarithmic growth phase were resuspended in serum-free culture medium, and the cell density was adjusted to 5 × 10⁻⁶. 4 Cells / 100 μL). 100 μL of cell suspension was seeded into the upper chamber of a Transwell chamber (supplier: Falcon). 500-600 μL of complete culture medium containing 10% fetal bovine serum was added to the lower chamber as a chemotactic agent. The experimental group received 20 μM tanidazole, while the control group received an equal volume of DMSO solvent. The culture plates were incubated at 37°C in a 5% CO2 cell culture incubator for 24 hours. After incubation, unmigrated cells were carefully wiped from the upper chamber membrane with a cotton swab. Cells that migrated to the lower chamber membrane were fixed with 4% paraformaldehyde for 15-30 minutes and then stained with 0.1% crystal violet solution for 20-30 minutes. After gentle rinsing with PBS and air-drying, multiple fields of view were randomly selected and photographed under an inverted microscope.

[0060] Result calculation: Migrating cells were counted in each field of view using ImageJ software. The mean cell count for each Transwell chamber was calculated, and the migration inhibition rate was calculated using the following formula: Migration inhibition rate (%) = [1 - (mean cell count in the tanflurane treatment group / mean cell count in the DMSO control group)] × 100%. The number of migrating cells in the tanflurane treatment group was significantly less than that in the DMSO control group ( p The value was <0.05 (Student's t-test), indicating that the tanidone effectively inhibited the migration ability of nasopharyngeal carcinoma cells. Figure 1 (D) Cell scratch healing assay for migration: Well-growing nasopharyngeal carcinoma cells were separated at an appropriate density (5 × 10⁻⁶). 5 Cells (per well) were seeded in 6-well plates and cultured in RPMI-1640 complete medium containing 10% fetal bovine serum. When cell confluence reached ≥90%, a sterile 200 μL pipette tip was used to create scratches perpendicular to the back of the wells on the monolayer of cells. Cells were gently washed 2-3 times with PBS to remove floating cells created by the scratches. The medium was then replaced with low-serum medium containing 1% fetal bovine serum, with 20 μM tanidazole or an equal volume of DMSO added as a solvent control. Cells were incubated at 37°C and 5% CO2. Observations were taken under an inverted microscope at 0 and 24 hours post-scraping, and images were taken at the same locations.

[0061] Results Calculation: ImageJ software was used to analyze scratch images taken at 0 hours and 24 hours, and the area of ​​the scratched region was measured. The scratch healing rate was calculated using the following formula: Scratch Healing Rate (%) = [(A0 - A] 24 [A0] × 100%. Where A0 represents the scratch area at 0 hours, A 24 The scratch area represents the area covered over 24 hours. The scratch healing rate in the tannic acid ester treatment group was significantly lower than that in the DMSO control group. p The value was <0.05 (Student's t-test), indicating that the tanidone effectively inhibited the migration ability of nasopharyngeal carcinoma cells. Figure 1 (China E) Example 3 The combination of tannic acid ester and cisplatin produces a synergistic effect. Set up the following experimental groups: Group A: Solvent control (DMSO) Group B: Cisplatin alone (concentration range: 10-80 μM) Group C: Tanifluoxetine alone (concentration range: 10-80 μM) Group D: Tanidazole and cisplatin were used in combination (molar ratio 1:1). Combination therapy involves administering medication simultaneously.

[0062] After culturing for 48-72 hours, cell viability was detected by the CCK-8 assay.

[0063] The Chou-Talalay method (using CompuSyn software) was used to calculate the Combination Index (CI) to quantitatively evaluate synergistic effects.

[0064] Effectiveness evaluation methods: CI < 0.9: indicates synergistic effect.

[0065] CI = 0.9-1.1: indicates an additive effect.

[0066] CI>1.1: indicates antagonistic effect.

[0067] Experimental results: The combined use of tannic acid ester and cisplatin at various concentration ratios resulted in CI values ​​significantly less than 0.9 (within the range of 0.63-0.74), indicating a clear synergistic effect between the two. Figure 1 (China F) Example 4 Tanidazole inhibits nasopharyngeal carcinoma tumor growth in vivo and exhibits a synergistic effect with cisplatin. 4.1 Test Objective To verify the inhibitory effect of tanidoxuridine on the growth of nasopharyngeal carcinoma tumors in animals, and to evaluate whether its combination with cisplatin can produce a synergistic antitumor effect.

[0068] 4.2 Test Methods (Mouse Subcutaneous Xenograft Model) Experimental animals: 4-6 week old female BALB / c nude mice were used.

[0069] Cell line and inoculation: HONE1 EBV cells in logarithmic growth phase were resuspended in a 1:1 mixture of PBS and Matrigel. 2 × 10⁶ cells were subcutaneously inoculated into the right axilla of each nude mouse. 6 100 cells (total volume 100 μL).

[0070] Grouping and drug administration: When the tumor volume grew to approximately 100 mm³, the mice were randomly divided into 4 groups (n=5): NC group (negative control group): daily intraperitoneal injection of an equal volume of solvent (2% DMSO, 50% PEG300, 5% Tween 80, 43% PBS).

[0071] Talniflumate group: daily intraperitoneal injection of tanniflumate (10 mg / kg, dissolved in the above solvent).

[0072] Cisplatin group: Cisplatin (5 mg / kg, dissolved in normal saline) was injected intraperitoneally every 3 days.

[0073] The combination therapy group (Talniflumate + Cisplatin) received daily intraperitoneal injections of 10 mg / kg, and cisplatin (5 mg / kg) every 3 days in combination with intraperitoneal injections.

[0074] Observation indicators: Tumor volume: The longest diameter (L) and shortest diameter (W) of the tumor were measured every 3 days using calipers, and the tumor volume was calculated using the formula: volume (mm³) = L × W² × 0.5.

[0075] Tumor weight: At the end of the experiment, all mice were euthanized, the tumors were completely removed and weighed.

[0076] 4.3 Effectiveness Evaluation Methods Plot the growth curves of tumor volume changes over time for each group.

[0077] At the end of the experiment, the differences between the average tumor volume and average tumor weight of each drug administration group and the NC group were compared, and the tumor inhibition rate was calculated.

[0078] By comparing the tumor-suppressing effects of the combination therapy group with the simple summation of the effects of each single drug group, and combining the combination index (CI<1) from previous in vitro experiments, the in vivo synergistic effect was comprehensively evaluated.

[0079] Use statistical methods (such as one-way ANOVA) to analyze the significant differences in data between groups.

[0080] 4.4 Experimental Results Tumor growth inhibition: Compared with the NC group, both the Talniflumate group and the Cisplatin group showed significant tumor inhibition effects (p<0.01). The combination therapy group showed the most significant tumor inhibition effect, with tumor volume and weight being significantly smaller than either single-drug group (p<0.001).

[0081] Synergistic effect verification: In vivo experimental results showed that the combined use of tanidoxime and cisplatin had a significantly better antitumor effect than the simple sum of their effects. This is corroborated by the in vitro CI value calculation results (CI<1), jointly confirming that the two have a clear synergistic antitumor effect both in vivo and in vitro. Figure 1 (China G) Conclusion: This embodiment fully demonstrates that tanidoxuridine monotherapy can effectively inhibit the growth of nasopharyngeal carcinoma tumors in vivo, and that its combination with cisplatin, a first-line chemotherapy drug, produces a strong synergistic effect, significantly enhancing the tumor-suppressing effect. This provides solid in vivo experimental evidence for the development of tanidoxuridine to overcome cisplatin resistance in nasopharyngeal carcinoma and improve the efficacy of combination chemotherapy.

[0082] The above description is merely a preferred embodiment of the present invention and is not intended to limit the invention. Various modifications and variations can be made to the present invention by those skilled in the art. Any modifications, equivalent substitutions, improvements, etc., made within the spirit and principles of the present invention should be included within the scope of protection of the present invention.

Claims

1. The application of talniflumate in the preparation of SFPQ inhibitors, characterized in that, The Chinese name of Talniflumate is Taniflumate, and its molecular formula is C 21 H 13 F3N2O4, and its chemical structural formula is as follows: 。 2. The use of Talniflumate in the preparation of drugs for the prevention and / or treatment of SFPQ-overexpressing solid tumors, characterized in that, The Chinese name of Talniflumate is taniflumate, and its molecular formula is C 21 H 13 F3N2O4, and its chemical structural formula is as follows: 。 3. The use of Talniflumate in the preparation of drugs for the prevention and / or treatment of nasopharyngeal carcinoma, characterized in that, The Chinese name of Talniflumate is taniflumate, and its molecular formula is C 21 H 13 F3N2O4, and its chemical structural formula is as follows: 。 4. The application according to claim 3, characterized in that, The nasopharyngeal carcinoma mentioned is EBERs-positive nasopharyngeal carcinoma.

5. A combination of Talniflumate and cisplatin.

6. The composition according to claim 5, characterized in that, The molar ratio of Talniflumate to cisplatin is 1:

1.

7. The composition according to claim 5, characterized in that, The use of a combination of talniflumate and cisplatin in the preparation of medicaments for the prevention and / or treatment of nasopharyngeal carcinoma.

8. The composition according to claim 5, characterized in that, Application of the combination of Talniflumate and cisplatin in the preparation of drugs for the treatment of drug-resistant nasopharyngeal carcinoma.

9. The composition according to claim 5, characterized in that, The drug-resistant nasopharyngeal carcinoma mentioned is cisplatin-resistant nasopharyngeal carcinoma.

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