Application of DL-3-phenyllactic acid in the preparation of drugs for treating cardiac myxoma

Abstract

This invention discloses the application of DL-3-phenyllactic acid in the preparation of drugs for treating cardiac myxoma. Based on metabolomics findings that the level of endogenous DL-3-phenyllactic acid in the serum of patients was significantly downregulated, this invention utilizes a cardiac myxoma organoid model derived from patient cardiac myxoma tissue for pharmacodynamic validation, confirming that DL-3-phenyllactic acid can dose-dependently inhibit the proliferation of cardiac myxoma organoids, with an IC50 value of [value missing]. 50 The effective molecular weight was 95.52 μM. Network pharmacology analysis suggests that its mechanism of action may involve key targets such as AKT1 and SRC. This invention reveals for the first time the therapeutic efficacy of DL-3-phenyllactic acid against cardiac myxoma, providing solid preclinical experimental evidence for its development into a drug for treating cardiac myxoma. This invention has non-obviousness and significant clinical application value.

Description

Technical Field

[0001] This invention specifically relates to the pharmaceutical application of a known compound, DL-3-phenyllactic acid, particularly its application in the preparation of a drug for treating cardiac myxoma, which falls under the field of medicine and health. Background Technology

[0002] Cardiac myxoma (CM) is the most common primary cardiac tumor in clinical practice. Although pathologically classified as benign, its clinical manifestations often pose a serious threat to the patient's life and health. From a pathophysiological perspective, the most dangerous characteristic of cardiac myxoma lies in the fragile texture and easy detachment of its tissue components, which can lead to tumor fragments breaking off and triggering systemic embolic events, including life-threatening complications such as cerebral embolism and coronary artery embolism. Even more seriously, some patients present with sudden death as their initial symptom. This unique biological behavior makes the clinical diagnosis and treatment of cardiac myxoma a unique challenge. Currently, surgical resection remains the only effective treatment for cardiac myxoma, and no drug treatment strategy has been proposed. However, surgical strategies currently face many challenges. Firstly, postoperative recurrence is becoming increasingly significant, especially in certain special populations, such as patients with familial Carney syndrome, where the recurrence rate can be as high as 22%. Secondly, cardiac myxomas are more common in middle-aged and elderly patients, who often have multiple underlying diseases and poor tolerance to open-chest surgery, leading to a higher risk of perioperative complications. Thirdly, for multiple tumors or those in special anatomical locations, such as those involving important conduction systems or valve structures, complete surgical resection is often difficult to achieve. It is worth noting that even with complete resection, a small percentage of patients still experience distant metastases. Compared to traditional surgery, targeted therapy has many potential advantages: its minimally invasive nature can significantly reduce treatment risks, especially suitable for elderly patients or those with multiple comorbidities; intervention targeting specific molecular pathways may be more effective in preventing recurrence; and systemic administration can simultaneously treat multiple lesions or micrometastases. In recent years, with the deepening research into the molecular mechanisms of cardiac myxomas, several potential therapeutic targets have been gradually revealed. Simultaneously, angiogenic factors and inflammatory mediators in the tumor microenvironment may also become new targets for intervention. Faced with these clinical challenges and opportunities, developing novel non-surgical therapies has become a key focus of current research on cardiac myxomas. In the field of biomedical research, research on organoid models constructed for benign tumors is relatively scarce, and organoids derived from benign cardiac tumors are even rarer. The emergence of organoid models aims to overcome the limitations of traditional research models. Traditional two-dimensional cell culture struggles to simulate the three-dimensional growth environment of cells in vivo and the complex intercellular interactions, while animal models suffer from high costs, lengthy processes, ethical controversies, and species differences. As a three-dimensional cell culture system, organoids simulate the in vivo microenvironment, prompting cells to form small tissues with specific structures and functions in vitro, providing a novel technological platform for biomedical research. As a preclinical research model, it helps to more accurately assess the safety and efficacy of new therapies, thereby accelerating the drug development process and advancing disease treatment research.

[0003] DL-3-phenyllactic acid, a naturally occurring organic acid with significant biological activity, is the racemic form of naturally occurring phenyllactic acid. It typically exists in various natural systems as a microbial metabolite. Its molecular structure simultaneously encompasses a hydrophobic benzene ring and hydrophilic hydroxyl and carboxyl groups, endowing it with unique amphiphilic properties, a structural feature that forms the basis of its diverse biological functions. Its value lies in its broad-spectrum and highly effective antibacterial and bacteriostatic abilities, exhibiting significant inhibitory effects against various Gram-positive bacteria, Gram-negative bacteria, and fungi. DL-3-phenyllactic acid is commonly used as a natural and safe preservative in the food, cosmetic, and pharmaceutical industries to extend product shelf life and improve hygiene and safety. It can also be used in agriculture and the feed industry as a biological antifungal agent and a regulator of animal gut health. It is worth noting that current research on the direct application of DL-3-phenyllactic acid in the treatment of human diseases is relatively scarce, with only a few studies exploring its potential value in the treatment of pulmonary fibrosis and acute lung injury.

[0004] There are currently no reports of DL-3-phenyllactic acid or its pharmaceutical compositions being developed as drugs for the treatment of cardiac myxoma. Summary of the Invention

[0005] This invention aims to address the clinical pain point of lacking targeted drugs for cardiac myxoma and proposes an innovative pharmaceutical use of DL-3-phenyllactic acid, namely its application in the preparation of drugs for treating cardiac myxoma.

[0006] This invention is achieved through the following technical solution:

[0007] The researchers of this invention conducted non-targeted metabolomics analysis on the serum of patients with cardiac myxoma and healthy controls. The results showed that the level of endogenous DL-3-phenyllactic acid in the serum of patients was significantly downregulated. Figure 1 , Figure 2 ).

[0008] This study successfully constructed a cardiac myxoma organoid model derived from patient cardiac myxoma tissue as an in vitro drug efficacy evaluation platform. Histological identification ( Figure 3 This model preserves the myxoid matrix and spindle cell morphology of the original tumor, and can highly simulate the histological characteristics of the primary tumor. Based on this model, this study used DL-3-phenyllactic acid for drug treatment, with exogenous addition concentrations of 0 μM, 10 μM, 20 μM, 40 μM, 80 μM, and 120 μM, covering low, medium, and high concentrations, for intervention. Experimental results ( Figure 5 , Figure 6The results showed that after 5 days of drug treatment, the proliferative activity of cardiac myxoma organoids in the 40 μM group was not significantly different from that in the control group (0 μM), with an average cell viability of approximately 100.62%, showing no significant inhibitory effect. The 80 μM group showed a 27.64% inhibition rate on cardiac myxoma organoid growth, with an average cell viability of approximately 72.36%, indicating mild inhibition. The 120 μM group showed a significantly enhanced inhibitory effect, with an inhibition rate as high as 77.62% and an average cell viability of approximately 22.38%. Pharmacodynamic experiments confirmed that DL-3-phenyllactic acid can significantly inhibit the proliferative activity of cardiac myxoma organoids in vitro in a dose-dependent manner. The calculated half-maximal inhibitory concentration (IC50) was [value missing]. 50 The value was 95.52 μM.

[0009] To more intuitively demonstrate the in vitro antitumor efficacy of DL-3-phenyllactic acid, cardiac myxoma organoids were treated with DL-3-phenyllactic acid at concentrations of 0 μM and 95.52 μM, and observed under a microscope. The results are as follows: Figure 7-10 As shown, compared with the 0 μM treatment group, DL-3-phenyllactic acid at a concentration of 95.52 μM showed a significant inhibitory effect on the proliferation of cardiac myxoma organoids.

[0010] To further explore the mechanism of action of DL-3-phenyllactic acid in the treatment of cardiac myxoma, this study conducted a systematic analysis using network pharmacology, identifying its core targets including AKT1, SRC, HSP90AA1, and NT5M. Figure 11 ).

[0011] Based on the above research findings, this invention claims to protect the use of DL-3-phenyllactic acid in the preparation of medicaments for the prevention and / or treatment of cardiac myxoma.

[0012] The beneficial effects of this invention lie in the first-time disclosure of a novel use of DL-3-phenyllactic acid in the preparation of drugs for treating cardiac myxoma, broadening the application scope of this compound. Its mechanism of action differs from known antibacterial effects; this discovery is not easily foreseen by those skilled in the art or simply deduced from existing technology, possessing outstanding substantive characteristics and significant innovation. In the specific implementation process, the research team successfully constructed a patient-derived cardiac myxoma organoid model for the first time, and used this model, which highly simulates clinicopathological features, for pharmacodynamic evaluation, giving the experimental results stronger clinical predictive significance and providing a reliable candidate compound and solid experimental basis for developing DL-3-phenyllactic acid into a new drug for treating cardiac myxoma. Network pharmacology studies revealed a potential novel drug mechanism of action for DL-3-phenyllactic acid. The results showed that DL-3-phenyllactic acid does not exert its effects through its known antibacterial mechanism, but rather through a multi-target, multi-pathway synergistic mode, further confirming the non-obviousness of its novel drug use. Attached Figure Description

[0013] Figure 1 HE staining was used to examine the similarity between the cardiac myxoma organoid model and the original cardiac myxoma tissue.

[0014] Figure 2 Results of differentially regulated metabolites in the serum of patients with cardiac myxoma compared to normal individuals.

[0015] Figure 3 The concentrations of serum DL-3-phenyllactic acid in the normal group and the tumor group were determined by metabolomics analysis.

[0016] Figure 4 The chemical structural formula is DL-3-phenyllactic acid.

[0017] Figure 5 The dose-dependent inhibition curve and IC50 of exogenous DL-3-phenyllactic acid on the growth of cardiac myxoma organoids. 50 value.

[0018] Figure 6 To evaluate the viability of cardiac myxoma organoid cells under different concentrations of DL-3-phenyllactic acid.

[0019] Figure 7 For control group and IC 50 Bar chart comparing cell viability in groups treated with DL-3-phenyllactic acid at different concentrations.

[0020] Figure 8 For control group and IC 50 Cell viability comparison of the DL-3-phenyllactic acid treatment group with the original data.

[0021] Figure 9Microscopic images of cardiac myxoma organoids in the group treated with 0 μM DL-3-phenyllactic acid.

[0022] Figure 10 For IC 50 Microscopic images of cardiac myxoma organoids in the DL-3-phenyllactic acid treatment group.

[0023] Figure 11 Visualization results for DL-3-phenyllactic acid-PPI. Detailed Implementation

[0024] The present invention will be described in more detail below with the aid of specific embodiments and accompanying drawings. It should be noted that these embodiments are for illustrative purposes only and are not intended to limit the scope of the invention. In the following embodiments, unless specific conditions are specified in the experimental methods, conventional conditions in the art are generally followed, or conditions recommended by the manufacturer are applied.

[0025] The phenyllactic acid involved in the examples (DL-3-Phenyllactic acid), CAS No.: 828-01-3, purity: >99.50%, structural formula ( Figure 4 ).

[0026] Example 1: Evaluation of the in vitro efficacy of DL-3-phenyllactic acid in inhibiting the growth of cardiac myxoma organoids.

[0027] (I) Using metabolomics technology to identify differentially expressed metabolites in the serum of patients with cardiac myxoma compared to normal individuals.

[0028] 1. Sample Pretreatment: Thirteen independent human serum samples (including control and experimental groups) were collected and frozen at -80℃. After thawing, the samples were vortexed for 10 seconds to mix, and 50 μL was added to a 1.5 mL centrifuge tube, along with 250 μL of 20% acetonitrile-methanol extraction buffer. The mixture was vortexed for 3 min, centrifuged at 12000 rpm and 4℃ for 10 min, and 250 μL of the supernatant was transferred to a new tube and incubated at -20℃ for 30 min. The mixture was then centrifuged twice under the same conditions (12000 rpm, 4℃, 10 min), and 180 μL of the supernatant was filtered through a protein precipitation plate to obtain the test solution, which was stored at -20℃.

[0029] 2. Chromatography-Mass Spectrometry Analysis: Analysis was performed using an ultra-high performance liquid chromatograph (Waters ACQUITY H-Class) tandem triple quadrupole-linear ion trap mass spectrometer (SCIEX QTRAP® 6500+). Chromatographic conditions: ACQUITY UPLC BEHAmide column (2.1 mm × 100 mm, 1.7 μm); mobile phase A was an aqueous solution of 10 mM ammonium acetate and 0.3% ammonia; mobile phase B was 90% acetonitrile / water; gradient program: 0–1.2 min to maintain 95% B, 8 min to decrease to 70% B, 9–11 min to maintain 50% B, 11.1–15 min to recover to 95% B; flow rate 0.4 mL / min, column temperature 40 °C, injection volume 2 μL. Mass spectrometry conditions: Electrospray ionization source positive / negative mode switching, ion source temperature 550℃, spray voltage ±5500V (positive / negative mode), curtain gas pressure 35psi; dynamic multi-reaction monitoring mode is adopted, and the declustering voltage and collision energy are optimized.

[0030] 3. Data Analysis and Quality Control: One sample was inserted for every 10 test samples for quality control. The proportion of metabolite detection coefficients of variation <0.3 exceeded 80%. After standardization by unit variance, principal component analysis was performed to assess differences between groups. Orthogonal partial least squares discriminant analysis was used to screen for differentially expressed metabolites. Before analysis, logarithmic transformation (log2) and mean centering were performed on the data. Significant differences were determined based on the variable importance projection (VIP) value and the change in Log2. The reliability of the model was verified by 200 permutation tests. Metabolites with VIP > 1 were considered significantly different metabolites. At the same time, a significant difference in marker content was also required if FC ≥ 2 or FC ≤ 0.5.

[0031] The results are as follows Figure 1 As shown, the differentially regulated metabolites in the serum of patients with cardiac myxoma, compared with normal individuals, include DL-3-phenyllactic acid.

[0032] (II) Construction of patient-derived cardiac myxoma organoids

[0033] Materials preparation: ① Prepare the required number of 24-well and 96-well plates and set them aside; ② Preheat the plates and cardiac myxoma organoid culture medium (containing 100 U / mL penicillin-streptomycin + 10 mM HEPES + 1×GlutaMAX + 10 μM Y27632) in a 37°C incubator; ③ Melt the BME gel in a 4°C refrigerator overnight to ensure it is in a liquid state when used.

[0034] Immediately place the collected fresh primary tissue blocks in tissue preservation solution.

[0035] Tumor tissue was pruned under sterile conditions to remove as much fat, muscle and other non-epithelial components as possible. The resulting tissue blocks were used to construct cardiac myxoma organoids.

[0036] Use a sterile scalpel to cut the trimmed tissue block into 1-3mm pieces. 3 The sample was then collected in a 15 mL centrifuge tube using tissue washing fluid. After centrifugation at 1000 rpm for 3 minutes at room temperature, the supernatant was discarded.

[0037] Wash the tissue again with tissue cleaning solution, then centrifuge and discard the supernatant.

[0038] Prepare a working solution by mixing the digestive enzyme dilution with the tissue digestive enzyme in equal proportions.

[0039] Add approximately 10 times the volume of the digestive enzyme working solution to the centrifuge tube according to the size of the tissue. Gently disperse the tissue precipitate with a pipette. Then place the centrifuge tube in a 37°C incubator and gently shake the centrifuge tube at 10-minute intervals to ensure uniform digestion of the tissue.

[0040] The digestion time depends on the degree of digestion of the tissue block. Once the tissue has been digested to the point of being clump-like and without obvious clumps, 1 / 10 volume of serum is added to stop the digestion process. The digestion time should not exceed 2 hours.

[0041] At the end of digestion, centrifuge at 1500 rpm for 3 minutes at room temperature, discard the supernatant, and collect the precipitate at the bottom.

[0042] If a large number of red blood cells are found in the precipitate, add an appropriate amount of red blood cell lysis buffer to the tube to resuspend the cells. Lyse the cells at room temperature for 5-10 minutes, then centrifuge the cell suspension at 1000 rpm for 3 minutes at room temperature and discard the supernatant.

[0043] Add 5 mL of cardiac myxoma organoid culture medium to the cell pellet and resuspend.

[0044] The cell suspension was filtered sequentially using 100μm and 40μm cell filters. The final cell suspension after filtration was centrifuged at 1500rpm for 3 minutes at room temperature, and the supernatant was discarded.

[0045] The cell pellet was resuspended at a BME matrix gel:culture medium ratio of 3:1 to achieve a cell density of 1×10⁻⁶ cells / mL. 5 -2×10 5 For 50 μL of BME matrix gel per cell, place it on ice for rapid processing to prevent solidification.

[0046] Drop the cell suspension into the center bottom of a preheated 24-well cell culture plate, adding approximately 50 μL of suspension to each well.

[0047] Incubate the culture plates in a cell culture incubator at 37°C and 5% CO2 for 20-30 minutes, observing them frequently. Once the BME has completely solidified, add 500 μL of preheated cardiac myxoma organoid culture medium to each well.

[0048] The culture medium for cardiac myxoma organoids was changed every 2-3 days, and the growth status of cardiac myxoma organoids was observed daily.

[0049] The results are as follows Figure 3 As shown, a cardiac myxoma organoid model was successfully constructed. HE staining showed that the cardiac myxoma organoid model had a high similarity to the original tissue.

[0050] (III) Treatment of cardiac myxoma organoids with complete culture medium containing DL-3-phenyllactic acid

[0051] Cardiac myxoma organoid seeding: Mix 8 μL of BME matrix gel with 1000 cells per well and seed in 96-well cell culture plates. Incubate the culture plates at 37°C, 5% CO2 for 20 minutes. After the BME matrix gel has completely solidified, slowly add 100 μL of pre-warmed cardiac myxoma organoid complete culture medium to each well.

[0052] Cardiac myxoma organoid culture and metabolite treatment: The growth status of cardiac myxoma organoids was observed daily under a microscope, and the culture medium was replaced with fresh cardiac myxoma organoid complete culture medium. Once the cardiac myxoma organoids had stabilized, the original culture medium was discarded and replaced with cardiac myxoma organoid complete culture medium containing different concentrations of DL-3-phenyllactic acid. The concentration gradients were set at 0 (control group), 10, 20, 40, 80, and 120 μM, with three replicates for each concentration. The culture plates were then returned to the incubator for further incubation.

[0053] Observation and recording of inhibitory effect: morphological changes of cardiac myxoma organoids were observed daily from the start of treatment. If a significant inhibitory effect was observed, the morphological characteristics of cardiac myxoma organoids in each concentration group were photographed and recorded under a microscope, and the treatment time and concentration were noted.

[0054] Cell viability assay: CellTiter-Glo® 3D Reagent was thawed overnight at 4°C. Before use, the reagent was placed in a 22°C water bath for approximately 30 minutes to equilibrate CellTiter-Glo® 3D Reagent to room temperature. The contents were gently mixed by inverting the container to obtain a homogenized solution. Five days after treatment with cardiac myxoma organoids, the cardiac myxoma organoid culture medium was discarded. Each well was gently washed once with 100 μL of pre-warmed PBS. After discarding the PBS, 100 μL of CellTiter-Glo® 3D reagent was added according to the manufacturer's instructions. The plate and its contents were equilibrated to room temperature for 30 minutes, and after thorough mixing for 5 minutes, the cells were lysed. The culture plate was then incubated at room temperature for another 25 minutes to stabilize the chemiluminescence signal. The chemiluminescence signal value of each well was then detected using a microplate reader, and the chemiluminescence value was recorded. The control group signal was taken as 100% cell viability, and the relative cell viability and inhibition rate of each metabolite treatment group were calculated.

[0055] IC 50 Concentration treatment experiments: Determining the IC50 of DL-3-phenyllactic acid in a cardiac myxoma organoid model. 50 After reaching a concentration of 95.52 μM, cardiac myxoma organoids were further treated using this concentration. Once the cardiac myxoma organoids had stabilized, the original culture medium was discarded and replaced with complete cardiac myxoma organoid culture medium containing 95.52 μM DL-3-phenyllactic acid, and culture continued. Morphological changes in the cardiac myxoma organoids were observed and recorded daily under a microscope, and microscopic images were taken for subsequent analysis. A control group (0 μM) was also set up for comparison. After 5 days of treatment, cell viability was assessed using the same CellTiter-Glo® 3D method as described above.

[0056] The results are as follows Figure 7-10 As shown, exogenous supplementation with DL-3-phenyllactic acid can significantly inhibit the proliferation and metabolic activity of cardiac myxoma organoids.

[0057] (iv) Elucidation of the potential drug mechanism of DL-3-phenyllactic acid based on network pharmacology

[0058] Target prediction: Using the SwissTargetPrediction and PharmMapper online platforms, the molecular structure of DL-3-phenyllactic acid was used as input to predict its potential targets. With a probability value > 0, a total of 239 high-confidence targets were obtained.

[0059] PPI Network Construction and Core Target Selection: The target list above was imported into the STRING database, the species was set to "Homo sapiens", and the minimum interaction confidence was 0.900 to obtain PPI network information. The results file was imported into Cytoscape software for visualization and node degree values ​​were calculated. The top 5 core targets were selected by sorting the degree values ​​in descending order: AKT1, SRC, HSP90AA1, NT5M, and BCL2L1. Figure 11 ).

[0060] Conclusion: Network pharmacology analysis suggests that DL-3-phenyllactic acid may inhibit cardiac myxoma growth by acting on key targets such as AKT1, SRC, HSP90AA1, NT5M, and BCL2L1, thereby regulating signaling pathways and tumor cell metabolic processes.

[0061] Based on the results and conclusions of the above experiments, this invention reveals for the first time the inhibitory effect of DL-3-phenyllactic acid on patient-derived cardiac myxoma organoids in an in vitro model. Through metabolomics, organoid models, and network pharmacology, a complete chain of evidence is formed, confirming that DL-3-phenyllactic acid has the potential to be developed into a therapeutic drug for cardiac myxoma, and has significant new drug development value and non-obviousness.

[0062] In summary, the above description is merely a specific embodiment of this application, intended to assist those skilled in the art in understanding or implementing this application. It will be apparent to those skilled in the art that various modifications can be made to these embodiments. The general principles defined herein may be implemented in other embodiments without departing from the spirit or scope of this application. Therefore, this application is not limited to the embodiments presented herein, but should be accorded the widest scope matching the principles and novel features claimed herein.

Claims

1. Application of DL-3-phenyllactic acid in the preparation of drugs for treating cardiac myxoma.

2. The use of DL-3-phenyllactic acid according to claim 1 in the preparation of a medicament for treating cardiac myxoma, characterized in that, DL-3-phenyllactic acid is a small molecule substance that is significantly reduced in the serum of patients with cardiac myxoma, as identified by metabolomics.

3. The use of DL-3-phenyllactic acid according to claim 1 in the preparation of a medicament for treating cardiac myxoma, characterized in that, The validation was achieved by constructing a cardiac myxoma organoid model derived from patient cardiac myxoma tissue.

4. The use of DL-3-phenyllactic acid according to claim 3 in the preparation of a medicament for treating cardiac myxoma, characterized in that, The method for constructing the cardiac myxoma organoid includes the following steps: a) Tissue pretreatment and digestion: Fresh tumor tissue was placed in a protective solution and stored at 4°C for no more than 72 hours. Under aseptic conditions, fat, muscle, and non-epithelial components were removed, and the tissue was cut into 1-3 mm pieces. 3 After washing and centrifuging the tissue blocks with washing solution, add 10 times the volume of digestive enzyme working solution and digest at 37°C for 10 minutes to 2 hours until flocculent. Add 1 / 10 volume of serum to stop digestion and centrifuge to collect the precipitate. b) Cell suspension preparation: The precipitate was resuspended in cardiac myxoma organoid culture medium, filtered sequentially through 100μm and 40μm filters, and the cells were collected by centrifugation. The cells were then resuspended on ice at a matrix gel:culture medium ratio of 3:1 until a density of 1×10⁶ cells / mL was achieved. 5 -2×10 5 1 cell / 50 μL; c) Matrix embedding and solidification: Add 50 μL of cell suspension to the bottom of the preheated culture plate wells and incubate at 37°C in a 5% CO2 incubator for 20-30 minutes until the matrix gel is completely solidified; d) Culture and maintenance of cardiac myxoma organoids: Add 500 μL of preheated cardiac myxoma organoid culture medium to each well, change the cardiac myxoma organoid culture medium every 2-3 days, and continue culturing to obtain the cardiac myxoma organoids.

5. The use of DL-3-phenyllactic acid according to claim 1 in the preparation of a medicament for treating cardiac myxoma, characterized in that, This was achieved by adding DL-3-phenyllactic acid to the cardiac myxoma organoid culture medium, wherein the concentration of DL-3-phenyllactic acid in the cardiac myxoma organoid culture medium was 10-120 μM.

6. The use of DL-3-phenyllactic acid according to claim 1 in the preparation of a medicament for treating cardiac myxoma, characterized in that, The specific steps are as follows: a) The cardiac myxoma organoids described in claim 3 were seeded into 96-well cell culture plates at a density of 1000 cells / 8 μL of BME matrix gel and incubated in a 37°C, 5% CO2 incubator for 20 minutes until the matrix gel solidified. 100 μL of cardiac myxoma complete culture medium was added to each well. b) Change the cardiac myxoma complete culture medium daily. After the cardiac myxoma organoids have grown stably, change it to the cardiac myxoma organoid culture medium containing DL-3-phenyllactic acid as described in claim 5. c) After culturing for another 5 days, the growth inhibition rate of cardiac myxoma organoids was determined using the CellTiter-Glo 3D cell viability assay kit, and the half-maximal inhibitory concentration (IC50) was calculated. 50 value; d) During drug treatment, the inhibitory effect of different concentrations of DL-3-phenyllactic acid on the growth of cardiac myxoma organoids was observed and recorded under a microscope; e) Setting DL-3-phenyllactic acid IC 50 The cardiac myxoma organoid culture medium at a certain concentration was used, with a 0 μM concentration group as a control. Cells were cultured for 5 days, and morphological changes in the cardiac myxoma organoids were observed and recorded daily under a microscope. Cell viability in the control group was detected using CellTiter-Glo 3D to verify IC50. 50 Concentration-based tumor-suppressing effect.

7. The use of DL-3-phenyllactic acid according to claim 1 in the preparation of a medicament for treating cardiac myxoma, characterized in that, The DL-3-phenyllactic acid inhibits the growth of cardiac myxoma organoids. 50 The value is 95.52 μM.

8. The use of DL-3-phenyllactic acid according to claim 1 in the preparation of a medicament for treating cardiac myxoma, characterized in that, Based on network pharmacology analysis, the mechanism of action of DL-3-phenyllactic acid in the preparation of drugs for treating cardiac myxoma involves the targets AKT1 and / or SRC and / or HSP90AA1 and / or NT5M.

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