Technical Field The present invention relates to a 2-phenyIpyridine derivative useful as a medicament, particularly a therapeutic or preventive agent for diseases in which xantine oxidase participates, such as hyperuricemia, gout,inflammatory bowel diseases, diabetic kidney diseases, and diabetic retinopathy.Background Art [0002]Abnormal increase in blood uric acid level, i.e., hyperuricemia is a disease which closely relates to gout, renal, dysfunction, urolithiasis, and the like (Shindan toChiryo, 2002, 90(2), 244-248 and Shindan to Chiryo, 2002,90(2), 220-224). Also, in organ transplantation (Ren. Fail. 2002 May; 24(3): 361-7) and chemotherapy of cancers (Am. J.Health Syst. Pharm. 2003 Nov 1; 60(21): 2213-22), it is known that serum uric acid level is remarkably increased andrenal dysfunction is induced (tumor lysis syndrome and thelike) . The therapeutic drugs for hyperuricemia are roughlydivided into uric acid-excretion accelerators and uric acidsynthesis inhibitors. However, since the action is reduced in. the uric acid-excretion accelerators when renal functiondecreases, allopurinol (Nippon Rinsho, 1996 Dec; 54(12):3364-8 and Nippon Rinsho, 2003; 61, Suppl. 1: 197-20) whichis a uric acid-synthesis inhibitor is suitably used forpatients having decreased renal function (Guideline fortherapy of hyperuricemia/gout, Japanese Society of Gout andNucleic Acid Metabolism, Therapeutic Guideline 2002) .Xanthine oxidase is an enzyme directing biosynthesis of uricacid, and xanthine oxidase inhibitors which inhibit theenzyme is effective, as uric acid-synthesis inhibitors, fortherapy of hyperuricemia and various diseases attributablethereto. Allopurinol employed in clinical use is only one xanthine oxidase inhibitor which is in practical use, at present.n the other hand, xanthine oxidase is known to havea role as an active oxygen-producing enzyme (Drug Me tab.Rev. 2004 May; 36(2): 363-75). Active oxygen is a exacerbation factor of morbid conditions, which causes DNAand cell damage and also induces inflammatory cytokine production (Free Radic. Biol. Med. 2001 May 15; 30(10): 1055-66). For example, it is known that active oxygen deeply participates in autoimmune and inflammatory diseasessuch as ulcerative colitis and Crohn's disease (Scand. J. Gastroenterol. 2001 Dec; 36(12): 1289-94) and ischemia re^jerfusion disorder (Biochem. Biophys. Res. Commun. 2004 Mar 5; 315(2): 455-62). Furthermore, recently, in diabetickidney diseases (Curr. Med. Res. Opin. 2004 Mar; 20(3) : 369- 79), heart failure (J. Physiol. 2004 Mar 16; 555 (Ft 3): 589-606, Epub 2003 Dex 23) , cerebrovascular disorder (Stroke, 1989 Apr; 20(4): 488-94), and the like, it is suggested thatactive oxygen participates in as one of exacerbation factors. Moreover, in diabetic retinopathy, it is known that an increase in vascular endothelial growth factor (VEGF) in the vitreous body deeply participates in morbid condition and an increase in expression of VEGF through oxidatin stress occurs under morbid conditions (Curr Drug Targets. 2005 Jun; 6(4): 511-24). Since a xanthine oxidase inhibitor inhibits production of active oxygen, it is effective in treatment of these diseases. Actually, it hasbeen reported that allopurinol is effective in ulcerativecolitis (Aliment. Pharmacol. Ther. 2000 Sep; 14(9): 1159-62), angiopathy involved in diabetes (Hypertension, 2000Mar; 35(3): 746-51), and chronic heart failure (Circulation,2002 Jul 9; 106(2): 221-6) in human. As above, although allopurinol which is a xanthine oxidase inhibitor is reported to have effectiveness for various diseases, severe adverse effects such as Stevens- Jolinson syndrome, toxic epidermal necrolysis, hepatopathy,and renal dysfunction have been reported (Nippon Rinsho,2003; 61, Suppl. 1: 197-201). As one cause thereof, it ispointed out that allopurinol has a nucleic acid-likestructure and inhibits pyrimidine metabolic pathway (LifeSci. 2000 Apr 14; 66(21): 2051-70). Accordingly, it is highly desired to develop a highly safe and highly effectivexanthine oxidase inhibitor having a non-nucleic acidstructure.[0003] Hitherto, compounds having xanthine oxidaseinhibitory activity have been reported. For example, as xanthine oxidase inhibitors, there have been reported phenyl-substituted azole compounds such as 2-phenylthiazole derivatives (Patent Documents 1, 2, and 3), 3- phenylisothiazole derivatives (Patent Documents 4 and 5) phenylpyrazole derivatives (Patent Documents 6, 7, and 8),2-phenyloxazole derivatives (Patent Document 9), and phenylimidazole derivatives (Patent Document 9). On the other hand, it is described that a compound represented by the following formula (II) has a uric acidexcreting action and is useful for therapy of hyperuricemia (Non-Patent Document 1) . However, there are neither disclosure nor suggestion of the xanthine oxidase-inhibitory ac tion and uric acid-synthesis inhibitory action in the do cument. Moreover, it is suggested that a compound represented by the following general formula (III) is effective as antiinflammatory, antipyretic, analgesic, and diuretic agents (Patent Document 10). wherein the groups COX and OY are ortho to each other and [A.r] is para to either COX or OY; [Ar] represents benzene or the like, R represents alkyl, halogen, alkoxy, cyano, nitro, or the like, a halogen atom, lower alkyl, or the like, X represents -OH, -NH2, alkylamino, or the like, Y represents a hydrogen atom, alkyl, alkenyl, aralkyl, or the like, and R1 represents a hydrogen atom or alkyl; see the publication foi further information. In addition, it is disclosed that a compound represented by the following formula (IV) has antiinflammatory and analgesic actions (Non-Patent However, in any of Patent Document 10 and Non-Patent Document 2, there are neither disclosure nor suggestion of the xanthine oxidase-inhibitory action and uric acidsynthesis inhibitory action. Patent Document 1: W092/09279 Patent Document 2: JP-A-2002-105067 Patent Document 3: W096/31211 Patent Document 4: JP-A-57-85379 Patent Document 5: JP-A-6-211815 Patent Document 6: JP-A-59-95272 Patent Document 7: W098/18765 Patent Document 8: JP-A-10-310578 Patent Document 9: JP-A-6-65210 Patent Document 10: DE2031230 Non-Patent Document 1: Annali di Chimica Applicata, Italy, 1931, Vol. 21, p. 553-558 Non-Patent Document 2: Journal of Medicinal Chemistry, USA, 1971, Vol. 14, p. 339-344 Disclosure of the Invention Problems that the Invention is to Solve [0007] An object of the invention is to provide a highly safe and novel therapeutic or preventive agent for hyperuricemia, gout, inflammatory bowel diseases, diabetic kidney diseases, or diabetic retinopathy based on an excellent xanthine oxidase-inhibitory action. Means for Solving the Problems [0008] As a result of extensive studies on compounds having a acanthine oxidase-inhibitory action, although a xanthine oxddase-inhibitory action has been hitherto not known on 2- phenylpyridinecarboxylic acid derivatives, the present in-ventors have confirmed that a 2-phenylpyridine derivative represented by the following general formula wherein the pyoridine ring is substituted with a carboxyl group or the Ii3ulfonyl ester formation. [0028] The compound (I) thus produced is isolated and purified as its free form or a salt thereof, the salt being produced by carrying out a usual salt formation treatment. The isolation and purification are carried out by employing usually used chemical techniques such as extraction, concentration, evaporation, crystallization, filtration, recrystallization and various types of chromatography. Various isomers can be isolated in the usual way making use of the difference in physicochemical properties between corresponding isomers. For example, optical isomers can be separated from each other by a general optical resolution method such as fractional crystallization after conversion of a racemic compound into a diastereomer salt with an optically active organic acid (tartaric acid or the like) or chromatography using a chiral packing material. A.ISO, an optical isomer can be produced starting from an appropriate optically active starting compound. In this connection, a mixture of diastereomers can be separated by fractional crystalization or chromatography. [0029] (Test method) The advantages of the compound of the invention are confirmed by the following pharmacological tests. 1. Xanthine oxidase-inhibitory activity (1) Preparation of test compound A test compound was dissolved in DMSO (manufactured by Nakarai) so as to be a concentration of 10 mM and then used after the concentration was adjusted to an aimed one at use. (2) Measuring method The evaluation of xanthine oxidase-inhibitory activity of the compound of the invention was carried out using a method described in a document (Free Radic. Biol. Med. 6, 607-615, 1992) with partial modification. Namely, xanthine oxidase (derived from butter milk, manufactured by Sigma) was adjusted to 0.03 units/ml using a 50 mM phosphate buffer and was added to a 96-well plate in an amount of 50 Hi/well. Each test compound diluted so as to be a final concentration was added thereto in an amount of 2 ill/well, followed by treatment at room temperature for 20 minutes. Pterin (manufactured by Sigma) was added thereto so as to be a final concentration of 5 pM, followed by reaction at room temperature for 10 minutes. Measurement was performed using a micropiate reader saphire (manufactured by Tecan) under conditions of excitation at 345 nm and emission at 390 run (pterin was oxidized by xanthine oxidase into i soxanthopterin, which emitted a light under the c onditions). The concentration of the test compound at which 50% inhibition was observed (IC50 value) was calculated, the emissions of isoxanthopterin under conditions of the presence or absence of xanthine oxidase being 0% inhibition and 100% inhibition, respectively. The compounds of the invention had good xanthine oxidase-inhibitory activity. The IC50 values of representative compounds of Examples are shown in the From the above test, it was confirmed that the compounds of the invention had potent xanthine oxidaseinhibitory activity. [0031] 2 . Serum uric acid-lowering action A test compound was orally administered compulsorily t o ICR mice using an oral sonde. After 2 hours, 6 hours, and, depending on the compound, further 24 hours from the administration, blood was collected from an abdominal aorta and then serum was separated in a usual manner. Serum uric acid was measured on an absorptiometer (SPECTRA MAX 190, manufactured by Molecular Device) by an uricase method using a uric acid-measuring kit (Uric Acid C-TestWako: Wako Pure Chemical Industries, Ltd.) and a uric acid-lowering ratio was determined according to the following equation. Uric acid-lowering ratio (%) = (Uric acid level of control animal - Uric acid level of test compound-administered animal) x 100/Uric acid level of control animal In the test, an excellent serum uric acid-lowering action of the compounds of the invention was confirmed. For example, the compounds of Examples 4, 35, and 44 showed a uxic acid-lowering ratio of 80% or more after 2 hours from the oral administration thereof in an amount of 1 mg/kg. Moreover, the compounds of the invention exhibited a highly long-acting action and, for example, 50% or more of uric acid-lowering ratio after 24 hours from the administration remained in the compounds of Examples 4, 6, 7, 44, 50, 51, 54, 56, 57, 58, 60, 62, and 84. From the above results, it was revealed that the compounds of the invention had a strong and long-acting s erum uric acid-lowering action. [0032] 3. Acetic acid-induced enteritis-suppressing action One ml of 3% acetic acid was administered into the rectum of a Wistar rat of 2 days of fasting. A group wherein 1 ml of physiological saline had been administered instead of acetic acid was separately prepared as a normal group. Thereafter, to the 3% acetic acid-administered group, a test compound or 0.5% methyl cellulose (control group) was orally administered once a day and dissection was performed on each administered group on fourth day. A part of the large intestine 2 to 7 cm from the anus side was cut out and incised. After feces were removed by means of tweezers, the part was washed and a score of morbid conditions was evaluated and tissue weight was measured. The score of morbid conditions and a tissue weight increasesuppressing ratio were calculated by the following methods. Score of morbid conditions: feces, general conditions, adhesion, perforation, cell death, ulcer, edema, and xaegacolon each was evaluated and point-rated with dividing i nto four stages. Tissue weight increase-suppressing ratio (%) = 100 - { (Tissue weight of test compound-administered group - Tissue weight of normal group) / (Tissue weight of control group rissue weight of normal group) x 100} As a result, as compared with the normal group wherein physiological saline had been administered into the rectum, deterioration of the score of morbid conditions and remarkable erosion and resulting intestinal tissue weight increase were observed in the 3% acetic acid-administered group. On the other hand, when the test compoundadministered group was compared with the control group, significant improvement in the score of morbid conditions and suppression of intestinal tissue weight increase were observed in the test compound-administered group in comparison with the control group. For example, the compounds of Examples 4 and 45 suppressed 70% or more of the intestinal tissue weight increase when administered in an amount of 10 mg/kg. From the above results, the effectiveness of the compound of the invention on ulcerative colitis was shown. [0033] 4. Trinitrobenzenesulfonic acid-induced enteritisinhibitory action The effectiveness of the compound of the invention on an enteritis model can be also evaluated by a model using trinitrobenzenesulfonic acid (TNBS) as an inducing agent instead of acetic acid (Cell. Mol. Biol, 38, 189-199, 1992). Thus, referring to the method described in the report, the enteritis-suppressing action of the compound of the invention was evaluated. Namely, TNBS or physiological saline as a normal grxoup was administered into the rectum of male Wistar rats of 200 to 250 g. Thereafter, a test compound or 0.5% methyl cellulose (control group) was orally administered once a day and dissection was performed on each administered group on 21st day. A part of the large intestine 2 to 7 cm from the anus side was cut out and incised. After feces were removed by means of tweezers, the part was washed and a score of morbid conditions was evaluated and tissue weight was measured. The score of morbid conditions and a tissue weight increase-suppressing ratio were calculated as in the evaluation method of the above acetic acid-induced enteritis-suppressing action. As a result, as compared with the normal group wherein physiological saline had been administered into the rectum, deterioration of the score of morbid conditions and remarkable erosion and resulting intestinal tissue weight increase were observed in the TNBS-administered group. On the other hand, when the test compound-administered group was compared with the control group, significant improvement in the score of morbid conditions and suppression of intestinal tissue weight increase were observed in the test compound-administered group in comparison with the control g- roup. For example, the compound of Example 4 suppressed 7 0% or more of the intestinal tissue weight increase when a.dministered in an amount of 3 mg/kg. From the above results, the effectiveness of the compound of the invention on ulcerative colitis was shown. As above, from the test results of 3 and 4, it was revealed that the compounds of the invention had a strong antiinflammatory action. [OO34] 5 . Pyrimidine synthetic pathway-inhibitory action Allopurinol which is an existing hyperuricemia therapeutic drug is known to cause renal dysfunction as an undesirable action. As mentioned previously, since allopurinol has a nucleic acid-like structure, as one cause thereof, it is presumed that it inhibits pyrimidine synthetic pathway. In recent studies on xanthine oxidase inhibitors, there have been desired compounds which do not influence pyrimidine synthetic pathway. For example, it has been reported that the comparative compound 3 has reduced BUN (Blood Urea Nitrogen) concentration-increasing action, which is an index of renal dysfunction, as compared with al-lopurinol (Research Communications in Molecular Pathology and. Pharmacology, 104(3), 293-305, (1999)). Thus, according to the method described in the document, the influence of the compounds of the invention on a BUN level was confirmed. As a result, it was found that the influence of the compounds of the invention on the BUN level was small. For e*xample, the compounds of Examples 4 and 45 exhibited no inhibitory action at an oral administration of 30 mg/kg. From the above results, since the compounds of the invention do not inhibit the pyrimidine synthetic pathway, there was revealed an advantage that the compounds do not exhibit adverse effects based thereon. [0035] 6. AKR1C3 inhibitory action AKR1C3 known as a molecule belonging to aldo-keto reductase is known as a multifunctional enzyme (Jikken Igaku 23, 90-97, 2005). There is expected the application of a compound inhibiting AKR1C3 to various morbid conditions including inflammatory diseases (Mol. Pharmacol 67, 60-68, 2O05) (Current Pharmaceutical Design 10, 3505-3524, 2004) (J. Biol. Cham 273, 1855-1888, 1998). As a result of testing the presence of AKR1C3 (17f)HSD5) inhibitory activity on the compounds of the invention according to the method described in DELFIA (registered trademark) Testosterone Reagents R050-201 (manufactured by Perkin Elmer) , it was found that the compounds surprisingly have inhibitory activity against the enzyme. For example, the compound of Example 4 showed an IC50 value of 1 pM or less. From the above results, the compound of the invention was suggested to be compounds having an inflammatory action independently of xanthine oxidase inhibition. Therefore, the compound of the invention is expected as an antiinflammatory drug having a high efficacy. [0036] 7. Diabetic retinopathy model The efficiency of the compound of the invention on diabetic retinopathy was tested by the method described in European Journal of Pharmacology 458 (2003) 283-289 (except that: the animal used in the experiment was male Wistar rat, 10 weeks old) . Streptozotocin (STZ) was administered to the animals to be tested and increase in blood sugar level was confirmed after 24 hours. Thereafter, the animals were divided into a 0.5% methyl cellulose-administered group (control group) and 3O mg/kg test compound-administered group and oral administration was performed once a day for 7 days. As a result, as compared with the normal rats, a remarkable increase of VEGF mRNA in the vitreous body was observed in the control group. On the other hand, in the group to which the compound of the invention had been administered, suppression of increase of VEGF mRNA was observed as compared with the control group. For example, the Example compound 4 exhibited a significant suppressing acti-on. These results showed the efficiency of the compound of: the invention on diabetic retinopathy. [0037] From the above tests, the following were confirmed: CL) the compound of the invention has a xanthine oxidaseinhi- bitory action and excellent uric acid-lowering action and antiinflammatory action based thereon; (2) the compound of the invention has little influence on the BUN level and hence can avoid adverse effects such as renal dysfunction based on the inhibition of pyrimidine metabolic pathway; (3) the compound of the invention inhibits not only xanthine oxidase but also AKR1C3 and has an excellent profile as an an tiinf lamma tory drug; and (4) the compound of the invention is also effective in diabetic complications such as diabetic retinopathy. Incidentally, the compound of the invention is superior to uric acid-excreting agents in view of the fact that the compound of the invention is also effective in hyperuricemia patients having decreased renal function. [0038] The pharmaceutical composition containing the compound (I) of the invention or a salt thereof as an active ingredient may be prepared using a carrier, an excipient, and other additives generally used in formulation. The administration may be in any form of oral administration by means of tablets, pills, capsules, granules, powders, or liquids or parenteral administration by means of injections such as intravenous injections or intramuscular injections, suppositories, subcutaneous preparations, transnasal preparations, or inhalations. The dose may be suitably determined, depending on individual cases in consideration of the symptom, the age and the sex of the patients of administration targets, but is, in general, from about 0.001 to 100 mg/kg per adult per day in the case of oral administration and this may be administered all at a time or may be divided into a few portions for administration in 2 to 4 times. In the case of intravenous administration, the dose is, in general, from about 0.0001 to 10 mg/kg per adult per time and administration was performed once a day or plurality of times per day. In the case of inhalation, the dose is, in general, from about 0. 0001 to 1 mg/kg per adult per time and administration was performed once a day or plurality of times per day. As the solid composition for oral administration in accordance with the invention, tablets, powders, granules, and the like are used. In such a solid composition, one or more active substances are mixed with at least one inactive excipient, for example, lactose, mannitol, glucose, hydroxypropyl cellulose, microcrystalline cellulose, starch, polyvinylpyrrolidone, magnesium metasilicate aluminate, or th.e like. According to usual methods, the composition may contain inactive additives, for example, a lubricant such as magnesium stearate, a disintegrator such as sodium ca-rboxymethylstarch, and a solubilizing agent. If necessary, the tablets or pills may be coated with sugar coating agents or gastrosoluble or enterosoluble coating ag-ents. [0039] The liquid composition for oral administration includes pharmaceutically acceptable emulsions, solutions, suspensions, syrups, and elixirs, and the like and contains inactive solvents generally used, for example, purified water and ethanol. The composition may contain an auxiliary agent such as a solubilizer, a wetting agent, and a suspending agent, a sweetener, a flavoring agent, an aromatic agent, and a preservative in addition to the inactive solvents. The injections for parenteral administration encompass aseptic, aqueous or non-aqueous solutions, suspensions, and emulsions. The solvents for aqueous solutions include, for example, distilled water for injections and physiological saline. The non-aqueous solvents include, for example, propylene glycol, polyethylene glycol, vegetable oils such as olive oil, alcohols such as ethanol, polysorbate 80 (name in Pharmacopeia) , and the like. Such a composition may further contain an isotonic agent, a preservative, a wetting agent, an emulsifier, a dispersant, a stabilizer, and a solubilizing agent. These may be sterilized, for example, by filtration through a bacteria-retaining filter, blending with germicides, or irradiation. These may be also prepared into aseptic solid compositions and the compositions may be used, after dissolution in aseptic water or aseptic solvents for injections prior to use. [0040] The transmucomembranous preparations such as inhalations and transnasal preparations are used in the form of solid, liquid, or semi-solid, and may be produced in accordance with hitherto known methods. For example, an excipient such as lactose or starch and further a pH regulating agent, an antiseptic, a surfactant, a lubricant, a stabilizer, and a thickening agent may be optionally added thereto. For the administration, an appropriate device for inhalation or blowing can be used. For example, using a known device such as a metered dose-inhaling device or a nebulizer, the compound may be administered solely or as a powder of formulated mixture, or as a solution or suspension in. combination with a pharmaceutically acceptable carrier. A dry powder-inhaling device or the like may be a device for single use or a device for several uses, where a dry power or- a capsule containing a power can be utilized. Alternatively, it may be in the form of a pressurized aenrosol spray wherein an appropriate propellant, for example, a suitable gas such as chlorofluoroalkane, hydrof luoroalkane or carbon dioxide is employed. In the production of suppositories, a low-melting waux, for example, a mixture of fatty acid glycerides or cocoa butter was melted, an active ingredient was added thereto, and the whole was homogeneously dispersed by stirring. Thereafter, the melt was poured into a suitable mold and solidified under cooling. The liquid preparations include solutions, suspensions, supported enemas, and emulsions, for example, water or aqueous propylene glycol solutions. [Examples] [0041] The following will explain the production methods of the compound (I) of the invention in further detail with reference to Examples. The invention is not limited to the invention of the compounds described in the following Examples. Also, production methods of starting materials are shown as Referential Examples. The following abbreviations are used in Referential Examples, Examples, and the following Tables. Ex: Example No.; REx: Referential Example No.; Dat: physicochemical data {F: FAB-MS (M+H)+, FN: FAB-MS (M-H)~, ES: ESI-MS (M+H) + , El: EI-MS (M) + , APN: API-ES-MS (M-H)~, [Compound where (Na) is indicated after the above Mass spectroscopic measured value represents one observed as Na salt and compound where (G-2W) is indicated thereafter represents one observed as glycerin adduct di-dehydrate]; NMR: 5 ppm of characteristic peaks in 1H-NMR in DMSO-d6, NMRC: 5 ppm of characteristic peaks in 1H-NMR in CDC13; Str: structural formula; Syn: Production method (each numeral indicates Example No., at which the compound was similarly produced); Sal: salt (compound not indicated represents a free compound); Me: methyl; Et : ethyl; nPr: n-propyl; iPr: isopropyl; nBu: n-butyl; iBu: isobutyl; tBu: tert-butyl; cBu: cyclobutyl; nPen: n-pentyl; iPen: isopentyl; cPen: cyclopentyl; nHex: n-hexyl, cHex: cyclohexyl; cHep: cycloheptyl; cOct: cyclooctyl, Bn: benzyl; Ph: phenyl; 2Py: 2-pyridyl, and 3Py: 3-pyridyl. [0042] Referential Example 1 5-Bromo-2-hydroxybenzonitrile, isobutyl bromide, and potassium carbonate were heated at 80°C in DMF in the presence of tetra-n-butylammonium bromide to obtain 5-bromo- 2-isobutoxybenzonitrile. F: 254, 256. [0043] Referential Example 2 After 2,2-dimethyl-l-propanol and sodium hydride were stirred at 0°C in DMF, 5-bromo-2-fluorobenzonitrile was added thereto, followed by reaction at room temperature to obtain 5-bromo-2-(2,2-dimethylpropoxy)benzonitrile. NMRC: 3.67 (2H, s), 6.83 (1H, d), 7.64 (1H, d). [0044] Re ferential Example 3 5-Bromo-2-fluorobenzonitrile and piperidine were heated at 80°C in DMSO in the presence of cesium carbonate to obtain 5-bromo-2-piperidin-l-ylbenzonitrile. F: 265. [0045] Referential Example 4 5-Bromo-2-isobutoxybenzonitrile and tr.iisopropylborate were dissolved in a mixed solvent of THF and toluene and an n-butyllithium - hexane solution was adcded dropwise to the solution at a temperature below -60°C. Af-ter the temperature was elevated to -20°C, 1M hydrochloric acid was added, followed by stirring at room temperature to ob-tain (3-cyano-4-isobutoxyphenyl)boronic acid. F: 220. [0046] Referential Example 5 Methyl 2-[4(benzyloxy)-3-cyanophenyl]isonicotinate and. pentamethylbenzene were stirred at room temperature in trdfluoromethanesulfonic acid to obtain methyl 2-(3-cyano-4- hydroxyphenyl)isonicotinate. F: 255. [0047] Referential Example 6 Methyl 3-fluoroisonicotinate was oxidized with 3- chloroperbenzoic acid, followed by heating in the presence of phosphoryl chloride. The product was separated by silica gel column chromatography to obtain methyl 2-chloro-5- fluoroisonicotinate (El: 189) and methyl 2-chloro-3- fluoroisonicotinate (El: 189). [0048] Referential Example 7 Methyl 2- (3-cyano-4-hydroxyphenyl)isonicotinate and N-chlorosuccinimide were stirred at room temperature in acetonitrile to obtain methyl 2-(3-chloro-5-cyano-4- hydroxyphenyl)isonicotinate. ES: 289. [0049] Referential Example 8 Methyl 2-(3-cyano-4-hydroxyphenyl)isonicotinate and N-bromosuccinimide were stirred at room temperature in acetonitrile to obtain methyl 2-(3-bromo-5-cyano-4- hydroxyphenyl)isonicotinate. FN: 333. [0050] Referential Example 9 Sodium hydride was added to a DMF solution of 2,3- difluorobenzonitrile and 2-(methylsulfonyl)ethanol, followed by stirring at room temperature to obtain 3-fluoro-2- hydr oxybenzonitrile. FN: 136. 3-Fluoro-2-hydroxybenzonitrile and Nbromosuccinimide were stirred at room temperature in acetonitrile to obtain 5-bromo-3-fluoro-2- hydroxybenzonitrile. El: 215, 217. [0051] Referential Example 10 (3-Cyano-4-benzyloxy-5-fluorophenyl)boronic acid and methyl 2-chloroisonicotinate were dissolved in a mixed solution of toluene and a 2M aqueous sodium carbonate solution, followed by heating under reflux for 3 hours in the presence of tetrakis (triphenylphosphine) palladium to obtain methyl 2-(3-cyano-4-benzyloxy-5- fluorophenyl)isonicotinate. F: 363. Methyl 2-(3-cyano-4-benzyloxy-5- fluorophenyl)isonicotinate is stirred at room temperature in methanol-THF (1:1) under a hydrogen atmosphere at normal pressure in the presence of palladium-carbon to obtain methyl 2-(3-cyano-5-fluoro-4-hydroxyphenyl)isonicotinate. FN: 271. [0052] Referential Example 11 Methyl 2- (3-cyano-4-hydroxyphenyl)isonicotinate and trifluoromethanesulfonic anhydride were reacted at 0°C in dichloromethane in the presence of diisopropylethylamine to obtain methyl 2-(3-cyano-4- {[(trifluoromethyl)sulfonyl]oxy}phenyl)isonicotinate. F: 387. Referential Example 12 Cesium fluoride and tetrakis(triphenylphosphine)- palladium were added to a 1,2-dimethoxyethane solution of (3-cyano-4-fluorophenyl)boronic acid and methyl 2- chloroisonicotinate, followed by reaction under heating to reflux to obtain methyl 2-(3-cyano-4- f luorop henyl) isonicotinate. F: 257. [0053] Referen tial Examples 13 to 35 The compounds of Referential Examples 13 to 16 were produced in a similar manner to the method of Referential Example I, the compounds of Referential Examples 17 to 21 were produced in a similar manner to the method of Referential Example 2, the compound of Referential Example 22 was produced in a similar manner to the method of Referential Example 3, and the compounds of Referential Examples 23 to 35 were produced in a similar manner to the method of Referential Example 4, using corresponding starting materials. The structure and physicochemical data of the compounds of Referential Examples 13 to 35 are shown in. the following Table 2. [0054] Example 1 (L) In a. mixed solution of 50 ml of toluene and 30 ml of a 2M aqueous sodium carbonate solution were dissolved 1.46 g off (3-cyano-4-isobutoxyphenyl)boronic acid and 1.86 g of methyl 2-chloroisonicotinate, and the resulting solution was heated st 100°C for 1 hour in the presence of 0.49 g of tetrakis (triphenylphosphine)palladium. The reaction 57-- solution was extracted with ethyl acetate and the organic layer was washed with brine and then dried and concentrated under reduced pressure. The residue was purified by silica gel column chromatography (hexane:ethyl acetate:chloroforms?0:15:15) to obtain 1.98 g of methyl 2- (3-cyano-4-isobutoxyphenyl)isonicotinate. (2) Then, 1.98 g of the compound was dissolved in a mixed solution of 30 ml of methanol and 70 ml of THF, and 9 ml of a 1M aqueous sodium hydroxide solution was added thereto, followed by heating at 50°C for 1 hour. After cooling, the resulting solution was neutralized with 1M hydrochloric acid and then extracted with chloroform, followed by washing with brine. After the solution was dried, concentration was performed under reduced pressure and the resulting residue was recrystallized from a mixed solvent of ethanol and water to obtain 1.66 g of 2-(3-cyano-4-isobutoxyphenyl)isonicotinic acid. [0055] Example 2 (1) In 5 ml of DMF were dissolved 82 mg of methyl 2-(3- cyano-4-hydroxyphenyl)isonicotinate and 66 mg of isopropyl iodide, and the resulting solution was heated at 80°C for 3 hours in the presence of 72 mg of potassium carbonate and 10 mg of tetra-n-butylammonium bromide. The reaction solution was cooled and then diluted with water, followed by extraction with ethyl acetate. The organic layer was washed with brine and then dried and concentrated under reduced pressure. The resulting residue was washed with a mixed solvent (hexane : ethyl acetate=10 : 1) to obtain 91 mg of methyl 2- (3-cyano-4-isopropoxyphenyl) isonicotinate . (2) Then, 86 mg of the compound was dissolved in a mixed solution of 3 ml of methanol and 3 ml of THF, and 0.35 ml of a 1M aqueous sodium hydroxide solution was added thereto, followed by heating at 60°C for 1 hour. After being cooled to room temperature, the resulting solution was diluted with diisopropyl ether and water and an aqueous layer was separated. The aqueous layer was neutralized with 1M hydrochloric acid and then extracted with ethyl acetate. After being washed with water, the organic layer was dried and concentrated under reduced pressure to obtain 55 mg of 2- (3-cyano-4-isopropoxyphenyl) isonicotinic acid. [0056] Example 3 (1) In 5 ml of THF were dissolved 63 mg of 3- (methyl thio) -1- propanol and 100 mg of methyl 2- (3-cyano-4- hydroxyphenyl) isonicotinate, and the resulting solution was heated at 0°C for 10 minutes in the presence of 0.15 ml of tributylphosphine and 149 mg of 1,1'- (azodicarbonyl) dipiperidine. Then, the reaction solution was warmed to room temperature and stirred all day and night. After removal of the solvent, water was added and extraction with ethyl acetate was performed. The resulting organic layer is washed with brine and then dried and concentrated under reduced pressure. The resulting residue was purified by silica gel column chromatography (chloroform:methanol=95:5) to obtain 92 mg of methyl 2-{3- cyano-4- [3- (methyl thio) propoxy] phenyl }isonicotinate . (2) Then, 92 mg of the compound was dissolved in a mixed solution of 3 ml of methanol and 3 ml of THF, and 0.32 ml of a 1M aqueous sodium hydroxide solution was added thereto, followed by heating at 60°C for 1 hour. After being cooled, the reaction solution was diluted with diisopropyl ether and an aqueous layer was separated. The aqueous layer was neutralized with 1M hydrochloric acid and then extracted with ethyl acetate. After washing with brine, the organic layer was dried and concentrated under reduced pressure to obtain 81 mg of 2-{3-cyano-4- [3- (methylthio) propoxy] phenyl } isonicotinic acid . [O057] Example 4 (1) In 7 ml of DMSO was dissolved 2.22 g of methyl 2- cyano-4-fluorophenyl)isonicotinate, and 2.44 ml of hexamethyleneimine was added thereto, followed by heating at 5Q°C for 5 hours. After cooling, the reaction solution was diluted with ethyl acetate and was washed with 1M hydrochloric acid, a saturated aqueous sodium hydrogen carbonate solution, and brine, successively. The organic layer was dried and then concentrated under reduced pressure and the resulting residue was dissolved in a mixed solvent of ethyl acetate and diisopropyl ether. Activated carbon was added thereto, followed by stirring for 1 hour. Then, the activated carbon was removed by filtration and washed with ethyl acetate. The resulting filtrate and washing liquid were combined and concentrated to obtain 2.58 g of methyl 2-(4-azepan-l-yl-3-cyanophenyl)isonicotinate. (2) Then, 2.49 g of the compound was dissolved in a mixed solvent of 15 ml of methanol and 30 ml of THF, and 11 ml of a 1M aqueous sodium hydroxide solution was added thereto, followed by heating at 80°C for 1 hour. After cooling, the reaction solution was concentrated under reduced pressure. Then, water was added, followed by washing with diisopropyl ether. The resulting aqueous layer was filtered and then neutralized with 1M hydrochloric acid. The precipitated crystals were collected Toy filtration and washed with water and ethanol, successively. The crude crystals were recrystallized from a mixed solvent of DMSO and water to obtain 2.07 g of a free compound of 2-(4-azepan-l-yl-3-cyanophenyl)isonicotinate. 295 mg of the free compound obtained in a similar manner was suspended in a mixed solvent of 4 ml of ethanol and 2 ml of THF, and 0.46 ml of a 4M hydrogen chloride-ethyl acetate solution was added thereto. After stirring at room temperature for 30 minutes, the precipitated crystals were collected by filtration to obtain 279 mg of 2-(4-azepan-lyl- 3-cyanophenyl)isonicotinic acid monohydrochloride. [0058] Example 5 (1) In 0.4 ml of 1,4-dioxane were dissolved 237 mg of methyl 2-(3-cyano-4-{[(trifluoromethyl)sulfonyl]oxy}phenyl)- isonicotinate and 0.4 ml of heptamethyleneimine, followed by heating at 90°C for 1 hour. After the reaction solution was cooled, purification by silica gel column chromatography (hexane:ethyl acetate:chloroform=80:10:10) was performed to obtain 23 mg of 2- (4-azocan-l-yl-3- cyanophenyl) isonicotinate. (2) Then, 22 mg of the compound was dissolved in a mixed solution of 2 ml of methanol and 2 ml of THF, and 0.15 ml of a 1M aqueous sodium hydroxide solution was added thereto, followed by reaction at room temperature for 2 0 hours. To the reaction solution were added 0.15 ml of 1M hydrochloric acid and 20 ml of water, and the resulting precipitate was collected by filtration. The precipitate was washed with water and then dried to obtain 16 mg of 2-(4-azocan-l-yl-3- cvanophenyl)isonicotinic acid. [O059] Example 6 (1) In 3 ml of DMSO was dissolved 247 mg of methyl 2-(3- c^ano-4-fluorophenyl)isonicotinate, and 0.31 ml of aminomethylcyclohexane was added thereto. After being stirred at 40°C for 17 hours, the reaction solution was diluted with ethyl acetate and washed with water and brine, successively. The organic layer was dried and concentrated under reduced pressure and then recrystallization was performed from a mixed solvent of diisopropyl ether and hexane to obtain 266 mg of methyl 2-{3-cyano-4- [ (cyclohexylmethyl) amino]phenyl}isonicotinate. (2) Then, 266 mg of the compound was dissolved in a mixed solvent of 5 ml of methanol and 10 ml of THF, and 1.14 ml of a 1M aqueous sodium hydroxide solution was added thereto, followed by heating at 80°C for 1 hour. After cooling, the reaction solution was diluted with water and washed with diethyl ether. The resulting aqueous layer was neutralized wi-th 1M hydrochloric acid and extracted with ethyl acetate and the organic layer was dried and concentrated under reduced pressure. The resulting residue was recrystallized from a mixed solvent of ethanol and water to obtain 199 mg of: 2-{3-cyano-4- [ (cyclohexylmethyl) amino]phenyl}isonicotinic acid. Then, 199 mg of the compound was dissolved in 10 ml off ethanol and 0.59 ml of a 1M aqueous sodium hydroxide solution was added thereto. After stirring at room temperature for 15 minutes, the reaction solution was concentrated. The resulting residue was washed with 2- pxropanol to obtain 181 mg of sodium 2-{3-cyano-4- [