Deoxyvasicinone derivatives, processes for their preparation and use in medicine

Abstract

The present application belongs to the technical field of pharmacotherapy, and particularly relates to a deoxyviburtine derivative, a preparation method thereof and application thereof in medicine. The structural formula of the deoxyviburtine derivative is shown in formula (A): wherein R is any one of phenyl, 4-methylphenyl, 4-tert-butylphenyl, 4-methoxyphenyl, 4-trifluoromethoxyphenyl, 4-bromophenyl, 4-fluorophenyl, 3-fluorophenyl, 2-fluorophenyl, 3-Cl, 4-F phenyl. The LPS-induced RAW264.7 cell experiment proves that the deoxyviburtine derivative can well inhibit the NO production in the cell, and the in-vivo experiment proves that the deoxyviburtine derivative can treat the adjuvant-induced arthritis rats. The deoxyviburtine derivative provided by the present application has the potential to develop into an anti-inflammatory drug and has the potential to develop into a drug for preventing or treating rheumatoid arthritis.

Description

Technical Field

[0001] This invention belongs to the field of pharmacotherapeutic technology, specifically relating to a deoxydaunocarbazone derivative, its preparation method, and its application in pharmaceuticals. Background Technology

[0002] Inflammation is a defensive response of the body's immune system to various damaging and invading microorganisms. Inflammation is divided into infectious inflammation caused by infection and non-infectious inflammation not caused by infection. In most cases, inflammation is beneficial, serving as an automatic defense mechanism of the body. However, sometimes inflammation can also have adverse effects on the body, such as attacking human tissues and inflammation occurring in some transparent tissues. Inflammation plays a crucial role in the development of circulatory diseases, such as atherosclerosis, blood viscosity, inflammatory bowel disease, rheumatoid arthritis, and essential hypertension. Meanwhile, certain types of malignant tumors are also known to be closely related to inflammatory mechanisms.

[0003] Rheumatoid arthritis (RA) is a chronic inflammation of one or more joints, accompanied by pain, erythema, swelling, and elevated temperature in the affected area. It is a persistent systemic autoimmune disease characterized by chronic inflammation of the synovial tissue and progressive erosion of adjacent cartilage and bone. If left untreated, RA can lead to cumulative joint damage and irreversible disability. During RA, many pro-inflammatory cytokines (NOs) are abnormally produced in serum and synovial fusion fluid. Therefore, new anti-inflammatory drugs can be developed to inhibit the production and release of pro-inflammatory substances.

[0004] However, existing anti-inflammatory drugs generally suffer from poor selectivity, toxic side effects, and drug resistance. Finding highly effective and low-potency anti-inflammatory drugs remains an important task. Summary of the Invention

[0005] To address the aforementioned technical problems, the present invention first provides a deoxydaunoside alkaloid derivative, the structural formula of which is shown in formula (A):

[0006]

[0007] Wherein, R is any one of phenyl, 4-methylphenyl, 4-tert-butylphenyl, 4-methoxyphenyl, 4-trifluoromethoxyphenyl, 4-bromophenyl, 4-fluorophenyl, 3-fluorophenyl, 2-fluorophenyl, 3-Cl, and 4-Fphenyl.

[0008] The preparation method of this deoxydextrin derivative includes the following steps:

[0009] S1. Using phosphorus oxychloride as a catalyst, 4-nitro-o-aminobenzoic acid and 2-pyrrolidone undergo a dehydration condensation reaction. Excess 4-nitro-o-aminobenzoic acid is neutralized by adding ammonia water, and the yellow solid reaction product 6-nitro-2,3-dihydropyrrolo[2,1-b]quinazolin-9(1H)-one is collected.

[0010] S2. Palladium on carbon is added as a catalyst and hydrazine hydrate is used as a reducing agent to reduce the yellow solid reaction product to the intermediate compound 6-amino-2,3-dihydropyrrolo[2,1-b]quinazoline-9(1H)-one;

[0011] S3. The intermediate compound is added to dichloromethane and reacted with benzenesulfonyl chloride with various substituents R (RT). The deoxydoxyduckbillone alkaloid derivative is obtained by column chromatography purification.

[0012] The preparation route can be represented as follows:

[0013]

[0014] The preparation route is primarily for illustrative purposes and not for limiting the invention.

[0015] Step i: Compound a (4-nitro-o-aminobenzoic acid) and compound b (2-pyrrolidone) were mixed in toluene, and phosphorus oxychloride was added as a catalyst. The mixture was then refluxed at 110°C for 4 hours. The toluene solution was discarded, and the reactants were poured into water. Concentrated ammonia was added to make the solution alkaline to remove excess 4-nitro-o-aminobenzoic acid. The yellow solid was collected by filtration and purified by silica gel column chromatography to obtain compound c (6-nitro-2,3-dihydropyrrolo[2,1-b]quinazolin-9(1H)-one).

[0016] Step ii: Compound c was completely dissolved in methanol, and then 10% palladium on carbon and hydrazine hydrate were added. The mixture was hydrogenated at 60°C for 4 hours. After the reaction was completed, the palladium on carbon was filtered off while hot, and the methanol and hydrazine hydrate were removed by rotary evaporation. The crude product was purified by silica gel column chromatography to obtain compound d (6-amino-2,3-dihydropyrrolo[2,1-b]quinazoline-9(1H)-one).

[0017] Step iii: Compound d was dissolved in dichloromethane, and benzenesulfonyl chloride containing various substituents R was added. The reaction was carried out at room temperature for 10 hours, and the reaction progress was monitored by thin-layer chromatography. The crude product was purified by column chromatography using a mixture of dichloromethane and methanol to obtain the deoxy-duckbillone alkaloid derivative e. The substituent R is any one of phenyl, 4-methylphenyl, 4-tert-butylphenyl, 4-methoxyphenyl, 4-trifluoromethoxyphenyl, 4-bromophenyl, 4-fluorophenyl, 3-fluorophenyl, 2-fluorophenyl, and 3-Cl,4-Fphenyl.

[0018] The present invention further provides the application of the deoxydaunoside derivative described above in the preparation of anti-inflammatory drugs.

[0019] The present invention also provides the use of the deoxydaunoside derivative described above in the preparation of drugs for the prevention or treatment of arthritis.

[0020] Preferably, the arthritis is rheumatoid arthritis.

[0021] Preferably, the R group of the deoxyduckbillone alkaloid derivative is a 4-fluorobenzenesulfonyl chloride group.

[0022] The present invention also provides an anti-inflammatory drug comprising a pharmaceutically effective dose of the deoxyduckbillone alkaloid derivative as described above and a pharmaceutically acceptable carrier.

[0023] Preferably, the pharmaceutically acceptable carrier includes one or more of the following functions: excipient, stabilizer, antioxidant, colorant, diluent, and sustained-release agent.

[0024] Preferably, the pharmaceutically acceptable carrier includes one or more excipients with functions such as excipients, stabilizers, antioxidants, colorants, diluents, and sustained-release agents; such as starch, lipids, waxes, dextrin, sucrose, lactose, microcrystalline cellulose, gelatin, citric acid, inorganic salts, hydroxypropyl methylcellulose, hydroxyethyl cellulose, etc.

[0025] Preferably, the drug is any one of injection, tablet, pill, capsule, suspension or emulsion.

[0026] The beneficial effects of this invention are as follows:

[0027] LPS-induced RAW264.7 cell experiments demonstrated that the deoxydaunoside derivative provided in this invention can effectively inhibit NO production in cells. In vivo experiments showed that the deoxydaunoside derivative provided in this invention can treat adjuvant-induced arthritis in rats. This indicates that the deoxydaunoside derivative provided in this invention shows promise as an anti-inflammatory drug and has the potential to be developed into a drug for the prevention or treatment of rheumatoid arthritis. Attached Figure Description

[0028] Figure 1 The effect of compound e7 on an arthritis model rat. Detailed Implementation

[0029] Unless otherwise stated, the terms used herein have the meanings commonly understood by those skilled in the art.

[0030] The technical solution of the present invention will be described in more detail below with reference to the embodiments.

[0031] Example 1

[0032] Synthesis of compound e1

[0033]

[0034] Following the previously described preparation route, compound d (201 mg, 1 mM) was dissolved in 10 mL of pyridine, followed by the addition of benzenesulfonyl chloride (846 mg, 4.8 mM), and the reaction was carried out at room temperature for 8–12 hours. The reaction progress was monitored by TLC. After the reaction was complete, insoluble impurities were removed by filtration, and the solvent was removed by rotary evaporation. Compound e1 was obtained by column chromatography using methanol:dichloromethane (1:9), as a white solid with a yield of 61%. 1 H NMR (500MHz, DMSO-d6) δ10.99(s,1H),7.96(d,J=8.7Hz,1H),7.63(t,J=7.3,7.3Hz,1H),7.58(t,J=7.3,7.3Hz,2H),7.27(d,J=2. 2Hz,1H),7.21(dd,J=8.7,2.2Hz,1H),3.98(t,J=7.4,7.1Hz,2H),3.01(t,J=7.9,7.9Hz,2H),2.11(p,J=7.7,7.7,7.7,7.7Hz,2H). 13 C NMR (126MHz, DMSO-d6) δ161.75,159.85,150.56,143.44,139.62,133.76,129.95,127.67,127.15,117.54,116.14,114.32,46.67,32.31,19.28.

[0035] Example 2

[0036] Synthesis of compound e2

[0037]

[0038] The method is the same as in Example 1, except that the R group is replaced with 4-methylbenzenesulfonyl chloride, yielding a white solid with a yield of 58%. 1H NMR (500MHz, DMSO-d6) δ10.91(s,1H),7.96(d,J=8.6Hz,1H),7.74(d,J=8.4Hz,2H),7.37(d,J=8.1Hz,2H),7.26(d,J=2.1Hz,1H),7. 20(dd,J=8.6,2.2Hz,1H),3.98(t,J=7.2,7.2Hz,2H),3.01(t,J=7.9,7.9Hz,2H),2.32(s,3H),2.11(p,J=7.7,7.7,7.7,7.7Hz,2H). 13 C NMR(126MHz,DMSO-d6)δ161.71,159.85,150.55,144.22,143.57,136.76,13 0.36,127.63,127.21,117.47,116.03,114.17,46.66,32.32,21.39,19.29.

[0039] Example 3

[0040] Synthesis of compound e3

[0041]

[0042] The method is the same as in Example 1, except that the R group is replaced with 4-tert-butylbenzenesulfonyl chloride, yielding a white solid with a yield of 69%. 1 H NMR (500MHz, DMSO-d6) δ10.99(s,1H),7.97(d,J=8.7Hz,1H),7.81(d,J=8.6Hz,2H),7.61(d,J=8.6Hz,1H),7.31(d,J=2.1Hz,1H),7. 23(dd,J=8.7,2.2Hz,1H), 3.98(t,J=7.4,7.1Hz,2H), 3.01(t,J=7.9,7.9Hz,2H), 2.12(p,J=7.7,7.7,7.7,7.7Hz,2H), 1.24(s,9H). 13 C NMR(126MHz,DMSO-d6)δ161.71,159.84,156.77,150.61,143.60,137.02,127.6 9,127.04,126.83,117.24,115.96,113.84,46.65,35.34,32.32,31.12,19.29.

[0043] Example 4

[0044] Synthesis of compound e4

[0045]

[0046] The method is the same as in Example 1, except that the R group is replaced with 4-methoxybenzenesulfonyl chloride, yielding a white solid with a yield of 53%. 1 H NMR (500MHz, DMSO-d6) δ10.84(s,1H),7.96(d,J=8.7Hz,1H),7.79(d,J=9.0Hz,2H),7.26(d,J=2.1Hz,1H),7.20(dd,J=8.6,2.2Hz,1 H),7.09(d,J=9.0Hz,2H),3.98(t,J=7.2,7.2Hz,2H),3.79(s,3H),3.02(t,J=7.9,7.9Hz,2H),2.12(p,J=7.8,7.8,7.7,7.7Hz,2H). 13 C NMR(126MHz,DMSO-d6)δ163.16,161.70,159.88,150.57,143.67,131.16,12 9.45,127.61,117.44,115.95,115.06,114.08,56.12,46.67,32.32,19.30.

[0047] Example 5

[0048] Synthesis of compound e5

[0049]

[0050] The method is the same as in Example 1, except that the R group is replaced with 4-trifluoromethoxybenzenesulfonyl chloride, yielding a white solid with a yield of 74%. 1 H NMR (500MHz, DMSO-d6) δ11.35(s,1H),7.98(t,J=7.3,7.3Hz,2H),7.72(dtd,J=9.3,5.1,5.1,1.6Hz,2H),7.43(q,J=7.5,7.5,7.4Hz,2H),7. 26(d,J=2.1Hz,1H),7.22(dd,J=8.6,2.2Hz,1H),3.98(t,J=7.2,7.2Hz,2H),3.02(t,J=7.9,7.9Hz,2H),2.12(p,J=7.7,7.7,7.7,7.7Hz,2H). 13C NMR (126MHz, DMSO-d6) δ161.89,159.80,150.38,142.92,136.87(d,J=8.6Hz),131.06,127.74,127.02( d, J=13.5Hz), 125.65 (d, J=3.6Hz), 117.90 (d, J=20.6Hz), 117.26, 116.13, 113.78, 46.72, 32.30, 19.26.

[0051] Example 6

[0052] Synthesis of compound e6

[0053]

[0054] The method is the same as in Example 1, except that the R group is replaced with 4-bromobenzenesulfonyl chloride, yielding a white solid with a yield of 65%. 1 H NMR (500MHz, DMSO-d6) δ11.12(s,1H),8.00(d,J=3.2Hz,1H),7.98(d,J=3.1Hz,1H),7.60(d,J=8.4Hz,2H),7.29(d,J=2.2Hz, 1H), 7.22 (dd, J=8.7, 2.2Hz, 1H), 3.99 (t, J=7.2, 7.2Hz, 2H), 3.03 (t, J=7.9, 7.9Hz, 2H), 2.13 (p, J=7.8, 7.8, 7.8, 7.8Hz, 2H). 13 CNMR(126MHz,DMSO-d6)δ161.86,159.81,150.56,143.09,138.50,129.85,127.82,122.09,117.62,116.40,114.51,46.70,32.34,19.30.

[0055] Example 7

[0056] Synthesis of compound e7

[0057]

[0058] The method is the same as in Example 1, except that the R group is replaced with 4-fluorobenzenesulfonyl chloride, yielding a white solid with a yield of 42%. 1H NMR (500MHz, DMSO-d6) δ11.00(s,1H),7.97(d,J=8.7Hz,1H),7.92(dd,J=8.9,5.1Hz,2H),7.43(t,J=8.9,8.9Hz,1H),7.26(d,J=2. 1Hz, 1H), 7.20 (dd, J=8.7, 2.2Hz, 1H), 3.99 (t, J=7.4, 7.1Hz, 2H), 3.02 (t, J=7.9, 7.9Hz, 2H), 2.13 (p, J=7.7, 7.7, 7.7, 7.7Hz, 2H). 13 C NMR(126MHz, DMSO-d6)δ164.96(d,J=252.2Hz),161.84,159.86,150.56,143.25,135.95(d,J=2.9Hz ),130.29(d,J=9.6Hz),127.75,117.66,117.20(d,J=23.0Hz),116.30,114.52,46.70,32.33,19.30.

[0059] Example 8

[0060] Synthesis of compound e8

[0061]

[0062] The method is the same as in Example 1, except that the R group is replaced with 3-fluorobenzenesulfonyl chloride, yielding a white solid with a yield of 43%. 1 H NMR (500MHz, DMSO-d6) δ11.09(s,1H),7.99(d,J=8.6Hz,1H),7.70(d,J=7.9Hz,1H),7.66(t,J=6.9,6.9Hz,1H),7.53(t,J=8.2,8.2Hz,1H), 7.29–7.26(m,1H),7.22(dd,J=8.7,2.1Hz,1H),3.99(t,J=7.2,7.2Hz,2H),3.02(t,J=7.8,7.8Hz,2H),2.12(p,J=7.7,7.7,7.6,7.6Hz,2H). 13C NMR (126MHz, DMSO-d6) δ162.14(d,J=249.1Hz),161.86,159.82,150.56,143.04,141.59(d,J=6.8Hz),132.47(d,J=8.0H z),127.81,123.51,123.49,121.06(d,J=21.0Hz),117.73,116.45,114.71,114.18(d,J=24.4Hz),46.70,32.33,19.29.

[0063] Example 9

[0064] Synthesis of compound e9

[0065]

[0066] The method is the same as in Example 1, except that the R group is replaced with 2-fluorobenzenesulfonyl chloride, yielding a white solid with a yield of 36%. 1 H NMR (500MHz, DMSO-d6) δ11.35(s,1H),7.99(d,J=4.2Hz,1H),7.97(d,J=5.4Hz, 1H),7.72(dddd,J=8.4,7.0,5.1,1.8Hz,1H),7.44(dd,J=4.7,3.7Hz,1H),7.42( d,J=7.6Hz,1H),7.26(d,J=2.1Hz,1H),7.22(dd,J=8.7,2.2Hz,1H),3.98(t,J=7 .3,7.2Hz,2H),3.02(t,J=7.9,7.9Hz,2H),2.12(p,J=7.7,7.7,7.7,7.7Hz,2H). 13 C NMR (126MHz, DMSO-d6) δ161.95,159.87,158.57(d,J=255.0Hz),150.39,142.92,136.90(d,J=8.6Hz),131.06,127.7 4,126.97(d,J=13.5Hz),125.66(d,J=3.6Hz),117.89(d,J=20.7Hz).,117.29,116.11,113.78,46.73,32.29,19.25.

[0067] Example 10

[0068] Synthesis of compound e10

[0069]

[0070] The method is the same as in Example 1, except that the R group is replaced with 3-Cl,4-fluorobenzenesulfonyl chloride, yielding a white solid with a yield of 31%. 1 H NMR (500MHz, DMSO-d6) δ11.14(s,1H),8.00(d,J=8.6Hz,1H),7.86(t,J=1.9,1.9Hz,1H),7.73(ddd,J=8.2,2.1,1.0Hz,1H),7.62(t,J=8.0,8.0Hz,1 H),7.27(d,J=2.2Hz,1H),7.23(dd,J=8.6,2.2Hz,1H),4.00(t,J=7.4,7. 2Hz, 2H), 3.04 (t, J=7.9, 7.9Hz, 2H), 2.14 (p, J=7.8, 7.8, 7.7, 7.7Hz, 2H). 13 C NMR (126MHz, DMSO-d6) δ162.13, 159.84, 147.50 (d, J = 683.3Hz), 143.04, 141.35, 134.52, 132.9 8(d,J=222.5Hz),127.91,126.63,125.94,117.82,116.39,114.44,49.06,46.82,32.32,19.26.

[0071] Example 11

[0072] Cell inhibitory activity assay method:

[0073] RAW 264.7 (mouse mononuclear macrophage leukemia cells) is one of the most commonly used in vitro models for osteoclast and inflammation research, and is widely used in the study of bone diseases such as rheumatoid arthritis, osteoporosis, osteolysis, and periodontitis.

[0074] RAW264.7 cells (5 × 10⁻⁶) 3 Cells were seeded per well in 96-well plates and incubated for 24 h. The culture medium was then discarded, and the cells were pretreated with a medium containing the compound (100 μM) for 24 h. MTT (5 mg / mL, 20 μL / well) solution was incubated in the dark for 4 h. The supernatant was discarded, and 150 μL of DMSO was added. The optical density was measured at 492 nm using a microplate reader.

[0075] Inhibition rate calculation method:

[0076]

[0077] Relative OD value of drug sensitivity wells = Absolute OD value of drug sensitivity wells - Absolute OD value of blank control wells

[0078] The toxicity test results of this series of derivatives on RAW264.7 cells are shown in Table 1.

[0079] Table 1 shows the survival rates of RAW264.7 cells for e1-e10.

[0080]

[0081] As shown in Table 1, most compounds exhibited low toxicity at 50 μM, with compound e3 showing weak cytotoxicity. Therefore, the anti-inflammatory activity of all compounds was further evaluated within the safe toxicity range.

[0082] Example 12

[0083] Several pro-inflammatory cytokines and mediators exist in rheumatoid arthritis (RA) and participate in the inflammatory response, leading to pain, bone and cartilage damage, and even severe disability. Endogenous nitrogen (NO) production is a key mediator in the RA inflammatory pathway, generating oxygen free radicals that contribute to cartilage and joint damage. In RA patients, serum and synovial fluid NO levels are elevated. Therefore, within the safe toxicity range, a 30 μM concentration was chosen to test the ability of all compounds to inhibit NO production, further evaluating their anti-inflammatory activity.

[0084] This embodiment tests the effect of deoxydaunoside derivatives on LPS-induced NO production in RAW264.7 cells, using indomethacin as a positive control.

[0085] RAW264.7 cells (6 × 10⁻⁶) 4 Cells were seeded at 1000 cells / well in 48-well plates and incubated for 24 h. Then, culture medium containing compounds (deoxydaunocarbazone derivatives e1-e10) was added for further incubation. After 1 h of incubation, LPS (1 μg / mL, 30 μL / well) was added to stimulate the cells for 24 h. Then, 50 μL of the supernatant was collected into 96-well plates, and Griess reagents I and II (50 μL / well) were added. Cells were incubated for 5 min, and absorbance was measured at 450 nm. The inhibitory activity of compounds e1-e10 on NO production is summarized in Table 2.

[0086] Table 2 shows the inhibitory effects of e1-e10 on NO release.

[0087]

[0088] As shown in Table 2, at a concentration of 30 μM, the deoxydaunoside derivatives E1-E10 all exhibited certain inhibitory effects on NO release, suggesting their potential as anti-inflammatory drugs. Among the tested compounds, E7 showed the strongest inhibitory effect, exceeding that of the positive control drug indomethacin.

[0089] Example 13

[0090] In vivo studies

[0091] Female rats, weighing 160-180g, were purchased from the Animal Experiment Center of Anhui University of Traditional Chinese Medicine. The temperature, relative humidity, and dark-light cycle in the animal room were maintained at 23℃-25℃, 40%-60%, and 12h daily, respectively. The animal experiments were approved by the Experimental Animal Ethics Committee of Anhui Medical University.

[0092] Inflammation was induced by intradermal injection of 0.1 mL Freund's complete adjuvant (FCA) into the left hind paw of rats. The same volume of saline was injected into the same site in the normal control group. Ten days after FCA injection, the rats were randomly divided into three groups. The experimental group was treated with compound e7 (30 mg / kg) for 14 days, the positive control group was treated with indomethacin (30 mg / kg) for 14 days, and the model group received saline as a control.

[0093] See results Figure 1 Using compound e7 and a positive control drug to treat an adjunct-induced arthritis (AIA) model in rats, the anti-inflammatory activity of compound e7 in vivo was confirmed. Compared with the model group, the treatment group showed reduced paw swelling and improved body weight.

[0094] Experiments show that most of the deoxyduckbillone alkaloid derivatives designed and synthesized in this invention exhibit effective NO release inhibitory activity. Among them, compound e7 showed the strongest NO release inhibitory activity against LPS-induced RAW264.7 cells at a concentration of 30 μM. Further in vivo studies showed that e7 could effectively alleviate paw swelling in a rat model of rheumatoid arthritis, and has the potential to be developed into an effective therapeutic drug for rheumatoid arthritis.

[0095] The above are merely preferred embodiments of the present invention and are not intended to limit the scope of the invention. Although the present invention has been described in detail with reference to the foregoing embodiments, those skilled in the art should understand that any modifications, equivalent substitutions, and improvements made within the spirit and principles of the present invention should be included within the scope of protection of the present invention.

Claims

1. A deoxydextrin ketone derivative, characterized in that, The structural formula of the deoxy-duckbill ketone derivative is shown in formula (A): （A） Wherein, R is any one of 4-methylphenyl, 4-trifluoromethoxyphenyl, and 4-fluorophenyl.

2. A method for preparing the deoxydextrin alkaloid derivative as described in claim 1, characterized in that, Includes the following steps: S1. Using phosphorus oxychloride as a catalyst, 4-nitro-o-aminobenzoic acid and 2-pyrrolidone undergo a dehydration condensation reaction. Excess 4-nitro-o-aminobenzoic acid is neutralized by adding ammonia water, and the yellow solid reaction product 6-nitro-2,3-dihydropyrrolo[2,1-b]quinazolin-9(1H)-one is collected. S2. Palladium on carbon is added as a catalyst and hydrazine hydrate is used as a reducing agent to reduce the yellow solid reaction product to the intermediate compound 6-amino-2,3-dihydropyrrolo[2,1-b]quinazoline-9(1H)-one; S3. The intermediate compound is added to dichloromethane and reacted with 4-methylbenzenesulfonyl chloride, 4-trifluoromethoxybenzenesulfonyl chloride or 4-fluorobenzenesulfonyl chloride in a substitution reaction. The deoxydoxyduckbillone derivative is obtained by column chromatography purification.

3. The use of a deoxydaunoside derivative as described in claim 1 in the preparation of anti-inflammatory drugs.

4. The use of a deoxydaunoside derivative as described in claim 1 in the preparation of a medicament for the prevention or treatment of arthritis.

5. The application as described in claim 4, characterized in that, The arthritis mentioned is rheumatoid arthritis.

6. The application as described in claim 4, characterized in that, The R group of the deoxydaunoside derivative is 4-fluorophenyl.

7. An anti-inflammatory drug comprising a pharmaceutically effective dose of the deoxyduckbillone alkaloid derivative as described in claim 1 and a pharmaceutically acceptable carrier.

8. The anti-inflammatory drug as described in claim 7, characterized in that, The pharmaceutically acceptable carriers include carriers that function as stabilizers, colorants, diluents, and sustained-release agents, or a combination thereof.

9. The medicament as described in claim 8, characterized in that, The drug is any one of the following: injection, tablet, pill, capsule, suspension, or emulsion.

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