CN110894182B - Anti-tumor compound aiming at Fyn-CD147 signal channel target spot and preparation method and application thereof - Google Patents
Anti-tumor compound aiming at Fyn-CD147 signal channel target spot and preparation method and application thereof Download PDFInfo
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- C—CHEMISTRY; METALLURGY
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- C07C49/00—Ketones; Ketenes; Dimeric ketenes; Ketonic chelates
- C07C49/76—Ketones containing a keto group bound to a six-membered aromatic ring
- C07C49/84—Ketones containing a keto group bound to a six-membered aromatic ring containing ether groups, groups, groups, or groups
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P35/00—Antineoplastic agents
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- C—CHEMISTRY; METALLURGY
- C07—ORGANIC CHEMISTRY
- C07C—ACYCLIC OR CARBOCYCLIC COMPOUNDS
- C07C45/00—Preparation of compounds having >C = O groups bound only to carbon or hydrogen atoms; Preparation of chelates of such compounds
- C07C45/61—Preparation of compounds having >C = O groups bound only to carbon or hydrogen atoms; Preparation of chelates of such compounds by reactions not involving the formation of >C = O groups
- C07C45/67—Preparation of compounds having >C = O groups bound only to carbon or hydrogen atoms; Preparation of chelates of such compounds by reactions not involving the formation of >C = O groups by isomerisation; by change of size of the carbon skeleton
- C07C45/68—Preparation of compounds having >C = O groups bound only to carbon or hydrogen atoms; Preparation of chelates of such compounds by reactions not involving the formation of >C = O groups by isomerisation; by change of size of the carbon skeleton by increase in the number of carbon atoms
- C07C45/72—Preparation of compounds having >C = O groups bound only to carbon or hydrogen atoms; Preparation of chelates of such compounds by reactions not involving the formation of >C = O groups by isomerisation; by change of size of the carbon skeleton by increase in the number of carbon atoms by reaction of compounds containing >C = O groups with the same or other compounds containing >C = O groups
- C07C45/74—Preparation of compounds having >C = O groups bound only to carbon or hydrogen atoms; Preparation of chelates of such compounds by reactions not involving the formation of >C = O groups by isomerisation; by change of size of the carbon skeleton by increase in the number of carbon atoms by reaction of compounds containing >C = O groups with the same or other compounds containing >C = O groups combined with dehydration
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Abstract
The invention relates to an anti-tumor compound aiming at Fyn-CD147 signal channel targets and a preparation method and application thereof. The anti-tumor compound is prepared by reacting 3-hydroxyacetophenone and 4-bromo-3, 5-dimethoxybenzaldehyde under the catalysis of alcohol and sodium alcoholate. The anti-tumor compound can effectively inhibit the proliferation of skin tumor cells, colon cancer cells, liver cancer cells and lung cancer cells, wherein the half inhibition concentrations of the human skin malignant melanoma cells SK-Mel-5 and SK-Mel-28 are 0.8956 mu M and 0.8257 mu M respectively, which shows that the anti-tumor compound has stronger capacity of inhibiting the growth and proliferation of tumors and inducing the apoptosis of tumor cells, and can be applied to the preparation of anti-tumor drugs. The anti-tumor compound has a structure represented by the following structural formula I:
。
Description
Technical Field
The invention relates to the field of medicines, in particular to an anti-tumor compound aiming at Fyn-CD147 signal channel targets, and a preparation method and application thereof.
Background
A tumor is a cell proliferative disease, and the tumor cells have three significant basic characteristics: immobility, mobility and loss of contact inhibition. On a cellular level, carcinogenesis is a very rare event. Genetically, cancer develops from a cell and from a cell that has lost control of proliferation. The human body has millions of cells, and billions of cells divide every day, and theoretically almost any cell may be cancerated by the change of genetic components, but this is not true in practice. Malignant transformation of a cell requires multiple genetic changes, i.e., multiple genetic mutations in a cell. Tumorigenesis is thus a progressive process involving multiple stages of reaction and accumulation of mutations. In this process, cancerous cell lines become increasingly uncontrolled by regulatory mechanisms within the receptor and gradually invade normal tissues. After malignant transformation of the cells, the cancer cells continue to accumulate mutations, which confer new properties on the mutated cells and make the cancer cells more dangerous. At present, the antitumor drugs are still few and expensive, and other antitumor compounds need to be further searched.
Disclosure of Invention
Based on the situation, the anti-tumor compound aiming at Fyn-CD147 signal channel targets and the preparation method and application thereof are needed.
An anti-neoplastic compound directed against the Fyn-CD147 signaling pathway target, said anti-neoplastic compound having a structure represented by structural formula I:
the invention also provides a preparation method of the anti-tumor compound, which comprises the following steps:
dissolving sodium alcoholate in alcohol, adding 3-hydroxyacetophenone and 4-bromo-3, 5-dimethoxybenzaldehyde to react for 40-60 hours, adjusting the pH value to 1-2, and extracting to obtain the anti-tumor compound.
In one embodiment, the molar ratio of the 3-hydroxyacetophenone to the 4-bromo-3, 5-dimethoxybenzaldehyde is (0.8-1.2): 1.
In one embodiment, the ratio of the mass of the sodium alkoxide to the volume of the alcohol is (52-56) mg:1 mL.
In one embodiment, the method further comprises the following steps: before the pH value is adjusted, 4-8 mL of water is added and the mixture is washed by ether for multiple times.
In one embodiment, the method further comprises the following steps: recrystallizing the anti-tumor compound with a mixture of ethanol and water.
In one embodiment, the extraction specifically comprises the following steps: the organic phases are extracted several times with 18-24 mL of ethyl acetate and combined.
The invention also provides application of the anti-tumor compound in preparing anti-tumor medicines.
The invention also provides an anti-tumor drug aiming at the Fyn-CD147 signal channel target spot, which comprises the anti-tumor compound, wherein the mass ratio of the anti-tumor compound in the anti-tumor drug is not more than 99%.
In one embodiment, the dosage form of the antitumor drug is injection, tablet, paste or suppository.
The anti-tumor compound is generated by the reaction of 3-hydroxyacetophenone and 4-bromo-3, 5-dimethoxybenzaldehyde under the catalysis of alcohol and sodium alcoholate, and the chemical reaction formula is shown as follows:
the anti-tumor compound can effectively inhibit the proliferation of skin tumor cells, colon cancer cells, liver cancer cells and lung cancer cells, wherein the semi-inhibition concentrations of the human skin malignant melanoma cells SK-Mel-5 and SK-Mel-28 are 0.8956 mu M and 0.8257 mu M respectively, the semi-inhibition concentration of the human skin malignant melanoma cells SK-Mel-5 and SK-Mel-28 is 0.95 mu M, the semi-inhibition concentration of the human skin malignant melanoma cells is 1.1 mu M, and the semi-inhibition concentration of the human skin malignant melanoma cells is 2.15 mu M, so that the anti-tumor compound has strong capacity of inhibiting the growth and proliferation of tumors and inducing the apoptosis of the tumor cells. The antitumor compound can weaken phosphorylation of FYN kinase on CD147 tyrosine, is an antitumor compound aiming at Fyn-CD147 signal channel targets, can be applied to preparation of antitumor drugs, provides new theoretical and experimental bases for prevention and treatment of tumors, and can be widely used as a tool molecule in tumor-related research.
Drawings
FIG. 1 is a graph showing the results of CCK-8 experiments on human skin malignant melanoma cells SK-Mel-5 at various concentrations of the antitumor compound of example 1;
FIG. 2 is a graph showing the results of CCK-8 experiments on human skin malignant melanoma cells SK-Mel-28 at various concentrations of the antitumor compound of example 1;
FIG. 3 is a graph showing the results of CCK-8 experiments on colon cancer cells HT29 at various concentrations of the anti-tumor compound of example 1;
FIG. 4 is a graph showing the results of CCK-8 experiments on hepatoma cells HepG2 with the anti-tumor compound of example 1 at different concentrations;
FIG. 5 is a graph showing the results of the CCK-8 assay for lung cancer cell A549 with the anti-tumor compound of example 1 at various concentrations;
FIG. 6 is a diagram showing the results of CCK-8 experiments on human malignant melanoma cells SK-Mel-5 at different concentrations of chalcone;
FIG. 7 is a diagram showing the results of CCK-8 experiments on human skin malignant melanoma cells SK-Mel-28 at different concentrations of chalcone;
FIG. 8 is a diagram showing the results of CCK-8 experiments on human malignant melanoma cells SK-Mel-28 at different concentrations for compounds of structural formula II;
FIG. 9 is a diagram showing the result of CCK-8 experiment on human skin malignant melanoma cell SK-Mel-28 at different concentrations by using the compound of structural formula III;
FIG. 10 is a diagram showing the results of an experiment in which FYN kinase and prokaryotic expression purified CD147 were subjected to in vitro phosphorylation reaction, and the inhibitory effect of an antitumor compound on CD147 phosphorylation was examined.
Detailed Description
In order that the invention may be more fully understood, a more particular description of the invention will now be rendered by reference to specific embodiments thereof that are illustrated in the appended drawings. This invention may, however, be embodied in many different forms and should not be construed as limited to the embodiments set forth herein. Rather, these embodiments are provided so that this disclosure will be thorough and complete.
Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. The terminology used in the description of the invention herein is for the purpose of describing particular embodiments only and is not intended to be limiting of the invention. As used herein, the term "and/or" includes any and all combinations of one or more of the associated listed items.
The anti-tumor compound aiming at the Fyn-CD147 signal channel target of one embodiment of the invention has a structure represented by the following structural formula I:
the preparation method of the antitumor compound provided by the embodiment of the invention comprises the following steps: dissolving sodium alcoholate in alcohol, adding 3-hydroxyacetophenone and 4-bromo-3, 5-dimethoxybenzaldehyde to react for 40-60 hours, adjusting the pH value to 1-2, and extracting to obtain the anti-tumor compound.
In one specific example, the molar ratio of 3-hydroxyacetophenone to 4-bromo-3, 5-dimethoxybenzaldehyde is (0.8-1.2): 1.
In one specific example, the ratio of the mass of the sodium alkoxide to the volume of the alcohol is (52-56) mg:1 mL.
In one specific example, the method further comprises the following steps: before the pH value is adjusted, 4-8 mL of water is added and washed by ether for multiple times, so that part of impurities can be removed, and the product purity is improved.
In one specific example, the method further comprises the following steps: the purity of the antitumor compound can be further improved by recrystallizing the antitumor compound with a mixture of ethanol and water.
In a specific example, the extraction specifically comprises the following steps: the organic phases are extracted several times with 18 to 24mL of ethyl acetate and combined.
The invention provides an application of the antitumor compound in preparing antitumor drugs. The antitumor compound has effects of inhibiting other skin tumors such as basal cell carcinoma, squamous cell carcinoma, colon cancer cell, hepatocarcinoma cell and lung cancer cell, etc., except malignant melanoma.
The invention also provides an anti-tumor drug aiming at the Fyn-CD147 signal channel target spot, which comprises the anti-tumor compound, wherein the mass percentage of the anti-tumor compound in the anti-tumor drug is not more than 99%. Optionally, the antitumor drug is in the form of injection, tablet, paste or suppository.
In a specific example, the anti-tumor drug further comprises a hardening agent and an analgesic. Optionally, the hardening agent is one or more of ethanol, propylene glycol, glycerol, isopropanol, and polyethylene glycol. Optionally, the analgesic agent is one or more of aspirin, ibuprofen, indomethacin, paracetamol, phenylbutazone, rofecoxib, and celecoxib.
In a specific example, the above antitumor drug further comprises a disintegrant and an absorbent. Optionally, the disintegrant is one or more of sodium hydroxymethyl starch, an effervescent disintegrant, and crospovidone. Optionally, the absorbent is one or more of calcium sulfate, calcium hydrogen phosphate, calcium carbonate and light magnesium oxide.
The anti-tumor compound is generated by the reaction of 3-hydroxyacetophenone and 4-bromo-3, 5-dimethoxybenzaldehyde under the catalysis of alcohol and sodium alcoholate, and the chemical reaction formula is shown as follows:
the anti-tumor compound can effectively inhibit the proliferation of skin tumor cells, colon cancer cells, liver cancer cells and lung cancer cells, wherein the semi-inhibition concentrations of the human skin malignant melanoma cells SK-Mel-5 and SK-Mel-28 are 0.8956 mu M and 0.8257 mu M respectively, the semi-inhibition concentration of the human skin malignant melanoma cells SK-Mel-5 and SK-Mel-28 is 0.95 mu M, the semi-inhibition concentration of the human skin malignant melanoma cells is 1.1 mu M, and the semi-inhibition concentration of the human skin malignant melanoma cells is 2.15 mu M, so that the anti-tumor compound has strong capacity of inhibiting the growth and proliferation of tumors and inducing the apoptosis of the tumor cells. The antitumor compound can weaken phosphorylation of FYN kinase on CD147 tyrosine, is an antitumor compound aiming at Fyn-CD147 signal channel targets, can be applied to preparation of antitumor drugs, provides new theoretical and experimental bases for prevention and treatment of tumors, and can be widely used as a tool molecule in tumor-related research.
The following are specific examples.
Example 1
432mg of sodium methoxide was dissolved in 8mL of anhydrous methanol and cooled to zero degree. Then 3-hydroxyacetophenone (278mg, 2mmol) and 4-bromo-3, 5-dimethoxybenzaldehyde (500mg, 2mmol) were added, warmed to room temperature and stirred for 48 hours. After concentration, 6mL of water is added, 1.6mL of ether is used for washing for three times, the pH value is adjusted to 1 by concentrated hydrochloric acid, ethyl acetate is used for extraction for three times, organic phases are combined, after concentration, mixed solution of ethanol and water is used for recrystallization, the target product which is light yellow crystal is obtained by 494mg, and the yield is 68% according to the actual yield divided by the theoretical yield. The nuclear magnetic resonance spectrum is:1H NMR(500MHz,DMSO)δ9.72(s,1H),7.85(d,J＝15.6Hz,1H),7.59(d,J＝15.6Hz,1H),7.54(d,J＝7.6Hz,1H),7.36(s,1H),7.28(t,J＝7.8Hz,1H),7.15(s,2H),6.96(d,J＝8.0Hz,1H),3.81(s,6H).13C NMR(125MHz,DMSO)δ189.7,158.2,157.3,144.0,139.4,135.8,130.3,123.6,120.8,120.2,115.2,105.9,102.8,57.2.ESI-HRMS m/z:363.0225，365.0210[M+H]。
example 2
332mg of sodium methoxide were dissolved in 8mL of anhydrous methanol and cooled to zero degrees. Then 3-hydroxyacetophenone (278mg, 2mmol) and 4-bromo-3, 5-dimethoxybenzaldehyde (500mg, 2mmol) were added, warmed to room temperature and stirred for 24 hours. After concentration, 6mL of water was added, the mixture was washed with 1.6mL of ether for three times, the pH was adjusted to 1 with concentrated hydrochloric acid, the mixture was extracted with ethyl acetate for three times (20 mL), the organic phases were combined, and after concentration, the mixture was recrystallized from a mixture of ethanol and water to obtain 436mg of the objective product as pale yellow crystals.
Example 3
432mg of sodium ethoxide was dissolved in 4mL of anhydrous ethanol and cooled to zero degree. Then 3-hydroxyacetophenone (278mg, 2mmol) and 3,4, 5-trimethoxybenzaldehyde (500mg, 2mmol) were added, warmed to room temperature and stirred for 48 hours. After concentration, 6mL of water is added, the mixture is washed with 1.6mL of ether for three times, the pH value is adjusted to 1 by concentrated hydrochloric acid, the mixture is extracted with ethyl acetate for three times by 20mL of ethyl acetate, organic phases are combined, and after concentration, the mixture of ethanol and water is recrystallized to obtain 290mg of a target product which is light yellow crystals.
Comparative example 1
To 4mL of anhydrous methanol were added 3-hydroxyacetophenone (278mg, 2mmol) and 4-bromo-3, 5-dimethoxybenzaldehyde (500mg, 2mmol), and the mixture was stirred at room temperature for 48 hours, whereby the desired product could not be obtained.
The anti-tumor compound obtained in example 1 was used for the CCK-8 test: respectively taking human skin malignant melanoma cells SK-Mel-5 and SK-Mel-28, preparing single cell suspension with culture medium containing 10% fetal calf serum, counting, inoculating 1000 cells per well to 96-well plate, each well volume being 100ul, adding anti-tumor compounds (50nM, 100nM, 500nM and 1 μ M) with different concentrations after adherence, adding maximum corresponding volume of drugs into DMSO group, measuring in 0h, 24h, 48h and 72h, adding 10ul CCK-8 before measurement, incubating for 2h, measuring absorption value of each well at 450nM wavelength on a microplate reader, recording result, and drawing cell growth curve with time as abscissa and absorption value as ordinate. As shown in FIGS. 1 and 2, the antitumor compound has good inhibitory effects on SK-Mel-5 and SK-Mel-28, and the half inhibitory concentrations are 0.8956 μ M and 0.8257 μ M, respectively. Respectively taking colon cancer cells HT29, liver cancer cells HepG2 and lung cancer cells A549, preparing single cell suspension by using a culture medium containing 10% fetal calf serum, counting, inoculating 1000 cells per hole to a 96-hole plate, adding anti-tumor compounds (1 mu M, 2.5 mu M, 5 mu M and 10 mu M) with different concentrations after adherence, adding the maximum corresponding volume of the drugs into a DMSO group, measuring at 0h, 24h, 48h and 72h, adding 10ul CCK-8 before measurement, incubating for 2h, measuring the absorption value of each hole at a wavelength of 450nm on an enzyme labeling instrument, recording the result, and drawing a cell growth curve by taking time as a horizontal coordinate and the absorption value as a vertical coordinate. The results are shown in fig. 3-5 respectively, and it can be seen that the antitumor compound also has certain inhibitory effects on colon cancer, liver cancer and lung cancer, and the half inhibitory concentrations are 0.95 μ M, 1.1 μ M and 2.15 μ M, respectively.
CCK-8 testing was performed using the backbone compound chalcone: respectively taking human skin malignant melanoma cells SK-Mel-5 and SK-Mel-28, preparing single cell suspension with culture medium containing 10% fetal calf serum, counting, inoculating 1000 cells per well to 96-well plate, each well volume being 100ul, adding chalcone (1 mu M, 5 mu M, 10 mu M and 20 mu M) with different concentrations after adherence, adding maximum corresponding volume of drug into DMSO group, performing determination in 0h, 24h, 48h and 72h, adding 10ul CCK-8 before determination, after incubating for 2 hours, determining absorption value of each well on a microplate reader at 450nm wavelength, recording result, and drawing cell growth curve with time as abscissa and absorption value as ordinate. As shown in FIGS. 6 and 7, the half inhibitory concentrations were 2.5. mu.M and 6.7. mu.M, respectively, and the effects were far inferior to those of the antitumor compounds of the present invention.
CCK-8 testing was performed using the compound of formula II: taking human skin malignant melanoma cells SK-Mel-28, preparing single cell suspension with culture medium containing 10% fetal calf serum, counting, inoculating 1000 cells per well to 96-well plate, each well volume is 100ul, adding the above compounds (1 uM, 5 uM and 20 uM) with different concentrations after adherence, adding maximum corresponding volume of the drugs into DMSO group, measuring at 0h, 24h, 48h and 72h, adding 10ul CCK-8 before measurement, incubating for 2 hours, measuring the absorption value of each well at 450nm wavelength on enzyme labeling instrument, recording the result, and drawing cell growth curve with time as abscissa and the absorption value as ordinate. As shown in FIG. 8, the half inhibitory concentration was 20.1. mu.M, and the effect was very poor, which was far from the antitumor compound of the present invention.
CCK-8 testing was performed using the compound of formula III below: taking human skin malignant melanoma cells SK-Mel-28, preparing single cell suspension with culture medium containing 10% fetal calf serum, counting, inoculating 1000 cells per well to 96-well plate, each well volume being 100ul, adding the above compounds (5 μ M, 10 μ M and 20 μ M) with different concentrations after adherence, adding maximum corresponding volume of the drug into DMSO group, performing determination in 0h, 24h, 48h and 72h, adding 10ul CCK-8 before determination, incubating for 2h, determining absorption value of each well at 450nm wavelength on enzyme labeling instrument, recording result, and drawing cell growth curve with time as abscissa and absorption value as ordinate. As shown in FIG. 9, the half inhibitory concentration was 20.7. mu.M, and the effect was very poor, which is far from the antitumor compound of the present invention.
In vivo experiments: in order to further explore the in vivo effect of the antitumor compound, a xenograft model is established by 5-6 weeks old nude mice, melanoma cells SK-Mel-5 with high proliferation speed are selected as inoculation cells, cells with good growth state, no pollution and strong activity are selected for amplification, and subcutaneous tumorigenesis is carried out on 40 nude mice. Continuously observing 7-10 days after inoculation until the size of the tumor reaches 50mm3～100mm3Selecting the nude mice meeting the above standard, and randomly dividing the nude mice into 3 groups: a control group, a 20mg/kg dose group and a 40mg/kg dose group, wherein each group comprises 6 animals, the animals are divided into groups and then are raised in cages, the anti-tumor compound is injected into the abdominal cavity continuously for treatment, the tumor volume is measured every other day until the tumor size of the control group reaches 1000mm3The experiment was terminated at this time, and the tumor bodies of the mice were removed for immunohistochemistry and Ki67 expression was detected.
The experimental results are as follows: after treatment, no mortality occurred in each group of nude mice, and the body weight average increased with the treatment time. The growth of tumors was significantly inhibited in the 20mg/kg dose group compared to the control group, whereas the growth was significantly inhibited in the 40mg/kg dose group compared to the 20mg/kg dose group. The above results can demonstrate that the anti-tumor compound of the present invention can effectively inhibit the growth of melanoma in vivo.
The invention further researches and screens the action mechanism of the anti-tumor compound, and finds that the anti-tumor compound mainly plays a role in aiming at Fyn-CD147 signal channel targets. By reacting Fyn kinase with purified CD147, the reaction system: fyn 1uL (100ng), CD147(5uL), 10 XKinase Buffer (2uL), ATP (1mM 1uL), an antitumor compound (5. mu.M 2. mu.L), reaction at 30 ℃ for 40 minutes, followed by Western Blot and Coomassie staining. The results are shown in fig. 10 (wherein anti-p is tyrosine phosphorylated antibody), which illustrates that the anti-tumor compound of the present invention can reduce phosphorylation of FYN kinase on CD147 tyrosine, thereby proving that the anti-tumor compound is an anti-tumor compound aiming at FYN-CD147 signal pathway target, providing new theoretical and experimental basis for prevention and treatment of tumor, and can be widely used as a tool molecule in tumor-related research.
The technical features of the embodiments described above may be arbitrarily combined, and for the sake of brevity, all possible combinations of the technical features in the embodiments described above are not described, but should be considered as being within the scope of the present specification as long as there is no contradiction between the combinations of the technical features.
The above-mentioned embodiments only express several embodiments of the present invention, and the description thereof is more specific and detailed, but not construed as limiting the scope of the invention. It should be noted that, for a person skilled in the art, several variations and modifications can be made without departing from the inventive concept, which falls within the scope of the present invention. Therefore, the protection scope of the present patent shall be subject to the appended claims.
Claims (10)
1. An anti-tumor compound directed to a Fyn-CD147 signal pathway target, wherein the anti-tumor compound has a structure represented by the following structural formula I:
2. a method for preparing the anti-neoplastic compound of claim 1, comprising the steps of:
dissolving sodium alkoxide in alcohol, adding 3-hydroxyacetophenone and 4-bromo-3, 5-dimethoxybenzaldehyde to react for 40-60 hours, adjusting the pH value to 1-2, and extracting to obtain the antitumor compound.
3. The method according to claim 2, wherein the molar ratio of the 3-hydroxyacetophenone to the 4-bromo-3, 5-dimethoxybenzaldehyde is (0.8-1.2): 1.
4. The method according to claim 2, wherein the ratio of the mass of the sodium alkoxide to the volume of the alcohol is (52 to 56) mg:1 mL.
5. The method of claim 2, further comprising the steps of: before the pH value is adjusted, 4-8 mL of water is added and the mixture is washed by diethyl ether for multiple times.
6. The method of claim 2, further comprising the steps of: recrystallizing the anti-tumor compound with a mixture of ethanol and water.
7. The preparation method according to claim 2, wherein the extraction specifically comprises the steps of: the organic phases are extracted several times with 18 to 24mL of ethyl acetate and combined.
8. Use of the anti-tumor compound of claim 1 in the preparation of an anti-tumor medicament.
9. An anti-tumor drug against Fyn-CD147 signal pathway targets, comprising the anti-tumor compound of claim 1, wherein the anti-tumor compound accounts for no more than 99% of the anti-tumor drug by mass.
10. The antitumor drug as claimed in claim 9, wherein the dosage form of the antitumor drug is injection, tablet, paste or suppository.
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| CN105967991A (en) * | 2016-05-12 | 2016-09-28 | 哈尔滨医科大学 | Compound with antitumor activity and preparation method and application of compound |
| CN106831375A (en) * | 2016-12-28 | 2017-06-13 | 哈尔滨医科大学 | A kind of Chalcone Compounds with antitumor activity and its production and use |
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| CN105967991A (en) * | 2016-05-12 | 2016-09-28 | 哈尔滨医科大学 | Compound with antitumor activity and preparation method and application of compound |
| CN106831375A (en) * | 2016-12-28 | 2017-06-13 | 哈尔滨医科大学 | A kind of Chalcone Compounds with antitumor activity and its production and use |
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