Application of compound in preparation of anti-anaphylaxis drugs
By preparing compound FIP22, IgE-mediated type I hypersensitivity reactions were inhibited, solving the problem of severe side effects of existing anti-allergy drugs and providing a safer treatment option for allergic reactions.
Patent Information
- Application Number
- CN202511440945.X
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2025-10-10
- Publication Date
- 2025-12-12
AI Technical Summary
Existing anti-allergy medications have serious side effects, affecting patients' physical and mental health.
Anti-allergic drugs can be prepared using specific compounds (such as compound FIP22) to provide a safer treatment option by inhibiting IgE-mediated type I hypersensitivity reactions, including inhibiting mast cell degranulation, histamine, β-aminohexosidase and prostaglandin D2 release.
Compound FIP22 effectively inhibits IgE-mediated type I hypersensitivity reactions, reduces allergy symptoms, lowers drug side effects, and provides a safer treatment option.
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Figure CN121102500A_ABST
Abstract
Description
Technical Field
[0001] This invention belongs to the field of biomedical technology, and more specifically, relates to the application of a compound in the preparation of anti-allergic drugs. Background Technology
[0002] Allergic diseases are primarily IgE-mediated type I hypersensitivity reactions or allergic reactions, including allergic rhinitis, allergic bronchial asthma (ASA), and food allergies. Allergic diseases affect 40% of the population; globally, approximately 400 million people suffer from allergic rhinitis (AR), 300 million from asthma, and 250 million from food allergies. Allergic diseases have been listed by the WHO as one of the six most common chronic diseases, making them a key area for research and prevention. Allergic diseases not only impact quality of life but can also be life-threatening, imposing a heavy economic burden on families and society.
[0003] Allergic reactions are an overreaction of the body's immune system to foreign substances (such as pollen, dust mites, and food). When these substances enter the body, the immune system misinterprets them as harmful, triggering an excessive immune response. During this process, large amounts of inflammatory mediators, such as histamine and leukotrienes, are released, leading to allergic symptoms. Common allergic symptoms include itchy, red, and swollen skin, sneezing, runny nose, coughing, and asthma. Severe allergic reactions can even cause shock and endanger life. Allergic reactions not only cause physical suffering but can also negatively impact mental health, leading to anxiety, depression, and other emotional problems.
[0004] Currently, preventing allergies involves two main approaches: first, identifying the allergen and avoiding or reducing direct contact with it; and second, alleviating allergy symptoms through medication. Current anti-allergy medications mainly include histamines, leukotriene inhibitors, and corticosteroids. However, these medications have serious side effects, including nausea, vomiting, drowsiness, fatigue, and cognitive decline. Therefore, most of these medications are primarily used as adjunctive therapy.
[0005] In recent years, researchers have been exploring areas where drugs have fewer side effects and better efficacy. Chemical drugs have gradually gained widespread attention, and it has been found that they have significant effects in treating allergies. Summary of the Invention
[0006] In order to overcome the problem of severe side effects in the existing anti-allergy drugs, the present invention aims to provide an application of a compound in the preparation of anti-allergy drugs.
[0007] The above-mentioned objective of this invention is achieved through the following technical solution: The use of a compound in the preparation of an anti-allergic drug, the chemical structure of which is shown in Formula I below: .
[0008] Furthermore, the Linker can be selected from any of the following structures: .
[0009] Furthermore, the Linker is selected from the following structure: .
[0010] Furthermore, the allergic reaction is a type I allergic reaction mediated by IgE antibodies.
[0011] Furthermore, the type I allergic reaction is one or more of allergic rhinitis, asthma, urticaria, anaphylactic shock, and allergic conjunctivitis.
[0012] Furthermore, the dosage form of the drug is tablets, powders, capsules, granules, oral liquids, or syrups.
[0013] Furthermore, the drug has the effect of inhibiting IgE-mediated serum histamine release.
[0014] Furthermore, the drug has the effect of inhibiting IgE-mediated β-aminohexosidase release.
[0015] Furthermore, the drug has the effect of inhibiting IgE-mediated prostaglandin D2 release.
[0016] Furthermore, the drug has the effect of inhibiting IgE-mediated release of leukotrienes LTC4.
[0017] The present invention has the following beneficial effects: The compound provided by this invention can effectively inhibit mast cell degranulation, thereby inhibiting the occurrence of IgE-mediated type I hypersensitivity reactions. Therefore, this compound can be used as an anti-drug hypersensitivity agent, providing more possible treatment options for the clinical treatment of drug hypersensitivity reactions. Attached Figure Description
[0018] Figure 1 The cytotoxicity of FIP22 synthesized in this embodiment of the invention; Figure 2 This invention demonstrates the inhibitory effect of the present invention on mast cell degranulation; Figure 3 This invention demonstrates the inhibitory effect of the present invention on passive cutaneous anaphylaxis in mice; Figure 4 This invention demonstrates the inhibitory effect of the present invention on systemic allergic reactions in mice. Detailed Implementation
[0019] The present invention will be further illustrated below with reference to specific embodiments, but these embodiments do not limit the present invention in any way. Unless otherwise specified, the reagents, methods, and equipment used in the present invention are conventional reagents, methods, and equipment in this technical field. Unless otherwise specified, the reagents and materials used in the following embodiments are commercially available.
[0020] Example 1: Synthesis of Compound IP5 .
[0021] Synthesis of compound IR1: IRO (2.2 g, 10.0 mmol) and propyl-2-amine hydrochloride (1.9 g, 20.0 mmol) were dissolved in N,N-dimethylformamide (8.8 mL), and N,N-diisopropylethylamine (6.5 g, 50.0 mmol) was added. The reaction was heated at 80 °C overnight and monitored by TLC. After the reaction was completed, the reaction solution was added to 90 mL of vigorously stirred water, and the crude product was purified by silica gel column chromatography (PE:EA = 30:1 to 5:1) to obtain IR1 (2.0 g, 63%).
[0022] IR1: 1H NMR (400 MHz, CDCl3) δ 8.65 (s, 1H), 6.52 (s, 1H), 4.32 (d, J= 7.1 Hz, 2H), 3.69 – 3.64 (m, 1H), 1.36 (d, J = 7.1 Hz, 3H), 1.28 (s, 3H),1.26 (s, 3H). ESI-MS m / z: 243.10 [M+H]+ 241.05 [MH]-. Synthesis of compound IR2: IR1 (4 g, 16.4 mmol), 1H-pyrrolo[2,3-b]pyridine-5-carboxylonitrile (2.4 g, 16.4 mmol), tris(dibenzylacetone)palladium (6.0 g, 6.5 mmol), and 4,5-bis(diphenylphosphino)-9,9-dimethyloxanthracene (3.8 g, 6.5 mmol) were suspended in anhydrous dioxane (150 mL) and cesium carbonate (16.1 g, 49.4 mmol). After purging the air three times with nitrogen, the reaction mixture was refluxed at 110 °C overnight. After the reaction was complete, the residue was removed by vacuum filtration with diatomaceous earth and then extracted with dichloromethane (3 × 200 mL). The organic layer was washed with brine, dried over anhydrous sodium sulfate, filtered, and concentrated. The crude product was purified by silica gel chromatography (PE:EA = 30:1 to 10:1) to obtain IR2 (3.6 g, 52%).
[0023] IR2: 1H NMR (400 MHz, CDCl3) δ 8.82 (s, 1H), 8.66 (d, J = 1.6 Hz, 1H), 8.56 (d, J = 3.9 Hz, 1H), 8.25 (s, 1H), 8.23 (d, J = 1.6 Hz, 1H), 8.17 (d, J = 6.2 Hz, 1H), 6.70 (d, J = 3.9 Hz, 1H), 4.36 (q, J = 7.1 Hz, 2H), 3.92 (dq,J = 13.0, 6.5 Hz, 1H), 1.42 (d, J = 7.1 Hz, 3H), 1.38 (d, J = 6.3 Hz, 6H).ESI-MS m / z: 350.30[M+H]+ 348.30[MH]-. Synthesis of compound IR3: IR2 (2.0 g, 5.74 mmol) was dissolved in a mixed solution of tetrahydrofuran (30 mL) and ethanol (6 mL), followed by the addition of lithium hydroxide (1.4 g, 57.4 mmol) and water (4 mL). The reaction was carried out overnight at 50 °C. After the reaction was complete, the solvent was evaporated, and the solid was extracted with ethyl acetate. The aqueous phase was collected, and the pH was adjusted to 3-4, resulting in the precipitation of a solid. The solid was filtered under reduced pressure to obtain a white filter cake, which was identified as IR3 (1.5 g, 83%).
[0024] IR3: 1H NMR (400 MHz, DMSO) δ 13.14 (s, 1H), 8.79 (s, 1H), 8.69 (s, 1H), 8.64 (s, 1H), 8.52 (d, J = 3.5 Hz, 1H), 8.27 (d, J = 7.0 Hz, 1H), 8.16(s, 1H), 6.86 (d, J = 3.6 Hz, 1H), 3.82 (dd, J = 12.7, 6.3 Hz, 1H), 1.32 (d,J = 6.3 Hz, 6H). ESI-MS m / z: 322.25[M+H]+ 320.15[MH]-. Synthesis of compound IR4: IR3 (1.0 g, 3.1 mmol), (1r,4r)-4-aminocyclohexane-1-carboxylic acid methyl ester (0.9 g, 4.6 mmol), and 2-(7-azabenzotriazole)-N,N,N',N'-tetramethylurea hexafluorophosphate (1.75 g, 4.6 mmol) were dissolved in N,N-dimethylformamide (50 mL), followed by the addition of N,N-diisopropylethylamine (3.2 g, 24.8 mmol). The reaction was carried out overnight at room temperature and monitored by TLC. After the reaction was complete, the reaction solution was added to 500 mL of vigorously stirred water, precipitating a milky white solid. The solid was filtered under reduced pressure to obtain the crude product, which was then purified by silica gel column chromatography (DCM:MeOH = 150:1–50:1) to obtain IR4 (0.8 g, 68%).
[0025] IR4: 1H NMR (400 MHz, CDCl3) δ 8.65 (d, J = 1.4 Hz, 1H), 8.49 (d, J =3.9 Hz, 1H), 8.37 (d, J = 7.1 Hz, 1H), 8.30 (s, 1H), 8.23 (d, J = 1.3 Hz,1H), 8.18 (s, 1H), 6.70 (d, J = 3.9 Hz, 1H), 5.95 (d, J = 7.5 Hz, 1H), 3.98 –3.80 (m, 2H), 3.69 (s, 3H), 2.30 (ddd, J = 12.1, 7.9, 3.5 Hz, 1H), 2.18 (d, J= 9.8 Hz, 2H), 2.09 (d, J = 13.7 Hz, 2H), 1.65 (s, 6H), 1.37 (s, 2H), 1.36(s, 2H). ESI-MS m / z: 461.15[M+H]+ 459.30[MH]-. Synthesis of compound IR5: IR4 (700 mg, 1.5 mmol) was dissolved in a mixed solution of tetrahydrofuran (100 mL) and methanol (10 mL), followed by the addition of lithium hydroxide (180 mg, 7.5 mmol) and water (10 mL). The reaction was carried out overnight at 50 °C. After the reaction was complete, the solvent was evaporated, and the solid was extracted with ethyl acetate. The aqueous phase was collected, and the pH was adjusted to 3-4, resulting in the precipitation of solid. The solid was filtered under reduced pressure to obtain a white filter cake, which was identified as IR5 (555 mg, 83%).
[0026] IR5: 1H NMR (400 MHz, DMSO) δ 12.05 (s, 1H), 8.78 (s, 1H), 8.65 (s,1H), 8.57 (d, J = 7.4 Hz, 1H), 8.55 (s, 1H), 8.51 (d, J = 3.4 Hz, 1H), 8.32(d, J = 7.5 Hz, 1H), 8.06 (s, 1H), 6.86 (d, J = 3.4 Hz, 1H), 3.75 (dd, J =12.7, 6.2 Hz, 2H), 3.33 (s, 1H), 1.95 (s, 2H), 1.91 (s, 2H), 1.41 (d, J =10.3 Hz, 2H), 1.36 (d, J = 9.5 Hz, 2H), 1.29 (s, 3H), 1.27 (s, 3H). ESI-MS m / z: 447.25[M+H]+ 445.25[MH]-.
[0027] Example 2 Synthesis of compound SP3 I. Synthesis of Compound SQ1
[0028] SQ0 (10.0 g, 0.06 mmol) was dissolved in glacial acetic acid (100 mL). After complete dissolution, 3-aminopiperidine-2,6-dione hydrochloride (11.0 g, 0.067 mmol) and sodium acetate (5.93 g, 0.072 mmol) were added. The mixture was heated under reflux at 120 °C overnight. The mixture was stirred at 120 °C for 4 hours. The mixture was cooled to room temperature. The solution was poured into ice water (200 mL). The mixture was stirred for 10 minutes. The mixture was filtered. The gray solid was purified by silica gel rapid column chromatography. The final product was brown solid SQ1 (yield: 90-92%).
[0029] SQ1: 1H NMR (400 MHz, DMSO) δ 11.09 (s, 1H), 7.93 (dd, J = 8.2, 4.5Hz, 1H), 7.76 (dd, J = 7.3, 2.0 Hz, 1H), 7.68 – 7.60 (m, 1H), 5.11 (dd, J =12.8, 5.4 Hz, 1H), 2.84 (ddd, J = 17.2, 13.9, 5.3 Hz, 1H), 2.56 (d, J = 19.4Hz, 1H), 2.45 (dt, J = 10.1, 8.7 Hz, 1H), 2.07 – 1.97 (m, 1H). ESI-MS m / z277.30 [M+H]+; 275.20 [MH]-. II. Synthesis of compound SP2 SQ1 (19.2 mmol) and the corresponding spirocyclic amine protected by tert-butyl formate (23.0 mmol) were dissolved in N,N-dimethylformamide (50 mL). After complete dissolution, N,N-diisopropylethylamine (28.8 mmol) was added, and the mixture was heated under reflux at 90 °C overnight, monitored by TLC. After the reaction was complete, the reaction solution was added to 400 mL of vigorously stirred water, precipitating a yellow solid. The solid was filtered under reduced pressure to obtain the crude product, which was then purified by silica gel column chromatography (DCM:MeOH = 200:1–30:1) to obtain the yellow intermediate SP2 (62–83%).
[0030] SP2: 1H NMR (400 MHz, CDCl3) δ 8.17 (s, 1H), 7.67 (dd, J = 8.5, 2.5Hz, 1H), 7.06 (dd, J = 13.3, 5.4 Hz, 1H), 4.93 (dd, J = 12.3, 5.3 Hz, 1H), 3.42 (dd, J = 9.0, 5.4 Hz, 8H), 3.12 (s, 1H), 2.89 – 2.74 (m, 3H), 1.67 –1.63 (m, 4H), 1.51 – 1.48 (m, 4H), 1.46 (s, 9H). ESI-MS m / z: 511.50 [M+H]+, 509.40 [MH]-. III. Synthesis of compound SP3:
[0031] SP2 was dissolved in dioxane hydrochloride and reacted overnight at room temperature. The reaction was monitored by TLC. After the reaction was completed, the solvent was removed by vacuum evaporation to obtain SP3 as a pale yellow solid.
[0032] Example 3 Synthesis of compound FIP22
[0033] IR5 (50 mg, 0.112 mmol), 2-(7-azabenzotriazole)-N,N,N',N'-tetramethylurea hexafluorophosphate (52 mg, 0.135 mmol), and half of the N,N-diisopropylethylamine (44 mg, 0.336 mmol) to be added were dissolved in N,N-dimethylformamide (5 mL). Then, intermediate SP3 (52 mg, 0.135 mmol) and the remaining half of the N,N-diisopropylethylamine solution in N,N-dimethylformamide were slowly added dropwise. The mixture was stirred overnight at room temperature and detected by TLC. After the reaction was complete, the reaction solution was added to 500 mL of vigorously stirred water, and a solid precipitated. The solid was filtered under reduced pressure to obtain the crude product. The crude product was purified by silica gel column chromatography (DCM:MeOH = 150:1–50:1) to obtain the target compound FIP22.
[0034] FIP22:1H NMR (400 MHz, DMSO) δ 11.08 (s, 1H), 8.78 (s, 1H), 8.63 (d,J = 1.4 Hz, 1H), 8.56 (s, 1H), 8.50 (d, J = 3.7 Hz, 1H), 8.33 (d, J = 7.1 Hz,1H), 8.06 (s, 1H), 7.63 (d, J = 8.4 Hz, 1H), 7.29 (s, 1H), 7.20 (d, J = 7.9Hz, 1H), 6.86 (d, J = 3.7 Hz, 1H), 5.07 (dd, J = 12.7, 5.2 Hz, 1H), 3.79 –3.69 (m, 2H), 3.46 (s, 8H), 2.88 (dd, J = 21.2, 9.3 Hz, 1H), 2.58 (d, J =20.5 Hz, 2H), 2.51 (s, 1H), 2.06 – 1.99 (m, 1H), 1.92 (s, 2H), 1.72 (s, 2H),1.56 (s, 4H), 1.45 (dd, J = 20.1, 10.4 Hz, 8H), 1.28 (d, J = 6.1 Hz, 6H),1.22 – 1.14 (m, 1H). 13C NMR (101 MHz, DMSO) δ 173.27, 173.21, 170.58,168.11, 167.43, 167.19, 155.38, 154.75, 151.31, 149.03, 147.72, 146.52,134.45, 134.17, 129.67, 125.39, 122.76, 118.73, 117.81, 117.76, 109.77,107.95, 103.59, 102.33, 96.75, 60.22, 55.38, 49.21, 48.45, 43.57, 43.26,41.13, 38.87, 37.30, 36.40, 35.13, 34.56, 31.76, 31.47, 30.37, 28.72, 22.68,22.52. HRMS (ESI) for C46H49N10O6 (M - H)-: calcd 837.3915; found, 837.3841.HPLC: tR 3.742 min, purity 99.7%.
[0035] Validation of the efficacy of compound FIP22 as a drug to inhibit allergic reactions
[0036] I. Validation of FIP22's Cytotoxicity
[0037] The cytotoxicity of FIP22 was evaluated using a CCK-8 assay in BMMCs. The specific experimental procedure is as follows: Collect cells in the logarithmic growth phase into centrifuge tubes and centrifuge at 1200 rpm / min for 4 min. Discard the supernatant, wash 2-3 times with sterile PBS, resuspend the cells in culture medium, gently and repeatedly pipette to mix, count the cells, adjust the cell density to 5×104 cells / mL, gently and repeatedly pipette to mix, and seed 100 μL into each well of a 96-well plate. For the control group, add 0.5 μL of DMSO to each well. For the experimental group, add 0.5 μL of different drug concentrations (1, 10, 50, 100, 200, 400 μm) sequentially according to the concentration gradient, with three replicates for each concentration. Add 100 μL of PBS buffer to the edge wells of the 96-well plate to reduce evaporation. After culturing in a 37 ℃, 5% CO2 incubator for 8 h, 10 μL of CCK-8 solution was added to each well, and the cells were incubated in a 37 ℃, 5% CO2 incubator for 1 h. The absorbance of each well was measured at 450 nm using a microplate reader, and the data were saved. The cell proliferation inhibition experiment was set up with the following three groups: Blank group (Ab): with culture medium and CCK-8 solution, without cells and drugs.
[0038] Control group (Ac): culture medium containing cells and CCK-8 solution, without drugs.
[0039] Experimental group (As): Added cell-containing culture medium, drugs and CCK-8 solution.
[0040] The absorbance of each well was obtained using a microplate reader. Cell viability was calculated by dividing the difference in absorbance between the experimental and blank wells by the difference between the control and blank wells, as shown in the following formula:
[0041] The results are as follows Figure 1 As shown, FIP22 did not produce significant toxicity to BMMCs at a concentration of 400 μM, indicating that FIP22 has very low cytotoxicity and high safety within this concentration range.
[0042] II. FIP22 inhibits mast cell degranulation. β-hexosinase (β-Hex) release rate can be used as an indicator of the degree of mast cell degranulation and can also be used to assess the effect of drugs on mast cell degranulation.
[0043] After treating the cells in the medium-sized dish with antibodies, wash the cells with HBSS buffer and prepare a 96-well plate. Divide the cells into groups and administer the drug accordingly, with three replicates per group. After separating the cells into groups, treat for 4 hours. Then, add 2 μL of antigen to each well for every 100 μL of cell suspension and incubate at 37 °C for 15 minutes. Transfer the incubated cells to EP tubes, centrifuge, collect the supernatant, and transfer the supernatant to a new 96-well plate. Add 50 μL of substrate (β-HEX) and 25 μL of supernatant to each well and incubate at 37 °C for 1 hour. Finally, add 175 μL of stop solution and measure the absorbance at 405 nm using a microplate reader.
[0044] The results are as follows Figure 2 As shown, allergy leads to increased degranulation of BMMCs, which can be inhibited by the addition of FIP22. Furthermore, the inhibitory effect of FIP22 on degranulation increases with increasing FIP22 dosage, indicating that FIP22 has a significant inhibitory effect at this concentration.
[0045] III. FIP22 Inhibits Passive Cutaneous Allergy in Mice BALB / c mice were randomly divided into five groups according to body weight: a blank control group, a model group, a low-dose FIP22 group, a high-dose FIP22 group, and an AICAR group, with 10 BALB / c mice in each group. Mice were first anesthetized with Supra-50. After anesthesia, 20 μL of IgE antibody at a concentration of 4 μg / mL was subcutaneously injected into the right ear of each mouse. The drug was administered 24 h later. The following day, the drug was administered via gavage at a dose of 0.1 mL / 10 g. Four hours after drug administration, 200 μL of physiological saline containing 60 μg of DNP-HSA and 1% Evans blue was injected via the tail vein.
[0046] One hour after each group of mice was given DNP-HSA, their ears were photographed, they were euthanized by cervical dislocation, their right ears were removed, and they were separated into different groups. The mice were then placed in test tubes containing 400 μL of N-formyldeacetylated colchicine and placed in a water bath at 63°C overnight.
[0047] Add 200 μL from the test tube to a 96-well plate, measure the absorbance of each well using a microplate reader at a wavelength of 630 nm, and calculate the amount of Evans blue leaching.
[0048] The results are as follows Figure 3As shown, compared with the control group, the extravasation of Evans blue in the ear tissue of mice in the model group was significantly increased, indicating the occurrence of an allergic reaction. Conversely, the extravasation of Evans blue in the low-dose FIP22 group and the FIP22 group was significantly reduced, indicating that FIP22 can inhibit passive cutaneous anaphylaxis in mice. Furthermore, with increasing dosage, the extravasation of Evans blue gradually decreased, indicating that FIP22 has a significant therapeutic effect on allergic diseases.
[0049] IV. FIP22 inhibits systemic allergic reactions in mice. Six-week-old BALB / c mice were used. ICR mice were randomly divided into five groups according to body weight: a blank control group, a model group, a low-dose FIP22 group, a high-dose FIP22 group, and an AICAR group, with eight BALB / c mice in each group. 100 μL of IgE antibody at a concentration of 20 μg / mL was injected via the tail vein first, followed by drug administration 24 h later. The next day, the drug was administered via gavage at a dose of 0.1 mL / 10 g. Four hours after drug administration, 200 μL of physiological saline containing 4 mg of DNP-HSA was injected via the tail vein. Blood was collected from the eyeball 15 min after DNP-HSA administration. After clotting for 2 h, serum was obtained by centrifugation.
[0050] Measure PGD2, LCT4, and histamine levels according to the ELISA kit instructions. Set up the standard and sample wells in the kit's accompanying plate. Add 50 μL of different concentrations of standard to the standard wells and 40 μL of sample diluent to the sample wells. In addition to the blank wells, add 10 μL of the test sample and 100 μL of horseradish peroxidase (HRP)-labeled antibody to the sample wells. Seal the plate with a sealing strip and incubate at 37°C for 1 h. After 1 h, discard the liquid in the plate. Prepare the washing buffer provided with the kit according to the instructions, and add 300 μL of the washing buffer. Repeat the washing process 4 times. After washing, invert the plate and pat dry with absorbent paper. Add 50 μL of substrate A and 50 μL of substrate B to each well. Incubate at room temperature in the dark for 15 min. After incubation, add 50 μL of stop solution to each well. Measure the absorbance of each well at 450 nm using a microplate reader and save the data.
[0051] The results are as follows Figure 4 As shown in the figure, A represents the concentration of LTC4 in serum; B represents the concentration of PGD2 in serum; and C represents the concentration of histamine in serum. The results indicate that FIP22 reduced the levels of histamine, LTC4, and PGD2 in serum, and its effect at high doses was close to that of a positive control drug, indicating that FIP22 can significantly and effectively inhibit systemic allergic reactions in mice.
[0052] The above embodiments are preferred embodiments of the present invention, but the embodiments of the present invention are not limited to the above embodiments. Any changes, modifications, substitutions, combinations, or simplifications made without departing from the spirit and principle of the present invention shall be considered equivalent substitutions and shall be included within the protection scope of the present invention.
Claims
1. Use of a compound in the manufacture of a medicament for the treatment of an allergic reaction, said compound having the chemical structure of Formula I: ###0001### Formula I wherein: R1 is selected from the group consisting of H, CH3, CH2CH3, CH2CH2CH3, CH2CH2CH2CH3, CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH3, CH2CH2CH2CH2CH2CH2CH2CH2 。 2. Use according to claim 1, characterized in that, 。 3. Use according to claim 2, characterized in that, 。 4. Use according to claim 1, characterized in that, 5. Use according to claim 4, characterized in that, 6. Use according to claim 1, characterized in that, 7. Use according to claim 1, characterized in that, 8. The use according to claim 1, characterized in that, 9. The use according to claim 1, characterized in that, 10. The use according to claim 1, characterized in that,