PHARMACEUTICALS CONTAINING XANTIN COMPOUNDS FOR THE PREVENTION OR TREATMENT OF URA-INDUCED DISEASES OR GOUT

Abstract

The invention relates to a compound with formula (I), its pharmaceutical salts, its solvates, or any of these preparations for the reduction of uric acid levels, for the prevention or reduction of inflammation, and for the prevention or treatment of urate disease or gout. Specifically, the invention relates to a compound with formula (I), its pharmaceutical salts, its solvates, or any of these preparations for the treatment or prevention of hyperuricemia, gout, gouty inflammatory disease, uric acid-induced pain and nephropathy, wherein R1 is a hydrogen, C1-4 alkyl or similar group, R2 is a C1-10 alkyl or similar group, R3 is a halogen or similar group.

Description

Prevention or treatment of uric acid or gouty diseases Technical field The present invention relates to the prevention or treatment of uric acid or gouty diseases. More specifically, the present invention relates to compounds or their compositions for treating or preventing uric acid or gouty diseases. In addition, the present invention also relates to methods for treating or preventing uric acid or gouty diseases, as well as the use of the compounds or compositions for reducing uric acid and anti-inflammatory effects, and the use of the compounds or compositions in the preparation of therapeutic or preventive agents for uric acid or gouty diseases. Background art High uric acid is a metabolic disease caused by the disorder of purine metabolism in the human body, resulting in an increase in blood uric acid. The daily production and excretion of uric acid in the body are approximately equal. In terms of production, one-third comes from food and two-thirds is synthesized in the body. The excretion pathway is that one-third is excreted through the intestine and two-thirds is excreted from the kidneys. As long as any one of the above-mentioned pathways has problems, it will cause an increase in uric acid. The increase in uric acid will hinder the process of blood secreting uric acid, resulting in the inability to excrete uric acid. Excessive uric acid can also cause other diseases, such as gout, kidney disease, and cardiovascular diseases. High uric acid can cause gout. Gout is a disorder of purine metabolism in the human body, resulting in an increase in blood uric acid and causing recurrent joint inflammation. High uric acid can also cause gouty nephropathy, which is caused by the excessive production of blood uric acid that is not excreted reasonably, resulting in renal damage caused by hyperuricemia. Severe high uric acid patients can lead to renal failure. Gout is a group of heterogeneous diseases caused by tissue damage due to increased blood uric acid, which is caused by disorders of purine metabolism in the body and / or reduced uric acid excretion, manifested as hyperuricemia. The normal plasma uric acid content in humans is 20 - 60mg / L. When it exceeds 80mg / L, urate crystals will deposit in joints, soft tissues, cartilage, kidneys and other parts, precipitating crystals, resulting in arthritis, urinary tract stones and kidney diseases, namely "gout disease". During an acute attack, urate microcrystals deposit in joints, causing local granulocyte infiltration and inflammatory reactions. Repeated attacks can deform joints and form "tophi", which have long been common diseases in the West and Japan. In recent years, gout has also become a prevalent disease in China (especially in coastal open areas). Existing research suggests that an acute gout attack is an acute inflammatory process induced by urate crystals. It starts from the interaction between urate crystals and resident monocytes / macrophages, undergoes a series of inflammatory reactions, and finally spontaneously resolves with the participation of multiple mechanisms. Most patients with gout The onset is related to the rate of change (increase or decrease) of serum uric acid levels, rather than to stable serum uric acid levels. The rapid fluctuation of serum uric acid levels can cause changes in the volume or shape of crystals, making them loose in the tissue matrix, promoting the release of urate crystals from the sites of gouty tophus deposition that have already formed, and it is the shed microcrystals or newly formed crystals locally that trigger the inflammatory response. The interaction between monocytes / macrophages and urate crystals is the main link in the initiation of acute gout. The interaction between urate crystals and resident macrophages triggers inflammation and induces the infiltration of neutrophils and monocytes, expanding the inflammatory response. The onset of acute gout involves multiple inflammatory factors, mainly including chemokines such as IL-1β, IL-6, IL-18, TNF-α, and IL-8 (CXCL-8). By measuring the levels of inflammatory factors and anti-inflammatory factors in the synovial fluid of patients at different stages of acute gout attacks, it was found that in the early and middle stages of inflammation, the levels of inflammatory factors such as IL-1β, IL-6, and TNF-α and the white blood cell levels in the synovial fluid were significantly increased. Currently, IL-1, also known as lymphocyte stimulating factor, is mainly produced by activated monocytes-macrophages. There are two different molecular forms of the IL-1 molecule, IL-1α and IL-1β. At low local concentrations, it co-stimulates the activation of antigen-presenting cells and T cells, promotes the proliferation of B cells and the secretion of antibodies, and conducts immune regulation. The precursor of IL-1β is produced by immune cells such as monocytes, macrophages, and dendritic cells, and is converted into active IL-1β by NALP3 inflammasome-activated protease-1 and released to mediate the inflammatory response. IL-1β can induce the release of IL-6 and IL-8 and mediate the infiltration of neutrophils. In addition, the rapid clinical response of acute gout patients to various IL-1 inhibitors also proves the key role of this factor in gout inflammation. Recent research data show that interleukin 1β (IL1β) plays an important role in the inflammatory process caused by monosodium urate (MSU) crystal deposition in gout patients (Ann Rheum Dis 2009; 68: 1613-1617.). TNF-α (tumor necrosis factor) is a polypeptide cytokine produced by monocytes and macrophages and plays an important role in inflammatory responses, the development of the immune system, programmed cell death, and lipid metabolism. TNF-α is also involved in the occurrence of diseases including asthma, Crohn's disease, rheumatoid arthritis, neuropathic pain, obesity, type II diabetes, autoimmune diseases, and tumors. In immune responses, TNF-α is a multifunctional regulator and even acts as a strong pyrogenic substance to stimulate neutrophils, change the characteristics of vascular endothelial cells, and regulate the metabolic activities of other tissues. IFN-γ (Interferon-γ) is a glycoprotein produced by T cells and natural killer cells in the immune system. The initiating effect of IFN-γ can promote macrophages to secrete higher levels of pro-inflammatory cytokines and lower levels of anti-inflammatory cytokines, and enhance the bactericidal and antitumor activities of macrophages. The common sign of gout patients is the pathological increase in the uric acid concentration in the blood. Although not all people with increased uric acid levels will develop gout, an increased uric acid level is still a prerequisite for gout. There are two reasons for the increase in uric acid concentration: one is the reduced excretion of uric acid in urine; the other is the enhanced biosynthesis of uric acid due to the lack of regulatory effects. Gout is divided into primary and secondary types. The former is mainly caused by enzyme defects and is often accompanied by hypertension, diabetes, hyperlipidemia, obesity, metabolic syndrome, and coronary heart disease, with a genetic tendency; the latter is caused by various reasons such as kidney diseases, blood diseases, and medications. If gout is not actively prevented or is treated improperly, gout attacks will become more and more frequent, the symptoms will deepen accordingly, and more and more joints will be affected, leading to a gout - heterogeneous disease. Urate crystals deposit in joints to form gouty acute arthritis; as multiple joints are simultaneously affected, gout will develop into chronic (long-term) arthritis. Repeated attacks can cause permanent joint damage, including long-term pain and stiffness, limited mobility, and joint deformity. When the condition progresses, crystals deposit in soft tissues and form masses called "tophi" under the skin. Crystal deposition in the kidneys can trigger kidney diseases, leading to acute uric acid nephropathy and chronic urate nephropathy, causing serious kidney damage and resulting in urinary system uric acid stones. Gouty arthritis has a high incidence, is difficult to cure, and recurs frequently. All kinds of difficult complications make patients extremely painful. This disease has been listed as one of the top ten stubborn diseases of mankind in the 21st century by the World Health Organization. Currently, multiple epidemiological studies have confirmed that serum uric acid is an independent risk factor for the onset of hypertension. For every 1 mg / dL increase in serum uric acid level, the relative risk of hypertension onset increases by 25%. Long-term hyperuricemia can damage the function of pancreatic β cells and induce diabetes, and studies have confirmed that long-term hyperuricemia has a causal relationship with impaired glucose tolerance and the onset of diabetes. Uric acid is an independent risk factor for coronary heart disease death: Studies have shown that regardless of gender, uric acid is an independent risk factor for coronary heart disease death in the general population. For every 1 mg / dL increase in serum uric acid, the risk of death increases by 48% in men and 126% in women. Serum uric acid > 6 mg / dL is an independent risk factor for coronary heart disease; serum uric acid > 7 mg / dL is an independent risk factor for stroke. Uric acid is closely related to kidney diseases. In addition to uric acid crystal deposition leading to renal arterioles and chronic In addition to interstitial inflammation exacerbating renal damage, many epidemiological investigations and animal studies have shown that uric acid can directly cause microvascular lesions in the afferent arterioles of glomeruli, leading to chronic kidney disease. Currently, there are not many varieties of anti-gout drugs. The main drugs for clinical treatment of gout are colchicine, drugs that inhibit uric acid synthesis (allopurinol, febuxostat), drugs that promote uric acid excretion (such as probenecid, sulfinpyrazone, benzbromarone, Lesinurad), non-steroidal anti-inflammatory drugs and hormones. In the acute onset period, colchicine, non-steroidal anti-inflammatory drugs and hormones are mainly used, and in the remission period, drugs that inhibit uric acid synthesis and drugs that promote uric acid excretion are mainly used. However, these drugs all have the defects of poor curative effect and large side effects in treatment. The first-line drugs for lowering uric acid recommended by the 2012 American College of Rheumatology (ACR) gout treatment guidelines are allopurinol and febuxostat. Febuxostat is recommended as a first-line drug for the first time. Probenecid is used as a first-line uric acid excretion-promoting drug for lowering uric acid treatment only when it is contraindicated or intolerant to at least one xanthine oxidase inhibitor. In addition, the ACR guidelines recommend that uric acid lowering treatment can be started after effective anti-inflammatory treatment begins. Therefore, there is still a need to research and develop new drugs that can treat or prevent uric acid-related or gout-related diseases. WO2005077950 discloses the compounds shown by general formula (I) of the present invention, which are used to treat diseases such as dyslipidemia and type II diabetes by activating the HM74A (also known as GPR109A) receptor. However, this patent document does not disclose or imply that the said compounds can be used to prevent or treat uric acid-related or gout-related diseases. WO2011057110 discloses that xanthine derivatives are used to prevent or treat diseases such as cerebral ischemia by activating the HM74A receptor. US20130150383 discloses the effect of xanthine compounds in the treatment of psoriasis. US2015080418A1 discloses the use of xanthine compounds in nerve tissue diseases. WO9316699A1 discloses the use of xanthine compounds in the treatment of fungal infections. WO9920280A1 discloses the use of xanthine compounds in the treatment of skin pruritus. EP0389282A2 discloses the effects of xanthine compounds in aspects such as brain metabolism, neuroprotection and vascular abnormalities. The literature (Expert Opin. Ther Patents 2009, 19(7), 957-967) discloses that xanthine derivatives activate GPR109A to treat diseases such as dyslipidemia and type II diabetes. The literature (Curr Atheroscler Rep 2013, 15: 325, 1-10) reported that GPR109A has the pharmacological effect of mediating vascular inflammation. The literature (PLoS One. 2014 Oct 17; 9(10): e109818) indicated that GPR109A has the effect of treating Parkinson's disease. However, these above-mentioned literatures have not reported the effect of xanthine compounds in reducing uric acid, preventing or treating gout. SUMMARY OF THE INVENTION The object of the present invention is to provide a new method for reducing uric acid, anti-inflammation, treating or preventing hyperuricemia, gout, gouty inflammation, pain and uric acid nephropathy. To achieve the above object, the inventors of the present invention conducted intensive research. As a result, unexpectedly, it was found that a class of xanthine compounds can reduce uric acid and have anti-inflammatory effects, and thus effectively prevent or treat hyperuricemia, gout, gouty inflammation, pain and uric acid nephropathy, thereby completing the present invention. Specifically, the present invention relates to the following technical solutions. (1) The use of the compound represented by formula (I), its pharmaceutically acceptable salt, its solvate or a pharmaceutical composition containing any one of them for reducing uric acid, anti-inflammation, and the use for preparing a drug for treating and / or preventing hyperuricemia, gout, gouty inflammation, pain and uric acid nephropathy, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by a halogen atom, cyano group, C 3-7 cycloalkyl; R3 is selected from a halogen atom, cyano group. (2) In the use of the above (1), R1 represents hydrogen or methyl, R2 represents ethyl, cyclopropyl ethyl, cyclopropyl methyl, propyl, 2-methylpropyl, butyl, 3-methylbutyl or pentyl, R3 represents a fluorine atom or a chlorine atom. (3) In the use of the above (1), the compound is selected from: 8-Chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, and 8-Chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione. (4) Use of the 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, their pharmaceutically acceptable salts, their solvates or pharmaceutical compositions containing any of them for reducing uric acid. (5) Use of 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, their pharmaceutically acceptable salts, their solvates or pharmaceutical compositions containing any of them for anti-inflammatory purposes. (6) 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6 dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, their pharmaceutically acceptable salts, their solvates or pharmaceutical compositions containing any of them in the preparation of a medicament for the treatment and / or prevention of hyperuricemia. (7) The use of 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, their pharmaceutically acceptable salts, their solvates, or a pharmaceutical composition containing any of them in the preparation of a medicament for the treatment and / or prevention of gout. (8) The use of 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, their pharmaceutically acceptable salts, their pharmaceutically acceptable salts, their solvates, or a pharmaceutical composition containing any of them in the preparation of a medicament for the treatment and / or prevention of gouty inflammation. (9) The 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, their pharmaceutically acceptable salts, their pharmaceutically acceptable salts, their solvates, or Use of a pharmaceutical composition containing any one of them in the preparation of a medicament for treating and / or preventing pain. (10) The 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, their pharmaceutically acceptable salts, their pharmaceutically acceptable salts, their solvates, or a pharmaceutical composition containing any one of them in the preparation of a medicament for treating and / or preventing uric acid nephropathy. (11) In the uses described in (1) to (10) above, the hyperuricemia includes primary hyperuricemia and secondary hyperuricemia. (12) In the uses described in (1) to (10) above, the gout includes primary gout and secondary gout. (13) In the uses described in (1) to (10) above, the gouty inflammation includes acute gouty arthritis, subcutaneous tophi, and chronic tophaceous arthritis. (14) In the uses described in (1) to (10) above, the pain includes acute pain, chronic pain, intractable pain, and cancer pain. (15) In the uses described in (1) to (10) above, the uric acid nephropathy includes acute uric acid nephropathy, chronic urate nephropathy, and uric acid urinary calculi. (16) A pharmaceutical composition comprising any one or more of the compound represented by formula (I), its pharmaceutically acceptable salts, and its solvates, and one or more pharmaceutical carriers. (17) The compound represented by formula (I), its pharmaceutically acceptable salt, or its solvate, which is used for preventing or treating uric acid or gouty diseases, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups, and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by halogen atoms, cyano groups, C 3-7 cycloalkyl; R3 is selected from halogen atoms, cyano groups. (18) The compound of (1) above, its pharmaceutically acceptable salt, or its solvate, wherein, R1 represents hydrogen or methyl, R2 represents ethyl, cyclopropyl ethyl, cyclopropyl methyl, propyl, 2-methylpropyl, butyl, 3-methylbutyl, or pentyl, R3 represents a fluorine atom or a chlorine atom. (19) The compound of (1) above, its pharmaceutically acceptable salt, or its solvate, wherein the compound is selected from: 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-Chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, and 8-Chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione. (20) The compound according to any one of (17) to (19) above, a pharmaceutically acceptable salt thereof or a solvate thereof, which is a hydrate. (21) The compound according to any one of (17) to (19) above, a pharmaceutically acceptable salt thereof or a solvate thereof, wherein the uric acid-related or gout-related disease is hyperuricemia, gout, gouty inflammation, pain or uric acid nephropathy. (22) The compound according to any one of (17) to (19) above, a pharmaceutically acceptable salt thereof or a solvate thereof, which is used for reducing the risk of occurrence of gout, hypertension, diabetes, hyperlipidemia, obesity, metabolic syndrome, coronary heart disease and kidney damage. (23) The compound according to (21) above, a pharmaceutically acceptable salt thereof or a solvate thereof, wherein the hyperuricemia includes primary hyperuricemia and secondary hyperuricemia. (24) The compound according to (21) above, a pharmaceutically acceptable salt thereof or a solvate thereof, wherein the gout includes primary gout and secondary gout. (25) The compound according to (21) above, a pharmaceutically acceptable salt thereof or a solvate thereof, wherein the gouty inflammation includes acute gouty arthritis, subcutaneous tophus and chronic tophaceous arthritis. (26) The compound according to (21) above, a pharmaceutically acceptable salt thereof or a solvate thereof, wherein the pain includes acute pain, chronic pain, intractable pain and cancer pain. (27) The compound according to (21) above, a pharmaceutically acceptable salt thereof or a solvate thereof, wherein the uric acid nephropathy includes acute uric acid nephropathy, chronic urate nephropathy and uric acid urinary calculi. (28) The compound represented by formula (I), a pharmaceutically acceptable salt thereof or a solvate thereof, which is used for reducing uric acid, wherein R1 is selected from hydrogen, C1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by a halogen atom, cyano group, C 3-7 cycloalkyl; R3 is selected from a halogen atom, cyano group. (29) The compound represented by formula (I), its pharmaceutically acceptable salt or solvate thereof, which is used for anti-inflammatory, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by a halogen atom, cyano group, C 3-7 cycloalkyl substituted; R3 is selected from a halogen atom, cyano group. (30) A pharmaceutical composition for preventing or treating uric acid or gouty diseases, which contains the compound represented by formula (I), its pharmaceutically acceptable salt or solvate thereof, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by a halogen atom, cyano group, C 3-7 cycloalkyl; R3 is selected from a halogen atom, cyano group. (31) The pharmaceutical composition of (30) above, wherein the uric acid-related or gout-related disease is hyperuricemia, gout, gouty inflammation, pain or uric acid nephropathy. (32) A pharmaceutical composition for reducing uric acid, which contains a compound represented by formula (I), a pharmaceutically acceptable salt thereof or a solvate thereof, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by a halogen atom, a cyano group, C 3-7 cycloalkyl; R3 is selected from a halogen atom, a cyano group. (33) A pharmaceutical composition for anti-inflammatory, which contains a compound represented by formula (I), a pharmaceutically acceptable salt thereof or a solvate thereof, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by a halogen atom, a cyano group, C 3-7 cycloalkyl; R3 is selected from a halogen atom, a cyano group. (34) A method for preventing or treating uric acid-related or gout-related diseases, which includes the step of administering a compound represented by formula (I), a pharmaceutically acceptable salt thereof or a solvate thereof to a mammal in need of such treatment, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C2-6 Alkenyl, C 2-6 Alkynyl, wherein the C 1-10 Alkyl, C 2-6 Alkenyl, C 2-6 Alkynyl is unsubstituted or optionally substituted by a halogen atom, a cyano group, C 3-7 Cycloalkyl; R3 is selected from a halogen atom, a cyano group. (35) The method according to (34) above, wherein the uric acid or gouty disease is hyperuricemia, gout, gouty inflammation, pain or uric acid nephropathy. (36) A method for reducing uric acid, comprising the step of administering a compound of formula (I), a pharmaceutically acceptable salt thereof or a solvate thereof to a mammal in need of such treatment, wherein R1 is selected from hydrogen, C 1-4 Alkyl, wherein the C 1-4 Alkyl is unsubstituted or Optionally substituted by one or more halogen atoms, a cyano group and CF3; R2 is selected from C 1-10 Alkyl, C 2-6 Alkenyl, C 2-6 Alkynyl, wherein the C 1-10 Alkyl, C 2-6 Alkenyl, C 2-6 Alkynyl is unsubstituted or optionally substituted by a halogen atom, a cyano group, C 3-7 Cycloalkyl; R3 is selected from a halogen atom, a cyano group. (37) A method for anti - inflammation, comprising the step of administering a compound of formula (I), a pharmaceutically acceptable salt thereof or a solvate thereof to a mammal in need of such treatment, wherein R1 is selected from hydrogen, C 1-4 Alkyl, wherein the C 1-4 Alkyl is unsubstituted or optionally substituted by one or more halogen atoms, a cyano group and CF3; R2 is selected from C 1-10 Alkyl, C 2-6 Alkenyl, C 2-6 Alkynyl, wherein the C 1-10 Alkyl, C 2-6 Alkenyl, C 2-6 Alkynyl is unsubstituted or optionally substituted by a halogen atom, a cyano group, C 3-7 Cycloalkyl; R3 is selected from a halogen atom, a cyano group. (38) The composition according to any one of (30) to (33) above, further comprising one or more other anti-hyperuricemic drugs, anti-gout attack drugs, and anti-inflammatory drugs. (39) A pharmaceutical kit, comprising: the composition according to any one of (30) to (33) above, and an instruction manual including information in one or more forms selected from the disease state targeted by administration of the pharmaceutical composition, storage information of the pharmaceutical composition, administration information, and usage instructions on how to administer the pharmaceutical composition. By adopting the above technical solution of the present invention, it has both anti-inflammatory effects, inhibits the occurrence and development of inflammation in hyperuricemic patients, and alleviates the inflammatory responses of gout patients, tophus patients, gouty arthritis patients, and uric acid nephropathy patients; and can also reduce the risk of occurrence of gout, hypertension, diabetes, hyperlipidemia, obesity, metabolic syndrome, coronary heart disease, and kidney damage by reducing uric acid, thereby achieving the purpose of alleviating the pain of patients and treating or preventing uric acid-related or gouty diseases. In particular, the inflammatory response is a disease state after the increase in uric acid. The compounds of the present invention have an unexpected effect of reducing uric acid, so the inflammatory response caused by the increase in uric acid can be fundamentally alleviated, thereby exerting an anti-inflammatory effect. Specific Embodiments The terms used in this specification have the following meanings. The term "halogen" refers to a fluorine atom, a chlorine atom, a bromine atom, an iodine atom, etc. Fluorine atoms and chlorine atoms are preferred. The term "C 1-10 alkyl" represents a straight-chain or branched-chain alkyl containing 1 to 10 carbon atoms, preferably a C 1-6 alkyl containing 1 to 6 carbon atoms. The "C 1-10 alkyl" includes, for example, methyl, ethyl, n-propyl, isopropyl, n-butyl, isobutyl, sec-butyl, tert-butyl, n-pentyl, isopentyl, 2-methylbutyl, neopentyl, 1-ethylpropyl, n-hexyl, isohexyl, 3-methylpentyl, 2-methylpentyl, 1-methylpentyl, 3,3-dimethylbutyl, 2,2-dimethylbutyl, 1,1-dimethylbutyl, 1,2-dimethylbutyl, 1,3-dimethylbutyl, 2,3-dimethylbutyl, 2-ethylbutyl, 1,2-dimethylpropyl, heptyl, octyl, nonyl, decyl, etc. The term "C 1-4 alkyl" represents a straight-chain or branched-chain alkyl containing 1 to 4 carbon atoms, such as methyl, ethyl, n-propyl, isopropyl, n-butyl, isobutyl, sec-butyl, tert-butyl, etc. The term "C 2-6"Alkenyl" refers to a straight-chain or branched alkenyl group with 2 to 6 carbon atoms containing a double bond, such as vinyl, 1-propenyl, 2-propenyl, 1-methylethenyl, 1-butenyl, 2-butenyl, 3-butenyl, 1-methyl-1-propenyl, 2-methyl-1-propenyl, 1-methyl-2-propenyl, 2-methyl-2-propenyl, 1-pentenyl, 2-pentenyl, 3-pentenyl, 4-pentenyl, 1-methyl-1-butenyl, 2-methyl-1-butenyl, 3-methyl-1-butenyl, 1-methyl-2-butenyl, 2-methyl-2-butenyl, 3-methyl-2-butenyl, 1-methyl-3-butenyl, 2-methyl-3-butenyl, 3-methyl-3-butenyl, 1,1-dimethyl-2-propenyl, 1,2-dimethyl-1-propenyl, 1,2-dimethyl-2-propenyl, 1-ethyl-1-propenyl, 1-ethyl-2-propenyl, 1-hexenyl, 2-hexenyl, 3-hexenyl, 4-hexenyl, 5-hexenyl, 1-methyl-1-pentenyl, 2-methyl-1-pentenyl, 3-methyl-1-pentenyl, 4-methyl-1-pentenyl, 1-methyl-2-pentenyl, 2-methyl-2-pentenyl, 3-methyl-2-pentenyl, 4-methyl-2-pentenyl, 1-methyl-3-pentenyl, 2-methyl-3-pentenyl, 3-methyl-3-pentenyl, 4-methyl-3-pentenyl, 1-methyl-4-pentenyl, 2-methyl-4-pentenyl, 3-methyl-4-pentenyl, 4-methyl-4-pentenyl, 1,1-dimethyl-2-butenyl, 1,1-dimethyl-3-butenyl, 1,2-dimethyl-1-butenyl, 1,2-dimethyl-2-butenyl, 1,2-dimethyl-3-butenyl, 1,3-dimethyl-1-butenyl, 1,3-dimethyl-2-butenyl, 1,3-dimethyl-2-butenyl, 2,2-dimethyl-3-butenyl, 2,3-dimethyl-1-butenyl, 2,3-dimethyl-2-butenyl, 2,3-dimethyl-3-butenyl, 3,3-dimethyl-1-butenyl, 3,3- dimethyl-2-butenyl, 1-ethyl-1-butenyl, 1-ethyl-2-butenyl, 1-ethyl-3-butenyl, 2-ethyl-1-butenyl, 2-ethyl-2-butenyl, 2-ethyl-3-butenyl, 1,1,2-trimethyl-2-propenyl, 1-ethyl-1-methyl-2-propenyl, 1-ethyl-2-methyl-1-propenyl, 1-ethyl-2-methyl-2-propenyl, 1,3-butadienyl, 1,3-pentadienyl, 1,4-pentadienyl, 2,4-pentadienyl, 1,4-hexadienyl, 2,4-hexadienyl, etc. The double bond can be optionally cis and trans. The term "C 2-6"Alkynyl" refers to a straight-chain or branched alkynyl group with 2-6 carbon atoms containing a triple bond, such as ethynyl, 1-propynyl, 2-propynyl, 2-butynyl, 3-butynyl, 1-methyl-2-propynyl, 2-pentynyl, 3-pentynyl, 4-pentynyl, 1-methyl-2-butynyl, 1-methyl-3-butynyl, 2-methyl-3-butynyl, 1,1-dimethyl-2-propynyl, 1-ethyl-2-propynyl, 2-hexynyl, 3-hexynyl, 4-hexynyl, 5-hexynyl, 1-methyl-2-pentynyl, 4-methyl-2-pentynyl, 1-methyl-3-pentynyl, 2-methyl-3-pentynyl, 1-methyl-4-pentynyl, 2-methyl-4-pentynyl, 3-methyl-4-pentynyl, 1,1-dimethyl-2-butynyl, 1,1-dimethyl-3-butynyl, 1,2-dimethyl-3-butynyl, 2,2-dimethyl-3-butynyl, 1-ethyl-2-butynyl, 1-ethyl-3-butynyl, 2-ethyl-3-butynyl, and 1-ethyl-1-methyl-2-propynyl, etc. The term "3-7 membered cycloalkyl" refers to a cyclic alkyl group derived by removing one hydrogen atom from the alkane part of 3-7 carbon atoms, including monocyclic cycloalkyl, fused cycloalkyl, bridged cycloalkyl, and spirocyclic cycloalkyl. The term "monocyclic cycloalkyl" refers to a 3-7 membered monocyclic cycloalkyl, including 3-7 membered saturated monocyclic cycloalkyl and 3-7 membered partially saturated monocyclic cycloalkyl. "3-7 membered saturated monocyclic cycloalkyl" means that the monocyclic ring is a fully saturated carbon ring, and its examples include but are not limited to: cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, cyclooctyl, methylcyclopropyl, dimethylcyclopropyl, methylcyclobutyl, dimethylcyclobutyl, methylcyclopentyl, dimethylcyclopentyl, methylcyclohexyl, dimethylcyclohexyl, etc. "3-7 membered partially saturated monocyclic cycloalkyl" means that the monocyclic ring is a partially saturated carbon ring, and its examples include but are not limited to cyclopropenyl, cyclobutenyl, cyclopentenyl, cyclohexenyl, 1,4-cyclohexadienyl, cycloheptenyl, 1,4-cycloheptadienyl, cyclooctenyl, 1,5-cyclooctadienyl, etc. The term "fused cycloalkyl" refers to a fused cycloalkyl formed by two or more cyclic structures sharing two adjacent carbon atoms with each other, including 6-7 membered saturated fused cycloalkyl and 6-7 membered partially saturated fused cycloalkyl. Examples of 6-7 membered saturated fused cycloalkyl include but are not limited to: bicyclo[3.1.0]hexyl, bicyclo[4.1.0]heptyl, bicyclo[2.2.0]hexyl, bicyclo[3.2.0]heptyl, bicyclo[4.2.0]octyl, etc. 6-7 membered partially saturated fused cycloalkyl means that at least one ring in the fused ring is a partially saturated carbon ring, and its examples include but are not limited to: bicyclo[3.1.0]hex-2-enyl, Bicyclo[4.1.0]hept-3-enyl, bicyclo[3.2.0]hept-3-enyl, bicyclo[4.2.0]oct-3-enyl, etc. The term "mammal" preferably refers to the human body. The term "treatment" refers to the complete or partial alleviation of symptoms associated with a disorder or disease, or the slowing or halting of the further development or worsening of these symptoms. The term "prevention" refers to preventing a disease or disorder in an object at risk of developing the disease or disorder. The term "uric acid disease" refers to diseases related to abnormal uric acid levels in the body, including but not limited to hyperuricemia or uric acid nephropathy. The term "gouty disease" refers to diseases related to gout, including but not limited to gout, gouty inflammation, or pain. Primary hyperuricemia is divided into molecular defects of unknown cause and congenital purine metabolism disorders: Congenital purine metabolism disorders are divided into the following four situations: (I) Increased activity of 5-phosphoribosyl-1-pyrophosphate synthetase (PRPPS), resulting in excessive synthesis of 5-phosphoribosyl-1-pyrophosphate synthetase and excessive uric acid production, with an X-linked genetic trait; (II) Partial deficiency of hypoxanthine-guanine phosphoribosyltransferase (HPRT), resulting in increased concentration of 5-phosphoribosyl-1-pyrophosphate synthetase and excessive uric acid production, with an X-linked genetic trait; (III) Complete deficiency of hypoxanthine-guanine phosphoribosyltransferase, resulting in excessive uric acid production due to increased purine synthesis, seen in Lesch-Nyhan syndrome, with an X-linked genetic trait; (IV) Deficiency of glucose-6-phosphatase: Excessive uric acid production due to increased purine synthesis and reduced renal clearance of uric acid, seen in glycogen storage disease type I, with an autosomal recessive genetic trait. Secondary hyperuricemia: Hyperuricemia caused by increased uric acid production or impaired uric acid excretion due to various acute and chronic diseases such as blood diseases or malignant tumors, chronic poisoning, drugs, or high-purine diets. Gout is a crystal-related arthropathy caused by the deposition of monosodium urate (MSU), directly related to hyperuricemia caused by purine metabolism disorders and / or reduced uric acid excretion, specifically referring to acute characteristic arthritis and chronic tophaceous disease, mainly including acute episodic arthritis, tophus formation, tophaceous chronic arthritis, urate nephropathy, and uric acid urinary stones. In severe cases, joint disability and renal insufficiency may occur. Primary gout is mostly hereditary, but only 10% - 20% of clinical cases have a family history of gout. Overproduction of uric acid accounts for 10% of the causes of primary hyperuricemia. The main reasons are defects in purine metabolic enzymes, deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT), and hyperactivity of phosphoribosyl pyrophosphate (PRPP) synthetase. Reduced renal excretion of uric acid in primary cases accounts for approximately 90% of primary hyperuricemia. The specific pathogenesis is unclear. It may be a polygenic hereditary disease, but organic kidney diseases should be excluded. Secondary gout refers to a clinical manifestation secondary to other diseases or caused by certain drugs. Myeloproliferative diseases such as leukemia, lymphoma, multiple myeloma, polycythemia vera, hemolytic anemia, and cancer can lead to accelerated cell proliferation, increased nucleic acid turnover, and increased uric acid production. Malignant tumors cause massive cell destruction after radiotherapy and chemotherapy for tumors, also increasing nucleic acid turnover and resulting in increased uric acid production. Kidney diseases including chronic glomerulonephritis, pyelonephritis, polycystic kidney, lead poisoning, and advanced hypertension can cause reduced glomerular filtration function, leading to decreased uric acid excretion and increased blood uric acid concentration. Drugs such as thiazide diuretics, furosemide, ethambutol, pyrazinamide, low-dose aspirin, and niacin can competitively inhibit the tubular excretion of uric acid and cause hyperuricemia. In addition, long-term use of immunosuppressants in kidney transplant patients can also cause hyperuricemia, possibly related to the inhibition of tubular uric acid excretion by immunosuppressants. Gouty inflammation is caused by the deposition of urate in the joint capsule, bursa, cartilage, bone, and other tissues, resulting in lesions and inflammatory reactions. It often has genetic and family factors, is more common in men over 40 years old, and is mostly seen in the metatarsophalangeal joint of the big toe. It can also occur in other larger joints, especially the ankle and foot joints. The main manifestation is severe pain in the joints, often occurring suddenly unilaterally. There is obvious swelling, heat, redness, and tenderness in the tissues around the joints. In acute gouty arthritis, most patients have no obvious symptoms before the attack, or only have fatigue, general discomfort, and joint tingling. The typical attack often wakes the patient up at night due to joint pain, and the pain intensifies progressively, reaching a peak in about 12 hours, presenting as tearing, knife-like, or biting pain, which is unbearable. The affected joint and the surrounding tissues are red, swollen, hot, painful, and have limited function. It usually resolves spontaneously within a few days or 2 weeks. The first attack mostly involves a single joint, with more than half occurring in the first metatarsophalangeal joint. In subsequent courses, some patients will involve this site. Secondly, joints such as the dorsal foot, heel, ankle, knee, wrist, and elbow are affected, and joints such as the shoulder, hip, spine, and temporomandibular joint are less affected. Multiple joints can be involved simultaneously, presenting as polyarthritis. Some patients may have systemic symptoms such as fever, chills, headache, palpitations, and nausea, accompanied by an increase in white blood cell count, an increase in erythrocyte sedimentation rate, and an increase in C-reactive protein, etc. During the intercritical period, a gout attack can last from several days to several weeks and then resolve spontaneously, usually without obvious... There are no obvious sequelae, or there may be local skin pigmentation, desquamation, pruritus, etc. Then it enters an asymptomatic remission period, lasting for several months, several years or more than ten years before recurrence. Most patients have a recurrence within 1 year, and the recurrence becomes more frequent, involving more and more joints, and the duration of symptoms becomes longer and longer. The affected joints generally develop from the lower limbs to the upper limbs, from the distal small joints to the large joints, with joints such as fingers, wrists and elbows being affected. In a few patients, the shoulders, hips, sacroiliac, sternoclavicular or spinal joints may be affected, and the bursae, tendons and tendon sheaths around the joints can also be involved, and the symptoms tend to be atypical. In a few patients, there is no remission period, and it shows chronic arthritis after the first onset. Chronic tophaceous stage. During the course of gout patients, a hard nodule called "tophus", also known as gout nodule, will appear. Subcutaneous tophi and chronic tophaceous arthritis are the results of long-term and significant hyperuricemia, with a large amount of sodium urate crystals deposited in the subcutaneous tissue, joint synovium, cartilage, bone and soft tissues around the joints. This kind of sodium urate crystal deposits in the soft tissue, causing chronic inflammation and fibrous tissue hyperplasia to form nodular swelling. Tophi are most common in the helix of the ear, and also more common in the first metatarsophalangeal joint of the big toe, fingers, wrists, elbows and knee joints, etc. In a few patients, they can appear in the nasal cartilage, tongue, vocal cords, eyelids, aorta, heart valves and myocardium. It invades the bone in the bones near the joints, forming bone deformities or damaging the bone. Such gout nodules can also be found in the synovial membrane, tendon sheath and cartilage near the joints. Tophi vary in size, from as small as sesame seeds to as large as eggs. Tophi can also occur in the internal organs, mainly in the renal parenchyma. Sometimes it can be seen in the ureter and bladder. It is rare in the liver, gallbladder, biliary tract and pancreas. There have been reports of finding urate crystals in saliva. No tophi have been seen in the brain, spleen and lungs. After the tophi appear, they gradually grow from small to large, the urate crystals gradually increase, and the internal pressure increases, often causing the local skin to bulge, tense, thin and shiny. Coupled with the erosive effect of urate crystals, the integrity of the skin covering it is damaged, and the anti-tensile property decreases. Once due to reasons such as friction, pressure, cold and trauma, it can ulcerate, and the "toothpaste-like" white urate crystal substance will leak out from the broken hole. The ulcerated area can form a sinus or fistula. The tissues around the opening show chronic inflammatory granulomas due to the irritation of urate crystals. It is prone to secondary bacterial infection, forming chronic suppurative lesions. Due to poor blood circulation, weak cell regeneration ability at the ulcerated area, combined with reasons such as infection and chronic granulomas, it is difficult to heal on its own. In severe cases, it can cause septicemia and lead to death. Tophi are the characteristic changes of gout. The formation of tophi is related to the course of the disease and the level of blood uric acid. The longer the course of the disease, the greater the probability of developing tophi. The longer the duration of hyperuricemia, the more likely to develop tophi. On the contrary, the more and larger the tophi are, it indicates that the hyperuricemia has not been well controlled, that is, the condition is more serious. For some patients, although the course of the disease has been very long, after treatment, the blood When uric acid remains within the normal range for a long time, tophaceous gout rarely occurs. The occurrence, number, and size of tophi are also direct indicators for clinicians to judge the severity of the condition and the satisfaction of treatment. The typical location for subcutaneous tophi is the auricle, and they are also commonly seen around joints with repeated attacks, as well as in areas such as the olecranon, Achilles tendon, and prepatellar bursa. They appear as yellowish-white neoplasms of varying sizes protruding under the skin, with a thin skin surface. After rupture, white powdery or pasty substances are discharged, and the wound does not heal for a long time. Subcutaneous tophi often coexist with chronic tophaceous arthritis. A large amount of tophi deposited in the joint can cause joint bone destruction, fibrosis of the surrounding tissues, and secondary degenerative changes, etc. The clinical manifestations include persistent joint swelling, pain, tenderness, deformity, and dysfunction. The symptoms in the chronic phase are relatively mild, but there can also be acute attacks. Urate nephropathy is renal damage caused by hyperuricemia due to excessive production or reduced excretion of uric acid, usually called gouty nephropathy. The clinical manifestations may include uric acid stones, low-molecular-weight proteinuria, edema, nocturia, hypertension, elevated blood and urine uric acid levels, and damage to the renal tubular function. This disease is common in Western countries and more prevalent in the northern part of China. There is no obvious seasonality. The incidence is high in obese people, those who like meat and alcohol. The male-to-female ratio is 9:1, and 85% are middle-aged and elderly people. If this disease can be diagnosed early and appropriate treatment (controlling hyperuricemia and protecting renal function) is given, the renal lesions can be alleviated or stop progressing. If treatment is delayed or inappropriate, the condition can deteriorate and develop into end-stage renal failure, requiring dialysis treatment. In chronic urate nephropathy, urate crystals deposit in the renal interstitium, leading to chronic tubulointerstitial nephritis. The clinical manifestations include a decline in urine concentrating function, with increased nocturia, low specific gravity urine, low-molecular-weight proteinuria, leukocyturia, mild hematuria, and cylindruria, etc. In the late stage, the glomerular filtration function can decline, resulting in renal insufficiency. Urate urinary tract stones occur when the concentration of uric acid in the urine increases to a supersaturated state and deposits in the urinary system to form stones. The incidence in gout patients is more than 20%, and it may occur before the onset of gouty arthritis. Smaller stones are in the form of gravel and are excreted with urine, often without symptoms; larger stones can block the urinary tract, causing renal colic, hematuria, dysuria, urinary tract infection, hydronephrosis, etc. There are many factors affecting the formation of kidney stones. Age, gender, race, genetics, environmental factors, eating habits, and occupation are related to the formation of stones. Metabolic abnormalities of the body, urinary tract obstruction, infection, foreign bodies, and the use of drugs are common causes of stone formation. It is known that there are 32 components of urinary stones, and the most common component is calcium oxalate. Stones composed of other components such as magnesium ammonium phosphate, uric acid, calcium phosphate, and cystine (an amino acid), etc., can also be mixtures of the above various components. Urate stones have persistently acidic urine, are characterized by being hard, smooth, granular, yellow or brownish-red, and have abnormal uric acid metabolism. In acute uric acid nephropathy, the levels of uric acid in blood and urine increase sharply, and a large amount of uric acid crystals deposit in the renal tubules, collecting ducts and other places, causing acute urinary tract obstruction. The clinical manifestations are oliguria, anuria, acute renal failure; a large number of uric acid crystals can be seen in the urine. It is mostly caused by secondary causes such as malignant tumors and their radiotherapy and chemotherapy (i.e., tumor lysis syndrome). The elevation of blood uric acid deposited in joints can cause gouty arthritis, further causing joint deformity; deposited in the kidneys can cause gouty nephropathy, uric acid stones, further causing uremia; the elevation of blood uric acid can stimulate the blood vessel wall to cause atherosclerosis and exacerbate coronary heart disease and hypertension; the elevation of blood uric acid can damage pancreatic B cells, thus inducing or exacerbating diabetes. Hyperuricemia is the pathogenesis basis of gout, but it is not enough to cause gout. Only when urate deposits in the body tissues and causes damage does gout occur; the higher the blood uric acid level, the greater the possibility of developing gout in the next 5 years. In the present invention, R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3, more preferably selected from hydrogen and unsubstituted C 1-4 alkyl, further preferably selected from hydrogen, methyl and ethyl, most preferably hydrogen or methyl. R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by halogen atoms, cyano groups, C 3-7 cycloalkyl, more preferably C 1-6 alkyl, further preferably ethyl, cyclopropyl ethyl, cyclopropyl methyl, propyl, 2-methylpropyl, butyl, 3-methylbutyl or pentyl, even more preferably C 3-6 alkyl, still more preferably C 4-5 alkyl, most preferably butyl or pentyl. R3 is selected from halogen atoms, cyano groups, preferably halogen atoms, more preferably fluorine atoms, chlorine atoms or bromine atoms, even more preferably fluorine atoms or chlorine atoms, most preferably chlorine atoms. The above various preferred schemes for the definitions of R1, R2 and R3 in the general formula (I) of the present invention are not exhaustive. The technical solutions obtained by arbitrarily deleting groups in their definitions and various preferred schemes are all included in the scope of the present invention. Moreover, the technical solutions obtained by arbitrarily combining the definitions of the above R1, R2 and R3, various preferred schemes and the technical solutions after arbitrarily deleting substituents in various preferred schemes are also included in the scope of the present invention. As a preferred embodiment of the present invention, wherein, R1 is selected from hydrogen or C 1-4 alkyl; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl; R3 is selected from a halogen atom, a cyano group. As another preferred embodiment of the present invention, wherein, R1 is selected from hydrogen or C 1-4 alkyl; R2 is selected from C 1-10 alkyl; R3 is selected from a halogen atom, a cyano group. As yet another preferred embodiment of the present invention, wherein, R1 is selected from hydrogen or C 1-4 alkyl; R2 is selected from C 1-6 alkyl; R3 is selected from a halogen atom. As another preferred embodiment of the present invention, wherein, R1 represents hydrogen or methyl, R2 represents ethyl, cyclopropyl ethyl, cyclopropyl methyl, propyl, 2-methylpropyl, butyl, 3-methylbutyl or pentyl, and R3 represents a fluorine atom or a chlorine atom. As yet another preferred embodiment of the present invention, wherein, R1 represents hydrogen or methyl, R2 represents propyl, 2-methylpropyl, butyl, 3-methylbutyl or pentyl, and R3 represents a fluorine atom or a chlorine atom. As yet another preferred embodiment of the present invention, wherein, R1 represents hydrogen or methyl, R2 represents propyl, butyl or pentyl, and R3 represents a chlorine atom. As examples of the preferred compounds among the compounds of the present invention, there may be mentioned: 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, and 8-Chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione. Pharmaceutically acceptable salts of the compounds represented by the general formula (I) are, for example, salts formed with alkali metals, alkaline earth metals, ammonium, alkylammonium, etc., and salts formed with inorganic acids or organic acids. These salts may include sodium salts, potassium salts, calcium salts, ammonium salts, aluminum salts, triethylammonium salts, acetate salts, propionate salts, butyrate salts, formate salts, trifluoroacetate salts, maleate salts, tartrate salts, citrate salts, stearate salts, succinate salts, ethyl succinate salts, lactate salts, gluconate salts, glucoheptonate salts, benzoate salts, methanesulfonate salts, ethanesulfonate salts, 2-hydroxyethanesulfonate salts, benzenesulfonate salts, p-toluenesulfonate salts, lauryl sulfate salts, malate salts, aspartate salts, glutamate salts, adipate salts, tris(hydroxymethyl)aminomethane salts, salts formed with cysteine, salts formed with N-acetylcysteine, hydrochloride salts, hydrobromide salts, phosphate salts, sulfate salts, hydroiodide salts, nicotinate salts, oxalate salts, picrate salts, thiocyanate salts, undecanoate salts, salts formed with acrylic acid polymers, salts formed with carboxyvinyl polymers, etc. Solvates of the compounds represented by the general formula (I) or their salts may include hydrates, etc., but are not limited thereto. The hydrate is preferably a monohydrate. In addition, in the compounds represented by the general formula (I) of the present invention, if there are chiral carbons, the present invention includes isomers formed based on any stereoconfiguration of these chiral carbons, for example, racemates or any one of the enantiomers. Moreover, the present invention includes all other stereoisomers that may occur. That is, the compounds of the present invention include all enantiomers, diastereomers, equilibrium compounds, mixtures of any ratio thereof, racemates, etc. The compounds of the general formula (I) of the present invention can be prepared by various known methods without particular limitation. For example, they can be prepared according to the following reaction steps as described in the following reaction roadmap, but the preparation method is not limited thereto. Reaction roadmap (Wherein, R1, R2, and R3 are defined as above, and X represents a halogen atom.) i) Alkylate starting material 1 with allyl bromide; ii) Diazotize with sodium nitrite and then hydrolyze to form intermediate B; iii) Halogenate with N-halosuccinimide at C 8 where R3 represents -F, -Cl, -Br, -I; iv) Alkylate at N 3 where R2 represents hydrogen or an alkyl group; v) Alkylate at N 1Upper alkylation, where R1 represents an alkane; vi) Removal of allyl vii) Alkylation on N 3 where R2 represents an alkane; viii) Alkylation on N 1 where R1 represents an alkane; ix) Formation of an aldehyde on C 8 ; x) Conversion of the aldehyde to a nitrile. Specifically, as shown in the above reaction pathway, when R3 represents a halogen atom, at 0 - 50 °C, preferably 20 - 30 °C, in a solvent such as DMSO, DMF, acetone, dioxane, acetonitrile, tetrahydrofuran, or N - methylpyrrolidone, preferably DMSO, raw material 1 is alkylated with allyl bromide to obtain intermediate A. Then, in a system of a dilute acid (such as acetic acid, dilute hydrochloric acid, or dilute sulfuric acid) and water, at 0 - 100 °C, preferably 20 - 60 °C, it is diazotized using sodium nitrite and then hydrolyzed to form intermediate B. Intermediate B is halogenated with a halogenated succinimide at 0 - 100 °C, preferably 20 - 60 °C, in DMF, DMSO, dioxane, acetonitrile, tetrahydrofuran, or N - methylpyrrolidone to obtain intermediate C. Intermediate C is alkylated with a halogenated hydrocarbon under the action of a base at 0 - 50 °C, preferably 25 °C, in DMF, DMSO, dioxane, acetonitrile, tetrahydrofuran, or N - methylpyrrolidone to obtain intermediate D. The preparation sequence of intermediate C and intermediate D can be interchanged. When R1 represents an alkyl group, intermediate D is alkylated with a halogenated hydrocarbon under the action of a base at 0 - 120 °C, preferably 50 - 100 °C, in DMF, DMSO, dioxane, acetonitrile, tetrahydrofuran, or N - methylpyrrolidone to obtain intermediate E. Intermediate D (where R1 represents a hydrogen atom) or intermediate E (where R1 represents an alkyl group) is reacted with morpholine or 1,3 - dimethylbarbituric acid in dichloromethane, chloroform, carbon tetrachloride, or acetone at 0 - 60 °C, preferably 20 - 30 °C, under inert gas protection, with or without a palladium catalyst, to remove the allyl group to obtain the compound shown in formula (I). When R3 represents a cyano group, intermediate B is alkylated with a halogenated hydrocarbon under the action of a base in DMF, DMSO, dioxane, acetonitrile, tetrahydrofuran or N-methylpyrrolidone at 0-50 °C, preferably 25 °C, to obtain intermediate C'. Intermediate C' is alkylated with a halogenated hydrocarbon under the action of a base in DMF, DMSO, dioxane, acetonitrile, tetrahydrofuran or N-methylpyrrolidone at 0-120 °C, preferably 50-100 °C, to obtain intermediate D'. Intermediate D is quenched with DMF, alcohols or water by an elimination reaction using LiHMDS or NaHMDS to obtain intermediate E'. Intermediate E' is reacted with hydroxylamine hydrochloride and pyridine in acetic anhydride, toluene or benzene to obtain intermediate F'. Intermediate F' is reacted with morpholine or 1,3-dimethylbarbituric acid in dichloromethane, chloroform, carbon tetrachloride or acetone at 0-60 °C, preferably 20-30 °C, under the protection of an inert gas, with or without a palladium catalyst, to remove the allyl group to obtain the compound represented by formula (I). The above-mentioned halogenated succinimides may be selected from chlorosuccinimide, bromosuccinimide, iodosuccinimide, etc. The above-mentioned bases may be selected from sodium carbonate, potassium carbonate, sodium bicarbonate, cesium carbonate, etc. The above-mentioned inert gases may be selected from nitrogen, argon, etc. The intermediates and target products obtained from the above reactions can be separated and purified according to need by conventional purification methods commonly used in organic synthetic chemistry, such as filtration, extraction, washing, drying, concentration, recrystallization, various chromatographic methods, etc. In addition, the intermediate can also be directly used in the next reaction without special purification. The obtained compound represented by the general formula (I) can also form acid addition salts, base addition salts, and various solvates, such as hydrates, according to conventional methods. Various isomers can be separated by conventional methods that utilize the differences in physical and chemical properties between the isomers. For example, a racemic mixture can be optically resolved by forming diastereomeric salts with a general optically active acid such as tartaric acid, or by a general racemic resolution method such as an optically active column chromatography method, to obtain an optically pure isomer. In addition, a diastereomeric mixture can be separated, for example, by fractional crystallization or various chromatographic methods. In addition, an optically active compound can also be prepared using an appropriate optically active starting material. The present invention includes a composition containing any one or more of the compounds represented by formula (I), their pharmaceutically acceptable salts, and their solvates. The composition may contain one or more pharmaceutical carriers. As the above carriers, for example, excipients and diluents include water, lactose, glucose, fructose, sucrose, sorbitol, mannitol, polyethylene glycol, propylene glycol, starch, gum, gelatin, alginate, calcium silicate, calcium phosphate, cellulose, aqueous syrup, methylcellulose, polyvinylpyrrolidone, talc, magnesium stearate, stearic acid, glycerol, sesame oil, olive oil, various oils such as soybean oil, etc. The present invention also includes a pharmaceutical composition of any of the above-mentioned compounds or their pharmaceutically acceptable salts or their solvates and one or more antihyperuricemic drugs, antigout attack drugs, and anti-inflammatory drugs. The antihyperuricemic drugs are selected from drugs that reduce uric acid production and uricosuric drugs, and the anti-inflammatory drugs include immunomodulatory non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids. The drugs that reduce uric acid production are selected from xanthine oxidase inhibitors, including allopurinol, febuxostat, pegloticase, a polyethylene glycol recombinant uricase, and the uricosuric drugs are selected from urate anion transporter 1 (URAT1) inhibitors, such as probenecid, benzbromarone, sulfinpyrazone, lesinurad. The antigout attack drug is selected from colchicine, and the non-steroidal anti-inflammatory drugs are selected from non-selective non-steroidal anti-inflammatory drugs and selective cyclooxygenase (COX-2) inhibitors. The non-selective non-steroidal anti-inflammatory drugs include aspirin, benorilate, indomethacin, glucosamine guanxin, sulindac, diclofenac sodium, ibuprofen, ibuprofen tablets, ketoprofen, naproxen, and piroxicam. The selective cyclooxygenase (COX-2) inhibitors are selected from celecoxib, rofecoxib, parecoxib, etc., and the glucocorticoids are selected from dexamethasone, hydrocortisone, cortisone, prednisone, prednisolone, methylprednisolone, prednisolone, prednisone, and betamethasone. The administration methods of the pharmaceutical composition of the present invention containing the compound represented by the above general formula (I) or its pharmaceutically acceptable salt and its solvate as the active ingredient can include oral administration through tablets, capsules, granules, powders, syrups, etc., or parenteral administration through intravenous injections, intramuscular injections, sterile powders for injection, concentrated solutions for injection, suppositories, inhalants, transdermal absorbents, eye drops, nasal drops, etc. In addition, when formulating pharmaceutical preparations of the above various dosage forms, the active ingredient can be used alone or appropriately combined with other pharmaceutically acceptable carriers, namely excipients, binders, extenders, disintegrants, surfactants, lubricants, dispersants, buffers, preservatives, flavoring agents, fragrances, coating agents, diluents, etc., and made into pharmaceutical preparations by conventional methods. The present invention also includes a medicine kit, which comprises: the above composition, and an instruction manual including information in one or more forms, the information being selected from the disease state targeted by administration of the pharmaceutical composition, storage information of the pharmaceutical composition, administration information, and instructions on how to administer the pharmaceutical composition. The dosage of the pharmaceutical composition of the present invention varies according to the patient's weight, age, gender, symptoms, etc., and can be appropriately selected according to oral administration or non-oral administration, etc. Next, through specific embodiments in the form of examples, the above content of the present invention will be further described in detail. However, it should not be understood that the scope of the above subject matter of the present invention is limited to the following examples. Experimental Example 1 Pharmacokinetic Experiment of Cynomolgus Monkeys Test articles: Compound A: Prepared through Example 2, Compound B: Prepared through Example 1, Compound C: Prepared through Example 3, Compound D: Prepared through Example 4; Animal experiment undertaking units: Shanghai Pharmaron Biotech Co., Ltd., Shandong Hongli Medical Animal Experiment Research Co., Ltd.; Animal source: Suzhou Xishan Zhongke Experimental Animal Co., Ltd.; Three cynomolgus monkeys were intravenously injected with 5 mg / kg of test article compounds A, B, D, and 3 mg / kg of test article compound C was intravenously injected. Blood was collected from the vein before administration and at 1 h, 3 h, 6 h, and 24 h after administration, and plasma was separated; analyzed by a 4000 Q Trap LC-MS / MS instrument; the concentration of the test substance was output using Analyst 1.6.1 of AB Company, and parameters such as mean, standard deviation, and coefficient of variation were calculated using Microsoft Excel (parameters directly output by Analyst 1.6.1 do not need to be calculated), and PK parameters were calculated using Pharsight Phoenix 6.2 software (NCA model). Half-life (t 1 / 2z (h)) Results: See Table 1 below. Table 1 t of compounds A, B, C, and D after IV administration in cynomolgus monkeys 1 / 2z (h) (Mean±SD) (n = 3) It can be seen from the test results that the half-lives (t 1 / 2z (h)) of compounds A, B, C, and D after IV administration in cynomolgus monkeys are quite different, and the time points for the uric acid-lowering experiment are set according to t 1 / 2z(h) Conduct the design. Experimental Example 2 Hypouricemic Experiment Test article: Compound A: Prepared through Example 2, Compound B: Prepared through Example 1, Compound C: Prepared through Example 3, Compound D: Prepared through Example 4; Experiment undertaking unit: Peli BioPharmaTech (Shanghai) Co., Ltd.; Animal source: Suzhou Xishan Zhongke Experimental Animal Co., Ltd.; Experimental method reference: Komoriya K, Osada Y, Hasegawa M, Horiuchi H, Kondo S, Couch RC, Griffin TB. Hypouricemic effect of allopurinol and the novel xanthine oxidase inhibitor TEI-6720 in chimpanzees. Eur J Pharmacol. 1993 Dec 21;250(3):455-60. Three cynomolgus monkeys were selected for each compound with numbers 1#, 2#, and 3# respectively. The test article was administered by intravenous injection. Blood was collected intravenously before administration and at 1 h, 3 h, 6 h, and 24 h after administration. Let it stand at room temperature, centrifuge to obtain serum, and detect the serum uric acid content. Serum uric acid reduction rate = (average uric acid content before administration - average uric acid content after administration) / average uric acid content before administration * 100%. Test results: Referring to the half-lives (t 1 / 2z (h)) of reference compounds A, B, C, and D after IV administration in cynomolgus monkeys, the serum uric acid content and serum uric acid reduction rate of Compound A before administration and at 3 h and 6 h after administration, the serum uric acid content and serum uric acid reduction rate of Compound B before administration and at 3 h after administration, the serum uric acid content and serum uric acid reduction rate of Compound C before administration and at 24 h after administration, and the serum uric acid content and serum uric acid reduction rate of Compound D before administration and at 3 h after administration were measured respectively. The specific results are shown in Tables 2 - 9 below. Table 2 Experimental results of Compound A in reducing serum uric acid Table 3 Serum uric acid reduction rate of Compound A Table 4 Experimental results of Compound B in reducing serum uric acid Table 5 Serum uric acid reduction rate of Compound B Table 6 Experimental results of Compound C in reducing serum uric acid Table 7 Serum uric acid reduction rate of Compound C Table 8 Experimental results of Compound D in reducing serum uric acid Table 9 Serum uric acid reduction rate of Compound D It can be seen from the test results that compared with before dosing, Compounds A, B, C, and D can significantly reduce the serum uric acid content of the test monkeys, indicating that the compounds shown in formula (I) have the uses of treating and / or preventing hyperuricemia, gout, gouty inflammation, and uric acid nephropathy. Experimental Example 3 Uric acid reduction experiment on a monkey hyperuricemia model Test articles: Compound A: Prepared by Example 2; Solvent: 5% glucose, purchased from Chenxin Pharmaceutical Co., Ltd., batch number 1312022142; Reagent: Uric acid (UA), purchased from Sigma-Aldrich Co., Ltd., batch number BCBM8832V; Animal experiment undertaking unit: Shandong Hongli Medical Animal Experiment Research Co., Ltd.; Animal source: Suzhou Xishan Zhongke Experimental Animal Co., Ltd.; Experimental method reference: Komoriya K, Osada Y, Hasegawa M, Horiuchi H, Kondo S, Couch RC, Griffin TB. Hypouricemic effect of allopurinol and the novel xanthine oxidase inhibitor TEI-6720 in chimpanzees. Eur J Pharmacol. 1993 Dec 21;250(3):455-60. Model group: Select 3 cynomolgus monkeys, numbered 1#, 2#, and 3# respectively, were subcutaneously injected with UA in the nape of the neck. Venous blood was collected before dosing and at 0.5 h, 1 h, 2 h, 4 h, 6 h, and 24 h after dosing. It was left to stand at room temperature, centrifuged to obtain serum, and the serum uric acid content was detected. Administration group: 3 cynomolgus monkeys numbered 1#, 2#, and 3# After 2 weeks of metabolic clearance in cynomolgus monkeys, the test article was administered by intravenous injection. Blood was collected from the vein before administration and 2 h after administration, and then UA was administered by subcutaneous injection in the nape of the neck. Blood was collected from the vein 1 h, 2 h, and 4 h after modeling. It was left standing at room temperature, centrifuged to obtain serum, and the serum uric acid content was detected. Serum uric acid reduction rate in normal monkeys after administration = (average uric acid content before administration - average uric acid content 2 h after administration) / average uric acid content before administration * 100%, Serum uric acid reduction rate in model monkeys after administration = (uric acid content after administration in the model group - uric acid content after administration in the administration group) / uric acid content in the model group * 100%. Test results: Referring to the half-life (t 1 / 2z 0.54 h) of uric acid (UA) in the cynomolgus monkeys after IV administration in the model group and the change trend of serum uric acid content, the time points for detecting serum uric acid content in the administration group were before administration, 2 h after administration, and 1 h, 2 h, and 4 h after UA modeling. The serum uric acid content and serum uric acid reduction rate in the model group and the administration group are shown in Tables 3-1, 3-2, and 3-3 below. Table 3-1 Experimental results of reducing serum uric acid in the model group Table 3-2 Experimental results of reducing serum uric acid in the administration group Table 3-3 Serum uric acid reduction rate in the administration group It can be seen from the test results that compared with the model group (itself), compound A can significantly reduce the serum uric acid content of the test monkeys, indicating that the compound shown in formula (I) has the use of treating and / or preventing hyperuricemia, gout, gouty inflammation, and uric acid nephropathy. Experimental example 4 MSU-induced gouty arthritis experiment Test article: Compound A: Prepared by Example 2, Compound B: Prepared by Example 1, Compound C: Prepared by Example 3; Solvent: Dimethyl sulfoxide, purchased from Sigma-Aldrich Co., Ltd., batch number SZBD133SV, Polyethylene glycol ester of 15-hydroxy stearic acid (Kolliphor HS 15), purchased from Beijing Fengli Jingqiu Trading Co., Ltd., batch number 19888216KO, 5% Glucose, purchased from Chenxin Pharmaceutical Co., Ltd., batch number 1312022142; Reagent: UA, purchased from Sigma - Aldrich Co., Ltd, batch number BCBM8832V; Male Wistar rats: Purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. The experimental method refers to: Hsin - Pai Lee, Shi - Ying Huang, Yen - You Lin. Soft Coral - Derived Lemnalol Alleviates Monosodium Urate - Induced Gouty Arthritis in Rats by Inhibiting Leukocyte Infiltration and iNOS, COX - 2 and c - Fos Protein Expression. Mar. Drugs 2013, 11, 99 - 113. Preparation of MSU crystals Weigh 1 g of uric acid and place it in 200 mL of boiling water. Heat it, add 2 mol / L NaOH until the pH reaches 9, the solution becomes clear. After cooling at room temperature overnight, filter to obtain MSU. Dry it at 60 °C for 24 h and sterilize it at a high temperature of 180 °C. After 1 - week of adaptive feeding of male Wistar rats, they were randomly grouped. One day in advance, the toe volume of the rats was measured. The model group was given 5 mL / kg of vehicle by subcutaneous injection, and the other dosing groups were given 5 mg / kg of the test article by subcutaneous injection. The rats were immediately anesthetized after dosing, and 0.09 mL of MSU suspension was injected into the left ankle joint cavity. The left toe volume of the rats was measured 9 h after the injection into the ankle joint cavity. Test results: See Table 10 below. Table 10 Experimental results of gouty arthritis (5 mg / kg) It can be seen from the test results that compared with the model group, Compounds A, B, and C can significantly inhibit the increase in the toe volume of the test rats, indicating that the compounds shown in formula (I) have the use for treating and / or preventing hyperuricemia, gout, gouty inflammation, and uric acid nephropathy. Experimental Example 5 MSU - induced gouty arthritis experiment Test article: Compound A: Prepared by Example 2, Compound C: Prepared by Example 3, Compound D: Prepared by Example 4; Solvent: Dimethyl sulfoxide, purchased from Sigma - Aldrich Co., Ltd, batch number SZBD133SV, Polyethylene glycol 15 - hydroxystearate (Kolliphor HS 15), purchased from Beijing Fengli Jingqiu Trading Co., Ltd, batch number 19888216KO, 5% Glucose, purchased from Chenxin Pharmaceutical Co., Ltd, batch number 1312022142; Reagent: UA, purchased from Sigma - Aldrich Co., Ltd, batch number BCBM8832V; Male Wistar rats: Purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. The experimental method refers to: Hsin - Pai Lee, Shi - Ying Huang, Yen - You Lin. Soft Coral - Derived Lemnalol Alleviates Monosodium Urate - Induced Gouty Arthritis in Rats by Inhibiting Leukocyte Infiltration and iNOS, COX - 2 and c - Fos Protein Expression. Mar. Drugs 2013, 11, 99 - 113. Preparation of MSU crystals Weigh 1 g of uric acid and place it in 200 mL of boiling water. Heat it, add 2 mol / L NaOH until the pH reaches 9, and the solution becomes clear. After cooling at room temperature overnight, filter to obtain MSU. Dry it at 60 °C for 24 h and sterilize it at 180 °C at high temperature. After male Wistar rats were adaptively fed for 1 week, they were randomly grouped, and the toe volume of the rats was measured one day in advance. The model group was subcutaneously injected with 15 mL / kg of the solvent, and the other drug - administered groups were subcutaneously injected with 15 mg / kg or 10 mg / kg of the test article. The rats were immediately anesthetized after administration, and 0.09 mL of MSU suspension was injected into the left ankle joint cavity. The left toe volume of the rats was measured 9 h after the injection into the ankle joint cavity. Test results: See Table 11 below. Table 11 Experimental results of gouty arthritis It can be seen from the test results that compared with the model group, compounds A, C, and D can significantly inhibit the increase in the toe volume of the test rats, indicating that the compounds shown in formula (I) have the uses of treating and / or preventing hyperuricemia, gout, gouty inflammation, and uric acid nephropathy. Put the gouty arthritis rats into a metabolic cage, stimulate the left foot palm of the rats with an electronic Von Frey analgesimeter, and record the maximum force value when the rats withdraw their feet, which is the pain threshold of the rats. Test results: See Table 12 below. Table 12 Experimental results of pain threshold It can be seen from the test results that compared with the model group, Compounds A, C, and D can significantly increase the pain threshold of the tested rats, indicating that the compounds shown in formula (I) have the uses of treating and / or preventing hyperuricemia, gout, pain, gouty inflammation, and uric acid nephropathy. Experimental Example 6 MSU-induced gouty arthritis experiment Test articles: Compound B: Prepared according to Example 1; Solvent: 5% glucose, purchased from Chenxin Pharmaceutical Co., Ltd., batch number 1312022142; Reagent: UA, purchased from Sigma-Aldrich Co., Ltd., batch number BCBM8832V; Male Wistar rats: Purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. The experimental method refers to: Hsin-Pai Lee, Shi-Ying Huang, Yen-You Lin. Soft Coral-Derived Lemnalol Alleviates Monosodium Urate-Induced Gouty Arthritis in Rats by Inhibiting Leukocyte Infiltration and iNOS, COX-2 and c-Fos Protein Expression. Mar. Drugs 2013, 11, 99-113. Preparation of MSU crystals Weigh 1 g of uric acid and place it in 200 mL of boiling water. Heat it and add 2 mol / L NaOH until the pH reaches 9. The solution becomes clear. After cooling at room temperature overnight, filter to obtain MSU. Dry it at 60 °C for 24 h and sterilize it at 180 °C at high temperature. After male Wistar rats are adaptively fed for 1 week, they are randomly grouped, and the toe volume of the rats is measured one day in advance. The model group is given 15 mL / kg of the solvent by subcutaneous injection, and the other dosing groups are given 15 mg / kg of the test article by subcutaneous injection. The rats are immediately anesthetized after dosing, and 0.09 mL of MSU suspension is injected into the left ankle joint cavity. The left toe volume of the rats is measured 9 h after the injection into the ankle joint cavity. Test results: See Table 13 below. Table 13 Experimental Results of Gouty Arthritis (15 mg / kg) It can be seen from the experimental results that compared with the model group, Compound B can significantly reduce the increase in the toe volume of the test rats, indicating that the compound shown in formula (I) has the use for treating and / or preventing hyperuricemia, gout, gouty inflammation and uric acid nephropathy. Put the rats with gouty arthritis into a metabolic cage, stimulate the left foot palm of the rats with an electronic Von Frey analgesimeter, and record the maximum force value when the rats withdraw their feet, which is the pain value of the rats. Experimental results: See Table 14 below. Table 14 Experimental Results of Pain Value (15 mg / kg) It can be seen from the experimental results that compared with the model group, Compound B can significantly reduce the pain of the test rats, indicating that the compound shown in formula (I) has the use for treating and / or preventing hyperuricemia, gout, pain, gouty inflammation and uric acid nephropathy. Experimental Example 7 LPS-induced TNF-α Release Experiment Test articles: Compound C: Prepared by Example 3 Compound D: Prepared by Example 4 Solvent: Dimethyl sulfoxide, purchased from Sigma-Aldrich Co., Ltd., batch number SZBD133SV Polyethylene glycol 15-hydroxystearate (Kolliphor HS 15), purchased from Beijing Fengli Jingqiu Trading Co., Ltd., batch number 19888216KO 5% Glucose, purchased from Chenxin Pharmaceutical Co., Ltd., batch number 1312022142 Reagent: Lipopolysaccharide (LPS), purchased from Sigma-Aldrich Co., Ltd., batch number 114M4009V Reagent: Phosphate buffer solution (PBS), purchased from Life Technologies, batch number 15552504 Male BALB / C mice: Purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. The experimental method refers to: Pascale Gaillard, Isabelle Jeanclaude-Etter, etc. Design and Synthesis of the First Generation of Novel Potent, Selective, and in Vivo Active (Benzothiazol-2-yl)acetonitrile Inhibitors of the c-Jun N-Terminal. J. Med. Chem. 2005, 48, 4596-4607. After adapting in the SPF-class animal house for 1 week, BALB / C mice were randomly divided into the corresponding model group and each dosing group according to body weight. The vehicle and the test article were subcutaneously injected at 10 mg / kg. 30 min after the injection of the vehicle or the test article, LPS was intraperitoneally injected at 15 mg / kg. 1 h after the administration of LPS, After the mice were anesthetized with sodium pentobarbital (intraperitoneally injected at 45 mg / kg), blood was collected by cardiac puncture, and the content of TNF-α (tumor necrosis factor) in plasma was detected using the Mouse TNF-α Elisa Ready-set-go kit. Test results: See Table 15 below. Table 15 Results of the LPS-induced TNF-α release experiment From the test results, it can be seen that compared with the model group, compounds C and D can significantly reduce the content of TNF-α in the plasma of the test mice, indicating that the compounds shown in formula (I) have the use for treating and / or preventing gouty inflammation. Experimental Example 8 ConA-induced IFNγ release test Test articles: Compound A: Prepared by Example 2, Compound C: Prepared by Example 3, Compound D: Prepared by Example 4; Vehicle: Dimethyl sulfoxide, purchased from Sigma-Aldrich Co., Ltd., batch number SZBD133SV, Polyethylene glycol 15-hydroxystearate (Kolliphor HS 15), purchased from Beijing Fengli Jingqiu Trading Co., Ltd., batch number 19888216KO, 5% glucose, purchased from Chenxin Pharmaceutical Co., Ltd., batch number 1312022142; Reagents: Concanavalin A (ConA), purchased from Sigma-Aldrich Co., Ltd., batch number SLBD7276V, Dulbecco's phosphate buffered saline (DPBS), purchased from Life Technologies, batch number 1627698; Male C57BL / 6 mice: purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. The experimental method refers to: Dalya R. Soond1, Elisa etc. PI3K p110δ regulates T cell cytokine production during primary and secondary immune responses in mice and humans. Blood. Author manuscript; available in PMC 2013 March 11. Gabriele Sass, Sonja Heinlein, etc. CYTOKINE EXPRESSION IN THREE MOUSE MODELS OF EXPERIMENTAL HEPATITIS. CYTOKINE, Vol. 19, No. 3 (7 August), 2002: pp 115 - 120. After C57BL / 6 adapted to the SPF - level animal house for 1 week, they were randomly divided into the corresponding model group and each dosing group according to body weight. After subcutaneous injection of the vehicle or the test article at 20 mg / kg for 30 min, ConA at 15 mg / kg was given via the tail vein. 3 h after ConA administration, the mice were anesthetized with sodium pentobarbital (intraperitoneal injection at 45 mg / kg), and blood was collected by cardiac puncture and placed in a centrifuge tube without anticoagulant. After standing at room temperature for 1 h, centrifugation was performed, and the serum was extracted and stored at - 80 °C. The content of IFNγ (interferon - γ) in the serum was detected using the Mouse IFNγ Elisa Ready - set - go kit. Test results: See Table 16 below. Table 16 Results of the ConA - induced IFNγ release experiment It can be seen from the test results that compared with the model group, compounds A, C, and D can significantly reduce the content of IFNγ in the serum of the test mice, indicating that the compounds shown in formula (I) have the use for treating and / or preventing gouty inflammation. Experimental Example 9 Air - sac inflammation experiment Test article: Compound A: Prepared according to Example 2, Solvent: Avicel RC-591, purchased from FMC BioPolymer, batch number DN14827450; Reagent: UA, purchased from Sigma-Aldrich; Male SD rats: Purchased from Shanghai Slake Laboratory Animal Co., Ltd. Experimental method: Preparation of MSU suspension: 1 g of uric acid was dissolved in 0.2 L of boiling water containing 6 mL of 1 N NaOH, the pH value was adjusted to 7.4, cooled to room temperature, and left overnight at 4 °C. The MSU crystals were centrifuged, evaporated to dryness, sonicated, and the length of the needle-shaped crystals was examined under a microscope to be 5-25 μm. 5 mg of the crystals were placed in a glass bottle and autoclaved. Sterile MSU crystals were added to 5 mL of sterile normal saline before balloon injection. After 1 week of adaptive feeding, male SD rats were randomly divided into 6 groups. After anesthesia, 24 mL of sterile air was injected into the back of the animals, and air was injected for the second time 4 days later. On the 7th day, the blank group and the model group were given 10 mL / kg of the solvent by gavage, the dexamethasone group was given 5 mg / kg of dexamethasone by intraperitoneal injection, the colchicine group was given 5 mg / kg of colchicine by gavage, and the high and low dose groups of Compound A were given 100 mg / kg and 30 mg / kg of Compound A by gavage, respectively. 1 h after administration, 5 mL of normal saline was injected into the back air sac of the rats in the blank group, and 5 mL of 1 mg / mL MSU crystal suspension was injected into the back air sac of the rats in the other groups. After 4 h, the lavage fluid in the air sac was taken. Part of the lavage fluid was used for cytological analysis, and the remaining lavage fluid was centrifuged at 8000 rpm for 15 min. The supernatant was stored at -80 °C for the detection of cytokines IL-1β, IL-6, KC and TNFα. The test results were expressed as mean±SEM and statistically analyzed by t-test. Test results: See Tables 17 and 18 below. Table 17 White blood cell count results (mean±SEM, n = 8) Note: Compared with the blank group: ** P < 0.01, *** P < 0.001; compared with the model group: ＄ P < 0.05, ＄＄ P < 0.01, ＄＄＄ P < 0.001 Table 18 Cytokine results (mean±SEM, n = 8) Note: Compared with the blank group: * P < 0.05, ***P < 0.001; compared with the model group: ＄ P < 0.05, ＄＄ P < 0.01, ＄＄＄ P < 0.001 From the experimental results, it can be seen that dexamethasone and colchicine can significantly inhibit the total number of cells and the number of neutrophils in the lavage fluid induced by MSU. Compound A can significantly inhibit the total number of cells and the number of neutrophils in the lavage fluid at oral doses of 30 mg / kg and 100 mg / kg. Dexamethasone can significantly inhibit the increase of IL-1β, IL-6, KC and TNFα induced by MSU, and compound A can significantly inhibit the increase of IL-6, KC and TNFα at an oral dose of 100 mg / kg. This experiment proves that compound A has good anti-inflammatory effects in the MSU-induced air sac test. Experimental Example 10 URAT1 (Urate Transporter 1) Experiment Test articles: Compound A: Prepared by Example 2, Compound B: Prepared by Example 1, Compound D: Prepared by Example 4; Experimental method: 1. Prepare a 5 mM stock solution of the compound with dimethyl sulfoxide (DMSO) for later use. There are 8 concentrations in this experiment, and the final concentrations are 5000 nM, 1250 nM, 312.5 nM, 78.1 nM, 19.5 nM, 4.9 nM, 1.2 nM, and 0.3 nM respectively. 2. Preparation method of buffer solution: Chloride-free HBSS buffer (125 mM sodium gluconate, 4.8 mM potassium gluconate, 1.3 mM calcium gluconate, 1.2 mM KH2PO4, 1.2 mM MgSO4, 5.6 mM glucose, 25 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES) (pH 7.4)); lysis solution (100 mM NaOH) 3. Obtain transfected cells stably expressing human urate transporter 1 (hURAT1): Place human embryonic kidney cells (HEK-293T) in a cell culture plate containing complete medium, incubate at 5% CO2 and 37 °C for 24 h, wash the cells with phosphate buffer (PBS), and digest with trypsin to prepare a single-cell suspension. Take 8×10 6The cells were placed in a cell culture plate, and then TransIT-293 Reagent: DNA complexes (1.5 ml of Opti-MEM I Reduced-Serum Medium, 15 μg of plasmid DNA, 45 μL of TransIT-293 Reagent, mixed well and incubated at room temperature for 30 min) were added dropwise to different regions of the cell culture plate. The cell culture plate was gently shaken to make the TransIT-293 Reagent: DNA complexes evenly distributed, and incubated at 5% CO2 and 37 °C for 48 h. In 4 hURAT1-transfected cells 14 14C-labeled uric acid uptake experiment: (1) hURAT1 transfected cells were seeded into a Poly-D-lysine 96-well microplate at a cell density of 6×10 4 / well and incubated overnight at 5% CO2 and 37 °C. (2) 12 h after the cells were seeded into the Poly-D-lysine 96-well microplate, the cells were washed 3 times with pre-warmed chlorine-free HBSS buffer, 200 μl / well, and the washing solution in the microplate was removed. (3) Chlorine-free HBSS buffer containing Uric acid[8-14C] (0.1 μCi / well) was added, 50 μl / well, and then the test compound was added, 5 μl / well, and incubated at 37 °C for 5 min. (4) The incubation buffer was removed and 100 μl of ice-cold chlorine-free HBSS buffer was added to terminate the Uric acid[8-14C] uptake reaction. (5) The plate was washed 3 times with chlorine-free HBSS buffer and the buffer in the wells was removed. (6) 50 μl / well of lysis buffer was added and shaken at 600 rpm for 10 min. (7) The microplate was placed on a centrifuge and centrifuged at 1000 rpm for 5 min, and then 45 μl of the supernatant was aspirated into an Isoplate-96 Microplate. (8) 150 μl / well of Ultima Gold TM XR scitillation cocktail was added and shaken at 600 rpm for 10 min. The Isoplate-96 microplate was placed in a MicroBeta Trilux (PerkinElmer) for detection 14 of the radioactivity of 14C. 5 Calculate the IC 50 value Inhibition rate (%) = (positive control signal intensity - compound signal intensity) / (positive control signal intensity - negative control signal intensity) × 100. Analysis was performed using GraphPad Prism 5.0 software to obtain the IC 50 value. Experimental results: See Table 19. Table 19 Results of the inhibitory effect of the compounds of the present invention on hURAT1 activity lesinurad*, this compound is a new drug for the treatment of gout developed by AstraZeneca and approved by the FDA in December 2015. Its chemical name is 2-[[5-bromo-4-(4-cyclopropyl-1-naphthalenyl)-4H-1,2,4-triazol-3-yl]thio]acetic acid. As can be seen from Table 19, the compounds of the present invention have good inhibitory effects on hURAT1 (human urate transporter 1). Example 1: Preparation of 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione (Compound B) (1) Preparation of 7-allyl-2-amino-1H-purin-6-(7H)-one Dissolve guanosine (2000 g, 7.07 mol) and allyl bromide (1950.5 g, 16.20 mol) in DMSO (100 mL). Under nitrogen protection, stir at room temperature for 18 hours. Add 37% concentrated hydrochloric acid (5 L) to the solution, stir for 1 hour, add 2 L of methanol, and then neutralize with 2N sodium hydroxide solution until a solid precipitates. Filter, and dry the filter cake in an oven to obtain a white solid (1210 g, yield 89.6%). (2) Preparation of 7-allyl-1H-purine-2,6-(3H,7H)-dione Dissolve 7-allyl-2-amino-1H-purin-6(7H)-one (1200 g, 6.28 mol) in acetic acid (3 L) and water (750 mL). Drop an aqueous solution (600 mL) of sodium nitrite (1732 g, 25.1 mol) into the above system, react and stir for 3 h, concentrate the reaction solution to one-third, let it stand, precipitate a solid, filter, and dry the filter cake to obtain a pale yellow solid (875 g, yield: 72.8%). (3) Preparation of 7-allyl-3-butyl-1H-purine-2,6-(3H,7H)-dione 7-Allyl-1H-purine-2,6-(3H,7H)-dione (400 g, 2.08 mol), n-butyl iodide (422 g, 2.29 mol) and potassium carbonate (345 g, 2.50 mol) were dissolved in anhydrous DMF (1.6 L). The reaction mixture was stirred for 24 h, ethyl acetate (2 L) and 2N dilute hydrochloric acid (500 mL) were added, and extraction was carried out. The organic phase was dried and concentrated to obtain a pale yellow solid (185 g, yield 35.9%). (4) Preparation of 7-allyl-3-butyl-8-chloro-1H-purine-2,6-(3H,7H)-dione 7-Allyl-3-butyl-1H-purine-2,6-(3H,7H)-dione (160 g, 0.645 mol) was dissolved in anhydrous DMF (800 mL), NCS (94.7 g, 0.71 mol) was added, and the reaction was stirred for 24 h under nitrogen protection. After concentration, 200 mL of ethyl acetate was added, and recrystallization was carried out. Filtration was carried out, and the filter cake was dried to obtain a pale yellow solid (110.2 g, yield 60.5%). (5) Preparation of 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione The crude product of 7-allyl-3-butyl-8-chloro-1H-purine-2,6-(3H,7H)-dione (565 mg, 2.0 mmol), tetrakis(triphenylphosphine)palladium (104 mg, 0.09 mmol) and morpholine (775 mg, 8.9 mmol) were dissolved in 20 mL of dichloromethane, and the reaction was carried out at room temperature for 12 h under nitrogen protection. After concentration, silica gel column chromatography (petroleum ether∶ethyl acetate = 1:1) was carried out to obtain 80 mg of a pale yellow solid, with a yield of 16.5%. Molecular formula: C9H 11 ClN4O2; Molecular weight: 242.1; Mass spectrum (M+H): 243.0 1 1H-NMR (DMSO-d6, 400 MHz): 0.85 (t, 3H), 1.23 - 1.27 (m, 2H), 1.54 - 1.59 (m, 2H), 3.81 (t, 2H), 11.17 (s, 1H), 14.25 (br.s, 1H). Example 2: Preparation of 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione (Compound A) (1) Preparation of 7-allyl-2-amino-1H-purin-6(7H)-one Guanosine (200 g, 0.707 mol) and allyl bromide (19.51 g, 0.162 mol) were dissolved in DMSO (1000 mL). Under nitrogen protection, the mixture was stirred at room temperature for 18 hours. 37% concentrated hydrochloric acid (500 mL) was added to the solution and stirred for 1 hour. Then 2 L of methanol was added, and the solution was neutralized with 2 N sodium hydroxide solution until a solid precipitated. The solid was filtered and dried in an oven to obtain a white solid (125 g, yield 92.5%). (2) Preparation of 7-allyl-1H-purine-2,6-(3H,7H)-dione 7-Allyl-2-amino-1H-purin-6-(7H)-one (120 g, 0.628 mol) was dissolved in acetic acid (1.5 L) and water (150 mL). An aqueous solution (300 mL) of sodium nitrite (173.2 g, 2.51 mol) was added dropwise to the above system, and the reaction was stirred for 3 h. The reaction solution was concentrated to one-third, allowed to stand, and a solid precipitated. The solid was filtered and dried to obtain a pale yellow solid (85 g, yield 70.5%). (3) Preparation of 7-allyl-8-chloro-1H-purine-2,6-(3H,7H)-dione 7-Allyl-1H-purine-2,6-(3H,7H)-dione (2.10 g, 10.9 mmol) was dissolved in anhydrous DMF (12 mL), and N-chlorosuccinimide (1.60 g, 12.0 mmol) was added. The reaction was stirred under nitrogen protection for 6 hours. The system was poured into water, extracted with ethyl acetate, and concentrated to obtain 1.20 g of a crude pale yellow solid. (4) Preparation of 7-allyl-3-pentyl-8-chloro-1H-purine-2,6-(3H,7H)-dione The crude product of 7-allyl-8-chloro-1H-purine-2,6-(3H,7H)-dione (750 mg) and sodium carbonate (383 mg, 3.61 mmol) were dissolved in anhydrous DMF (10 mL), and 1-iodopentane (690 mg, 3.48 mmol) was added. The reaction was stirred for 24 hours. The system was poured into water, and ethyl acetate (100 mL) and 2 N dilute hydrochloric acid (50 mL) were added for extraction. The organic phase was dried and concentrated to obtain 500 mg of a crude pale yellow oil. (5) Preparation of 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione For the specific method, refer to (5) in Example 1. The target compound (80 mg) was obtained with a yield of 4.6%. Molecular formula: C 10 H 13 ClN4O2; Molecular weight: 256.1; Mass spectrum (M+H): 257.1 1 1H-NMR (DMSO-d6, 600 MHz): 0.83 (t, 3H), 1.19 - 1.29 (m, 4H), 1.57 - 1.60 (m, 2H), 3.84 (t, 2H), 11.19 (s, 1H), 14.38 (br.s, 1H). Example 3: Preparation of 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione (Compound C) (1) Preparation of 8-chloro-1-methyl-3-butyl-7-(2-propen-1-yl)-1H-purine-2,6-(3H,7H)-dione 8-Chloro-3-butyl-7-(2-propen-1-yl)-1H-purine-2,6-(3H,7H)-dione (565 mg, 2.0 mmol) and potassium carbonate (304 mg, 2.2 mmol) were added to N,N-dimethylformamide (15 mL), then methyl iodide (341 mg, 2.4 mmol) was added. The reaction was carried out at 80 °C for 12 hours, dissolved in ethyl acetate, washed once with 2N dilute hydrochloric acid solution and saturated brine successively, dried, concentrated, and 400 mg of a crude brown product was obtained. (2) Preparation of 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione The crude product of 8-chloro-1-methyl-3-butyl-7-(2-propen-1-yl)-1H-purine-2,6-(3H,7H)-dione (400 mg), tetrakis(triphenylphosphine)palladium (104 mg, 0.09 mmol) and morpholine (775 mg, 8.9 mmol) were dissolved in 20 mL of dichloromethane. The reaction was carried out at room temperature for 12 hours under nitrogen protection, concentrated, and purified by silica gel column chromatography (petroleum ether∶ethyl acetate = 2∶1) to obtain 112 mg of a pale yellow solid. The overall yield of the two steps was 23.1%. Overall yield: 23.1%. Molecular formula: C 10 H 13 ClN4O2; Molecular weight: 256.1; Mass spectrum (M+H): 257.0 1H-NMR (DMSO-d6, 400 MHz): 0.88 (t, 3H), 1.27 - 1.32 (m, 2H), 1.60 - 1.65 (m, 2H), 3.23 (s, 3H), 3.92 (t, 2H), 14.45 (s, 1H). Example 4: Preparation of 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione (Compound D) The specific method was referred to Examples 1 - 3, and 120 mg of the target compound was obtained with a two-step yield of 26.3%. Molecular formula: C 11 H 15 ClN4O2; Molecular weight: 270.1; Mass spectrum (M + H): 271.1 1 H-NMR (DMSO-d6, 400 MHz): 0.86 (t, 3H), 1.25 - 1.33 (m, 4H), 1.62 - 1.67 (m, 2H), 3.23 (s, 3H), 3.92 (t, 2H), 14.45 (br.s, 1H). Example 5: Preparation of 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione (Compound E) The specific method was referred to Examples 1 - 3. 1 H-NMR (DMSO-d6, 400 MHz): 0.90 (d, 6H), 1.47 - 1.62 (m, 3H), 3.86 (t, 2H), 11.18 (br.s, 1H), 14.38 (br.s, 1H). Example 6: Preparation of 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione (Compound F) The specific method was referred to Examples 1 - 3. 1 H-NMR (DMSO-d6, 400 MHz): 0.00 - 0.06 (m, 2H), 0.36 - 0.42 (m, 2H), 0.67 - 0.77 (m, 1H), 1.60 (q, 2H), 4.06 - 4.10 (m, 2H). Example 7: Preparation of 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione monohydrate (1) Preparation of 7-allyl-2-amino-1H-purin-6(7H)-one Dissolve guanosine (4000 g, 14.1 mol) and allyl bromide (3900 g, 32.2 mol) in 11 L of DMSO, stir at room temperature for 24 hours. Add 7500 mL of 37% concentrated hydrochloric acid to the solution, stir for 1 hour, add 20 L of methanol, and then neutralize with saturated sodium hydroxide solution until a solid precipitates. Filter, wash the solid with water, and dry the filter cake in an oven to obtain a white solid (1585 g, yield 58.7%). (2) Preparation of 7-allyl-1H-purine-2,6-(3H,7H)-dione Dissolve 7-allyl-2-amino-1H-purin-6-(7H)-one (1584 g, 8.29 mol) in acetic acid (8.5 L) and water (1500 mL). Dropwise add an aqueous solution of sodium nitrite (2277 g, 33 mol) into the above system, stir the reaction overnight. There is a solid, filter, wash the solid with water, and dry the filter cake to obtain a white solid (1086 g, yield 68.2%). (3) Preparation of 7-allyl-8-chloro-1H-purine-2,6-(3H,7H)-dione Dissolve 7-allyl-1H-purine-2,6-(3H,7H)-dione (2166.3 g, 11.3 mmol) in anhydrous DMF (8 L), add N-chlorosuccinimide (1657 g, 12.4 mmol), stir the reaction under nitrogen protection for 24 hours. Add EA, cool, filter by suction, wash the solid with EA, and dry to obtain a white solid (1804 g, yield 70.6%). (4) Preparation of 7-allyl-3-pentyl-8-chloro-1H-purine-2,6-(3H,7H)-dione Dissolve 7-allyl-8-chloro-1H-purine-2,6-(3H,7H)-dione (200 g, 0.88 mol) in anhydrous DMF (1.2 L), add sodium carbonate (116.6 g, 1.1 mol), add 1-iodopentane (173 g, 0.87 mol), stir the reaction for 4 days. Pour the system into water, a solid precipitates, filter by suction, wash the solid with n-hexane slurry, filter by suction, and dry to obtain a white solid (197 g, yield 75.2%). (5) Preparation of 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione monohydrate Dissolve 7-allyl-3-pentyl-8-chloro-1H-purine-2,6-(3H,7H)-dione (96 g, 0.32 mol), tetrakis(triphenylphosphine)palladium (13 g, 0.011 mmol), and N,N-dimethylbarbituric acid (253 g, 1.62 mol) in 1 L of dichloromethane. React at room temperature for 12 hours under nitrogen protection. Filter by suction. Dissolve the solid in an aqueous sodium hydroxide solution, wash with dichloromethane. Adjust the pH of the aqueous phase to 4 with dilute HCl. A solid precipitates. Filter by suction and dry the solid to obtain 60 g of a white solid with a yield of 67.7%. Molecular formula: C 10 H 15 ClN4O3; Molecular weight: 274.1; Mass spectrum (M+H): 257.1 1 1H-NMR (DMSO-d6, 400 MHz): 0.84 - 0.86 (t, 3H), 1.28 (m, 4H), 1.63 (m, 2H), 3.85 (t, 2H), 11.22 (s, 1H), 14.38 (br.s, 1H).

Claims

1. A compound represented by the following formula (I), a pharmaceutically acceptable salt thereof, or a solvate thereof, which is used for preventing or treating uric acid and / or gouty diseases, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups, and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by a halogen atom, a cyano group, or a C 3-7 cycloalkyl; R3 is selected from a halogen atom and a cyano group.

2. The compound, a pharmaceutically acceptable salt thereof, or a solvate thereof according to claim 1, wherein, R1 represents hydrogen or methyl, R2 represents ethyl, cyclopropyl ethyl, cyclopropyl methyl, propyl, 2-methylpropyl, butyl, 3-methylbutyl or pentyl, R3 represents a fluorine atom or a chlorine atom.

3. The compound, a pharmaceutically acceptable salt thereof, or a solvate thereof according to claim 1, wherein, The compound is selected from: 8-chloro-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-butyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-pentyl-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(2-methylpropyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-3-(cyclopropylmethyl)-3,7-dihydro-1H-purine-2,6-dione, 8-chloro-1-methyl-3-(3-methylbutyl)-3,7-dihydro-1H-purine-2,6-dione, and 8-chloro-1-methyl-3-(2-cyclopropylethyl)-3,7-dihydro-1H-purine-2,6-dione.

4. The compound, a pharmaceutically acceptable salt thereof, or a solvate thereof according to any one of claims 1 to 3, which is a hydrate.

5. The compound, a pharmaceutically acceptable salt thereof, or a solvate thereof according to any one of claims 1 to 4, wherein, The uric acid or gouty disease is hyperuricemia, gout, gouty inflammation, pain or uric acid nephropathy.

6. The compound, a pharmaceutically acceptable salt thereof, or a solvate thereof according to claim 5, wherein, The hyperuricemia includes primary hyperuricemia and secondary hyperuricemia.

7. The compound, pharmaceutically acceptable salt or solvate thereof according to claim 5, wherein, The gout includes primary gout and secondary gout.

8. The compound, pharmaceutically acceptable salt or solvate thereof according to claim 5, wherein, The gouty inflammation includes acute gouty arthritis, subcutaneous tophus and chronic tophaceous arthritis.

9. The compound, pharmaceutically acceptable salt or solvate thereof according to claim 5, wherein, The pain includes acute pain, chronic pain, intractable pain and cancer pain.

10. The compound, pharmaceutically acceptable salt or solvate thereof according to claim 5, wherein, The uric acid nephropathy includes acute uric acid nephropathy, chronic urate nephropathy and uric acid urolithiasis.

11. The compound represented by the following formula (I), pharmaceutically acceptable salt or solvate thereof, which is used for reducing uric acid, wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by halogen atoms, cyano groups, C 3-7 cycloalkyl; R3 is selected from halogen atoms, cyano groups.

12. The compound represented by the following formula (I), pharmaceutically acceptable salt or solvate thereof, which is used for anti - inflammation. wherein R1 is selected from hydrogen, C 1-4 alkyl, wherein the C 1-4 alkyl is unsubstituted or optionally substituted by one or more halogen atoms, cyano groups and CF3; R2 is selected from C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl, wherein the C 1-10 alkyl, C 2-6 alkenyl, C 2-6 alkynyl is unsubstituted or optionally substituted by halogen atoms, cyano groups, C 3-7 cycloalkyl; R3 is selected from halogen atoms, cyano groups.

13. A pharmaceutical composition comprising the compound, pharmaceutically acceptable salt or solvate thereof according to any one of claims 1 - 12. A method for preventing or treating a disease, comprising the step of administering to a mammal in need of such treatment a compound, a pharmaceutically acceptable salt thereof or a solvate thereof according to any one of claims 1-12.