CASPASE INHIBITORS BASED ON PYRIDAZINONE SCAFFOLD TECHNICAL FIELD The present invention relates to a pyridazinone derivative or pharmaceutical!y acceptable salt thereof as an inhibitor against various caspases including caspase-I [interleukin-lp-converting enzyme, ICE], caspase-3 [apopain/CPP-32], caspase-8, and caspase-9, and a pharmaceutical composition for the inhibition of caspase comprising the same. BACKGROUND ART Caspase is a new kind of cysteine protease in the form of 1X2P2 tetramer discovered during the last 10 years. About 14 kinds thereof have been known until now. Caspase-1 (ICE), one of them, is a kind of cytokine and participates in converting the biologically inactive prointerleukin-lp to the active interleukin-1 p. Interleukin-1 consists of interleukin-la and interleukin-1p, both of which are synthesized in monocytes in the form of 3IKDa precursor. Only prointerleukin-1 p is activated by ICE. The positions hydrolyzed by caspase-1 are Asp27-Gly2Band Asp,16-Ala"7. The hydrolysis of the latter position gives interleukin-1 p. Interleukin-1 p has been reported to act as an important mediator in causing inflammation (1,3). Caspase-1 has been discovered for the first time in 1989, and the three dimensional structure thereof was determined by X-ray crystal lographic method by two independent study groups. Caspase-3(CPP-32) is broadly studied for its role or mechanism for action, and its three dimensional structure was determined in 1996(2). Caspase-3(apopain) activated from procaspase-3 is hydrolyzed in the position of (P4)Asp-X-X-Asp(P]) motif, and the known substrates include poly(ADP-ribose) polymerase, Ul 70,000 Mr small nuclear ribonucleoprotein, catalytic subunit of 460,000 Mr DNA-dependent protein kinase, etc. The X-ray structure of caspase-7 has been reported to be very similar to that of caspase-3(4). Caspase-8 and 9 are present in the upstream of caspase-3,6,7, and all of these caspases are known to participate in the apoptosis cascade. The X-ray structure of caspase-8 was determined in 1999(5), and particularly the inhibitors thereof may be advantageously used for treating die diseases related to apoptosis. Caspase inhibitors mean those compounds that inhibit the activity of caspase, and so control such symptoms as inflammation, apoptosis, etc. caused by the caspase activity. Diseases or symptoms that may be treated or attenuated by administering the inhibitors include the following: dementia, cerebral stroke, brain impairment due to AIDS, diabetes, gastric ulcer, cerebral injury by hepatitis virus, hepatitis-induced hepatic diseases, acute hepatitis, fulminant hepatic failure, sepsis, organ transplantation rejection, rheumatic arthritis, ischemic cardiac diseases, and liver cirrhosis(6). Among the caspase inhibitors known until now. the most noted irreversible inhibitors are the following: Both the above inhibitors exhibit their activity based on the common mechanism that they irreversibly inactivate the enzyme to suppress the cell apoptosis (irreversible, broad-spectrum inhibitor). It has been reported that irreversible inhibitor has much more effective inhibitory activity than reversible inhibitor (7). Both IDN-1965 of IDUN Co. and MX-1013 of Maxim Co. are reported to show activity in cell apoptosis model for hepatic injury (8, 9). These compounds are now in the stage of preclinical test. The irreversible inhibitor IDN-6556 is now in the stage of phase II clinical trial as a therapeutic agent for hepatic injury (10, 11). References: (1) Inflammation: Basic Principles and Clinical Correlates, 2nded., ed by Gallin, Goldstein and Snyderman. Raven Press Ltd., New York. 1992, pp211-232; Blood, 1996, 87(6), 2095-2147. (2) Wilson, K. P. et al, Nature, 1994, 370. 270; Walker, N. P. C. et al. Cell, 1994, 78, 343; Nature Structural Biology, 1996, 3(7), 619. (3) Thornberry, N. A. et al, Nature, 1992, 356. 768; Nature Biotechnology, 1996, 14, 297; Protein Science, 1995, 4, 3; Nature, 1995, 376(July 6), 37; Protein Science, 1995, 4, 2149. (4) Wei, Y. et al, Chemistry and Biology, 2000, 7, 423. (5) Blanchard H. et al, Structure, 1999, 7, 1125; Blanchard H. et al, J. of Mol. Biol, 2000, 302, 9. (6) References for caspase related diseases Dementia: Arch Neurol 2003 Mar;60(3):369-76, Caspase gene expression in the brain as a function of the clinical progression of Alzheimer disease. Pompl PN, Yemuf S, Xiang Z, Ho L, Haroutunian V, Purohit D, Mohs R, Pasinetti GM. Cerebral stroke: Proc Natl Acad Sci USA 2002 Nov 12;99(23): 15188-93, Caspase activation and neuroprotection in caspase-3-deficient mice after in vivo cerebral ischemia and in vitro oxygen glucose deprivation. Le DA, Wu Y, Huang Z, Matsushita K, Plesnila N, Augustinack JC, Hyman BT, Yuan J, Kuida K, Flavell RA, Moskowitz MA. Brain impairment due to AIDS: J Neurosci 2002 May 15;22(I0):4015-24, Caspase cascades in human immunodeficiency virus-associated neurodegeneration. Garden GA, Budd SL, Tsai E, Hanson L, Kaul M, D'Emilia DM, Friedlander RM, Yuan J, Masliah E, Lipton SA. Diabetes: Diabetes 2002 Jun;51(6):1938-48, Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathway. Cai L, Li W, Wang G, Guo L, Jiang Y, Kang YJ. Gastric ulcer: J Physiol Pharmacol 1998 Dec;49(4):489-500, Role of basic fibroblast growth factor in the suppression of apoptotic caspase-3 during chronic gastric ulcer healing. Slomiany BL, Piotrowski J, Slomiany A. Cerebral injury by hepatitis virus: J Viral Hepat 2003 Mar;10(2):81-6, Cerebral dysfunction in chronic hepatitis C infection. Forton DM, Taylor-Robinson SD, Thomas HC. Fulminant hepatic failure: Gastroenterology 2000 Aug;lI9(2):446-60, Tumor necrosis factor alpha in the pathogenesis of human and murine fulminant hepatic failure. Streetz K, Leifeld L, Gmndmann D, Ramakers J, Eckert K, Spengler U, Brenner D, Manns M, Trautwein C. Sepsis: Nat Immunol 2000 Dec;l(6):496-501, Caspase inhibitors improve survival in sepsis: a critical role of the lymphocyte. Hotchkiss RS, Chang KC, Swanson PE, Tinsley KW, Hui JJ, Klender P, Xanthoudakis S, Roy S, Black C, Grimm E, Aspiotis R, Han Y, Nicholson DW, Karl IE. Organ transplantation rejection: Xenotransplantation 2001 May;8(2):tl5-24, In vitro prevention of cell-mediated xeno-graft rejection via the Fas/FasL-pathway in CrmA-transducted porcine kidney cells. Fujino M, Li XK, Suda T, Hashimoto M, Okabe K, Yaginuma H, Mikoshiba K, Guo L, Okuyama T, Enosawa S. Amemiya H, Amano T, Suzuki S. Rheumatic arthritis: Prog Med Chem 2002;39:1-72, Caspase inhibitors as anti-inflammatory and antiapoptotic agents. Graczyk PP. Ischemic cardiac diseases: Am J Physiol Heart Circ Physiol 2002 Sep;283(3):H990-5, Hypoxia-induced cleavage of caspase-3 and DFF45/ICAD in human failed cardiomyocytes. Todor A, Sharov VG, Tanhehco EJ, Silverman N, Bemabei A, Sabbah HN. Anti-inflammation: J Immunol 2003 Mar 15;I70(6):3386-91, A broad-spectrum caspase inhibitor attenuates allergic airway inflammation in murine asthma model. Iwata A, Nishio K, Winn RK, Chi EY, Henderson WR Jr, Harlan JM. Hepatitis-induced hepatic diseases: i)J Viral Hepat. 2003 Sep;10(5):335-42. Apoptosis in hepatitis C Kountouras J, Zavos C, Chatzopoulos D.; ii) Apoptosis. 2003 Dec;8(6):655-63. Apoptosis participates to liver damage in HSV-induced fulminant hepatitis. Pretet JL, Pelletier L, Bernard B, Coumes-Marquet S, Kantelip B, Motigin C; iii) Proc Natl Acad Sci USA. 2003 Jun 24;100(13):7797-802. Caspase 8 small interfering RNA prevents acute liver failure in mice. Zender L, Hutker S, Liedtke C, Tillmann HL, Zender S, Mundt B, Waltemathe M, Gosling T, Flemming P. Malek NP, Trautwein C, Manns MP, Kuhnel F, Kubicka S. Liver cirrhosis: i) J Pharmacol Exp Ther. 2004 Mar;308(3):l 191-6, The caspase inhibitor Idn-6556 attenuates hepatic injury and fibrosis in the bile duct iigated mouse. Canbay A., Fledstein A., Baskin-Bey E., Bronk FS. Gores GJ.; ii) Hepatology. 2004 Feb;39(2):273-8, Apoptosis: the nexus of liver injury and fibrosis. Canbay A, Friedman S, Gores GJ.; iii) Hepatology. 2003 Nov;38(5): 1188-98, Kupffer cell engulfment of apoptotic bodies stimulates death ligand and cytokine expression. Canbay A, Feldstein AE, Higuchi H, Werneburg N, Grambihler A, Bronk SF, Gores GJ. (7) Wu J. et al, Methods: A Companion to Methods in Enzymohgy, 1999, 17, 320. (8) Hoglen N. C. et al, / of Pharmacoloy and Experimental Therapeutics, 2001, 297,811. (9) Jaeschke H. et al, Toxicology and Applied Pharmacology, 2000, 169, 11. (10) Hoglen N.C. et al, /. Pharmacol Exp. Ther.. 2004, 309(2):634. Characterization of IDN-6556 (3-[2-(2-tert-butyl-phenylaminooxaIyl)-amino]- propionylamino]-4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid): a liver-targeted caspase inhibitor. (11) Canbay A. et al, /. Pharmacol. Exp. Then, 2004, 308(3), 1191. The caspase inhibitor IDN-6556 attenuates hepatic injury and fibrosis in the bile duct Iigated mouse. DETAILED DESCRIPTION OF INVENTION [Technical Subject] The present inventors have extensively studied to design novel compounds which can be used as an effective and more selective inhibitor against caspases. [Means for Solving the Subject! To achieve such a subject, the present inventors synthesized various compounds, and determined their binding ability and inhibitory activity for caspases. As a result, the inventors have discovered that a compound of the following formula (1) does meet such requirements, and completed the present invention. [Formula l] in which R, R1, R\R3, R4, R5, R6, R7 and X are defined below. Therefore, the present invention provides the novel pyridazinone derivative of formula (1) or pharmaceutically acceptable salt thereof having effective inhibitory activity against caspases. It is another object of the present invention to provide a pharmaceutical composition for inhibiting caspase, specifically a composition for preventing inflammation and apoptosis, comprising the compound of formula (1) or pharmaceutically acceptable salt thereof as an active ingredient together with the pharmaceutically acceptable carrier. [Advantageous Effect! The compound of formula (I) according to the present invention has an excellent inhibitory activity against caspase, and so can be advantageously used for the treatment of various diseases and symptoms mediated by caspase. [Best Mode for Carrying Out the Invention] First of all, the important terms in the present invention are defined as follows: a) Q-Q-alkyl: Straight-chain or branched hydrocarbons having 1 to 5 carbon atoms, that include methyl, ethyl, n-propyl, i-propyl, n-butyi, i-butyl, t-butyl, etc., but are not limited thereto. b) GrCio-cycloalkyl: Cyclic hydrocarbons having 3 to 10 carbon atoms, that include cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, etc., but are not limited thereto. c) Aryl: Aryl group includes all the aromatic, heteroaromatic and their partially reduced derivatives. The aromatic group means a 5 to 15-membered single or fused unsaturated hydrocarbon. The heteroaromatic group means the aromatic group containing I to 5 hetero atoms selected from a group consisting of oxygen, sulfur, and nitrogen. The aryl group includes phenyl, naphthyl, indolyl, quinolinyl, isoquinolyl, imidazolinyl, isoxazolyl, oxazolyl, thiazolyl, etc., but is not limited thereto. One or more hydrogens in said C|-C5-alkyl, C3-Ci0-cycloalkyl or aryl group may be replaced with a group(s) selected from the following: acyl, amino, carboalkoxy, carboxy, carboxyamino, cyano, halo, hydroxy, nitro, thio, alky], cycloalkyl, alkoxy, aryl, aryloxy, sulfoxy, and guanido group. d) Natural amino acid includes the following: Glycine, Alanine, Valine, Leucine, Isoleucine, Serine, Threonine, Cysteine, Methionine, Proline, Aspartic acid, Asparagine, Glutamic acid, Glutamine, Lysine, Arginine, Histidine, Phenylalanine, Tyrosine, and Tryptophan. Further, the present specification includes the following abbreviations: N-bromosuccinimide: NBS 0-(7-azabenzotriazol-3-yl)-N,N,N',N'-tetramethyluroniumhexafluorophosphate]: HATU N,N-dimethyl formamide: DMF Dimethylsulfoxide: DMSO N-methylmorpholine: NMM 2,2'~Azobis(2-methyl propionitrile): AIBN 2,2,6,6-TetramethyI-l-piperidinyIoxy, free radical: TEMPO Lithium bis(trimethylsilyl)amide: LiHMDS N-(2-Hydroxyethyl)piperazine-N'-(2'-ethanesulfonic acid): HEPES 3-[(3-Cholamidopropyl)dimethylamino]-1 -propanesulfonate: CHAPS Ethylenediaminetetraacetic acid: EDTA Dithiolhreitol: DTT The present invention will be explained more in detail below. One aspect of the present invention relates to the pyridazinone derivative of the following formula (1): [Formula 1] in which I ) R1 represents H, C]-Cs-alkyl, Cj-Cio-cycloalkyl, aryl, or a side chain residue of all the natural amino acids, II ) R2 represents H, Ci-C5-alkyl, QrQo-cycloalkyl, aryl, or a side chain residue of all the natural amino acids, III JR3 represents H,Ci-C5-alkyl, hydroxy, C|-C5-alkoxy, or halogen, IV) R4represents H, Ci-Cj-alkyl, CrCm-cycloalkyl, or aryl, V ) R' represents H, Cj-Cs-alkyl, C^-Cio-cycloaikyl, or aryl, .) R° and R7 independently of one another each represent H, C]-C5-alkyl, C3-Cio-cycloaIky], or aryl, i) X represents -CH2OR9 (R9 is CrC5-alkyl, C3-C,0-cycloalkyl, or aryl), -CH2OC(=O)R10(R10is Ci-Cs-alkyl, C3-C,o-cycloalkyl, or aryl), -CHrOP(=0}Rn:(Rn is C|-C5-alkyl, QrCio^ycloalkyl, or aryl), or -CH2-W (W is halogen), or pharmaceutical^ acceptable salt thereof, which is useful as an inhibitor for caspase. In the compound of formula (1) according to the present invention, R1 preferably represents a side chain residue of all the natural amino acids, more preferably -CH^COOH. The compound of formula (1) may include the two kinds of stereoisomers, or mixtures thereof (diastereomeric mixtures) when the carbon to which Rl is attached becomes a stereocenter due to the R1 group. The compound of formula (1) may include an ester form (-CO2Y wherein Y is C,-C5-alkyl), a sulfonamide form (-CONHSO:Z wherein Z is Ci-Cs-alkyl), and a pharmaceutically acceptable salt form, when R1 is a side chain residue of an amino acid containing carboxyl moiety; or the compound of formula (1) may also exist in the form of a pharmaceutical ly acceptable salt when R1 is a side chain residue of an amino acid containing a base moiety. The compound of the present invention (formula la) may exist in the form of a cyclic ketal (formula lb) when R1 is -CH2COOH, and so a skilled artisan may understand that the cyclic ketal form (formula lb) may also be covered by the present invention. Formula la Formula lb Also, the equilibrium forms of said compounds should be understood to cover their tautomeric forms. R preferably represents Ci-Cs-alkyl, more preferably methyl, ethyl, n-propyl, i-propyl, n-butyl, i-butyl, or t-butyl. The compound of formula (I) may include the two kinds of stereoisomers, or mixtures thereof (diastereomeric mixtures) when the carbon to which R2 is attached becomes a stereocenter due to the R2 group. The compound of formula (1) may include an ester form (-CO2Y wherein Yis Ci-C5-alkyl), a sulfonamide form (-CONHSO2Z wherein Z is Ci-Cs-alkyl), and a pharmaceutically acceptable salt form, when R" is a side chain residue of an amino acid containing carboxyl moiety; or the compound of formula (1) may also exist in the form of a pharmaceutic ally acceptable salt when R2 is a side chain residue of an amino acid containing a base moiety. R3 preferably represents H, O-CValkyl. G-CValkoxy, or halogen, more preferably H, methyl, ethyl, n-propyl, i-propyl, n-butyl, i-butyl, or t-butyl, methoxy, ethoxy, fluoro, or chloro. R4 preferably represents H. R5 preferably represents Ci-C5-alkyl substituted by substituted or unsubstituted C3-Cio-cycloalkyl or by substituted or unsubstituted aryl; or represents substituted or unsubstituted aryl. R! more preferably represents Ci-Cs-alkyl substituted by C3-Cio-cycloalkyl which is unsubstituted or substituted by one or more substituents selected from the group consisting of Ci-Cs-alkyl, hydroxy, Q-Cralkoxy and halogen, or by aryl which is unsubstituted or substituted by one or more substituents selected from the group consisting of C|-C5-alkyl, hydroxy, C|-C5-alkoxy and halogen; or represents aryl which is unsubstituted or substituted by one or more substituents selected from the group consisting of Ci-Cs-atkyl, hydroxy, C|-C5-alkoxy and halogen. For example, Rs is phenyl, naphthyl, indolyl, quinolinyl, isoquinolyl, imidazolinyl, isoxazolyl, oxazolyl or thiazolyl, or is methyl substituted by phenyl, naphthyl, indolyl, quinolinyl, isoquinolyl, imidazolinyl, isoxazolyl, oxazolyl, thiazolyl or cyclohexyl, each of which is unsubstituted or substituted by one or more substituents selected from the group consisting of methyl, ethyl, n-propyl, i-propyl, n-butyl, i-butyl, t-butyl, methoxy, ethoxy, trihalomethyl and halogen. R6 and R7 each preferably represent H. R preferably represents aryl substituted by one or more halogens, more preferably phenyl substituted by one or more fluorines, and most preferably 2,3,5,6-tetrafluorophenyl, 2,3,6-trifluorophenyl or 2,6-difluorophenyl. Rt0 preferably represents aryl substituted by one or more halogens, more preferably phenyl substituted by one or more chlorines, most preferably 2,6-dichlorophenyl. R11 preferably represents aryl, more preferably phenyl. W preferably represents F. The most preferred compounds are those selected from the following group: 5-fluoro-342-(5-methyl-3-oxo-2-phenyl-2,3-dihydro-pyridazin-4-yl)-butyrylamin o]-4- oxo-pentanoic acid (1); 3-[2-(2-benzyl-5-methyl-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyryIamino]-5-fluor 0-4- oxo-pentanoic acid (2); 3-[2-(2-benzyl-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyrylamino]-5-fluoro-4-oxo-pentanoic acid (3); 3-[2-(2-benzyl-5-ch]oro-3-oxo-2,3-dihydrO'pyridazin-4-y])-butyrylamino]-5-fluor o-4- oxo-pentanoic acid (4); 3-[2-(2'benzyI-5-methoxy-3-oxo-2,3'dihydro-pyridazin-4-yl)-butyrylamino]-5-flu oro-4-oxo-pentanoic acid (5); 3-2-[2-(2-tert-butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamino-5-fl uoro-4-oxo-pentanoic acid (6); 3-2-[2-(3-tert-butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yI]-butyrylamino-5-fl uoro-4-oxo-pentanoic acid (7); 5-fluoro-3-2-[2-(2-melhyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamin o-4- oxo-pentanoic acid (8); 5-fluoro-3-2-[2-(3-methyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamin o-4- oxo-pentanoic acid (9); 5-fluoro-3-2-[2-(3-methoxy-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-y]]-butyrylam ino-4-oxo-pentanoic acid (10); 5-fluoro-3-[2-(2-naphthalen-l-ylmethyl-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyry 1 amino]-4-oxo-pentanoic acid (11); 5-fluoro-3-[2-(2-naphthalen-2-ylmethyl-3-oxo-2,3'dihydro-pyridazin-4-yl)-butyry 1 amino]-4-oxo-pentanoic acid (12); 5-fluoro-3-2-[2-(2-melhyI-oxazol-4-ylmethyl)-3-oxo-2,3-dihydro-pyridazin-4-yI]- butyrylamino-4-oxo-pentanoic acid (13); 5 -fl uoro- 3 -2- [2-(2-methy l-thiazol-4-y lmethy 1)- 3 -oxo-2,3-dihydro-py ridazin-4-y 1 ] - butyryIamino-4-oxo-pentanoic acid (14); 3-2-[2-(3,5-dimethyI-isoxazol-4-ylmethyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-but yryl amino-5-fluoro-4-oxo-pentanoic acid (15); 3-[2-(2-cyclohexylmethyl-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyrylamino]-5-flu oro-4-oxo-pentanoic acid (16); 5-fluoro-3-[2-(2-isoquinolin-l-ylmethyl-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyry 1 amino]-4-oxo-pentanoic acid (17); 3-{2-[2-(2-chIoro-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamino}-5-flu oro-4-oxo-pentanoic acid (18); 3-{2-[2-(3-chloro-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamino}-5-flu oro-4-oxo-pentanoic acid (19); 3-)2-[2-(3-bromo-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamino}-5-flu oro-4-oxo-pentanoic acid (20); 5-fluoro-4-oxo-3-!2-[3-oxo-2-(2-trifluoromethyl-benzyl)-2,3-dihydro-pyridazin-4 -yl]- butyrylamino)-pentanoic acid (21); 5-fluoro-4-oxo-3-{2-[3-oxo-2-(3-txifluoromethyl-benzyl)-2,3-dihydro-pyridazin-4 -yl]- butyry!amino)-pentanoic acid (22); 2,6-dichloro-benzoic acid (S)-3-{(R)-2-[2-(2-tert-butyl-benzyl)-3-oxo-2,3-dihydro- pyridazin-4-yl]-butyrylamino)-4-carboxy-2-oxo-butyl ester and 2,6-dichloro-benzoic acid (S)-3-{(S)-2-[2-(2-tert-butyt-benzyl)-3-oxo-2,3'dihydro-pyridazin-4-yl]-butyrylamino)-4- carboxy-2-oxo-butyl ester (23-1, 23-2); (S)-3-)(R)-2-[2-(2-tert-butyl'benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyryla mino} -4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid and (S)-3-{(S)-2-[2-(2-tert-butyl-benzyl)- 3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamino}-4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid (24-1, 24-2); (S)-3-((R)-2-[2-(3-tert-butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyryla mino}-4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid and (S)-3-{0 = 3:2:1), Li0H.H2O (165 mg, 3.0 eq) was added thereto, and the mixture was heated for about 2 h while stirring. The reaction mixture was neutralized by \N aqueous hydrochloric acid solution, distilled under reduced pressure to almost thoroughly remove tetrahydrofuran. The residue was dissolved in excess ethyi acetate (50 mL), washed with aqueous sodium chloride solution, dried (anhydrous Na2SC>4), and concentrated under reduced pressure to give 356mg (Yield 100%) of the title compound. This compound was used in the next reaction without further purification. Preparation 2-4) 3-t2-(2-Benzyl-5-methyI-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyrylamino]-5-f luoro-4-oxo-pentanoic acid tert-butyl ester A mixture of the carboxylic acid derivative of Preparation 2-3) (153 mg, 0.535 mmol), 3-amino-5-fluoro-4-hydroxy-pentanoic acid tert-butyl ester (see Tetrahedron Letters, 1994, 55(52), 9693-9696, 133 mg, 1.2 eq) and HATU (265 mg, 1.3 eq) was cooled to 0°C, triethylamine (0.30 mL, 4.0 eq) was added thereto in DMF solvent (5 mL), and the mixture was reacted for one day. The solvent was distilled under reduced pressure. The residue was extracted with ethyl acetate (30 mL x 2), washed with water, aqueous sodium hydrogen carbonate solution and aqueous sodium chloride solution, dried (anhydrous Na2S04), and concentrated under reduced pressure. The residue was separated by column chromatography (40-60% ethyl acetate-hexane) to give 233 mg (92%) of 3-[2-(2-benzyl-5-methyl-3-oxo-2,3-dihydro-pyridazin-4-yl)butyrylamino]-5-fluoro-4-hydr oxy-pentanoic acid tert-butyl ester. To this compound and Dess-Martin reagent (312 mg, 3.0 eq) was added anhydrous dichloromethane (4 mL), which was then stirred for 1 h at room temperature. The reaction was stopped by isopropyl alcohol (1 mL). The solid was removed by celite fiitration under reduced pressure, and extracted with ethyl acetate (20 mL x 2), The extract was washed with water, saturated aqueous sodium hydrogen carbonate solution and aqueous sodium chloride solution, dried (anhydrous Na^SC^), and concentrated under reduced pressure. The residue was separated by column chromatography (30-40% ethyl acetate-hexane) to give 201 mg (79%) of the title compound. 'H-NMR (500MHZ, CDCl3) 5 8.13(br s, 1H), 7.62(s, 1H), 7.38-7.25(m, 5H), 5.38-5.20(m, 2H), 5.20-4.80(m, 2H), 4.80-4.68(m, 1H), 3.76(m, 1H), 2.88-2.57(m, 2H), 2.26(s, 3H), 2.26-1.98(m, 2H), 1.41(m, 9H), 0.87(m, 3H) Example 2) 3-[2-(2-Benzyl-5-methyl-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyrylaniiiio]-5-f luoro-4-oxo-pentanoic acid The compound of Preparation 2-4) (198 mg, 0.418 mmol) was dissolved in dichloromethane (4 mL), and trifluoroacetic acid (2 mL) was added at 0°C. The mixture was stirred for 1 h, during which it was slowly warmed to room temperature. The mixture was concentrated under reduced pressure, and separated by column chromatography (10% methanol-dichloromethane) to give 175 mg (stoichiometric yield, white powder) of the title compound. lH-NMR (500MHz, DMSO-, 8.70-8.63(dd, 1H), 7.85(m, 1H), 7.78(m, 1H), 7.30(m, IH), 5.24-4.97(m, 4H). 4.59-4.46{m, 1H), 3.63(m, IH), 2.82-2.47(m, 2H), 2.30(s, 3H), 1.73-1.63(m, 2H), 0.83(m, 3H) Preparation 14-1) 2-[2-(2-Methyl-thiazo]-4-ylmethyl)-3-oxo-2,3-dihydro-pyridazin-4-yI]-butyric acid ethyl ester The compound of Preparation 6-6) (98 mg, 0.47 mmol) and 4-bromomethyl-2-methyJ-thiazoie (112 mg, 1.3 eq, Lancaster) were reacted according to the same procedure as Preparation 2-1) to give the title compound (101 mg, 67%). 'H-NMR (500MHZ, CDC13) 5 7.79(d, IH), 7.20(d, IH), 7.05(s, IH), 5.45-5.37(ABq, 2H), 4.20-4.10(m, 2H), 3.88(t, IH), 2.68 (s, 3H), 1.96 & l.Slftwo m, 2H), 1.22{t, 3H), 0.95(t, 3H) Preparation 14-2) 5-Fluoro-3-2-[2-(2-methyl-thiazol-4-ylmethyl)-3-oxo-2,3-dihydro-pyridazin-4-yi]-butyrylamino-4-oxo-pentanoic acid tert-butyl ester The compound of Preparation 14-1) (101 mg, 0.31 mmol) was reacted according to the same procedure as Preparation 3-5) to give the title compound (32 mg, 21%). 'H-NMR (500MHz, CDC13) 5 7.83(two d, IH), 7.58(m, 2H), 7.20-7.03(m, 2H), 5.51-4.69(m, 5H), 3.75(m, IH), 2.93-2.62(m, 2H), 2.64(m, 3H), 2.12(m, IH), 1.66(m, IH), 1.41 & I.38(m, 9H),0.94(m, 3H) Example 14) 5-Fluoro-3-2-[2-(2-methyl-thiazol -4-y I methyl )-3-oxo-2,3-dihy dro-py r idazin-4-yl]-butyrylamino-4-oxo-pentanoicacid The compound of Preparation 14-2) (32 mg, 0.066 mmoi) was reacted according to the same procedure as Example 2) to give the title compound (16 mg, 58%). 'H-NMR (500MHZ, CDCb) 5 7.82(m, 1H), 7.80-7.76(dd, 1H), 7.25(s, 1H), 7.12(m, 1H), 6.07-6.91(m, 1H), 5.15-4.57(m, 4H), 3.90(m, 1H), 2.92-2.75(m, 2H), 2.67(s, 3H), 2.22-1,67(m, 2H), 0.97(m, 3H) Preparation 15-1) 2-[2-(3,5-Dimethyl-isoxazol-4-ylmethyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-bu tyric acid ethyl ester The compound of Preparation 6-6) (96 mg, 0.46 mmol) and 4-chloromethyl-3,5-dimethyl-isoxazole (86 mg, 1.3 eq, Aldrich) were reacted according to the same procedure as Preparation 2-1) to give the title compound (119 mg, 82%). 'H-NMR (500MHZ, CDC13) 5 7.71(d, 1H), 7.18(d, 1H), 5.10-5.02(ABq, 2H), 4.20-4.10(m, 2H), 3.85(t, 1H), 2.46(s, 3H), 2.32(s, 3H), 1.98-1.74(two m, 2H), 1.22(t, 3H), 0.95(t, 3H) Preparation 15-2) 3-2-[2-(3,5-Dimethyl-isoxazol-4-y]methyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamino-5-fluoro-4-oxo-pentanoic acid tert-butyl ester The compound of Preparation 15-1) (119 mg, 0.37 mmol) was reacted according to the same procedure as Preparation 3-5) to give the title compound (47 mg, 40%). 'H-NMR (400MHZ, CDC13) 5 7.79(two d, 1H), 7.48(m, IH), 7.21(d, 2H), 5.30-4.79(m, 5H), 3.77(m, IH), 2.97-2.69(m, 2H), 2.54(two s, 3H), 2.36(s, IH), 2.16(m, IH), 1.72(m, 1H), 1.47 & 1.42(two s, 9H), 0.99(m, 3H) Example 15) 3-2-[2-(3,5-Dimethyl-isoxazol-4-ylmethyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyrylamino-5-fluoro-4-oxo-pentanoic acid The compound of Preparation 15-2) (47 mg, 0.098 mmol) was reacted according to the same procedure as Example 2) to give the title compound (27 mg, 66%). 'H-NMR (500MHZ, DMSO~d6) 5 8.64(br s, IH), 7.86(dd, IH), 7.28(m, IH), 5.32-4.91(m, 2H), 5.08-4.96(m, 2H), 4.56-4.47(m, IH), 3.66(m, IH), 2.63-2.32(m, 2H), 2.37(s, 3H), 2.16{s, 3H), 1.72-1.63(m, 2H), 0.82(m, 3H) Preparation 16-1) 2-(2-Cyclohexylmethyl-3-oxo-2,3-dihydro-pyridazin-4-y!)-butyric acid ethyl ester The compound of Preparation 6-6) (101 mg, 0.48 mmol) and bromomethyl-cyclohexane (111 mg, 1.3 eq, Aldrich) were reacted according to the same procedure as Preparation 2-1) to give the title compound (82 mg, 56%). 'H-NMR (500MHZ, CDC13) 6 7.71(d, 1H), 7.16(d, 1H), 4.20-4.10(m, 2H), 4.14-3.94(m, 2H), 3.86(1, IH), 1.98-1.74(two m, 2H), I.72-t.60(broad m, 5H), 1.23(t, 3H), 1.20-1.16(broadm, 3H), 1.05-1.00(m, 2H), 0.96(t, 3H) Preparation 16-2) 3-[2-(2-Cyclohexylmethyl-3-oxo-2,3-dihydro-pyridazin-4->,l)-butyrylamino]-5 -fIuoro-4-oxo-pentanoic acid tert-butyl ester The compound of Preparation 16-1) (80 mg, 0.26 mmol) was reacted according to the same procedure as Preparation 3-5) to give the title compound (106 mg, 88%). 'H-NMR (500MHz, CDCI3) 5 7.77(m, IH), 7.64(m, IH), 7.l4(m, IH), 5.29-4.724), and concentrated under reduced pressure to give 2,6-dichloro-benzoic acid (S)-4-tert-butoxycarbonyl-3-{2-[2-(2-tert-butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl] -butyryl amino |-2-hydroxy-butyl ester. To this compound and Dess-Martin reagent (260 mg, 2.0 eq) was added anhydrous dichloromethane (4 mL), which was then stirred for 0.5 h at room temperature. The reaction was stopped by isopropy] alcohol (1 mL). The solid was removed by ceiire nitration under reduced pressure, and extracted witn etnyl acetate (20 mL x 2). The extract was washed with water, saturated aqueous sodium hydrogen carbonate solution and aqueous sodium chloride solution, dried (anhydrous Na^SO*), and concentrated under reduced pressure. The residue was separated by column chromatography (20-25% ethyl acetate-hexane) to give 163 mg (78%) of the title compound. 'H-NMR (500MHZ, CDC13) 5 7.84 (m, 1H), 7.62(m, 1H), 7.43(t, 1H), 7.34-7.25(m, 4H), 7.16(m, 1H), 7.06(t, 1H), 6.83-6.74(two d, 1H), 5.86-5.52(m, 2H), 5.22-4.81(m, 3H), 3.86(m, 1H), 2.89-2.62(m, 2H), 2.02(m, 1H), 1.75 (m, 1H), 1.49 & 1.48(twos, 9H), 1.41 & 1.37(twos, 9H), 0.99(m, 3H) Example 23-1) and 23-2) 2,6-Dichloro-benzoic acid (S)-3-{(R)-2-[2-(2-tert-butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl}-butyrylamino j-4-carboxy-2-oxo-butyl ester and 2,6-Dichloro-benzoic acid {S)-3-{(S)-2-[2-(2-tert-butyI-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl}-butyrylamino} -4-carboxy-2-oxo-butyl ester The compound of Preparation 23-3) (159 mg, 0.29 mmo!) was reacted according to the same procedure as Example 2) to give the title compound as a mixture of two diastereomers, which was then separated by Prep-TLC (70% EtOAc/Hexane) to give 62 mg (42%) and 50 mg (34%) of each diastereomer. The compound with lower polarity on TLC was assigned as Example 23-1 and the compound with higher polarity as Example 23-2, but their specific diastereomer forms were not identified. Compound with lower polarity: 'H-NMR (500MHZ, DMSO-rfs) 5 8.78(br, 1H), 7.93(m, 1H), 7.56-7.52(m, 3H), 7.40(m, 1H), 7.34ft, 1H), 7.1 l(m, 1H), 7.05(m, 1H), 6.67(d, 1H), 5.58-5.42(ABq, 2H), 5.30-4.60(br m, 3H), 4.58 & 4.50(two br m, 1H), 3.72(m, 1H), 2.70-2.50(br, 2H), 1.82-1.63{m, 2H), 1.40(m, 9H), 0.85(m, 3H) (Example 23-J) Compound with higher polarity: 'H-NMR (500MHZ, DMSO-40 5 8.74(br, 1H). 7.93(m, 1H), 7.57-7.51(m, 3H), 7.40(d, 1H), 7.34(d, 1H), 7.1 l(m, 1H), 7.02(m, 1H), 6.67(d, 1H), 5.56-5.43(ABq, 2H), 5.26-5.00(br m, 2H), 4.72(m, 1H), 3.70(m, 1H), 2.76-2.50(br, 2H), 1.82-1.63(m, 2H), 1.38(s, 9H), 0.85(1, 3H) (Example 23-2) Preparation 24-1) tert-butyl (3S)-3-amino-4-hydroxy-5-(2,3,5,6-tetrafluorophenoxy)pentanoate N-benzyloxycarbonyJ-p -r-butyl-aspartic acid (J 7.9 g, 55.5 mmol) and 2,3,5,6-tetrafluorophenol were reacted according to the same procedure as Preparation 23-1) and 23-2) to give 13.2 g (68%) of the title compound. 'H-NMR (400 MHz, DMSO-d6) 5 8.2 (br, 2H), 7.6-7.5(m, 1H), 5.9(m, 1H), 4.3-4.1(m, 3H), 3.6(m, 1H), 2.7(m, 1H), l,4(s,9H) Preparation 24-2) {S)-3-{(R)-2-[2-(2-tert-Butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyr ylamino)-4-oxo-S-(2,3,5,6-tetrafluoro-phenoxy)-pentanoJc acid tert-butyl ester and; (S)-3-{(S)-2-[2-(2-tert-Butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyry lamino}-4-oxo-5-{2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid tert-butyl ester The compound of Preparation 6-8) (104 mg, 0.29 mol) was hydrolyzed according to the same procedure as Preparation 2-3) to give the carboxylic acid derivative. A mixture of this carboxylic acid derivative (95 mg, 0.29 mmol), the compound of Preparation 24-1) (113 mg, 1.2 eq) and HATU (143 mg, 1.3 eq) was cooled to 0°C, triethylamine (0.16 mL, 4.0 eq) was added thereto in DMF solvent (5 mL), and the mixture was reacted for 2 h. The solvent was distilled under reduced pressure. The residue was extracted with ethyl acetate (30 mL x 2), washed with water, aqueous sodium hydrogen carbonate solution and aqueous sodium chloride solution, dried (anhydrous Na^SO^, concentrated under reduced pressure, and preliminarily purified by Prep-TLC (500% EA/Hexane) to give 172 mg (89%) of (S)-3-{2-[2-(2-tert-butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]'butyrylaminoJ-4-hydr oxy-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid tert-butyl ester. To this compound and Dess-Martin reagent (220 mg, 2.0 eq) was added anhydrous dichloromethane (4 mL), which was then stirred for 1 h at room temperature. The reaction was stopped by isopropyl alcohol (1 mL). The solid was removed by celite filtration under reduced pressure, and extracted with ethyl acetate (20 mL x 2). The extract was washed with water, saturated aqueous sodium hydrogen carbonate solution and aqueous sodium chloride solution, dried (anhydrous Na.2SOi), and concentrated under reduced pressure. The residue was purified by Prep-TLC (30% EA/Hexane) to give 74 mg (38%) of the title diastereomer with lower polarity and 67 mg (35%) with higher polarity. Diastereomer with lower polarity; 'H-NMR (500MHz. CDCh) 5 7.83(d, 1H), 7.59(d, 1H), 7.42(d, 1H), 7.22(d, 1H), 7.17(t, 1H), 7.06(t, 1H), 6.76(m, 1H), 6.73(d, 1H), 5.65(Abq, 2H), 5.I9-5.02(Abq, 2H), 4.75(m, 1H), 3.81(dd, IH), 2.76(dd, 1H), 2.59(dd, 1H), 2.19(m, 1H), 1.73(m, 1H), 1.48(s, 9H), 1.34(s, 9H),0.98(t,3H) Diastereomer with higher polarity: 'H-NMR (500MHz, CDClj) 8 7.83(d, IH), 7.61(d, IH), 7.39(d, IH), 7.23(d, IH), 7.14(t, IH), 7.05(t, IH), 6.78(d, IH), 6.72(m, IH), 5.74-5.58(Abq, 2H), 5.07-4.83(Abq, 2H), 4.82(m, IH), 3.80(dd, 3H), 2.89(dd, IH), 2.68(dd, IH), 2.16(m, )H), 1.75(m. !H), 1.48(s, 9H), 1.39(s, 9H), 0.96(t, 3H) Example 24-1) and 24-2) (S)-3-{(R)-2-[2-(2-tert-Butyl-benzyI)-3-oxo-2,3-dihydro.pyridaziii-4-yI]-butyr ylamino}-4-oxO'5-(2,3,5,6-tetrafluorO'phenoxy)-pentanoic acid and (S)-3-{(S)-2-[2-(2-tert-Butyl-beozyl)-3-oxo-2,3-dihydro-pyridazin-4.yl]-butyry lamino} -4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid The compound with lower polarity prepared in Preparation 24-2) (74 mg, 0.11 mmol) was reacted according to the same procedure as Example 2) to give one of the title compounds (58 mg, 87%) which was assigned as Example 24-1). 'H-NMR (500MHZ, CDCb) 5 7.9] (d, 1H), 7.43(d, IH), 7.39(bs, IH), 7.18(t. 1H). 7.05{t, IH), 6.75(m, IH), 6.70(d, IH), 5.65(s, 2H), 5.40-4.50(m, 3H), 3.95(m, IH), 3.01(m, IH), 2.55(m, IH), 2.13(m, IH), 1.73(m, IH), 1.47(s, 9H), 0.97(t, 3H) (Example 24-1) The compound with higher polarity prepared in Preparation 24-2) (67 mg, 0.10 mmol) was reacted according to die same procedure as Example 2) to give the other of the title compounds (60 mg, 98%) which was assigned as Example 24-2). 'H-NMR (500MHz, CDCI3) S 7.91(d, IH), 7.42(d, IH), 7.3I(bs, IH), 7.16(t, IH), 7.03(t, 1H), 6.75(m, )H), 6.70(d, 1H), 5.65(s, 2H). 4.89-4.03(m, 3H), 3.76(m, 1H), 2.99(m, lH),2.70(m, 1H), 2.12(m, 1H), 1.75(m, 1H), 1.48(s, 9H), 0.97(t, 3H) (Example 24-2) Preparation 25-1) (S)-3-{2-[2-(3-tert-Butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yI]-butyryla mino}-4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid tert-butyl ester The compound of Preparation 7-2) (135 mg, 0.38 mmol) was reacted according to the same procedure as Preparation 24-2) to give the title compound (198 mg, 79%). 'H-NMR (50OMHZ, CDCI3) 5 7.79(two d, 1H), 7.63(m, 1H), 7.42(two s, 1H), 7.32-7.14(m, 4H), 6.73(m, 1H), 5.43-5.2 l(m, 2H), 5.20-4.71(m, 3H), 3.77(m, 1H), 2.93-2.59(m, 2H), 2.15(m, 1H), 1.69(m, 1H), 1.43 & 1.40(two s, 9H),1.29(s, 9H), 0.95(m, 3H) Example 25-1) and 25-2) (S)-3-{(R)-2-[2-(3-tert-Butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyr ylamino)-4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid and (S)-3-{(S)-2-[2-(3-tert-Butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyry lamino}-4-oxo-5-(2,3,5,6-tetrafluoro-phenoxy)-pentanoic acid The compound of Preparation 25-1) (75 mg, 0.11 mmoi) was reacted according to the same procedure as Example 2) to give the title compound as a mixture of two diastereomers, which was then separated by Prep-TLC (70% EtOAc/Hexane) to give 31 mg (44%) of a diastereomer with lower polarity (Example 25-1} and 33 mg (48%) of a diastereomer with higher polarity (Example 25-2). Diastereomer with lower polarity: 'H-NMR (500MHZ, DMSO-40 5 S.70(m, 1H), 7.87(d, 1H), 7.50(m, 1H), 7.30(s, 1H), 7.24(d, 2H), 7.18(m, 1H), 6.97(m, 1H), 5.24-5.03(m, 4H), 4.64-4.52(m, 1H), 3.6S(m, !H), 2.68-2.58(m, 2Hj, I.73(m, IH), I.63(m, IH), 1.19(s, 9H), 0.82(m, 3H) (Example 25-1) Diastereomer with higher polarity: 'H-NMR (500MHZ, DMSO-ck) 5 8.66(m, IH), 7.87(d, IH), 7.50(m, IH), 7.30(s, IH), 7.25(two d, 2H), 7.16(m, IH), 6.96(m, IH), 5.23-4.90(m, 4H), 4.63-4.54(m, IH), 3.68(m, IH), 2.68-2.50(m, 2H), 1.73(m, IH), 1.63(m, 1H), 1.19(s, 9H), 0.82(m, 3H) (Example 25-2) Preparation 26-1) (S)-2-Amino-succinic acid 4-tert-butyl ester 1-methyl ester hydrochloride To Cbz-Asp(0-tert-Bu)-OH.H20 (5.00 g, 14,6 mmol) and K2C03 (4.05 g, 2.0 eq) were added DMF (100 mL) and Mel (2.74 mL, 3 eq), which was then stirred for 2-3 h at room temperature. The solvent was distilled under reduced pressure. The residue was extracted with ethyl acetate (100 mL x 2), washed with water, aqueous sodium hydrogen carbonate solution and aqueous sodium chloride solution, dried (anhydrous Na2S04), and concentrated under reduced pressure. The residue was purified by column chromatography (30% ethyl acetate/he xane) to give (S)-2-benzyIoxycarbonylamino-succinic acid 4-tert-butyl ester 1-methyl ester in a stoichiometric yield. This compound was dissolved inMeOH {100 mL), c-HCl (1.1 mL, 1.0 eq) was added, and subjected to debenzyloxycarbonylation (Pd/C) for 40 min under hydrogen balloon, whereby giving 3.28 g (96%) of the title compound. Preparation 26-2) (S)-2-{2-E2-(2-tert-Butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyryla minoj-succinic acid 4-tert-butyl ester 1-methyl ester The compound of Preparation 6-8) was hydrolyzed according to the same procedure as Preparation 2-3) to give the carboxylic acid derivative. A mixture of this carboxylic acid derivative (938 mg, 2.86 mmol), the compound of Preparation 26-1) (753 mg, 1.1 eq) and HATU (1.41 g, 1.3 eq) was cooled to 0°C, triethylamine (2.00 mL, 5.0 eq) was added thereto in DMF solvent (18 mL), and the mixture was reacted for I h at room temperature. The solvent was distilled under reduced pressure. The residue was extracted with ethyl acetate (50 mL x 2), washed with water, aqueous sodium hydrogen carbonate solution and aqueous sodium chloride solution, dried (anhydrous Na?S04>, and concentrated under reduced pressure. The residue was purified by column chromatography (50% ethyl acetate-hexane) to give 1.24 g (84%) of the title compound. 'H-NMR (400MHZ, CDC13) 5 7.84(dd, 1H), 7.48(d, 1H), 7.41-7.32(dd, 1H), 7.30(d, 1H), 7.23(m, 1H), 7.14(m, IH), 6.92-6.83(dd, IH), 5.76-5.65(m, 2H), 4.82(m, 1H), 3.91(m, 1H), 3.76,3.6S(two s, 3H), 2.92-2.63(m, 2H), 2.19(m, 1H), 1.76(m, 1H), 1.55(s, 9H), 1.46,1.42(two s, 9H), 1.02(m, 3H). Preparation 26-3) (S)-S-Bromo-3-{2-[2-(2-tert-butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl)-butyryIamino}-4-oxo-pentanoic acid tert-butyl ester The compound of Preparation 26-2) (1.24 g, 2.41 mmol) was hydrolyzed according to the same procedure as Preparation 2-3) to give the carboxylic acid derivative (1.15 g, 95%). To this carboxylic acid derivative (1.15 g, 2.30 mmol) and NMM (0.28 mL, 2.53 mmol) was added anhydrous tetrahydrofuran (20 mL) under nitrogen atmosphere, which was maintained at O'C. Isobutylchioroformate (0.31 mL, 2.42 mmol) was added, and the mixture was stirred for about 30 min. To the reaction mixture maintained at 0°C was added diazomethane-ether solution (synthesized from 4.0 eq of l-methyl-3-nitro-l-nitroso-guanidine, 40 mL), which was then stirred for 4 h at 0°C to give the diazoketone derivative. 30% HBr/AcOH (1.02 mL, 2.0 eq) was added thereto at 0°C, and stirred for 30 min. The reaction mixture was extracted with ethyl acetate, washed with water, twice with saturated aqueous sodium hydrogen carbonate solution, and aqueous sodium chloride solution, dried (anhydrous Na2SO,|), and concentrated under reduced pressure to give the bromomethylketone derivative (1.30 g, 98%). This compound was used in the next reaction without further purification. 'H-NMR (500MHz, CDClj) 6 7.84(dd, 1H), 7.63-7.58(dd, 1H), 7.43(d, 1H), 7,25-7.17(m, 2H), 7.09(m, 1H), 6.83-6.75{dd, 1H), 5.74-5.62{m, 2H), 4.9l,4.82(two m, lH),4.12-3.93(m, 2H), 3.79(m, 1H), 2.91-2.60(m, 2H), 2. J7(m, JH), 1.74(m. !H), 1.49(s, 9H), 1.40,1.36(two s, 9H), 0.97(m, 3H). Preparation 26-4) (S)-3-{2-[2-(2-tert-Butyl-benzyl)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyryla mino}-4-oxo-5-(2,3,6-trifluoro-phenoxy)-pentanoic acid tert-butyl ester The compound of Preparation 26-3) (100 mg, 0.17 mmol) and 2,3,6-trifluorophenol (31 mg, 1.2 eq) were dissolved in dimethylformamide (2 mL), KF (25 mg, 2.5 eq) was added thereto, and the mixture was stirred for 4 h at room temperature. The residue obtained by concentration under reduced pressure was extracted with ethyl acetate, washed with water, twice with saturated aqueous sodium hydrogen carbonate solution, and aqueous sodium chloride solution, dried (anhydrous Na^SCXO, and concentrated under reduced pressure. The residue was purified by Prep-TLC (70% ethyl acetate/hexane) to give 77 mg (69%) of the title compound. 'H-NMR (500MHZ, CDCl3) 5 7.82(m, 1H), 7.56(in, 1H), 7.42(t, 1H), 7.23(t, 1H), 7.16(m, 1H), 7.06(m, 1H), 6.82-6.73(m, 3H), 5.76-5.55(m, 2H), 5.10-4.78(m, 3H), 3.82(m, 1H), 2.94-2.60(m, 2H), 2.16(m, 1H), 1.73(m, 1H), 1.46(s, 9H), L39,1.34(two s, 9H), 0.95(m, 3H). Example 26-1) and 26-2) (S)-3-{(R)-2-[2-(2-tert-Butyl-benzy1)-3-oxo-2,3-dihydro-pyridazin-4-yl]-butyr ylamino}-4-oxo-5-(2,3,6-trifluoro-phenoxy)-pentanoic acid and (S).3-j(S)-2-[2-f2-tert-Buty]-benzy])-3-oxo-2,3-dihydro-pyridazin-4->']]-but3'ry lamino}-4-oxo-5-(2,3.6-trifluoro-phenoxy)-pentanoicacid The compound of Preparation 26-4) (77 mg, 0.12 mmol) was reacted according to the same procedure as Example 2) to give the title compound as a mixture of two diastereomers, which was then separated by Prep-TLC (50% ethyl acetate/hexane) to give 24 mg (34%) of a diastereomer with lower polarity (Example 26-1) and 17 mg (24%) of a diastereomer with higher polarity (Example 26-2). Diastereomer with lower polarity: 'H-NMR (500MHz, CDC13) 5 7.89(d, IH), 7.43(d, 1H), 7.30(m, 1H), 7.18(t, 1H), 7.05