A tryptamine compound and its preparation method and application

Abstract

The present invention discloses a tryptamine compound and a preparation method and application thereof. The tryptamine compound can be used to prepare a drug for preventing and / or treating cancer; the cancer is at least one of breast cancer, liver cancer, lung cancer, colorectal cancer, leukemia, pancreatic cancer, glioma, osteosarcoma, cervical cancer, ovarian cancer, kidney cancer and esophageal cancer. The present invention screens the activity of multiple compounds and finds for the first time that the three tryptamine compounds provided by the present invention have excellent inhibitory activity against multiple different types of human cancer cells, providing an optional solution for a broad-spectrum anticancer drug.

Description

Technical Field

[0001] The present invention relates to the field of anti-tumor drugs, and in particular to a tryptamine compound and a preparation method and application thereof. Background Art

[0002] Cancer is a disease that seriously threatens human health. Its morbidity and mortality continue to rise, becoming an important public health issue worldwide. Existing cancer treatments include surgery, radiotherapy, chemotherapy, and targeted therapy, but these methods are often accompanied by certain side effects, and some patients may develop resistance to existing therapies. Therefore, developing new anticancer drugs to improve efficacy and reduce side effects is an important direction in the current field of tumor research.

[0003] Indole derivatives are a class of natural products with multiple biological activities. Their unique structure endows them with multiple biological activities. In recent years, studies have found that some indole derivatives have significant anti-tumor activity and can inhibit the growth and metastasis of tumor cells through multiple mechanisms.

[0004] Although some tryptamine compounds have achieved positive results in anti-tumor research, there are still few literatures on their structural improvement, synthesis methods and clinical applications. Therefore, the synthesis of new tryptamine compounds and their research in cancer treatment will help promote the development and application of anti-cancer drugs. Summary of the invention

[0005] In view of the deficiencies of the prior art, the present invention provides a novel tryptamine compound and its application in the preparation of a drug for preventing and / or treating cancer.

[0006] In order to solve the above technical problems, the technical solution of the present invention is as follows: a tryptamine compound, wherein the tryptamine compound is compound I, compound II and compound III, and the structural formulas are shown in formula I, formula II or formula III respectively:

[0007] Formula I Formula II Formula III.

[0008] The present invention also provides the use of the tryptamine compound in preparing a drug for preventing and / or treating cancer, wherein the cancer is at least one of breast cancer, liver cancer, lung cancer, colorectal cancer, leukemia, pancreatic cancer, glioma, osteosarcoma, cervical cancer, ovarian cancer, kidney cancer and esophageal cancer.

[0009] That is, the cancer cells that the tryptamine compounds can inhibit are at least one of human breast cancer cells, human liver cancer cells, human leukemia cells, human cervical cancer cells, human lung cancer cells, human colorectal cancer cells, human kidney cancer cells, human ovarian cancer cells, human glioma cells, human pancreatic cancer cells, human osteosarcoma cells and human esophageal cancer cells.

[0010] Preferably, the cancer is breast cancer.

[0011] As a further description of the above scheme: the tryptamine compound is used in combination with a pharmaceutically acceptable carrier. That is, when compound I-III is used as a drug, it can be used directly or in the form of a pharmaceutical composition. It can be administered to patients in need of treatment orally or by injection, and can be made into a variety of forms of drugs for use, with a wide range of applications.

[0012] As a further description of the above scheme: the tryptamine compound uses the compound with the structure shown in Formula I-III or its pharmaceutically acceptable salt as the active ingredient.

[0013] As a further description of the above scheme: the mass fraction of the active pharmaceutical ingredient is 0.01% to 99%. Preferably, the mass fraction of the active pharmaceutical ingredient is 0.01% to 30%.

[0014] The present invention also provides a method for preparing the tryptamine compound, and the specific process is as follows:

[0015] Preferably, the preparation method of the compound I is as follows: dissolving compound 1 in acetonitrile, adding 3-5 molar times of 8-12% NaClO aqueous solution; stirring at room temperature for 1-2 hours, extracting with acetonitrile after phase separation, combining the acetonitrile layers to obtain an acetonitrile solution of compound 2; then adding catalyst Pd / C and ammonium formate, stirring at room temperature for 1.5-3 hours, the reaction is completed, and after extraction, purification is performed by silica gel column chromatography to obtain compound I; the molar ratio of compound 2 to ammonium formate is 1:1.5-3;

[0016] The structural formulas of the compounds 1 and 2 are as follows:

[0017] .

[0018] Preferably, the preparation method of the compound II is as follows: dissolving the raw material compound 3 in acetonitrile, adding 3-5 molar times of 8-12% NaClO aqueous solution, stirring at room temperature for 1-2 hours, extracting with acetonitrile after phase separation, combining the acetonitrile layers to obtain an acetonitrile solution of compound 4, and then adding 2.5-4 molar times of 4,5-dichloro-o-phenylenediamine, stirring at room temperature for 1-3 hours, and filtering to obtain compound II;

[0019] The structural formulas of the compounds 3 and 4 are as follows:

[0020] .

[0021] Preferably, the preparation method of the compound III is as follows: dissolving compound 5 in acetonitrile, adding 3-5 molar times of 8-12% NaClO aqueous solution; stirring at room temperature for 1-2 hours, extracting with acetonitrile after phase separation, combining the acetonitrile layers to obtain an acetonitrile solution of compound 6; then adding 2-4 molar times of 5-bromoindole and 1-1.5 molar times of 1N H2SO4 aqueous solution, stirring at room temperature for 2-4 hours, extracting and purifying by silica gel column chromatography to obtain compound III;

[0022] The structural formulas of the compounds 5 and 6 are as follows:

[0023] .

[0024] Compared with the prior art, the present invention has the following beneficial effects: the present invention screens the activity of tryptamine compounds and finds for the first time that tryptamine compounds such as structural formula I-III have excellent inhibitory activity against various types of human cancer cells, providing an alternative for broad-spectrum anticancer drugs. At the same time, the synthesis method of the tryptamine compounds is simple and has a high yield. BRIEF DESCRIPTION OF THE DRAWINGS

[0025] Figure 1 It is the structural formula of tryptamine compounds I-III;

[0026] Figure 2 The results of the inhibition of tryptamine compounds I-III on human breast cancer cell lines HCC1806 (left) and HCC1937 (right), ***p<0.001;

[0027] Figure 3 It is the structural formula of tryptamine compounds IV-IX. DETAILED DESCRIPTION

[0028] The technical solution of the present invention is further described in detail below in conjunction with the accompanying drawings and specific embodiments, but the present invention is not limited to the following technical solution.

[0029] The human liver cancer cells described in the following examples are human liver cancer cells Huh-7, the human lung cancer cells are human lung cancer cells H460, the human breast cancer cells are human breast cancer cells HCC1937 and HCC1806, the human leukemia cells are human leukemia cells HL-60, the human cervical cancer cells are human cervical cancer cells Hela, the human colorectal cancer cells are human colorectal cancer cells HCT116, the human renal cancer cells are human renal cancer cells 786-0, the human ovarian cancer cells are human ovarian cancer cells Hey, the human glioma cells are human glioma cells T98G, the human pancreatic cancer cells are human pancreatic cancer cells SW1990, the human osteosarcoma cells are human osteosarcoma cells MG63, and the esophageal cancer cells are Eca-190. The conventional cancer cells used above are all from the Kunming Institute of Zoology, Chinese Academy of Sciences.

[0030] Unless otherwise specified, the reagents in the embodiments of the present invention can be purchased from commercial sources. RPMI1640 culture medium, DMEM culture medium, and fetal bovine serum were purchased from Biological Industries; phosphate buffered saline (PBS) and 0.25% trypsin (containing EDTA) were purchased from Gibco.

[0031] The cell lines were cultured in DMEM or RPMI1640 medium containing 10% fetal bovine serum at 37°C, 5% CO2 and 90% humidity.

[0032] The structural formula of the tryptamine compounds used in the following examples is as follows: Figure 1 shown.

[0033] Example 1 Synthesis of Tryptamine Compounds I-III

[0034] The specific process for the synthesis of compound I is as follows:

[0035]

[0036] Compound 1 (349 mg, 1.0 mmol) was dissolved in 10 mL of acetonitrile, and 10% NaClO aqueous solution (1.48 mL, 4.0 mmol) was added. The reaction was stirred at room temperature for 1-1.5 hours, and thin layer chromatography (petroleum ether: ethyl acetate = 2:1 (volume ratio)) showed that the reaction was complete. After phase separation, it was extracted with 2 mL of acetonitrile, and the acetonitrile layers were combined to obtain an acetonitrile solution of the intermediate (compound 2), and then 10% Pd / C 38 mg and formic acid amine (126 mg, 2.0 mmol) were added, and the reaction was stirred at room temperature for 2 hours. After the reaction was completed, the resulting solution was diluted with ethyl acetate (20 mL), and then extracted and washed with an appropriate amount of water. The organic layer after extraction was added with anhydrous sodium sulfate to dry, filtered, and concentrated under reduced pressure in a rotary evaporator to obtain a crude product. Purification was performed using silica gel column chromatography with petroleum ether / ethyl acetate = 3:1 to obtain 322 mg of the target product (compound I) with a yield of 92%.

[0037] The structural characterization of compound I is as follows:

[0038] 1 H NMR (500 MHz, DMSO-d6) δ 11.58 (s, 1H), 7.61 (d, J = 8.3 Hz, 2H), 7.38–7.34 (m, 3H), 7.22 (d, J = 2.1 Hz, 1H), 7.00 – 6.95 (m, 1H), 4.19 – 4.08 (m, 2H), 2.70–2.60 (m, 2H), 2.32 (s, 3H).

[0039] 13 C NMR (126 MHz, DMSO-d6) δ 145.24, 143.13, 137.54, 132.22, 130.60,130.11, 127.94, 127.06, 124.90, 120.01, 117.02, 114.27, 103.97, 56.56, 22.87,21.51.

[0040] HRMS (ESI): calcd for C 17 H 15 ClN2O2S [M + H] + m / z 347.0616, found347.0611.

[0041] The specific process for the synthesis of compound II is as follows:

[0042]

[0043] The raw material compound 3 (260 mg, 1.0 mmol) was dissolved in 10 mL of acetonitrile, and a 10% NaClO aqueous solution (1.48 mL, 4.0 mmol) was added. The reaction was stirred at room temperature for 1-1.5 hours, and thin layer chromatography (petroleum ether: ethyl acetate = 4:1 (volume ratio)) showed that the reaction was complete. After phase separation, it was extracted with 2 mL of acetonitrile, and the acetonitrile layers were combined to obtain an acetonitrile solution of the intermediate (compound 4), and 4,5-dichloro-o-phenylenediamine (531 mg, 3.0 mmol) was added, and the reaction was stirred at room temperature for 2 hours. The target product (Compound II) was directly filtered to obtain 364 mg, with a yield of 84%.

[0044] The structural characterization of compound II is as follows:

[0045] 1 H NMR (500 MHz, DMSO-d6) δ 8.49 (s, 1H), 7.71 (d, J = 7.1 Hz, 1H), 7.45 (s, 1H), 7.42 (t, J = 8.1 Hz, 1H), 7.22 (t, J = 7.8 Hz, 2H), 7.19 (s,1H), 6.81 (t, 1H), 2.83 – 2.74 (m, 2H), 1.90 – 1.78 (m, 1H), 1.67 – 1.53 (m,1H), 1.27 (s, 9H).

[0046] 13 C NMR (126 MHz, DMSO-d6) δ 161.24, 155.78, 142.28, 133.36, 130.56,130.35, 128.68, 125.74, 125.13, 124.69, 121.05, 120.47, 117.03, 113.61,78.19, 61.53, 34.83, 33.58, 28.59, 28.31.

[0047] HRMS (ESI): calcd for C 21 H 22 Cl2N4O2 [M + H] + m / z 433.1193, found433.1183.

[0048] The specific process for the synthesis of compound III is as follows:

[0049]

[0050] The raw material compound 5 (314 mg, 1.0 mmol) was dissolved in 10 mL of acetonitrile, and a 10% NaClO aqueous solution (1.48 mL, 4.0 mmol) was added. The reaction was stirred at room temperature for 1-1.5 hours, and thin layer chromatography (petroleum ether: ethyl acetate = 2:1 (volume ratio)) showed that the reaction was complete. After phase separation, it was extracted with 2 mL of acetonitrile, and the acetonitrile layers were combined to obtain an acetonitrile solution of the intermediate (compound 6), and 5-bromoindole (588 mg, 3.0 mmol) and 1N H2SO4 aqueous solution (2 mL, 1.0 mmol) were added, and the reaction was stirred at room temperature for 3 hours. The degree of reaction was detected by thin layer chromatography. After the intermediate reaction was complete, the resulting solution was diluted with ethyl acetate, and then extracted and washed with an appropriate amount of water. The organic layer after extraction was dried with anhydrous sodium sulfate, filtered, and concentrated under reduced pressure in a rotary evaporator to obtain a crude product. The product was purified by silica gel column chromatography with petroleum ether / ethyl acetate = 3:2 (volume ratio) to obtain 334 mg of the target product (Compound III) with a yield of 64%.

[0051] The structural characterization of compound III is as follows:

[0052] TLC: Rf = 0.16 (petroleum ether / ethyl acetate = 3:2)

[0053] 1 H NMR (500 MHz, DMSO-d6) δ 11.29 (d, J = 2.1 Hz, 1H), 10.66 (s, 1H), 7.63 (s, 1H), 7.55 (d, J = 7.9 Hz, 2H), 7.38 – 7.29 (m, 3H), 7.28 – 7.23 (m,1H), 7.21 (d, J = 2.4 Hz, 1H), 7.13 (dd, J = 8.6, 1.9 Hz, 1H), 7.09 (s, 1H), 7.03 (d, J = 7.3 Hz, 1H), 7.00 – 6.92 (m, 2H), 2.60 (t, J = 11.1 Hz, 1H),2.48 – 2.37 (m, 2H), 2.35 (s, 3H), 2.33 – 2.29 (m, 1H).

[0054] 13C NMR (126 MHz, DMSO-d6) δ 179.39, 143.28, 142.23, 137.69, 135.93,132.56, 130.19, 128.98, 126.97, 125.50, 124.66, 124.22, 122.58, 122.04,114.29, 113.94, 111.78, 110.23, 50.97, 40.09, 35.79, 21.49.

[0055] HRMS (ESI): calcd for C 25 H 22 BrN3O3S[M + H] + m / z 524.0638, found 524.0641.

[0056] Example 2 Antitumor activity test of natural products with antitumor activity

[0057] The CCK-8 method was used to detect cell growth inhibition. The CCK-8 reagent contains WST-8 (chemical name: 2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfonic acid benzene)-2H-tetrazolyl monosodium salt), which can be reduced to a highly water-soluble orange-yellow formazan product by dehydrogenase in the presence of the electron coupling reagent 1-methoxy-5-methylphenazine dimethyl sulfate (1-Methoxy PMS) by mitochondrial dehydrogenase. The amount of formazan generated is proportional to the number of living cells. Therefore, this characteristic can be used to directly analyze cell proliferation and toxicity. An absorption peak is generated at a wavelength of 450 nm. The more and faster the cell proliferation, the darker the color; the greater the cell toxicity, the lighter the color. The CCK8 detection reagent was purchased from Shanghai Biyuntian Biotechnology Co., Ltd., catalog number C0039.

[0058] The tryptamine compounds (Ⅰ, Ⅱ, Ⅲ) were dissolved in DMSO (dimethyl sulfoxide), and then DMSO was used to prepare DMSO solutions with concentrations of 1 mM, 100 μM, and 10 μM, respectively.

[0059] Breast cancer cells HCC1937 and HCC1806 (4×10 3 / well) were inoculated in 96-well plates, 99 μl of culture medium was added, and the plates were cultured in a 37°C 5% CO2 constant temperature incubator for 24 h. Then, 1 μl of four different concentrations of tryptamine compounds (Ⅰ, Ⅱ, Ⅲ) dissolved in DMSO was added to the cell culture in each well. In the control group, only the same volume of DMSO was added to the cell culture, so that the concentrations of each compound in the cell culture solution were 10 μM, 1 μM, and 0.1 μM, respectively, and the plates were placed in an incubator for incubation for 72 h. Then 10 μL of CCK-8 solution was added to each well, and the plates were cultured in an incubator for 0.5-4 hours (different cell culture times), and the absorbance at 450 nm was measured. The percentage of the absorbance value of the experimental group relative to the absorbance value of the control group represents the cell survival rate or the cell proliferation level, that is, the control group defaults to 100% ( Figure 2 ).

[0060] Calculation formula: cell survival rate = [(As-Ab) / (Ac-Ab)] × 100%;

[0061] Inhibition rate = [(Ac-As) / (Ac-Ab)] × 100%;

[0062] As: absorbance of experimental wells (containing cells, culture medium, CCK-8 solution and drug solution);

[0063] Ac: absorbance of control well (containing cells, culture medium, CCK-8 solution, but no drug);

[0064] Ab: absorbance of blank well (containing culture medium and CCK-8 solution, but not cells or drugs).

[0065] The results are as follows Figure 2 As shown, compounds Ⅰ, Ⅱ, and Ⅲ exhibited breast cancer inhibitory activity at a concentration of 10 μM, and the survival rates of both breast cancer cells were below 50%.

[0066] According to the above test method, similar tryptamine compounds IV-IX (structures such as Figure 3 The inhibitory effect on cancer cell growth was weak and the anti-tumor activity was low (see Table 1).

[0067] Table 1 Inhibition rate of tryptamine compounds IV-IX on cancer cell growth

[0068]

[0069] Example 3

[0070] Tryptamine compounds Ⅰ, Ⅱ and Ⅲ were dissolved in DMSO, and then DMSO was used to prepare DMSO solutions with concentrations of 10 mM, 1 mM, 100 μM, 10 μM and 1 μM, respectively.

[0071] Human breast cancer cells HCC1806 (4×10 3 / well) were inoculated in 96-well plates, each well contained 100 μL of cell culture medium, and cultured in a 37°C 5% CO2 constant temperature incubator for 24 hours, and then 1 μL of DMSO containing different concentrations of compounds was added to the cells in each well, so that the final concentrations were 100 μM, 10 μM, 1 μM, 100 nM, and 10 nM; the control group was only added with 1 μL of DMSO to the cell culture, and then placed in an incubator for 72 hours, and CCK8 was used to detect the proliferation effect. The results are shown in Table 2.

[0072] Table 2 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ, cisplatin, cyclophosphamide and talazoparib on human breast cancer cell line HCC1806 50 (μM)

[0073]

[0074] According to the results in Table 2, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human breast cancer cell line HCC1806, IC 50 They are 1.045μM, 1.772μM and 1.867μM respectively, and have better effects and lower dosages than the breast cancer chemotherapy drugs currently used in clinical practice (cisplatin and lapatinib).

[0075] Example 4

[0076] The human breast cancer cell line HCC1806 was replaced with the human breast cancer cell line HCC1937. Other details were the same as those in Example 3. 50 The results of the values ​​are shown in Table 3.

[0077] Table 3 IC50 of tryptamine compounds Ⅰ, Ⅱ and Ⅲ on human breast cancer cell line HCC1937 50 (μM)

[0078]

[0079] According to the results in Table 3, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human breast cancer cell line HCC1937, IC 50 They are 1.389 μM, 2.020 μM and 2.749 μM respectively.

[0080] Example 5

[0081] The human breast cancer cells HCC1806 were replaced with human breast cancer cells MDA-MB-231. Other aspects were the same as those in Example 3. 50 The results of the values ​​are shown in Table 4.

[0082] Table 4 IC50 of tryptamine compounds Ⅰ, Ⅱ, and Ⅲ on the growth inhibition of human breast cancer cell line MDA-MB-231 50 (μM)

[0083]

[0084] According to the results in Table 4, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human breast cancer cell line MDA-MB-231, IC 50 They are 5.872 μM, 2.916 μM and 2.202 μM respectively.

[0085] Example 6

[0086] The human breast cancer cell line HCC1806 was replaced with the human liver cancer cell line Huh-7. Other details were the same as those in Example 3. 50 The results of the values ​​are shown in Table 5.

[0087] Table 5 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on human hepatoma cell line Huh-7 50 (μM)

[0088]

[0089] According to the results in Table 5, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human liver cancer cell line Huh-7, IC 50 They are 1.042 μM, 1.762 μM and 2.657 μM respectively.

[0090] Example 7

[0091] The human breast cancer cells HCC1806 were replaced with human lung cancer cells H460. Other aspects were the same as those in Example 3. 50 The results of the values ​​are shown in Table 6.

[0092] Table 6 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on human lung cancer cell line H460 50 (μM)

[0093]

[0094] According to the results in Table 6, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human liver cancer cell line H460, IC 50 They are 0.357 μM, 3.373 μM and 2.716 μM respectively.

[0095] Example 8

[0096] The human breast cancer cells HCC1806 were replaced with human myeloid leukemia cells HL-60. Others were the same as in Example 3. 50 The results of the values ​​are shown in Table 7.

[0097] Table 7 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on the growth inhibition of human myeloid leukemia cell line HL-60 50 (μM)

[0098]

[0099] According to the results in Table 7, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human myeloid leukemia cell line HL-60, IC 50 They are 1.542 μM, 2.047 μM and 5.145 μM respectively.

[0100] Example 9

[0101] The human breast cancer cells HCC1806 were replaced with human cervical cancer cells Hela cells. Others were the same as in Example 3. 50 The results of the values ​​are shown in Table 8.

[0102] Table 8 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on human cervical cancer cell line Hela 50 (μM)

[0103]

[0104] According to the results in Table 8, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human cervical cancer cell Hela cell line, IC 50 They are 1.213 μM, 4.156 μM and 4.391 μM respectively.

[0105] Example 10

[0106] The human breast cancer cell line HCC1806 was replaced by the human colorectal cancer cell line HCT116. Other details were the same as those in Example 3. 50 The results of the values ​​are shown in Table 9.

[0107] Table 9 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on human colorectal cancer cell line HCT11650 (μM)

[0108]

[0109] According to the results in Table 9, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cancer cell toxicity against human colorectal cancer cell line HCT116, IC 50 They are 1.064 μM, 2.679 μM and 3.814 μM respectively.

[0110] Embodiment 11

[0111] The human breast cancer cell line HCC1806 was replaced with the human renal cancer cell line 786-0. Other details were the same as those in Example 3. 50 The results of the values ​​are shown in Table 10.

[0112] Table 10 The half-maximal growth inhibition concentration IC of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on human renal cancer cell line 786-0 50 (μM)

[0113]

[0114] According to the results in Table 10, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human renal cancer cell line 786-0, IC 50 They are 3.883 μM, 2.066 μM and 6.212 μM respectively.

[0115] Example 12

[0116] The human breast cancer cells HCC1806 were replaced with human ovarian cancer cells Hey. Other aspects were the same as those in Example 3. 50 The results of the values ​​are shown in Table 11.

[0117] Table 11 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on human ovarian cancer cell line Hey 50 (μM)

[0118]

[0119] According to the results in Table 11, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human ovarian cancer cell Hey cell line, IC 50 They are 0.923 μM, 3.317 μM and 1.175 μM respectively.

[0120] Embodiment 13

[0121] The human breast cancer cells HCC1806 were replaced with human osteosarcoma cells MG63. Other aspects were the same as those in Example 3. 50 The results of the values ​​are shown in Table 12.

[0122] Table 12 IC50 of tryptamine compounds Ⅰ, Ⅱ, Ⅲ on human osteosarcoma cell line MG63 50 (μM)

[0123]

[0124] According to the results in Table 12, tryptamine compounds Ⅰ, Ⅱ, and Ⅲ have strong cytotoxic activity against human osteosarcoma cell line MG63, IC 50 They are 2.032 μM, 3.814 μM and 0.986 μM respectively.

[0125] Embodiment 14

[0126] Human breast cancer cells HCC1806 were replaced by human glioma cells T98G, human pancreatic cancer cells SW1990, and human esophageal cancer cells Eca-190. Others were the same as in Example 3. Half-maximum growth inhibition concentration IC values ​​of tryptamine compounds I-III on various cancer cells 50 The results of the values ​​are shown in Tables 13 to 15.

[0127] Table 13 IC50 of tryptamine compounds I on various cancer cells 50 (μM)

[0128]

[0129] According to the results in Table 13, tryptamine compound I has strong cancer cell cytotoxicity against human glioma cells T98G, human pancreatic cancer cells SW1990 and human esophageal cancer cells Eca-190, IC 50 They are 1.62 μM, 4.23 μM and 6.22 μM respectively.

[0130] Table 14 IC50 of tryptamine compounds II on various cancer cells 50 (μM)

[0131]

[0132] According to the results in Table 14, tryptamine compound II has strong cancer cell cytotoxicity against human glioma cell T98G, human pancreatic cancer cell SW1990 and human esophageal cancer cell Eca-190, IC 50 They are 6.12 μM, 5.51 μM and 4.12 μM respectively.

[0133] Table 15 IC50 of tryptamine compound III on various cancer cells 50 (μM)

[0134]

[0135] According to the results in Table 15, tryptamine compound III has strong cancer cell cytotoxicity against human glioma cells T98G, human pancreatic cancer cells SW1990 and human esophageal cancer cells Eca-190, IC 50 They are 1.21M, 6.25μM and 7.02μM respectively.

[0136] In summary, tryptamine compounds I, II, and III have excellent inhibitory activity against a variety of different types of human cancer cells, providing an option for broad-spectrum anticancer drugs.

[0137] It should be noted that the embodiments described above are only used to explain the present invention and do not constitute any limitation to the present invention. The present invention has been described with reference to typical embodiments, but it should be understood that the words used therein are descriptive and explanatory words, rather than restrictive words. The present invention may be modified as specified within the scope of the claims of the present invention, and the present invention may be revised without departing from the scope and spirit of the present invention. Although the present invention described therein relates to specific methods, materials and embodiments, it does not mean that the present invention is limited to the specific examples disclosed therein, but rather, the present invention extends to all other methods and applications with the same functions.

Claims

1. Use of a tryptamine compound in the preparation of a drug for preventing and / or treating cancer, characterized in that: The tryptamine compound is compound I, compound II or compound III, and the structural formula is shown in formula I, formula II or formula III respectively: Formula I Formula II Formula III The cancer is at least one of breast cancer, liver cancer, lung cancer, colorectal cancer, leukemia, pancreatic cancer, glioma, osteosarcoma, cervical cancer, ovarian cancer, kidney cancer and esophageal cancer.

2. The use of the tryptamine compound according to claim 1 in the preparation of a drug for preventing and / or treating cancer, characterized in that: The cancer is breast cancer.

3. The use of the tryptamine compound according to claim 1 in the preparation of a drug for preventing and / or treating cancer, characterized in that: The tryptamine compound is used in combination with a pharmaceutically acceptable carrier.

4. The use of the tryptamine compound according to claim 1 in the preparation of a drug for preventing and / or treating cancer, characterized in that: The drug uses the compound with the structure shown in Formula I-III or its pharmaceutically acceptable salt as the active ingredient.

5. Use of the tryptamine compound according to claim 4 in the preparation of a drug for preventing and / or treating cancer, characterized in that: The mass fraction of the active pharmaceutical ingredient is 0.01% to 99%.

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