1,2,3-TRIAZOLE DERIVATIVES AS IL4i1 INHIBITORS

Abstract

The invention relates to compounds of Formula (I) wherein R1, R2, R3, R4, R5, A and X are as described in the description; to their preparation, to pharmaceutically acceptable salts thereof, to pharmaceutical compositions containing one or more compounds of Formula (I), to pharmaceutical combinations and to the use of such compounds as medicaments, especially as IL4i1 inhibitors.

Description

[0001] ID 409A 1,2,3-Triazole derivatives as IL4i1 inhibitorsThe present invention relates to 1,2,3-triazole derivatives of Formula (I), and their use aspharmaceuticals. The invention also concerns related aspects including processes for the preparation of the compounds, pharmaceutical compositions containing one or more compounds of Formula (I), and especially their use as IL4i1 inhibitors. IL-4 induced gene-1 (IL4i1, FIG1) was first reported as a gene of unknown function that isinduced by IL-4 in B cells (Chu, C. C. et al., Proc. Natl. Acad. Sci. U. S. A. 94, 2507–2512(1997)). In subsequent years, it was found that IL4i1 is an L-amino-acid oxidase (LAAO), a family of flavin adenine dinucleotide dependent enzymes that are found throughout evolution, from bacteria to mammals. IL4i1 can oxidize L-phenylalanine, its main substrate, into the α-keto acid phenylpyruvate (PPA) liberating ammonia (NH3) and hydrogen peroxide (H2O2) (Boulland, M.-L. et al. Blood 110, 220–227 (2007)). Low activity towards other amino acids such as L-tyrosine, L-leucine, L-tryptophan, L-arginine and L-methionine have also been described (Boulland, M.-L. et al.Blood 110, 220–227 (2007), Sadik, A. et al. Cell 182, 1252-1270.e34 (2020), Molinier-Frenkel,V. et al. Genes Immun.17, 148–152 (2016), Choueiry, F. et al. Cancers 13, 2146, (2021)).Human IL4i1 mRNA sequence encodes a protein of 567 amino acids, containing an amino- terminal signal peptide for the secretion, a large central domain for LAAO activity, and a carboxy-terminal domain (Chavan, S. S. et al. Biochim. Biophys. Acta BBA - Gene Struct.Expr.1576, 70–80 (2002)). Five isoforms of IL4i1 are encoded by the human gene leading tothe same secreted protein. Isoform 1 is expressed in lymphoid tissue (Chavan, S. S. et al.Biochim. Biophys. Acta BBA - Gene Struct. Expr. 1576, 70–80 (2002)) and humanspermatozoa (Houston, B. et al. Reprod. Camb. Engl. 149, 587–596 (2015)). Isoform 2 isexpressed in rare cells of the central nervous system (Wiemann, S. et al. BMC Biol. 3, 16(2005)) and in human spermatozoa (Houston, B. et al. Reprod. Camb. Engl. 149, 587–596(2015)), whereas little is known about the other isoforms. IL4i1 is mainly expressed by macrophages and dendritic cells and stimulated by microbial derived products or inflammatory stimuli (TLR, IL-1β, Type I and II interferons) (Marquet, J.et al. Eur. J. Immunol. 40, 2557–2568 (2010)). It has been also described that B cells (Bod,L. et al. J. Immunol. Baltim. Md 1950200, 1027–1038 (2018)), Th17 cells (Santarlasci, V. etal. Eur. J. Immunol. 44, 654–661 (2014)) and some Tregs (Scarlata, C.-M. et al. Eur. J.Immunol. 45, 474–479 (2015)) can produce IL4i1. IL4i1 can be found intracellularly mainly inthe lysosomes of expressing cells (Mason, J. M. et al. J. Immunol. Baltim. Md 1950 173, 4561–4567 (2004)) but also as a glycosylated enzyme (Boulland, M.-L. et al.Blood 110, 220–227 (2007)).IL4i1 has been described to display antimicrobial properties by limiting the growth of Gram negative and Gram positive bacteria mainly attributed to oxidative stress due to the productionof H2O2 (Puiffe, M.-L. et al. PLOS ONE 8, e54589 (2013)). It is also described as animmunoregulator by regulating the activation and / or the function of different types of immunecells such as T cells (Boulland, M.-L. et al. Blood 110, 220–227 (2007), Cousin, C. et al. Eur.J. Immunol. 45, 1772–1782 (2015), Lasoudris, F. et al. Eur. J. Immunol. 41, 1629–1638(2011), Aubatin, A. et al. Eur. J. Immunol. 48, 106–119 (2018), Puiffe, M.-L. et al. Front.Immunol.11, 600012 (2020)), Th17 cells (Santarlasci, V. et al. Eur. J. Immunol.44, 654–661(2014), Cousin, C. et al. Eur. J. Immunol. 45, 1772–1782 (2015)), B cells (Bod, L. et al. J.Immunol. Baltim. Md 1950 200, 1027–1038 (2018)) and macrophages (Yue, Y. et al. PloSOne 10, e0142979 (2015)).On T cells, IL4i1 inhibits CD8+ T cell proliferation, cytotoxicity and IFN-γ production and enhance the differentiation of CD4 to Tregs. These effects are linked to the generation ofH2O2 since they can be neutralized by catalase (Boulland, M.-L. et al. Blood 110, 220–227(2007), Cousin, C. et al. Eur. J. Immunol. 45, 1772–1782 (2015), Mazzoni, A. et al. J. Clin.Med.10, 2111 (2021), Ramspott, J. P. et al. J. Invest. Dermatol.138, 2625–2634 (2018)).On Th17, IL4i1 inhibits Th17 expansion through a reduction of CD3 chains expression in the T-cell receptor complex and by maintaining in the same cells a high expression of Tob1, whichinhibits cell cycle entry (Santarlasci, V. et al. Eur. J. Immunol. 44, 654–661 (2014),Annunziato, F. et al. Trends in Immunology 33, 505-512 (2012)).On B cells, IL4i1 leads to a reduced B cell infiltration, proliferation and differentiation towards plasma cells that produce antibodies partially through H2O2 production (Bod, L. et al. J.Immunol. Baltim. Md 1950200, 1027–1038 (2018)).On macrophages, IL4i1 enhances the polarization towards an anti-inflammatory M2phenotype (Yue, Y. et al. PloS One 10, e0142979 (2015)).In the context of cancer, IL4i1 is overexpressed in many tumor types as reported in theliterature (Rao, D. et al. Int. Immunopharmacol. 111, 109091 (2022)) and in The CancerGenome Atlas (TCGA) database. In particular, B cell lymphomas, endometrial carcinoma, triple negative breast and ovarian cancer have the highest level of expression of IL4i1 (TheICGC / TCGA Pan-Cancer Analysis of Whole Genomes Consortium Nature 578, 82–93 (2020),https: / / doi.org / 10.1038 / s41586-020-1969-6). Moreover, this high expression of IL4i1 is associated with a poor prognosis in various cancer types such as hepatocellular carcinoma(Rao, D. et al. Int. Immunopharmacol. 111, 109091 (2022)), triple negative breast cancer(Komatsu, M. et al. Int. J. Oncol. 42, (2013)), ovarian cancer (Zhao, H. et al. J.Transl. Med. 19, 454 (2021), Grobben, Y. et al. Cancers 15, 893 (2023)), clear cell renal cellcarcinoma (Liu, M. et al. Sci. Rep.10, 12949 (2020)), cutaneous melanoma (Ramspott, J. P.et al. J. Invest. Dermatol. 138, 2625–2634 (2018)), lung adenocarcinoma (Li, T. et al.MedComm 4, e355 (2023)) or thyroid cancer (Zhu, L. et al. BMC Endocr. Disord. 23, 148(2023)) and is expected to be a relevant therapeutic target for these patients. Inside the tumor, IL4i1 is expressed mainly by tumor infiltrating macrophages and dendritic cells and in some cases by tumor cells themselves (Carbonnelle-Puscian, A. et al. Leukemia 23, 952–960 (2009)). Mechanistically, IL4i1 exerts pro-tumoral activities by acting through an autocrine or a paracrine way on the immune cells to suppress anti-tumor immunity but also on tumor cells by activating AHR, through Trp metabolism, leading to an increase in cell motility and metastases formation (Sadik, A. et al. Cell 182, 1252-1270.e34 (2020)). Moreover, in advanced melanoma, anti PD-1 monoclonal antibody nivolumab can induceIL4i1 expression (Sadik, A. et al. Cell 182, 1252-1270.e34 (2020)). On the other hand, IL4i1enhances PD-L1 expression in lung adenocarcinoma (Zhu, J. et al. Immunogenetics 75, 17–25 (2023). These data suggest the potential of targeting IL4i1 for the treatment of various cancer types. However, currently, there are no specific IL4i1 inhibitors available. Thus, the IL4i1 inhibitors described in this patent application may be useful alone or in combination with immune checkpoint inhibitors, especially PD1 and PD-L1 inhibitors, for the treatment of cancer where IL4i1 is highly expressed or active.It has now been found that 1,2,3-triazole derivatives of Formula (I) are potent IL4i1 inhibitorswhich may be useful for the prevention and / or treatment of diseases or disorders related to the IL4i1 enzyme, such as especially cancers. 1) In a first embodiment, the present invention relates to compounds of Formula (I) wherein A represents -CH2-; -N(RA)-, wherein RArepresents hydrogen or (C1-4)alkyl; or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; X represents -O-, -S-, or -NH-; R1represents (C1-6)alkyl; (C2-4)alkenyl; (C2-4)alkynyl which is independently unsubstituted or mono-substituted with aryl; (C1-4)fluoroalkyl; (C1-4)hydroxyalkyl; (C1-4)alkoxy-(C1-4)alkyl; (C1-4)alkyl-carbonyl; (C1-4)alkoxy-carbonyl; amino-carbonyl; (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; (C3-8)heterocyclyl; (2-oxoimidazolidin-1-yl)methyl; aryl; aryl-(C1-4)alkyl; or heteroaryl; R2represents (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted with halogen; ferrocenyl; aryl which is independently unsubstituted or substituted with 1 to 5 substituents independently selected from the group consisting of deuterium, (C1-4)alkyl, (C2- 4)alkynyl, (C1-4)alkoxy, (C1-4)alkyl-carbonyl, cyano, halogen, (C1-4)fluoroalkyl, and (C1-4)hydroxyalkyl; or heteroaryl which is independently unsubstituted or mono- or di-substituted with halogen; R3represents hydrogen, (C1-4)alkyl, or halogen (especially hydrogen or fluoro); R4represents hydrogen, deuterium, (C1-4)alkyl, or (C1-4)fluoroalkyl (especially hydrogen, deuterium, or (C1-4)alkyl); and R5represents hydrogen, or deuterium; and to the salts (in particular pharmaceutically acceptable salts) of the compounds; with the proviso that the compound is not: N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-propyl-1,3,4-oxadiazol-2- amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-ethyl-1,3,4-thiadiazol-2- amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-(cyclopropylmethyl)-1,3,4- oxadiazol-2-amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-(tetrahydrofuran-2-yl)-1,3,4- oxadiazol-2-amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-(difluoromethyl)-1,3,4- thiadiazol-2-amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-isopropyl-1,3,4-thiadiazol-2- amine; 5-methyl-N-(1-(1-phenyl-1H-1,2,3-triazol- -1,3,4-thiadiazol-2-amine; 5-(difluoromethyl)-N-((1-(4-methoxyphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-thiadiazol-2- amine; and N-((1-(3-methoxyphenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-methyl-1,3,4-oxadiazol-2-amine. Definitions provided herein are intended to apply uniformly to the compounds of Formula (I) as defined in any one of embodiments 1) to 62), and, mutatis mutandis, throughout the description and the claims unless an otherwise expressly set out definition provides a broader or narrower definition. It is well understood that a definition or preferred definition of a term defines and may replace the respective term independently of (and in combination with) any definition or preferred definition of any or all other terms as defined herein. The compounds of Formula (I) as defined in any one of embodiments 1) to 62), may contain one or more stereogenic or asymmetric center(s), such as one or more asymmetric carbon atom(s). The compounds of Formula (I) may thus be present as mixtures of stereoisomers or in stereoisomerically enriched form, preferably as pure stereoisomers. Mixtures of stereoisomers may be separated in a manner known to a person skilled in the art. The term "enriched", for example when used in the context of enantiomers, is understood in the context of the present invention to mean especially that the respective enantiomer is present in a ratio (mutatis mutandis: purity) of at least 70:30, and notably of at least 90:10 (mutatis mutandis: purity of 70% / 90%) with respect to the respective other enantiomer. Preferably the term refers to the respective essentially pure enantiomer. The term “essentially”, for example when used in a term such as "essentially pure" is understood in the context of the present invention to mean especially that the respective stereoisomer / composition / compound etc. consists in an amount of at least 90, especially of at least 95, and notably of at least 99 per cent by weight of the respective pure stereoisomer / composition / compound etc. In this patent application, a dotted line shows the point of attachment of the radical drawn. For example, the radical group that is attached to the rest of the molecule via one of the carbon atoms of a cyclopentadienyl ring. The term "halogen" means fluorine, bromine, or iodine, preferably fluorine or chlorine. In case R1represents a cycloalkyl group which is substituted with halogen the term “halogen” means preferably fluorine or chlorine, and more preferably fluorine. In case R2represents a cycloalkyl group which is substituted with halogen the term “halogen” means preferably fluorine or chlorine, and more preferably fluorine. In case R2represents an aryl group which is substituted with halogen the term “halogen” means preferably fluorine, chlorine, or bromine, and more preferably fluorine or chlorine. In case R2represents a heteroaryl group which is substituted with halogen the term “halogen” means preferably fluorine, chlorine, or bromine, and more preferably chlorine. In case R3represents halogen the term “halogen” means preferably fluorine or chlorine, and more preferably fluorine. The term "alkyl", used alone or in combination, refers to a straight or branched saturated hydrocarbon chain containing one to six carbon atoms, preferably one to four carbon atoms. The term "(Cx-y)alkyl" (x and y each being an integer), refers to an alkyl group as defined before containing x to y carbon atoms. For example a (C1-6)alkyl group contains from one to six carbon atoms. Representative examples of (C1-6)alkyl groups are methyl, ethyl, n-propyl, iso-propyl, n-butyl, iso-butyl, sec.-butyl, tert.-butyl, the isomeric pentyls (especially pent-1-yl, 2-methyl-but-2-yl, pent-3-yl), and the isomeric hexyls (especially hex-1-yl, hex-2-yl, hex-3-yl, 2-methyl-pent-2-yl, 2,3-dimethyl-but-2-yl, 3-methyl-pent-3-yl). Representative examples of (C1-4)alkyl groups are methyl, ethyl, n-propyl, iso-propyl, n-butyl, iso-butyl, sec.-butyl and tert.- butyl. In case RArepresents (C1-4)alkyl the term means preferably methyl, ethyl, n-propyl or iso-propyl, more preferably methyl or ethyl, and most preferably methyl. In case R1represents (C1-6)alkyl the term means preferably methyl, ethyl, n-propyl, iso-propyl, n-butyl, iso-butyl, sec.-butyl, tert.-butyl, 2-methyl-but-2-yl, pent-3-yl, hex-2-yl, hex-3-yl, 2-methyl-pent-2-yl, 2,3- dimethyl-but-2-yl or 3-methyl-pent-3-yl, more preferably methyl, ethyl, iso-propyl, iso-butyl, sec.-butyl or tert.-butyl, and most preferably methyl, iso-propyl or tert.-butyl. In case R1represents (C1-4)alkyl the term means preferably methyl, ethyl, n-propyl, iso-propyl, n-butyl, iso-butyl, sec.-butyl or tert.-butyl, more preferably methyl, ethyl, iso-propyl, sec.-butyl or tert.- butyl, and most preferably methyl, iso-propyl or tert.-butyl. In case R1represents a cycloalkyl group which is substituted with (C1-4)alkyl the term "(C1-4)alkyl" means preferably methyl, ethyl, n-propyl, or iso-propyl, more preferably methyl or ethyl, and most preferably methyl. In case R2represents an aryl group which is substituted with (C1-4)alkyl the term "(C1-4)alkyl" means preferably methyl, ethyl, n-propyl, or iso-propyl, more preferably methyl or ethyl, and most preferably methyl. In case R3represents (C1-4)alkyl the term means preferably methyl, ethyl, n-propyl, or iso-propyl, more preferably methyl or ethyl, and most preferably methyl. In case R4represents (C1-4)alkyl the term methyl, ethyl, n-propyl, or iso-propyl, more preferably methyl or ethyl, and most preferably methyl. The term "(C1-4)fluoroalkyl" refers to an alkyl group as defined before containing one to four carbon atoms in which one or more (and possibly all) hydrogen atoms have been replaced with fluorine. The term "(Cx-y)fluoroalkyl" (x and y each being an integer) refers to a fluoroalkyl group as defined before containing x to y carbon atoms. For example a (C1-4)fluoroalkyl group contains from one to four carbon atoms in which one to nine hydrogen atoms have been replaced with fluorine. Representative examples of (C1-4)fluoroalkyl groups include fluoromethyl, difluoromethyl, trifluoromethyl, 1-fluoroethyl, 2-fluoroethyl, 1,1-difluoroethyl, 2,2- difluoroethyl, 2,2,2-trifluoroethyl and 2-fluoro-prop-2-yl. Preferred are (C1)fluoroalkyl groups such as fluoromethyl, difluoromethyl, and trifluoromethyl. In case R1represents (C1-4)fluoroalkyl the term means preferably difluoromethyl, trifluoromethyl, 1-fluoroethyl, 1,1- difluoroethyl or 2-fluoro-prop-2-yl, more preferably difluoromethyl or 2-fluoro-prop-2-yl and most preferably 2-fluoro-prop-2-yl. In case R2represents an aryl group which is substituted with (C1-4)fluoroalkyl the term “(C1-4)fluoroalkyl" means preferably fluoromethyl, difluoromethyl, trifluoromethyl, 1-fluoroethyl, 2-fluoroethyl, 1,1-difluoroethyl, 2,2-difluoroethyl or 2,2,2-trifluoroethyl, more preferably fluoromethyl, difluoromethyl or trifluoromethyl, and most preferably trifluoromethyl. In case R4represents (C1-4)fluoroalkyl the term “(C1-4)fluoroalkyl" means preferably fluoromethyl, difluoromethyl, trifluoromethyl, 1-fluoroethyl, 2- fluoroethyl, 1,1-difluoroethyl, 2,2-difluoroethyl or 2,2,2-trifluoroethyl, more preferably fluoromethyl, difluoromethyl or trifluoromethyl, and most preferably trifluoromethyl. The term "(Cx-y)hydroxyalkyl" (x and y each being an integer) refers to an alkyl group as defined before containing x to y carbon atoms wherein one hydrogen atom has been replaced by a hydroxy group. For example a (C1-4)hydroxyalkyl group contains from one to four carbon atoms in which one hydrogen atom has been replaced by a hydroxy group. Representative examples of "(C1-4)hydroxyalkyl" are hydroxymethyl, 1-hydroxyethyl, 2-hydroxyethyl, 1- hydroxyprop-1-yl, 2-hydroxyprop-1-yl, 3-hydroxyprop-1-yl, 1-hydroxyprop-2-yl, 2- hydroxyprop-2-yl, 1-hydroxybut-1-yl, 2-hydroxybut-1-yl, 3-hydroxybut-1-yl, 4-hydroxybut-1-yl, 1-hydroxybut-2-yl, 2-hydroxybut-2-yl, 3-hydroxybut-2-yl, 4-hydroxybut-2-yl, 1-hydroxy-2- methyl-prop-1-yl, 2-hydroxy-2-methyl-prop-1-yl, 3-hydroxy-2-methyl-prop-1-yl and 1-hydroxy- 2-methyl-prop-2-yl, and preferably hydroxymethyl, 1-hydroxyethyl, 2-hydroxyethyl, 1- hydroxyprop-1-yl, 2-hydroxyprop-1-yl, 3-hydroxyprop-1-yl, 1-hydroxyprop-2-yl and 2- hydroxyprop-2-yl. In case R1represents (C1-4)hydroxyalkyl the term means preferably hydroxymethyl, 1-hydroxyethyl, 2-hydroxyethyl, 1-hydroxyprop-1-yl, 2-hydroxyprop-1-yl, 3- hydroxyprop-1-yl, 1-hydroxyprop-2-yl, 2-hydroxyprop-2-yl, 1-hydroxybut-2-yl, 2-hydroxybut- 2-yl, 3-hydroxybut-2-yl, 4-hydroxybut-2- hydroxy-2-methyl-prop-1-yl, or 1-hydroxy-2- methyl-prop-2-yl, more preferably hydroxymethyl, 1-hydroxyethyl, 2-hydroxyethyl, 1- hydroxyprop-1-yl, 2-hydroxyprop-1-yl, 3-hydroxyprop-1-yl, 1-hydroxyprop-2-yl or 2- hydroxyprop-2-yl, and most preferably hydroxymethyl or 2-hydroxyprop-2-yl. In case R2represents an aryl group which is substituted with (C1-4)hydroxyalkyl the term "(C1-4)hydroxyalkyl" means preferably hydroxymethyl, 1-hydroxyethyl, 2-hydroxyethyl, 1- hydroxyprop-1-yl, 2-hydroxyprop-1-yl, 3-hydroxyprop-1-yl, 1-hydroxyprop-2-yl or 2- hydroxyprop-2-yl, more preferably hydroxymethyl, 1-hydroxyethyl or 2-hydroxyethyl, and most preferably hydroxymethyl. The term "alkenyl", used alone or in combination, refers to a straight or branched hydrocarbon chain containing two to four carbon atoms and one carbon-carbon double bond. The term "(Cx-y)alkenyl" (x and y each being an integer), refers to an alkenyl group as defined before containing x to y carbon atoms. For example a (C2-4)alkenyl group contains from two to four carbon atoms. Representative examples of (C2-4)alkenyl are vinyl (ethenyl), prop-1-en-1-yl, prop-2-en-1-yl, prop-1-en-2-yl, but-1-en-1-yl, but-2-en-1-yl, but-3-en-1-yl, but-1-en-2-yl, but- 2-en-2-yl, but-3-en-2-yl, 2-methyl-prop-1-en-1-yl and 2-methyl-prop-2-en-1-yl. In case R1represents (C2-4)alkenyl the term means preferably vinyl, prop-1-en-1-yl, prop-2-en-1-yl or prop-1-en-2-yl, more preferably vinyl, prop-2-en-1-yl or prop-1-en-2-yl, and most preferably vinyl. The term “alkynyl”, used alone or in combination, refers to a straight or branched chain hydrocarbon group containing two to four carbon atoms wherein said hydrocarbon group contains at least one carbon-carbon triple bond. The term “(Cx-y)alkynyl” (x and y each being an integer), refers to an alkynyl group as defined before, containing x to y carbon atoms. For example a (C2-4)alkynyl group contains from two to four carbon atoms. Representative examples of (C2-4)alkynyl are ethynyl, prop-1-yn-1-yl, prop-2-yn-1-yl, but-2-yn-1-yl, but-1-yn- 1-yl, but-3-yn-1-yl and but-1-yn-3-yl. In case R1represents (C2-4)alkynyl the term means preferably ethynyl, prop-1-yn-1-yl, prop-2-yn-1-yl, but-2-yn-1-yl, but-1-yn-1-yl or but-3-yn-1- yl, more preferably ethynyl, prop-1-yn-1-yl or prop-2-yn-1-yl, and most preferably ethynyl. In case R2represents an aryl group which is substituted with (C2-4)alkynyl the term "(C2-4)alkynyl" means preferably ethynyl, prop-1-yn-1-yl, prop-2-yn-1-yl, but-2-yn-1-yl, but-1-yn-1-yl or but- 3-yn-1-yl, more preferably ethynyl, prop-1-yn-1-yl or prop-2-yn-1-yl, and most preferably ethynyl. The (C2-4)alkynyl group may be unsubstituted or substituted as specifically defined. Preferred examples of unsubstituted or substituted (C2-4)alkynyl groups representing R1are ethynyl and 2-phenyl-ethynyl, most preferred is ethynyl. The term "alkoxy", used alone or in refers to an alkyl-O- group wherein the alkyl group is as defined before. The term "(Cx-y)alkoxy" (x and y each being an integer) refers to an alkoxy group as defined before containing x to y carbon atoms. For example a (C1-4)alkoxy group means a group of the formula (C1-4)alkyl-O- in which the term "(C1-4)alkyl" has the previously given significance. Representative examples of (C1-4)alkoxy groups are methoxy, ethoxy, n-propoxy, iso-propoxy, n-butoxy, iso-butoxy, sec.-butoxy and tert.-butoxy. In case R1represents a cycloalkyl group which is substituted with (C1-4)alkoxy the term "(C1-4)alkoxy" means preferably methoxy, ethoxy, n-propoxy or iso-propoxy, more preferably methoxy or ethoxy, and most preferably methoxy. In case R2represents an aryl group which is substituted with (C1-4)alkoxy the term "(C1-4)alkoxy" means preferably methoxy, ethoxy, n-propoxy or iso- propoxy, more preferably methoxy or ethoxy, and most preferably methoxy. The term "(Cxa-ya)alkoxy-(Cx-y)alkyl" (x, xa, y and ya each being an integer) refers to an alkyl group as defined before wherein one hydrogen atom has been replaced by (Cxa-ya)alkoxy as defined before containing xa to ya carbon atoms. For example a (C1-4)alkoxy-(C1-4)alkyl group refers to an (C1-4)alkyl group as defined before containing one to four carbon atoms wherein one hydrogen atom has been replaced with (C1-4)alkoxy as defined before containing one to four carbon atoms. In case R1represents (C1-4)alkoxy-(C1-4)alkyl the term means preferably methoxymethyl, ethoxymethyl, 1-methoxy-ethyl, 2-methoxy-ethyl, 1-ethoxy-ethyl or 2-ethoxy- ethyl, more preferably methoxymethyl, ethoxymethyl, 2-methoxy-ethyl or 2-ethoxy-ethyl, and most preferably methoxymethyl. The term "cycloalkyl", used alone or in combination, refers to a saturated, mono- or bicyclic carbocyclic ring containing three to eight carbon atoms. A monocyclic carbocyclic ring contains preferably three to six carbon atoms, a bicyclic carbocyclic ring preferably five to eight carbon atoms. Bicyclic carbocyclic rings may be spiro bicyclic rings, wherein the two rings share one single carbon atom; fused bicyclic rings, wherein the two rings share two adjacent carbon atoms; or bridged bicyclic rings, wherein the two rings share at least three carbon atoms (preferably the two rings share three or four carbon atoms, more preferably the two rings share three carbon atoms) of which two carbon atoms are bridgehead atoms that are separated by a bridge containing at least one carbon atom. The term "(Cx-y)cycloalkyl" (x and y each being an integer), refers to a cycloalkyl group as defined before containing x to y carbon atoms. For example a (C3-8)cycloalkyl group contains from three to eight carbon atoms. Representative examples of cycloalkyl groups are monocyclic rings such as cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, cyclooctyl; spiro bicyclic rings such as spiro[2.2]pentyl, spiro[3.2]hexyl, spiro[4.2]heptyl, spiro[5.2]octyl, spiro[3.3]heptyl, spiro[4.3]octyl; fused bicyclic rings such as bicyclo[1.1.0]butyl, bicyclo[2.1.0]pentyl, bicyclo[3.1.0]hexyl, bicyclo[4.1.0] bicyclo[5.1.0]octyl, bicyclo[2.2.0]hexyl, bicyclo[3.2.0]heptyl, bicyclo[4.2.0]octyl, bicyclo[3.3.0]octyl; and bridged bicyclic rings such as bicyclo[1.1.1]pentyl, bicyclo[2.1.1]hexyl, bicyclo[3.1.1]heptyl, bicyclo[4.1.1]octyl, bicyclo[2.2.1]heptyl, bicyclo[3.2.1]octyl and bicyclo[2.2.2]octyl. In case R1represents (C3-8)cycloalkyl the term means preferably cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, spiro[4.2]heptyl, spiro[5.2]octyl, spiro[3.3]heptyl, spiro[4.3]octyl, bicyclo[1.1.0]butyl, bicyclo[2.1.0]pentyl, 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, bicyclo[3.3.0]octyl, bicyclo[1.1.1]pentyl, bicyclo[2.1.1]hexyl, bicyclo[3.1.1]heptyl, bicyclo[4.1.1]octyl, bicyclo[2.2.1]heptyl, bicyclo[3.2.1]octyl or bicyclo[2.2.2]octyl, more preferably cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, bicyclo[3.1.0]hexyl, bicyclo[4.1.0]heptyl, bicyclo[1.1.1]pentyl, bicyclo[2.2.1]heptyl, bicyclo[3.2.1]octyl or bicyclo[2.2.2]octyl, and most preferably cyclopropyl, cyclobutyl, bicyclo[3.1.0]hexyl or bicyclo[1.1.1]pentyl. In case R2represents (C3-8)cycloalkyl the term means preferably cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, spiro[4.2]heptyl, spiro[5.2]octyl, spiro[3.3]heptyl, spiro[4.3.]octyl, bicyclo[1.1.0]butyl, bicyclo[2.1.0]pentyl, 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, bicyclo[3.3.0]octyl, bicyclo[1.1.1]pentyl, bicyclo[2.1.1]hexyl, bicyclo[3.1.1]heptyl, bicyclo[4.1.1]octyl, bicyclo[2.2.1]heptyl, bicyclo[3.2.1]octyl or bicyclo[2.2.2]octyl, more preferably cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, bicyclo[1.1.1]pentyl or bicyclo[2.2.1]heptyl, and most preferably cyclohexyl or bicyclo[1.1.1]pentyl. The (C3-8)cycloalkyl group may be unsubstituted or substituted as specifically defined. Preferred examples of unsubstituted or substituted (C3-8)cycloalkyl groups representing R1are cyclopropyl, 1-hydroxy-cyclopropyl, cyclobutyl, 3,3- dimethyl-cyclobutyl, 3-methoxy-cyclobutyl, 3,3-difluoro-cyclobutyl, bicyclo[3.1.0]hexyl, bicyclo[1.1.1]pentyl, and especially cyclopropyl, cyclobutyl, 3,3-dimethyl-cyclobutyl, and bicyclo[1.1.1]pentyl. Preferred examples of unsubstituted or substituted (C3-8)cycloalkyl groups representing R2are cyclohexyl, 4,4-difluoro-cyclohexyl, and bicyclo[1.1.1]pentyl. The term "(Cxa-ya)cycloalkyl-(Cx-y)alkyl" (x, xa, y and ya each being an integer) refers to an (Cx-y)alkyl group as defined before containing x to y carbon atoms wherein one hydrogen atom has been replaced by (Cxa-ya)cycloalkyl as defined before containing xa to ya carbon atoms. For example a (C3-8)cycloalkyl-(C1-4)alkyl group refers to an (C1-4)alkyl group as defined before containing one to four carbon atoms (preferably methyl) wherein one hydrogen atom has been replaced with (C3-8)cycloalkyl as defined before containing three to eight carbon atoms (preferably cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, bicyclo[3.1.0]hexyl, bicyclo[4.1.0]heptyl, bicyclo[1.1.1]pentyl, bicyclo[2.2.1]heptyl, bicyclo[3.2.1]octyl or bicyclo[2.2.2]octyl, and more preferably cyclobutyl, cyclopentyl or cyclohexyl). In case R1represents (C3-8)cycloalkyl-(C1-4)alkyl the term means preferably cyclopropyl-methyl, 1-cyclopropyl-ethyl, 2-cyclopropyl-ethyl, 1-cyclopropyl-propyl, 2-cyclopropyl-propyl, 3- cyclopropyl-propyl, 1-cyclopropyl-1-methyl-ethyl, 2-cyclopropyl-1-methyl-ethyl, cyclobutyl- methyl, 1-cyclobutyl-ethyl, 2-cyclobutyl-ethyl, 1-cyclobutyl-propyl, 2-cyclobutyl-propyl, 3- cyclobutyl-propyl, 1-cyclobutyl-1-methyl-ethyl, 2-cyclobutyl-1-methyl-ethyl, cyclopentyl- methyl, 1-cyclopentyl-ethyl, 2-cyclopentyl-ethyl, 1-cyclopentyl-propyl, 2-cyclopentyl-propyl, 3- cyclopentyl-propyl, 1-cyclopentyl-1-methyl-ethyl, 2-cyclopentyl-1-methyl-ethyl, cyclohexyl- methyl, 1-cyclohexyl-ethyl, 2-cyclohexyl-ethyl, 1-cyclohexyl-propyl, 2-cyclohexyl-propyl, 3- cyclohexyl-propyl, 1-cyclohexyl-1-methyl-ethyl or 2-cyclohexyl-1-methyl-ethyl, more preferably cyclopropyl-methyl, 1-cyclopropyl-ethyl, 2-cyclopropyl-ethyl, cyclobutyl-methyl, 1- cyclobutyl-ethyl, 2-cyclobutyl-ethyl, cyclopentyl-methyl, 1-cyclopentyl-ethyl, 2-cyclopentyl- ethyl, cyclohexyl-methyl, 1-cyclohexyl-ethyl or 2-cyclohexyl-ethyl, and most preferably cyclopropyl-methyl, 1-cyclopropyl-ethyl or cyclopentyl-methyl. The term “alkyl-carbonyl”, used alone or in combination, refers to an alkyl-C(O)- group wherein the alkyl group is as defined before, which is attached to the rest of the molecule via the carbonyl-C-atom. The term “(Cx-y)alkyl-carbonyl” (x and y each being an integer) refers to an alkyl-carbonyl group as defined before containing in the alkyl radical x to y carbon atoms. For example a (C1-4)alkyl-carbonyl group contains in the alkyl radical one to four carbon atoms. Representative examples of (C1-4)alkyl-carbonyl groups are methyl-carbonyl, ethyl- carbonyl, n-propyl-carbonyl, iso-propyl-carbonyl, n-butyl-carbonyl, iso-butyl-carbonyl, sec.- butyl-carbonyl and tert.-butyl-carbonyl. In case R1represents (C1-4)alkyl-carbonyl the term means preferably methyl-carbonyl, ethyl-carbonyl, n-propyl-carbonyl, iso-propyl-carbonyl, n- butyl-carbonyl, iso-butyl-carbonyl, sec.-butyl-carbonyl or tert.-butyl-carbonyl, more preferably methyl-carbonyl or ethyl-carbonyl, and most preferably methyl-carbonyl. In case R2represents aryl which is substituted with (C1-4)alkyl-carbonyl the term “(C1-4)alkyl-carbonyl” means preferably methyl-carbonyl, ethyl-carbonyl, n-propyl-carbonyl, iso-propyl-carbonyl, n- butyl-carbonyl, iso-butyl-carbonyl, sec.-butyl-carbonyl or tert.-butyl-carbonyl, more preferably methyl-carbonyl or ethyl-carbonyl, and most preferably methyl-carbonyl. The term “alkoxy-carbonyl”, used alone or in combination, refers to an alkoxy-C(O)- group wherein the alkoxy group is as defined before, which is attached to the rest of the molecule via the carbonyl-C-atom. The term “(Cx-y)alkoxy-carbonyl” (x and y each being an integer) refers to an alkoxy-carbonyl group as defined before containing in the alkoxy radical x to y carbon atoms. For example a (C1-4)alkoxy-carbonyl group contains in the alkoxy radical one to four carbon atoms. Representative examples of (C1-4)alkoxy-carbonyl groups are methoxy- carbonyl, ethoxy-carbonyl, n-propoxy- iso-propoxy-carbonyl, n-butoxy-carbonyl, iso- butoxy-carbonyl, sec.-butoxy-carbonyl and tert.-butoxy-carbonyl. In case R1represents (C1- 4)alkoxy-carbonyl the term means preferably methoxy-carbonyl, ethoxy-carbonyl, n-propoxy- carbonyl, iso-propoxy-carbonyl, n-butoxy-carbonyl, iso-butoxy-carbonyl, sec.-butoxy- carbonyl or tert.-butoxy-carbonyl, more preferably methoxy-carbonyl or ethoxy-carbonyl, and most preferably ethoxy-carbonyl. The term “amino-carbonyl”, used alone or in combination, refers to an amino-C(O)- group (H2N-C(O)-) wherein the amino group is attached to the rest of the molecule via the carbonyl- C-atom. The term "cyano" refers to a group -CN. The term “aryl”, used alone or in combination, means a phenyl or a naphthyl group (preferably a phenyl group). The aryl group is unsubstituted or substituted as explicitly defined. In case R1represents aryl the term means preferably phenyl or naphthyl and more preferably phenyl. In case R1represents (C2-4)alkynyl which is substituted with aryl the term “aryl” means preferably phenyl or naphthyl and more preferably phenyl. In case R2represents aryl the term means preferably phenyl or naphthyl and more preferably phenyl. The aryl group representing R2is unsubstituted or substituted as explicitly defined. Preferred examples of unsubstituted or substituted aryl groups representing R2are phenyl, pentadeutero-phenyl (phenyl-d5), methyl-phenyl (especially 3-methyl-phenyl, and 4-methyl-phenyl), ethynyl-phenyl (especially 4-ethynyl-phenyl), methoxy-phenyl (especially 4-methoxy-phenyl), acetyl-phenyl (especially 4-acetyl-phenyl), cyano-phenyl (especially 2-cyano-phenyl, and 4-cyano-phenyl), fluoro- phenyl (especially 2-fluoro-phenyl, 3-fluoro-phenyl, and 4-fluoro-phenyl), chloro-phenyl (especially 2-chloro-phenyl, and 4-chloro-phenyl), trifluoromethyl-phenyl (especially 4- trifluoromethyl-phenyl), and hydroxymethyl-phenyl (especially 3-hydroxymethyl-phenyl). The term "aryl-(Cx-y)alkyl" (x and y each being an integer) refers to an alkyl group as defined before containing x to y carbon atoms wherein one hydrogen atom has been replaced by an aryl group as defined before. For example an aryl-(C1-4)alkyl group contains from one to four carbon atoms in which one hydrogen atom has been replaced by an aryl group. Representative examples of "aryl-(C1-4)alkyl" are aryl-methyl, 1-aryl-ethyl, 2-aryl-ethyl, 1-aryl- prop-1-yl, 2-aryl-prop-1-yl, 3-aryl-prop-1-yl, 1-aryl-prop-2-yl, 2-aryl-prop-2-yl, 1-aryl-but-1-yl, 2-aryl-but-1-yl, 3-aryl-but-1-yl, 4-aryl-but-1-yl, 1-aryl-but-2-yl, 2-aryl-but-2-yl, 3-aryl-but-2-yl, 4-aryl-but-2-yl, 1-aryl-2-methyl-prop-1-yl, 2-aryl-2-methyl-prop-1-yl, 3-aryl-2-methyl-prop-1-yl and 1-aryl-2-methyl-prop-2-yl, wherein aryl represents independently from each other phenyl or naphthyl (preferably phenyl). Preferred examples of "aryl-(C1-4)alkyl" are phenyl-methyl, 1- phenyl-ethyl, 2-phenyl-ethyl, 1-phenyl- 2-phenyl-prop-1-yl, 3-phenyl-prop-1-yl, 1- phenyl-prop-2-yl, and 2-phenyl-prop-2-yl; especially phenyl-methyl. The term “(C3-8)heterocyclyl”, used alone or in combination, refers to a saturated mono- or bi- cyclic moiety of 3 to 8 ring members containing, in addition to carbon atoms, one or two heteroatoms independently selected from nitrogen, oxygen and sulfur. A monocyclic heterocyclic ring contains preferably three to six members, a bicyclic heterocyclic ring preferably five to eight members. Bicyclic heterocyclic rings may be spiro bicyclic rings, fused bicyclic rings, or bridged bicyclic rings. Representative examples of such heterocyclyl groups are aziridinyl, azetidinyl, pyrrolidinyl, piperidinyl, azepanyl, oxiranyl, oxetanyl, tetrahydrofuranyl, tetrahydro-2H-pyranyl, thiiranyl, thietanyl, tetrahydro-thiophenyl, tetrahydro-2H-thiopyranyl, imidazolidinyl, piperazinyl, diazepanyl, oxazolidinyl, morpholinyl, oxazepanyl, thiazolidinyl, thiomorpholinyl, dioxolanyl, dithiolanyl, dioxanyl, dithianyl, azaspiro[2.4]heptanyl, oxaspiro[2.4]heptanyl, azaspiro[2.5]octanyl, oxaspiro[2.5]octanyl, azaspiro[3.3]heptanyl, oxaspiro[3.3]heptanyl, azaspiro[3.4]octanyl, oxaspiro[3.4]octanyl, azabicyclo[3.1.0]hexanyl, oxabicyclo[3.1.0]hexanyl, azabicyclo[4.1.0]heptanyl, oxabicyclo[4.1.0]heptanyl, azabicyclo[3.2.0]heptanyl, oxabicyclo[3.2.0]heptanyl, azabicyclo[4.2.0]octanyl, oxabicyclo[4.2.0]octanyl, azabicyclo[3.3.0]octanyl, oxabicyclo[3.3.0]octanyl, azabicyclo[2.2.1]heptanyl, oxabicyclo[2.2.1]heptanyl, azabicyclo[2.2.2]octanyl, and oxabicyclo[2.2.2]octanyl. Preferred examples of term “(C3- 8)heterocyclyl” are oxiranyl, oxetanyl, 2H-pyranyl, tetrahydro- thiophenyl, tetrahydro-2H-thiopyranyl, dioxolanyl, dithiolanyl, dioxanyl, dithianyl, and azaspiro[3.3]heptanyl. More preferred are oxetanyl, dioxolanyl and dithiolanyl; most preferred are oxetanyl and dithiolanyl (and especially oxetan-3-yl). The term “heteroaryl”, used alone or in combination, means a 5- to 10-membered monocyclic or bicyclic aromatic ring containing 1, 2 or 3 heteroatoms independently selected from oxygen, nitrogen and sulfur. Preferred is a 5- or 6-membered monocyclic heteroaryl group. Examples of such heteroaryl groups are furanyl, oxazolyl, isoxazolyl, oxadiazolyl, thienyl, thiazolyl, isothiazolyl, thiadiazolyl, pyrrolyl, imidazolyl, pyrazolyl, triazolyl, pyridyl, pyrimidyl, pyridazinyl, pyrazinyl, indolyl, isoindolyl, benzofuranyl, isobenzofuranyl, benzothiophenyl, indazolyl, benzimidazolyl, benzoxazolyl, benzisoxazolyl, benzothiazolyl, benzoisothiazolyl, benzotriazolyl, benzo[2,1,3]oxadiazolyl, benzo[2,1,3]thiadiazolyl, benzo[1,2,3]thiadiazolyl, quinolinyl, isoquinolinyl, cinnolinyl, quinazolinyl, quinoxalinyl and phthalazinyl. In case R1represents heteroaryl the term means preferably a 5- or 6-membered monocyclic aromatic ring containing 1, 2 or 3 heteroatoms (preferably 1 or 2 heteroatoms) independently selected from oxygen, nitrogen and sulfur (preferably from nitrogen and sulfur). Preferred examples of R1representing heteroaryl are furanyl, isoxazolyl, oxadiazolyl, thienyl, thiazolyl, isothiazolyl, thiadiazolyl, pyrrolyl, imidazolyl, pyrazolyl, triazolyl, pyridyl, pyrimidyl, pyridazinyl, and pyrazinyl; most preferred are thiazolyl (especially thiazol-5-yl) and pyridyl (especially pyridin-4-yl). In case R2represents heteroaryl the term means preferably a 5- or 6-membered monocyclic aromatic ring containing 1, 2 or 3 heteroatoms (preferably 1 or 2 heteroatoms) independently selected from oxygen, nitrogen and sulfur. Preferred examples of R2representing heteroaryl are furanyl, oxazolyl, isoxazolyl, oxadiazolyl, thienyl, thiazolyl, isothiazolyl, thiadiazolyl, pyrrolyl, imidazolyl, pyrazolyl, triazolyl, pyridyl, pyrimidyl, pyridazinyl, and pyrazinyl; most preferred are furanyl (especially furan-3-yl), thienyl (especially thiophen- 3-yl), and pyridyl (especially pyridin-3-yl). The heteroaryl groups representing R2are unsubstituted or substituted as explicitly defined. Examples of such unsubstituted or substituted heteroaryl groups are furanyl (especially furan-3-yl), thienyl (especially thiophen- 3-yl), 2-chloro-thienyl (especially 2-chloro-thiophen-4-yl), and pyridyl (especially pyridin-3-yl). 2) A further embodiment of the invention relates to compounds of Formula (I) according to embodiment 1), wherein A represents -CH2-; -N(RA)-, wherein RArepresents hydrogen or (C1-4)alkyl; or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; X represents -O-, or -S-; R1represents (C1-6)alkyl; (C2-4)alkynyl; (C1-4)fluoroalkyl; (C1-4)alkoxy-(C1-4)alkyl; (C3- 8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; (C3-8)heterocyclyl; aryl; aryl-(C1-4)alkyl; or heteroaryl; R2represents (C3-8)cycloalkyl; ferrocenyl; aryl which is independently unsubstituted or substituted with 1 to 3 substituents (especially 1 or 2 substituents) independently selected from the group consisting of (C1-4)alkyl, (C2-4)alkynyl, cyano, and halogen; pentadeutero- phenyl; or heteroaryl which is independently unsubstituted or mono- or di-substituted with halogen; R3represents hydrogen, (C1-4)alkyl, or halogen (especially hydrogen or fluoro); R4represents hydrogen, deuterium, (C1-4)alkyl, or (C1-4)fluoroalkyl (especially hydrogen, deuterium, or (C1-4)alkyl); and R5represents hydrogen, or deuterium; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 3) A further embodiment of the invention to compounds of Formula (I) according to any one of embodiments 1) or 2), wherein A represents -CH2-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 4) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 2), wherein A represents -N(RA)-, wherein RArepresents hydrogen or (C1-4)alkyl; or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 5) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 2), wherein A represents -NH-; or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 6) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 2), wherein A represents -N(RA)-, wherein RArepresents hydrogen or (C1-4)alkyl (especially methyl); and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 7) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 2), wherein A represents -NH-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 8) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 2), wherein A represents -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 9) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 8), wherein X represents -O-, or -S-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 10) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 8), wherein X represents -O-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 11) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 8), wherein X represents -S-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 12) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 11), wherein R1represents (C1-6)alkyl; (C2-4)alkynyl; (C1-4)fluoroalkyl; (C1-4)alkoxy-(C1-4)alkyl; (C3-8) which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; (C3- 8)heterocyclyl; aryl; aryl-(C1-4)alkyl; or heteroaryl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 13) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 11), wherein R1represents (C1-6)alkyl; (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; or (C3-8)heterocyclyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 14) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 11), wherein R1represents (C1-6)alkyl; (C3-8)cycloalkyl; (C3- 8)cycloalkyl-(C1-4)alkyl; or (C3-8)heterocyclyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 15) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 11), wherein R1represents (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1-4)alkoxy, and halogen (especially cyclopropyl, cyclobutyl, 3,3-dimethyl-cyclobutyl, or bicyclo[1.1.1]pentyl); and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 16) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 11), wherein R1represents aryl; aryl-(C1-4)alkyl; or heteroaryl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 17) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 16), wherein R2represents (C3-8)cycloalkyl; ferrocenyl; aryl which is independently unsubstituted or substituted with 1 to 3 substituents (especially 1 or 2 substituents) independently selected from the group consisting of (C1-4)alkyl, (C2-4)alkynyl, cyano, and halogen; pentadeutero-phenyl; or heteroaryl which is independently unsubstituted or mono- or di-substituted with halogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 18) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 16), wherein R2represents aryl which is independently unsubstituted or substituted with 1 or 2 substituents independently selected from the group consisting of (C1-4)alkyl, (C2-4)alkynyl, halogen; pentadeutero-phenyl; or heteroaryl which is independently unsubstituted or mono- or di-substituted with halogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 19) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 16), wherein R2represents phenyl which is unsubstituted or mono-substituted with (C1-4)alkyl (especially methyl) or halogen (especially fluoro); or pentadeutero-phenyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 20) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 16), wherein R2represents phenyl or pentadeutero-phenyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 21) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 20), wherein R3represents hydrogen or halogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 22) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 20), wherein R3represents hydrogen or fluoro; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 23) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 20), wherein R3represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 24) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 23), wherein R4represents hydrogen, deuterium, or methyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 25) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 23), wherein R4represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 26) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) to 25), wherein R5represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 27) A further embodiment of the invention relates to compounds of Formula (I), wherein A represents -CH2-; -N(RA)-, wherein RArepresents hydrogen or (C1-4)alkyl; or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; X represents -O-, -S-, or -NH-; R1represents (C2-6)alkyl (especially iso-propyl, and tert.-butyl); (C2-4)alkenyl; (C2-4)alkynyl which is independently unsubstituted or mono-substituted with aryl; (C1- 4)fluoroalkyl; (C1-4)hydroxyalkyl; (C1-4)alkoxy-(C1-4)alkyl; (C1-4)alkyl-carbonyl; (C1-4)alkoxy- carbonyl; amino-carbonyl; (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; (C3-8)heterocyclyl; (2-oxoimidazolidin-1-yl)methyl; aryl; aryl-(C1-4)alkyl; or heteroaryl; R2represents (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted with halogen; ferrocenyl; aryl which is independently unsubstituted or substituted with 1 to 5 substituents independently selected from the group consisting of deuterium, (C1-4)alkyl, (C2-4)alkynyl, (C1-4)alkyl-carbonyl, cyano, fluoro, (C1-4)fluoroalkyl, and (C1-4)hydroxyalkyl; or heteroaryl which is independently unsubstituted or mono- or di-substituted with halogen; R3represents hydrogen, (C1-4)alkyl, or halogen (especially hydrogen or fluoro); R4represents hydrogen, deuterium, or (C1-4)alkyl; and R5represents hydrogen, or deuterium; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 28) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 27), wherein A represents -NH- (preferred); or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; X represents -O-; R1represents (C2-6)alkyl (especially ethyl, n-propyl, iso-propyl, and tert.-butyl); (C2-4)alkynyl; (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; or (C3-8)heterocyclyl; R2represents phenyl which is unsubstituted (preferred) or substituted with 1 or 2 substituents independently selected from the group consisting of (C1-4)alkyl, (C2-4)alkynyl, cyano, and fluoro; pentadeutero-phenyl; or heteroaryl which is independently unsubstituted (preferred) or mono-substituted with halogen; R3represents hydrogen, or halogen (especially hydrogen or fluoro); R4represents hydrogen, deuterium, or (C1-4)alkyl; and R5represents hydrogen, or deuterium; and to the salts (in particular salts) of the compounds. 29) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), 27) or 28), wherein A represents -NH- (preferred); or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 30) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), 27) or 28), wherein A represents -NH-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 31) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), 27) or 28), wherein A represents -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 32) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 31), wherein X represents -O-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 33) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 32), wherein R1represents (C2-6)alkyl (especially ethyl, n-propyl, iso-propyl, and tert.-butyl); (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl- (C1-4)alkyl; or (C3-8)heterocyclyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 34) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 32), wherein R1represents (C2-6)alkyl (especially ethyl, n-propyl, iso-propyl, and tert.-butyl); (C3-8)cycloalkyl; (C3-8)cycloalkyl-(C1-4)alkyl; or (C3-8)heterocyclyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 35) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 32), wherein R1represents (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, (C1-4)alkoxy, and halogen (especially cyclopropyl, cyclobutyl, 3,3-dimethyl-cyclobutyl, or bicyclo[1.1.1]pentyl); and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 36) A further embodiment of the invention to compounds of Formula (I) according to any one of embodiments 1), 27) or 29) to 32), wherein R1represents aryl; aryl-(C1-4)alkyl; or heteroaryl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 37) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 36), wherein R2represents phenyl which is unsubstituted (preferred) or substituted with 1 or 2 substituents independently selected from the group consisting of (C1-4)alkyl, (C2-4)alkynyl, cyano, and fluoro; pentadeutero-phenyl; or heteroaryl which is independently unsubstituted (preferred) or mono-substituted with halogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 38) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 36), wherein R2represents phenyl which is unsubstituted or mono-substituted with (C1-4)alkyl (especially methyl) or fluoro; or pentadeutero-phenyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 39) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 36), wherein R2represents phenyl or pentadeutero- phenyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 40) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 39), wherein R3represents hydrogen or halogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 41) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 39), wherein R3represents hydrogen or fluoro; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 42) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 39), wherein R3represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 43) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 42), wherein R4represents hydrogen, deuterium, or methyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 44) A further embodiment of the invention to compounds of Formula (I) according to any one of embodiments 1), or 27) to 42), wherein R4represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 45) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1), or 27) to 44), wherein R5represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 46) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 27), wherein A represents -NH-; X represents -O-; R1represents (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted with (C1-4)alkyl; R2represents phenyl which is unsubstituted or mono-substituted with fluoro; or pentadeutero- phenyl; R3represents hydrogen, or fluoro; R4represents hydrogen, deuterium, or (C1-4)alkyl; and R5represents hydrogen, or deuterium; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 47) A further embodiment of the invention relates to compounds of Formula (I) according to embodiment 46), wherein R1represents (C3-8)cycloalkyl which is independently unsubstituted or di-substituted with methyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 48) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 46) or 47), wherein R2represents phenyl or pentadeutero-phenyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 49) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 46) to 48), wherein R3represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 50) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 46) to 49), wherein R4represents hydrogen, deuterium, or methyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 51) A further embodiment of the invention to compounds of Formula (I) according to any one of embodiments 46) to 49), wherein R4represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 52) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 46) to 51), wherein R5represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 53) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 27), wherein A represents -NH- (preferred); or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; X represents -O-; R1represents ethyl, iso-propyl, tert.-butyl, ethynyl, cyclopropyl, cyclobutyl, 3,3-dimethyl- cyclobutyl, 3-methoxy-cyclobutyl, 3,3-difluoro-cyclobutyl, bicyclo[3.1.0]hexyl (especially 3- bicyclo[3.1.0]hexyl), bicyclo[1.1.1]pentyl (especially 1-bicyclo[1.1.1]pentyl), cyclopropyl- methyl, 1-cyclopropyl-ethyl, cyclopentyl-methyl, or oxetanyl (especially 3-oxetanyl); R2represents phenyl which is unsubstituted (preferred) or substituted with 1 or 2 substituents independently selected from the group consisting of methyl, ethynyl, cyano, and fluoro; pentadeutero-phenyl; furanyl (especially furan-3-yl); thienyl (especially thiophen-3-yl); or 2- chloro-thienyl (especially 2-chloro-thiophen-4-yl); R3represents hydrogen or fluoro; R4represents hydrogen, deuterium, or methyl; and R5represents hydrogen, or deuterium; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 54) A further embodiment of the invention relates to compounds of Formula (I) according to embodiment 53), wherein A represents -NH-; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 55) A further embodiment of the invention relates to compounds of Formula (I) according to embodiment 53), wherein A represents -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 56) A further embodiment of the invention to compounds of Formula (I) according to any one of embodiments 53) to 55), wherein R1represents cyclopropyl, cyclobutyl, 3,3- dimethyl-cyclobutyl, or 1-bicyclo[1.1.1]pentyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 57) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 53) to 56), wherein R2represents phenyl or pentadeutero-phenyl; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 58) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 53) to 57), wherein R3represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 59) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 53) to 58), wherein R4represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 60) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 53) to 59), wherein R5represents hydrogen; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. 61) A further embodiment of the invention relates to compounds of Formula (I) according to any one of embodiments 1) or 27), wherein A represents -NH-; X represents -O-; R1represents cyclopropyl, cyclobutyl, 3,3-dimethyl-cyclobutyl, or 1-bicyclo[1.1.1]pentyl; R2represents phenyl; 4-fluorophenyl; or pentadeutero-phenyl; R3represents hydrogen; R4represents hydrogen, or deuterium, or methyl; and R5represents hydrogen, or deuterium; and to the salts (in particular pharmaceutically acceptable salts) of the compounds. The invention, thus, relates to compounds of Formula (I) as defined in embodiment 1) or 27), and to such compounds further limited by the characteristics of any one of embodiments 2) to 26) and 28) to 61), under consideration of their respective dependencies; to pharmaceutically acceptable salts thereof; and to the use of such compounds as further described below. For avoidance of doubt, especially the following embodiments relating to the compounds of Formula (I) are thus and intended and herewith specifically disclosed in individualized form: 1, 2+1, 3+1, 3+2+1, 4+1, 4+2+1, 5+1, 5+2+1, 6+1, 6+2+1, 7+1, 7+2+1, 8+1, 8+2+1, 9+1, 9+2+1, 9+5+1, 9+5+2+1, 9+7+1, 9+7+2+1, 10+1, 10+2+1, 10+5+1, 10+5+2+1, 10+7+1, 10+7+2+1, 11+1, 11+2+1, 11+5+1, 11+5+2+1, 11+7+1, 11+7+2+1, 12+1, 12+2+1, 12+5+1, 12+5+2+1, 12+7+1, 12+7+2+1, 12+10+1, 12+10+2+1, 12+10+5+1, 12+10+5+2+1, 12+10+7+1, 12+10+7+2+1, 13+1, 13+2+1, 13+5+1, 13+5+2+1, 13+7+1, 13+7+2+1, 13+10+1, 13+10+2+1, 13+10+5+1, 13+10+5+2+1, 13+10+7+1, 13+10+7+2+1, 14+1, 14+2+1, 14+5+1, 14+5+2+1, 14+7+1, 14+7+2+1, 14+10+1, 14+10+2+1, 14+10+5+1, 14+10+5+2+1, 14+10+7+1, 14+10+7+2+1, 15+1, 15+2+1, 15+5+1, 15+5+2+1, 15+7+1, 15+7+2+1, 15+10+1, 15+10+2+1, 15+10+5+1, 15+10+5+2+1, 15+10+7+1, 15+10+7+2+1, 16+1, 16+2+1, 16+5+1, 16+5+2+1, 16+7+1, 16+7+2+1, 16+10+1, 16+10+2+1, 16+10+5+1, 16+10+5+2+1, 16+10+7+1, 16+10+7+2+1, 17+1, 17+2+1, 17+5+1, 17+5+2+1, 17+7+1, 17+7+2+1, 17+10+1, 17+10+2+1, 17+10+5+1, 17+10+5+2+1, 17+10+7+1, 17+10+7+2+1, 17+13+1, 17+13+2+1, 17+13+5+1, 17+13+5+2+1, 17+13+7+1, 17+13+7+2+1, 17+13+10+1, 17+13+10+2+1, 17+13+10+5+1, 17+13+10+5+2+1, 17+13+10+7+1, 17+13+10+7+2+1, 17+15+1, 17+15+2+1, 17+15+5+1, 17+15+5+2+1, 17+15+7+1, 17+15+7+2+1, 17+15+10+1, 17+15+10+2+1, 17+15+10+5+1, 17+15+10+5+2+1, 17+15+10+7+1, 17+15+10+7+2+1, 18+1, 18+2+1, 18+5+1, 18+5+2+1, 18+7+1, 18+7+2+1, 18+10+1, 18+10+2+1, 18+10+5+1, 18+10+5+2+1, 18+10+7+1, 18+10+7+2+1, 18+13+1, 18+13+2+1, 18+13+5+1, 18+13+5+2+1, 18+13+7+1, 18+13+7+2+1, 18+13+10+1, 18+13+10+2+1, 18+13+10+5+1, 18+13+10+5+2+1, 18+13+10+7+1, 18+13+10+7+2+1, 18+15+1, 18+15+2+1, 18+15+5+1, 18+15+5+2+1, 18+15+7+1, 18+15+7+2+1, 18+15+10+1, 18+15+10+2+1, 18+15+10+5+1, 18+15+10+5+2+1, 18+15+10+7+1, 18+15+10+7+2+1, 19+1, 19+2+1, 19+5+1, 19+5+2+1, 19+7+1, 19+7+2+1, 19+10+1, 19+10+2+1, 19+10+5+1, 19+10+5+2+1, 19+10+7+1, 19+10+7+2+1, 19+13+1, 19+13+2+1, 19+13+5+1, 19+13+5+2+1, 19+13+7+1, 19+13+7+2+1, 19+13+10+1, 19+13+10+2+1, 19+13+10+5+1, 19+13+10+5+2+1, 19+13+10+7+1, 19+13+10+7+2+1, 19+15+1, 19+15+2+1, 19+15+5+1, 19+15+5+2+1, 19+15+7+1, 19+15+7+2+1, 19+15+10+1, 19+15+10+2+1, 19+15+10+5+1, 19+15+10+5+2+1, 19+15+10+7+1, 19+15+10+7+2+1, 20+1, 20+2+1, 20+5+1, 20+5+2+1, 20+7+1, 20+7+2+1, 20+10+1, 20+10+2+1, 20+10+5+1, 20+10+5+2+1, 20+10+7+1, 20+10+7+2+1, 20+13+1, 20+13+2+1, 20+13+5+1, 20+13+5+2+1, 20+13+7+1, 20+13+7+2+1, 20+13+10+1, 20+13+10+2+1, 20+13+10+5+1, 20+13+10+5+2+1, 20+13+10+7+1, 20+13+10+7+2+1, 20+15+1, 20+15+2+1, 20+15+5+1, 20+15+5+2+1, 20+15+7+1, 20+15+7+2+1, 20+15+10+1, 20+15+10+2+1, 20+15+10+5+1, 20+15+10+5+2+1, 20+15+10+7+1, 20+15+10+7+2+1, 21+1, 21+2+1, 21+5+1, 21+5+2+1, 21+7+1, 21+7+2+1, 21+10+1, 21+10+2+1, 21+10+5+1, 21+10+5+2+1, 21+10+7+1, 21+10+7+2+1, 21+13+1, 21+13+2+1, 21+13+5+1, 21+13+5+2+1, 21+13+7+1, 21+13+7+2+1, 21+13+10+1, 21+13+10+2+1, 21+13+10+5+1, 21+13+10+5+2+1, 21+13+10+7+1, 21+13+10+7+2+1, 21+15+1, 21+15+2+1, 21+15+5+1, 21+15+5+2+1, 21+15+7+1, 21+15+7+2+1, 21+15+10+1, 21+15+10+2+1, 21+15+10+5+1, 21+15+10+5+2+1, 21+15+10+7+1, 21+15+10+7+2+1, 21+20+1, 21+20+2+1, 21+20+5+1, 21+20+5+2+1, 21+20+7+1, 21+20+7+2+1, 21+20+10+1, 21+20+10+2+1, 21+20+10+5+1, 21+20+10+5+2+1, 21+20+10+7+1, 21+20+10+7+2+1, 21+20+13+1, 21+20+13+2+1, 21+20+13+5+1, 21+20+13+5+2+1, 21+20+13+7+1, 21+20+13+10+1, 21+20+13+10+2+1, 21+20+13+10+5+1, 21+20+13+10+5+2+1, 21+20+13+10+7+1, 21+20+13+10+7+2+1, 21+20+15+1, 21+20+15+2+1, 21+20+15+5+1, 21+20+15+5+2+1, 21+20+15+7+1, 21+20+15+7+2+1, 21+20+15+10+1, 21+20+15+10+2+1, 21+20+15+10+5+1, 21+20+15+10+5+2+1, 21+20+15+10+7+1, 21+20+15+10+7+2+1, 22+1, 22+2+1, 22+5+1, 22+5+2+1, 22+7+1, 22+7+2+1, 22+10+1, 22+10+2+1, 22+10+5+1, 22+10+5+2+1, 22+10+7+1, 22+10+7+2+1, 22+13+1, 22+13+2+1, 22+13+5+1, 22+13+5+2+1, 22+13+7+1, 22+13+7+2+1, 22+13+10+1, 22+13+10+2+1, 22+13+10+5+1, 22+13+10+5+2+1, 22+13+10+7+1, 22+13+10+7+2+1, 22+15+1, 22+15+2+1, 22+15+5+1, 22+15+5+2+1, 22+15+7+1, 22+15+7+2+1, 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In the list above the numbers refer to the embodiments according to their numbering provided hereinabove whereas “+” indicates the dependency from another embodiment. The different individualized embodiments are separated by commas. In other words, “3+2+1” for example refers to embodiment 3) depending on embodiment 2), depending on embodiment 1), i.e. embodiment “3+2+1” corresponds to the compounds of embodiment 1) further limited by the features of the embodiments 2) and 3). 62) Another embodiment relates to compounds of Formula (I) according to embodiment 1), which are selected from the following compounds: 5-cyclopropyl-N-((1-(4,4-difluorocyclohexyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine; N-((1-(bicyclo[1.1.1]pentan-1-yl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol- 2-amine; 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(2-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(3-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(m-tolyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(p-tolyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-(4-chlorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(4-(trifluoromethyl)phenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol- 2-amine; 4-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1-yl)benzonitrile; (3-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1- yl)phenyl)methanol; 2-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1-yl)benzonitrile; N-((1-(2-chlorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(4-methoxyphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine; 5-cyclopropyl-N-((1-(phenyl-d5)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(furan-3-yl)-1H-1,2,3- 4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(thiophen-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-(5-chlorothiophen-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol-2- amine; 5-cyclopropyl-N-((1-(pyridin-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-ferrocenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(cyclopentylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(cyclopropylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(1-cyclopropylethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 2-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)propan-2-ol; 1-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)cyclopropan-1-ol; 5-phenyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclobutyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-methyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(thiazol-5-yl)-1,3,4-oxadiazol-2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(2-azaspiro[3.3]heptan-6-yl)-1,3,4-oxadiazol-2- amine; 5-isopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(pyridin-4-yl)-1,3,4-oxadiazol-2-amine; 5-(tert-butyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(methoxymethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-benzyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(2-fluoropropan-2-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(oxetan-3-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(3,3-difluorocyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine; 5-(3-methoxycyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(3,3-dimethylcyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine; 5-(bicyclo[1.1.1]pentan-1-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine; 5-(bicyclo[3.1.0]hexan-3-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine; ethyl 5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazole-2-carboxylate; (5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)methanol; 5-(difluoromethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-ethynyl-N-((1-phenyl-1H-1,2,3-triazol-4- -1,3,4-oxadiazol-2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(phenylethynyl)-1,3,4-oxadiazol-2-amine; 1-((5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2- yl)methyl)imidazolidin-2-one; 5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazole-2-carboxamide; 1-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)ethan-1-one; 5-(cyclopentylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-thiadiazol-2-amine; N-((1-cyclohexyl-1H-1,2,3-triazol-4-yl)methyl)-5-(cyclopentylmethyl)-1,3,4-oxadiazol-2- amine; (R)-5-cyclopropyl-N-(1-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2-amine; (S)-5-cyclopropyl-N-(1-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((5-fluoro-1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl-d2)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-methyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 2-cyclopropyl-5-(2-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazole; 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-4H-1,2,4-triazol-3-amine; 5-cyclopropyl-N-(2-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((5-methyl-1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 1-(4-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1- yl)phenyl)ethan-1-one; 5-cyclopropyl-N-((1-(4-ethynylphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(1,3-dithiolan-2-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; and 5-(1,3-dioxolan-2-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; and to the salts (in particular pharmaceutically acceptable salts) of such compounds. The present invention also includes isotopically labelled, especially2H (deuterium) labelled compounds of Formula (I), which compounds are identical to the compounds of Formula (I) except that one or more atoms have each been replaced by an atom having the same atomic number but an atomic mass different from the atomic mass usually found in nature. Isotopically labelled, especially2H (deuterium) labelled compounds of Formula (I) and salts thereof are within the scope of the present invention. Substitution of hydrogen with the heavier isotope2H (deuterium) may lead to greater metabolic stability, resulting e.g. in increased in- vivo half-life or reduced dosage requirements, or may lead to reduced inhibition of cytochrome P450 enzymes, resulting e.g. in an improved safety profile. In one embodiment of the invention, the compounds of Formula (I) isotopically labelled, or they are labelled only with one or more deuterium atoms. In a sub-embodiment, the compounds of Formula (I) are not isotopically labelled at all. Isotopically labelled compounds of Formula (I) may be prepared in analogy to the methods described hereinafter, but using the appropriate isotopic variation of suitable reagents or starting materials. Where the plural form is used for compounds, salts, pharmaceutical compositions, diseases or the like, this is intended to mean also a single compound, salt, pharmaceutical composition, disease or the like. Any reference to a compound of Formula (I) as defined in any one of embodiments 1) to 62) is to be understood as referring also to the salts (and especially the pharmaceutically acceptable salts) of such compounds, as appropriate and expedient. The term "pharmaceutically acceptable salts" refers to salts that retain the desired biological activity of the subject compound and exhibit minimal undesired toxicological effects. Such salts include inorganic or organic acid and / or base addition salts depending on the presence of basic and / or acidic groups in the subject compound. For reference see for example ‘Handbook of Pharmaceutical Salts. Properties, Selection and Use.’, P. Heinrich Stahl, Camille G. Wermuth (Eds.), Wiley-VCH, 2008 and ‘Pharmaceutical Salts and Co-crystals’, Johan Wouters and Luc Quéré (Eds.), RSC Publishing, 2012. Whenever the word “between” is used to describe a numerical range, it is to be understood that the end points of the indicated range are explicitly included in the range. For example: if a temperature range is described to be between 40 ºC and 80 ºC, this means that the end points 40 ºC and 80 ºC are included in the range; or if a variable is defined as being an integer between 1 and 4, this means that the variable is the integer 1, 2, 3, or 4. Unless used regarding temperatures, the term “about” (or alternatively “around”) placed before a numerical value “X” refers in the current application to an interval extending from X minus 10% of X to X plus 10% of X, and preferably to an interval extending from X minus 5% of X to X plus 5% of X. In the particular case of temperatures, the term “about” (or alternatively “around”) placed before a temperature “Y” refers in the current application to an interval extending from the temperature Y minus 10 ºC to Y plus 10 ºC, and preferably to an interval extending from Y minus 5 ºC to Y plus 5 ºC. Besides, the term “room temperature” as used herein refers to a temperature of about 25 °C. The compounds of formula (I) as defined in any one of embodiments 1) to 62) and their pharmaceutically acceptable salts can be used as medicaments, e.g. in the form of pharmaceutical compositions for enteral (such as especially oral) or parenteral administration (including topical application or inhalation). The production of the pharmaceutical can be effected in a manner which will be familiar to any person skilled in the art (see for example Remington, The Science and Practice of Pharmacy, 21st Edition (2005), Part 5, “Pharmaceutical Manufacturing” [published by Lippincott Williams & Wilkins]) by bringing the described compounds of Formula (I) or their pharmaceutically acceptable salts, optionally in combination with other therapeutically valuable substances, into a galenical administration form together with suitable, non-toxic, inert, therapeutically compatible solid or liquid carrier materials and, if desired, usual pharmaceutical adjuvants. The present invention also relates to a method for the prevention or treatment of a disease or disorder mentioned herein comprising administering to a subject a pharmaceutically active amount of a compound of Formula (I) as defined in any one of embodiments 1) to 62) either alone or in combination with other pharmacologically active compounds and / or therapies. The meaning of the term “prevention” may also be understood as “prophylaxis”. For avoidance of any doubt, if compounds are described as useful for the prevention or treatment of certain diseases, such compounds are likewise suitable for use in the preparation of a medicament for the prevention or treatment of said diseases. Another aspect of the invention concerns a method for the prophylaxis or the treatment of a disease or disorder as mentioned below in a patient comprising the administration to said patient of a pharmaceutically active amount of a compound of Formula (I) as defined in any one of embodiments 1) to 62) or a pharmaceutically acceptable salt thereof. The compounds according to Formula (I) as defined in any one of embodiments 1) to 62) may be used in the prevention and / or treatment of diseases or disorders related to the IL4i1 enzyme; such as especially cancers. Cancers may be defined as cancers displaying IL4i1-expressing cells including skin cancer including melanoma; metastatic melanoma; lung cancer including non-small cell lung cancer; bladder cancer including urinary bladder cancer; urothelial cell carcinoma; renal carcinomas including renal cell carcinoma; metastatic renal cell carcinoma; metastatic renal clear cell carcinoma; gastro-intestinal cancers including colorectal cancer; metastatic colorectal cancer; familial adenomatous polyposis (FAP); esophageal cancer; gastric cancer; gallbladder cancer; cholangiocarcinoma; hepatocellular carcinoma; pancreatic cancer such as pancreatic adenocarcinoma or pancreatic ductal carcinoma; endometrial cancer; ovarian cancer; cervical cancer; neuroblastoma; prostate cancer including castrate-resistant prostate cancer; brain tumors including brain metastases, malignant gliomas, glioblastoma multiforme, medulloblastoma, meningiomas, neuroblastoma, astrocytoma; breast cancer including triple negative breast carcinoma; oral tumors; tumors; thoracic cancer; head and neck cancer; mesothelioma; leukemias including acute myeloid leukemia, and adult T-cell leukemia; carcinomas; adenocarcinomas; thyroid carcinoma including papillary thyroid carcinoma; choriocarcinoma; sarcomas including Ewing’s sarcoma; osteosarcoma; rhabdomyosarcoma; Kaposi’s sarcoma; lymphoma including Burkitt’s lymphoma, Hodgkin’s lymphoma, MALT lymphoma; multiple myelomas; and virally induced tumors. Further, cancers may be defined as cancers displaying IL4i1-expressing cells including brain cancers, skin cancers, bladder cancers, ovarian cancers, breast cancers, gastric cancers, pancreatic cancers, prostate cancers, colon cancers, blood cancers, lung cancers and bone cancers. Examples of such cancer types include neuroblastoma, intestine carcinoma such as rectum carcinoma, colon carcinoma, familiar adenomatous polyposis carcinoma and hereditary non-polyposis colorectal cancer, esophageal carcinoma, labial carcinoma, larynx carcinoma, hypopharynx carcinoma, tongue carcinoma, salivary gland carcinoma, gastric carcinoma, adenocarcinoma, medullary thyroid carcinoma, papillary thyroid carcinoma, renal carcinoma, kidney parenchymal carcinoma, ovarian carcinoma, cervix carcinoma, uterine corpus carcinoma, endometrium carcinoma, chorion carcinoma, pancreatic carcinoma, prostate carcinoma, testis carcinoma, breast carcinoma, urinary carcinoma, melanoma, brain tumors such as glioblastoma, astrocytoma, meningioma, medulloblastoma and peripheral neuroectodermal tumors, Hodgkin lymphoma, non-Hodgkin lymphoma, Burkitt lymphoma, acute lymphatic leukemia (ALL), chronic lymphatic leukemia (CLL), acute myeloid leukemia (AML), chronic myeloid leukemia (CML), adult T-cell leukemia lymphoma, diffuse large B-cell lymphoma (DLBCL), hepatocellular carcinoma, gall bladder carcinoma, bronchial carcinoma, small cell lung carcinoma, non-small cell lung carcinoma, multiple myeloma, basalioma, teratoma, retinoblastoma, choroid melanoma, seminoma, rhabdomyosarcoma, craniopharyngioma, osteosarcoma, chondrosarcoma, myosarcoma, liposarcoma, fibrosarcoma, Ewing sarcoma and plasmacytoma. Cancers displaying IL4i1-expressing cells may notably be defined as solid tumors that have specific genetic features, called mismatch repair deficiency and high microsatellite instability; skin cancer, in particular advanced melanoma, Merkel cell carcinoma, and cutaneous squamous cell carcinoma; lung cancer (non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC)); rectal squamous cell carcinoma; bladder cancer; advanced cervical cancer; endometrial cancer; advanced gastric cancer; head and neck cancer; esophageal carcinoma; triple negative breast cancer; renal cell carcinoma; metastatic colorectal cancer with mismatch repair deficiency (dMMR) or high microsatellite instability (MSI-H); primary mediastinal large B-cell lymphoma; advanced liver cancer; and Hodgkin’s lymphoma. Cancers may especially be defined as displaying IL4i1-expressing cells including solid tumors such as ovarian carcinoma, thyroid cancer, melanoma, non-small cell lung cancer (NSCLC), pancreatic adenocarcinoma, testicular germ cell tumors, mesothelioma, colon carcinoma, triple negative breast cancer, clear cell renal cell carcinoma, hepatocellular carcinoma, glioblastoma, endometrial cardinoma as well as lymphomas, in particular B-cell lymphoid malignancies, B-cell lymphoma, Primary Mediastinal large B-cell lymphoma (PMBL), classical Hodgkin lymphoma (cHL), Nodular Lymphocyte predominant Hodgkin’s lymphoma (NLPHL), non-mediastinal diffuse large B-Cell Lymphoma (DLBCL), and Small Lymphocytic Lymphoma / chronic Lymphocytic Leukemia (SLL / CLL), follicular lymphoma, marginal zone lymphoma. One or more compounds of Formula (I) may be used in the prevention and / or treatment of any cancer, notably the cancers mentioned hereinabove, either alone, or in combination with further pharmacologically active compounds and / or therapies selected from the group comprising surgery, radiotherapy, chemotherapy, hormonal therapy, immunotherapy, targeted therapy, cell therapy, gene therapy, cancer vaccines, virotherapy, and any combination thereof (and especially radiotherapy, chemotherapy, hormonal therapy, immunotherapy, targeted therapy, cell therapy, gene therapy, cancer vaccines, virotherapy, and any combination thereof). The terms "radiotherapy" or "radiation therapy" or "radiation oncology", refer to the medical use of ionizing radiation in the prevention (adjuvant therapy) and / or treatment of cancer; including external and internal radiotherapy. The term "targeted therapy" refers to the prevention / prophylaxis (adjuvant therapy) and / or treatment of cancer with one or more anti-neoplastic agents such as small molecules or antibodies which act on specific types of cancer cells or stromal cells. Some targeted therapies block the action of certain enzymes, proteins, or other molecules involved in the growth and spread of cancer cells. Other types of targeted therapies help the immune system kill cancer cells (immunotherapies); or deliver toxic substances directly to cancer cells and kill them. An example of a targeted therapy which is in particular suitable to be combined with the compounds of the present invention is immunotherapy, especially immunotherapy targeting the programmed death 1 (PD-1) receptor or its ligand PD-L1. Immunotherapy further refers to (i) an agonist of a stimulatory (including a co-stimulatory) receptor or (ii) an antagonist of an inhibitory (including a co­ inhibitory) signal on T cells, both of which result in amplifying antigen-specific T cell responses (often referred to as immune checkpoint regulators). Certain of the stimulatory and inhibitory molecules are members of the immunoglobulin super family (IgSF). important family of membrane-bound ligands that bind to co-stimulatory or co-inhibitory receptors is the B7 family, which includes B7-1, B7- 2, B7-H1 (PD-L1), B7-DC (PD-L2), B7-H2 (ICOS-L), B7-H3, B7-H4, B7-H5 (VISTA), and B7- H6. Another family of membrane bound ligands that bind to co­stimulatory or co-inhibitory receptors is the TNF family of molecules that bind to cognate TNF receptor family members, which includes CD40 and CD40L, OX-40, OX-40L, CD70, CD27L, CD30, CD30L, 4-lBBL, CD137 (4-lBB), TRAIL / Apo2-L, TRAILR1 / DR4, TRAILR2 / DR5, TRAILR3, TRAILR4, OPG, RANK, RANKL, TWEAKR / Fnl4, TWEAK, BAFFR, EDAR, XEDAR, TACI, APRIL, BCMA, LTpR, LIGHT, DcR3, HVEM, VEGI / TLlA, TRAMP / DR3, EDAR, EDAl, XEDAR, EDA2, TNFRl, Lymphotoxin a / TNFp, TNFR2, TNFa, LTPR, Lymphotoxin a 1p2, FAS, FASL, RELT, DR6, TROY, NGFR. When used in combination with the compounds of Formula (I), the term "targeted therapy" especially refers to agents such as: a. Epidermal growth factor receptor (EGFR) inhibitors or blocking antibodies (for example Gefitinib, Erlotinib, Afatinib, Icotinib, Lapatinib, Panitumumab, Neratinib, Osimertinib, Dacomitinib, Almonertinib, Tucatinib, Zalutumumab, Nimotuzumab, Matuzumab and Cetuximab) as well as trastuzumab (HERCEPTIN); b. Biologics targeting CD20 (for example Rituximab) c. RAS / RAF / MEK pathway inhibitors (for example Vemurafenib, Sorafenib, Dabrafenib, GDC-0879, PLX-4720, Encorafenib (LGX818), RG7304, Trametinib (GSK1120212), Cobimetinib (GDC-0973 / XL518), Binimetinib (MEK162, ARRY-162), Selumetinib (AZD6244)), Sotorasib, Adagrasib, as well as various mutant KRAS-specific, pan RAS, SOS1, SHP2 inhibitors, (Punekar et al., Nature Rev Clin Oncology, 2022, 19(10):637-655); d. Janus kinase (JAK) inhibitors ( for example Ruxolitinib, Itacitinib, Momelotinib, Fedratinib); e. Aromatase inhibitors (for example Exemestane, Letrozole, Anastrozole, Vorozole, Formestane, Fadrozole); f. signal transduction inhibitors (STI). A "signal transduction inhibitor" is an agent that selectively inhibits one or more vital steps in signaling pathways in the normal function of cancer cells, thereby leading to apoptosis. Suitable STIs include but are not limited to: (i) bcr / abl kinase inhibitors such as, for example, STI 571 (GLEEVEC®), Dasatinib, Ponatinib, Imatinib, Nilotinib, Radotinib,; (ii) inhibitors of Akt family kinases or the Akt pathway, such as, for example, Everolimus, and Temsirolimus; (iii) cell cycle kinase inhibitors such as, for example, Palbociclib, Ribociclib, and Abemaciclib; (iv) phosphatidyl inositol kinase inhibitors such as, for example,Copanlisib, Duvelisib, Idelalisib, Leniolisib, Alpelisib, and Umbralisib; (v) ALK inhibitors, such as, for example, Crizotinib, Ceritinib, Alectinib, Lorlatinib; (vi) BTK inhibitors, such as, for example, Ibrutinib, Acalabrutinib, Zanubrutinib; (vii) IDH inhibitors, such as, for example, Enasidenib, Ivosidenib; (viii) RET inhibitors, such as, for example, Selpercatinib; (ix) BCL-2 inhibitors, such as, for example, Venetoclax; (x) c-MET inhibitors, such as, for example, Capmatinib, Tepotinib; g. Angiogenesis inhibitors, especially VEGF signalling inhibitors such as Bevacuzimab (Avastin), Ramucirumab , Sorafenib or Axitinib; h. Poly-ADP-Ribose-Polymerase (PARP) inhibitors, such as Olaparib, Niraparib, Rucaparib, Talazoparib; i. Proteasome inhibitors (for example: Bortezomib, Carfilzomib, Ixazomib); j. HDAC inhibitors (for example: Vorinostat, Romidepsin, Belinostat, Panobinostat, Tucidinostat); EZH2 inhibitors (for example: Tazemetostat); k. Immune Checkpoint inhibitors (for example: anti-PD1 antibodies such as Pembrolizumab (Lambrolizumab, MK-3475), Nivolumab, Pidilizumab (CT-011), AMP- 514 / MEDI0680, PDR001, SHR-1210; REGN2810, BGBA317, PF-06801591, MGA- 012, TSR042, JS-001, BCD100, IBI-308, BI-754091, Toripalimab; fusion proteins targeting PD-1 such as AMP-224; small molecule anti-PD1 agents such as for example compounds disclosed in WO2015 / 033299, WO2015 / 044900 and WO2015 / 034820; anti-PD-L1 antibodies, such as BMS-936559, atezolizumab (MPDL3280A, RG7446), avelumab (MSB0010718C), durvalumab (MEDI4736); anti- PD-L2 antibodies, such as AMP224; anti-CTLA-4 antibodies, such as ipilimumab, tremelimumab; anti-Lymphocyte-activation gene 3 (LAG-3) antibodies, such as Relatlimab (BMS-986016), IMP701, IMP731, MK-4280, ImmuFact IMP321; anti T cell immunoglobulin mucin-3 (TIM-3) antibodies, such as MBG453, TSR-022; anti T cell immunoreceptor with Ig and ITIM domains (TIGIT) antibodies, such as RG6058 (anti- TIGIT, MTIG7192A); anti- Killer-cell immunoglobulin-like receptors (KIR) antibodies, such as Lirilumab (IPH2102 / BMS-986015), antagonists of Galectins (such as Galectin-1, Galectin-9), anti B and T lymphocyte attenuator (BTLA) antibodies such as JS004; l. Vaccination approaches (for cell vaccination, DNA, RNA, peptide or protein vaccination (for example with gp100 peptide or MAGE-A3 peptide) as well as recombinant viruses; m. Re-introduction of patient derived or allogenic (non-self) cancer cells genetically modified to secrete immunomodulatory factors such as granulocyte monocyte colony stimulating factor (GMCSF) gene-transfected tumor cell vaccine (GVAX) or Fms- related tyrosine kinase 3 (Flt-3) ligand gene-transfected tumor cell vaccine (FVAX), or Toll like receptor enhanced GM-CSF tumor based vaccine (TEGVAX); n. T-cell based adoptive immunotherapies, including chimeric antigen receptor (CAR) engineered T-cells (for example Tisagenlecleucel, Axicabtagene ciloleucel, Brexucabtagene autoleucel, Lisocabtagene maraleucel, Idecabtagene vicleucel, Ciltacabtagene autoleucel); o. Cytokine or immunocytokine based therapy (for example Interferon alpha, interferon beta, interferon gamma, interleukin 2, interleukin 6, interleukin 10, interleukin 15, TGF- β); p. Toll-like receptor (TLR) agonists (for example resiquimod, imiquimod, motolimod, glucopyranosyl lipid A, CpG oligodesoxynucleotides); q. Thalidomide analogues (for example Lenalidomide, Pomalidomide); r. Activators of T-cell co-stimulatory receptors (for example anti-CD137 / 4-1BB antibodies, such as BMS-663513 (urelumab), Utomilumab (PF-05082566) and second generation 4-1BB agonistic drugs (Claus et al., MABS 2023, VOL. 15(1):1- 22); anti-OX40 / CD134 (Tumor necrosis factor receptor superfamily, member 4) (such as RG7888 (MOXR0916), 9B12; MEDI6469, GSK3174998, MEDI6383, MEDI0562), anti OX40-Ligand / CD252; anti-glucocorticoid-induced TNFR family related gene (GITR) (such as TRX518, MEDI1873, MK-4166, BMS-986156, BMS-986153), anti- CD40 (TNF receptor superfamily member 5) antibodies (such as Dacetuzumab (SGN- 40), HCD122, CP-870,893, RG7876, ADC-1013, APX005M, SEA-CD40); anti-CD40- Ligand antibodies (such as BG9588); anti-CD27 antibodies such as Varlilumab; anti- CD28 antibodies; anti-ICOS antibodies; s. Molecules binding a tumor specific antigen as well as a T-cell surface marker such as bispecific antibodies or antibody fragments, antibody mimetic proteins such as designed ankyrin repeat proteins (DARPINS), bispecific T-cell engager (BITE), for example Blinatumomab, Tebentafusp, and others (Wei et al., Frontiers in Immunology, 2022,13:1035276),; t. Antibodies or small molecular weight inhibitors targeting colony-stimulating factor-1 receptor (CSF-1R) (for example Emactuzumab (RG7155), Cabiralizumab (FPA-008), PLX3397). u. Agents targeting immune cell check points on natural killer cells such as antibodies against Killer-cell immunoglobulin-like receptors (KIR) for example Lirilumab (IPH2102 / BMS-986015); v. Agents targeting the Adenosine receptors or the ectonucleases CD39 and CD73 that convert adenosin triphosphate (ATP) to Adenosine, such as MEDI9447 (anti-CD73 antibody), PBF-509; CPI-444 (Adenosine A2a receptor antagonist); w. antagonists to chemokine receptors including CCR2 or CCR4; x. modulators of the complement system; y. agents that deplete or inhibit T regulatory cells (e.g., using an anti-CD25 monoclonal antibody (e.g., daclizumab) or by ex vivo anti-CD25 bead depletion) or reverse / prevent T cell anergy or exhaustion; z. Antibody-drug conjugates, such as, for example, Mirvetuximab soravtansine, Tisotumab vedotin-tftv, Loncastuximab tesirine-lpyl, Belantamab mafodotin-blmf, Sacituzumab govitecan, Trastuzumab deruxtecan, Enfortumab vedotin, Polatuzumab vedotin-piiq, Moxetumomab pasudotox, Inotuzumab ozogamicin, Trastuzumab emtansine, Brentuximab vedotin, Gemtuzumab ozogamicin; aa. Radioligand therapies, such as, for example,177Lu-Lutathera,177Lu-PSMA-617 When used in combination with the compounds of Formula (I), immune checkpoint inhibitors (for example those listed under section k) above), and especially those targeting the programed cell death receptor 1 (PD-1 receptor) or its ligand PD-L1, are preferred. The term "chemotherapy" refers to the treatment of cancer with one or more cytotoxic anti- neoplastic agents ("cytotoxic chemotherapy agents"). Chemotherapy is often used in conjunction with other cancer treatments, such as radiation therapy or surgery. The term especially refers to conventional chemotherapeutic agents which act by killing cells that divide rapidly, one of the main properties of most cancer cells. Chemotherapy may use one drug at a time (single-agent chemotherapy) or several drugs at once (combination chemotherapy or polychemotherapy). Chemotherapy that convert to cytotoxic activity only upon light exposure is called photochemotherapy or photodynamic therapy. The term “cytotoxic chemotherapy agent” or “chemotherapy agent” as used herein refers to an active anti-neoplastic agent inducing apoptosis or necrotic cell death. When used in combination with the compounds of Formula (I), the term especially refers to conventional cytotoxic chemotherapy agents such as: 1) alkylating agents (including, without limitation, nitrogen mustards, ethylenimine derivatives, alkyl sulfonates, nitrosoureas and triazenes) such as uracil mustard, mechlorethamine, chlorambucil, cyclophosphamide, ifosfamide, streptozocin, carmustine, lomustine, melphalan, busulfan, procarbazine, dacarbazine, temozolomide, pipobroman, triethylene-melamine, triethylenethiophosphoramine, thiotepa or altretamine; in particular temozolomide); 2) platinum drugs (for example cisplatin, carboplatin or oxaliplatin); 3) antimetabolite drugs (for example 5-fluorouracil, floxuridine, pentostatine, capecitabine, 6-mercaptopurine, methotrexate, gemcitabine, cytarabine, fludarabine or pemetrexed); 4) anti-tumor antibiotics (for example daunorubicin, doxorubicin, epirubicin, idarubicin, actinomycin-D, bleomycin, mitomycin-C or mitoxantrone); 5) mitotic inhibitors (for example paclitaxel, docetaxel, ixabepilone, vinblastine, vincristine, vinorelbine, vindesine or estramustine); or 6) topoisomerase inhibitors (for example etoposide, teniposide, topotecan, irinotecan, diflomotecan or elomotecan). Also suitable are cytotoxic agents such as biological response modifiers; growth inhibitors; antihormonal therapeutic agents; leucovorin; tegafur; and haematopoietic growth factors. When used in combination with the compounds of Formula (I), preferred cytotoxic chemotherapy agents are the above-mentioned alkylating agents (notably fotemustine, cyclophosphamide, ifosfamide, carmustine, dacarbazine and prodrugs thereof such as especially temozolomide or pharmaceutically acceptable salts of these compounds; in particular temozolomide); mitotic inhibitors (notably paclitaxel, docetaxel, ixabepilone or pharmaceutically acceptable salts of these compounds; in particular paclitaxel); platinum drugs (notably cisplatin, oxaliplatin and carboplatin); as well as etoposide and gemcitabine. 1) Chemotherapy may be given with a curative intent or it may aim to prolong life or to palliate symptoms. 2) Combined modality chemotherapy is the use of drugs with other cancer treatments, such as radiation therapy or surgery.3) Induction chemotherapy is the first line treatment of cancer with a chemotherapeutic drug. This type of chemotherapy is used for curative intent.4) Consolidation chemotherapy is given after remission in order to prolong the overall disease-free time and improve overall survival. The drug that is administered is the same as the drug that achieved remission. 5) Intensification chemotherapy is identical to consolidation chemotherapy but a different drug than the induction chemotherapy is used.6) Combination chemotherapy involves a patient with two o more different drugs simultaneously. The drugs differ in their mechanism and side effects. The biggest advantage is minimising the chances of resistance developing to any one agent. Also, the drugs can often be used at lower doses, reducing toxicity.7) Neoadjuvant chemotherapy is given prior to a local treatment such as surgery, and is designed to shrink the primary tumor. It is also given to cancers with a high risk of micrometastatic disease. 8) Adjuvant chemotherapy is given after a local treatment (radiotherapy or surgery). It can be used when there is little evidence of cancer present, but there is risk of recurrence. It is also useful in killing any cancerous cells that have spread to other parts of the body. These micrometastases can be treated with adjuvant chemotherapy and can reduce relapse rates caused by these disseminated cells. 9) Maintenance chemotherapy is a repeated low-dose treatment to prolong remission. 10) Salvage chemotherapy or palliative chemotherapy is given without curative intent, but simply to decrease tumor load and increase life expectancy. For these regimens, a better toxicity profile is generally expected.

[0002] Preparation of compounds of Formula A further aspect of the invention is a process for the preparation of compounds of Formula (I). Compounds according to Formula (I) of the present invention can be prepared from commercially available or well known starting materials according to the methods described in the experimental part; by analogous methods; or according to the general sequence of reactions outlined below, wherein R1, R2, R3, R4, R5, A, and X are as defined for Formula (I) if not specifically stated otherwise. Other abbreviations used herein are explicitly defined, or are as defined in the experimental section. In some instances the generic groups R1, R2, R3, R4, R5, A, and X might be incompatible with the assembly illustrated in the schemes below and so will require the use of protecting groups (PG). The use of protecting groups is well known in the art (see for example “Protective Groups in Organic Synthesis", T.W. Greene, P.G.M. Wuts, Wiley-Interscience, 1999). For the purposes of this discussion, it will be assumed that such protecting groups as necessary are in place. The starting materials, the intermediates and the final products of the reactions described below may be isolated and purified if desired using conventional techniques, including but not limited to filtration, distillation, crystallization, chromatography, and the like and may be characterized using conventional means, including physical constants and spectral data. The compounds obtained may also be converted into salts, especially pharmaceutically acceptable salts thereof in a manner known per se. Compound identifiers Ax, Bx, Cx and Dx (x being an integer) as used in the general preparation routes below refer only to the structures in this section and do not apply to compounds disclosed elsewhere in this application. Unless specified otherwise, the reactions described herein take place at atmospheric pressure at a temperature in the range from about -78 °C to about 150 °C. General preparation routes: Compounds of Formula (I) wherein cycloalkyl can be prepared as illustrated in Scheme 1. Intermediate A2 can be assembled by a substitution reaction with NaN3 from A1 wherein Y is Br, I, OMs, OTs or OTf. The triazole compound A3 can be obtained by azide- alkyne cycloaddition catalyzed by Cu salts, such as for instance Cu(OAc)2.H2O. The removal of the Boc protecting group in the presence of an acid such as TFA or HCl provides the requisite amine A4. Treatment of A4 with TCDI and hydrazide A5 wherein R1is alkyl, cycloalkyl, heterocyclyl, aryl or heteroaryl, under the influence of a base such as TEA or DIPEA and in a solvent such as THF or 1,4-dioxane gives A6. Treatment of A6 with TsCl and a base, such as pyridine, TEA or DIPEA in a solvent, such as THF or 1,4-dioxane leads to the desired product A7. Alternatively, intermediate A4 reacts with A8 (wherein Y is Br, I, OMs, OTs or OTf and X is O, S or NH) via a nucleophilic substitution reaction in the presence of a base such as K2CO3, Cs2CO3, TEA, DBU or DIPEA and in a solvent such as DMF or DMSO to the desired product A9. Compounds of Formula (I) wherein R2is aryl or heteroaryl can be prepared as illustrated in Scheme 2. Intermediate B2 can be assembled by an Ullmann or Chan-Lam coupling with NaN3from B1 wherein Y is Br, I, or B(OH)2by catalysis with a Cu salts such as Cu(OAc)2·H2O. The triazole compound B3 can be obtained by addition of the respective alkyne in an azide- alkyne cycloaddition in a one-pot synthesis. The removal of the Boc protecting group in the presence of an acid such as TFA or HCl provides the requisite amine B4. Treatment of B4 with TCDI and hydrazide B5 wherein R1is alkyl, cycloalkyl, heterocyclyl, aryl or heteroaryl, under the influence of a base such as TEA or DIPEA and in a solvent such as THF or 1,4- dioxane gives B6. Treatment of B6 with TsCl and a base, such as pyridine, TEA or DIPEA in a solvent, such as THF or 1,4-dioxane leads to the desired product B7. Alternatively, intermediate B4 reacts with B8 (wherein Y is Br, I, OMs, OTs or OTf and X is O, S or NH) via a nucleophilic substitution reaction in the of a base such as K2CO3, Cs2CO3, TEA, DBU or DIPEA and in a solvent such as DMF or DMSO to the desired product B9. Compounds of Formula (I) wherein R2is cycloalkyl, aryl or heteroaryl can also be prepared as illustrated in Scheme 3. Intermediate C1 can be synthesized using the same procedures as for A3 or B3 in Scheme 1 or Scheme 2. The removal of the Boc protecting group in the presence of an acid such as TFA or HCl provides the requisite amine C2. Treatment of C2 with thiophosgene and hydrazine in a solvent such as CH2Cl2, CHCl3 or DCEgives C3. Treatment of C3 with an acid C4 wherein R1is alkyl, alkenyl, alkynyl, fluoroalkyl, hydroxyalkyl, alkoxy-alkyl, cycloalkyl, cycloalkyl-alkyl, heterocyclyl, aryl aryl-alkyl, or heteroaryl and EDCI in a solvent such as CH2Cl2, CHCl3 or DCE leads to the desired productC5. Compounds of Formula (I) wherein R2is aryl or heteroaryl can also be prepared as illustrated in Scheme 4. Intermediate D4 can be synthesized by condensation of D1 with tert-butanesulfinamide, nucleophilic addition reaction with Grignard reagents such as R4MgBr, wherein R4represents (C1-4)alkyl, or (C1-4)fluoroalkyl, and deprotection in the presence of an acid such as hydrochloric acid. Intermediate D6 can be synthesized using the same procedures as for the synthesis of A4 or B4 in Scheme 1 or Scheme 2. The desired product D11 can be synthesized using the same procedures as for the synthesis of A7 / A9, B7 / B9, or C5 in Scheme 1, Scheme 2, or Scheme 3 starting from intermediate D4 (A represents -NH-) or D6 (A represents -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom). Intermediate D7 can be synthesized using the same procedures as for the synthesis of A3 or B3 in Scheme 1 or Scheme 2, but using methyl pent-4-ynoate instead of N-Boc-propargylamine. After hydrolysis of D7 with a base such as LiOH and condensation with a hydrazide R1C(O)NHNH2, intermediate D9 can be obtained. The desired product D11, wherein A represents -CH2-, can be synthesized from D9 by cyclization with TsCl and a base such as TEA, DIPEA or DBU. Further, the product D11, wherein A represents -N(RA)- and RArepresents (C1-4)alkyl, can be synthesized by nucleophilic substitution of halogenated hydrocarbons with D10 which can be prepared in analogy to the synthesis of A7 / A9, B7 / B9, or C5 in Scheme 1, Scheme 2, or Scheme 3. Experimental section: Abbrevations (as used herein and in the description above): Ac acetyl Boc tert.-butyloxycarbonyl CDI 1,1'-carbonyldiimidazole DAST diethylaminosulfur trifluoride DBU 1,8-Diazabicyclo[5.4.0]undec-7-ene DCE dichloroethane DCM dichloromethane DIPEA N-ethyldiisopropylamine DMF dimethylformamide DMP Dess–Martin periodinane DMSO dimethylsulfoxide EDCI 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride Et ethyl EtOAc ethyl acetate h hour(s) HATU 2-(7-Aza-1H-benzotriazole-1-yl)-1,1,3,3-tetramethyluronium hexafluorophosphate LC liquid chromatography Me methyl MS mass spectroscopy min minute(s) NIS N-Iodosuccinimide NMP N-methyl-2-pyrrolidone NMR Nuclear magnetic resonance PE petroleum ether PG protecting group Ph phenyl rpm rotation(s) per minute rt. room temperature TBAF tetra-n-butylammonium fluoride TCDI 1,1'-thiocarbonyldiimidazole TEA triethylamine TFA trifluoroacetic acid THF tetrahydrofuran TLC thin layer chromatography TMS trimethylsilyl Ts tosyl (p-toluenesulfonyl) I. Chemistry The following examples illustrate the preparation of biologically active compounds of the invention but do not at all limit the scope thereof. General remarks: All solvents and reagents are used as obtained from commercial sources unless otherwise indicated. Temperatures are indicated in degrees Celsius (°C). Unless otherwise indicated, the reactions take place at room temperature (rt.) under an argon or nitrogen atmosphere and are run in a flame dried round-bottomed flask equipped with a magnetic stir bar. In mixtures, relations of parts of solvent or eluent or reagent mixtures in liquid form are given as volume relations (v / v), unless indicated otherwise. Characterization methods used: LC-MS LC / MS analyses were performed on Agilent 1200HPLC-6110 MS system. The column temperature was 35 °C. The LC retention times were obtained using the following elution conditions: Analytical HPLC on an Eclipse Plus-C18, (4.6x100 mm, 5 um); detection at 254 nM and MS; Gradient of water / 0.1% HCOOH (A) and CH3OH (B). The eluent flow rate was 1 mL / min and the characteristics of the eluting mixture proportion in function of the time t from start of the elution are summarized in the table below (a linear gradient being used between two consecutive time points): t (min) 0 6 11 Solvent A (%) 95 5 5 Solvent B (%) 5 95 95 Flash chromatography: Flash column chromatography was performed using a Isolera One system from Biotage. TLC analysis: Thin layer chromatography (TLC) analysis was performed using glass support (silica gel coated) silica gel 60 matrix (fluorescent indicator F254) from Yantai Jiangyou Silica Gel Development Company. Preparative chiral chromatography methods used: Preparative chiral purifications were performed on a Autoprep HPLC (PDR-separations.) system. The following parameters were used: A Superchiral R-OJ (Chiralway Biotech Co.,ltd.) column (21x250mm, 5 um) was used; detection at 254 nM and analysis using Shimadzu LC- 20A (Superchiral R-OJ, 4.6 x150mm, 5 um, 0.8 ml / min, 35 °C); the eluent was MeOH / Diethanolamine = 100 / 0.05 (v / v) and the flow rate was 15 mL / min; the column temperature was 35 °C. NMR1H-NMR spectra were recorded at rt with a Brucker NMR 400 / 600 spectrometer 1H (400 / 600 MHz) equipped with a Bruker's DCH cryoprobe. Chemical shifts are reported in ppm downfield from tetramethylsilane using residual as internal reference. The multiplicity is described as singulet s, doublet d, triplet t, quadruplet q, hextet h, or multiplet m. Broad signals are indicated as br. X-ray crystallography The X-ray crystallography data was recorded by a Bruker D8 VENTURE featured with PHOTON III photon-counting detector, radiated by CuKα (λ = 1.54178). Example 1 Synthesis of 5-cyclopropyl-N-((1-(4,4-difluorocyclohexyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: and NaN3(195 mg, 3 mmol) in DMSO (5 mL) was prepared at room temperature. The resulting mixture was heated to 90 °C for 2 hours. After it was cooled to room temperature, N-Boc- propargylamine (310 mg, 2 mmol), Cu(OAc)2.H2O (40 mg, 0.2 mmol) and L-ascorbic acid sodium salt (79 mg, 0.4 mmol) were added. The crude reaction mixture was stirred at rt. for 16 hours and diluted with EtOAc (15 mL) and water (30 mL). The aqueous layer was further extracted with EtOAc (15 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. The crude residue was purified by flash chromatography (petroleum ether / EtOAc, 2 / 1 v / v) to provide the desired product 1a as a white solid (291 mg, 46% yield).1H NMR (400 MHz, Chloroform-d) δ 7.49 (s, 1H), 5.10 (s, 1H), 4.46 – 4.40 (m, 1H), 4.38 (d, J = 6.0 Hz, 2H), 2.22 – 2.15 (m, 2H), 1.95 – 1.88 (m, 2H), 1.77 – 1.67 (m, 4H), 1.44 (s, 9H). LC / MS (m / z): 317.2 [M+H]+Step 2: (626 mg, 5 mmol) in CH3CN (15 mL) was added CuBr2(1675 mg, 7.5 mmol). The mixture turned black and was further stirred for 5 min at room temperature.tBuONO (purity: technical, ≥90% (GC), 1.4 mL, 10 mmol) was added and stirred at room temperature h and then heated at 50°C for 4 hours. The solvent was then evaporated in vacuo. Water (50 mL) and EtOAc (50 mL) were added and the mixture was filtered through celite and washed with EtOAc. The EtOAc layer was separated, and the aqueous layer was extracted with EtOAc (15 mL × 2). The combined organic layers were dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (petroleum ether / EtOAc, 10 / 1 v / v) to give 1b as colorless oil or solidat low temperature (425 mg, 45%).1H NMR (400 MHz, Chloroform-d) δ 2.17 (tt, J = 8.2, 5.3 Hz, 1H), 1.23 – 1.12 (m, 4H). LC / MS (m / z): 189.1 [M+H]+Step 3: were added and the mixture was stirred at room temperature. After the reaction was complete as determined by TLC analysis (about 2 hours), the mixture was concentrated under vacuo to dryness. The crude product was used without further purification. Then, 1b (95 mg, 0.5 mmol), K2CO3 (138 mg, 1 mmol) and DMF (5 mL) were added and the mixture was heated to 120 °C for 2 hours. After the reaction was cooled to room temperature, 50 mL of water was added. The aqueous layer was extracted three times with ethyl acetate (15 mL × 3). The combined organic phase was washed with saturated brine (15 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was purified by flash chromatography (DCM / MeOH, 20 / 1 v / v) to give 1 as white solid (122 mg, 75%).1H NMR (400 MHz, Chloroform-d) δ 7.71 (s, 1H), 5.24 (s, 1H), 4.59 (d, J = 6.2 Hz, 2H), 4.56 – 4.49 (m, 1H), 2.32 – 2.13 (m, 6H), 2.06 – 1.89 (m, 3H), 1.05 – 0.96 (m, 4H). LC / MS (m / z): 325.2 [M+H]+Example 2 Synthesis of N-((1-(bicyclo[1.1.1]pentan-1-yl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl- 1,3,4-oxadiazol-2-amine Step 1: mmol), and CuSO4·5H2O (50 mg, 0.2 mmol) were suspended in methanol (10 mL), and imidazole-1- sulfonyl azide hydrochloride (503 mg, 2.4 mmol) was added at rt. The mixture was stirred for 16 hours. Then N-Boc-propargylamine 2 mmol) and L-ascorbic acid sodium salt (79 mg, 0.4 mmol) were added. The crude reaction mixture was stirred at rt. for another 16 hours and diluted with EtOAc (10 mL) and water (30 mL). The aqueous layer was further extracted with EtOAc (10 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. The crude residue was purified by flash chromatography (petroleum ether / EtOAc, 2 / 1 v / v) to provide the desired product 2a as white solid (349 mg, 66%).1H NMR (400 MHz, Chloroform-d) δ 7.49 (s, 1H), 5.11 (s, 1H), 4.38 (d, J = 6.0 Hz, 2H), 2.69 (s, 1H), 2.38 (s, 6H), 1.44 (s, 9H). LC / MS (m / z): 265.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (72% yield).1H NMR (400 MHz, Chloroform- d) δ 6.85 (s, 1H), 5.20 (s, 1H), 4.17 (s, 2H), 2.29 (s, 1H), 1.97 (s, 6H), 1.60 – 1.52 (m, 1H), 0.63 – 0.55 (m, 4H). LC / MS (m / z): 273.2 [M+H]+Example 3 Synthesis of 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine Step 1: mmol) NaN3, 5 mL H2O and 5 mL CH3CN were added. The mixture was stirred at room temperature under air and 40 mg (0.2 mmol) Cu(OAc)2·H2O was added subsequently. The reaction was stirred for 6 hours and monitored by TLC analysis. Then, 79 mg L-ascorbic acid sodium salt (0.4 mmol) and 310 mg N-Boc-2-propyn-1-amine (2 mmol) were added to the reaction. The mixture was stirred at room temperature for 16 hours with a cap.50 mL of water was added to quench the reaction and the aqueous layer was extracted three times with EtOAc (15 mL × 3). The combined organic phase was washed with saturated brine (15 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was purified by flash chromatography (petroleum ether / EtOAc, 2 / 1 v / v) to give 3a as a white solid (395 mg, 72%).1H NMR (400 MHz, Chloroform-d) δ , 7.72 (d, J = 8.2 Hz, 2H), 7.56 – 7.49 (m, 2H), 7.47 – 7.41 (m, 1H), 5.21 (s, 1H), 4.48 (d, J = 6.0 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 275.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (88% yield).1H NMR (600 MHz, Chloroform- d) δ 8.15 (s, 1H), 7.73 – 7.69 (m, 2H), 7.53 – 7.48 (m, 2H), 7.46 – 7.41 (m, 1H), 5.43 (s, 1H), 4.68 (d, J = 6.0 Hz, 2H), 2.01 – 1.95 (m, 1H), 1.04 – 0.98 (m, 4H). LC / MS (m / z): 283.2 [M+H]+Example 4 Synthesis of 5-cyclopropyl-N-((1-(2-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: with the procedure described in Step 1 of Example 3 as a white solid (55% yield).1H NMR (400 MHz, Chloroform-d) δ 8.04 (s, 1H), 7.97 – 7.89 (m, 1H), 7.48 – 7.37 (m, 1H), 7.35 – 7.27 (m, 2H), 5.18 (s, 1H), 4.49 (d, J = 6.0 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 293.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (68% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.22 (s, 1H), 7.96 – 7.81 (m, 1H), 7.45 (s, 1H), 7.38 – 7.24 (m, 2H), 5.94 (s, 1H), 4.71 (s, 2H), 1.99 (s, 1H), 1.01 (d, J = 7.2 Hz, 4H). LC / MS (m / z): 301.0 [M+H]+Example 5 Synthesis of 5-cyclopropyl-N-((1- -1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: with the procedure described in Step 1 of Example 3 as a white solid (68% yield).1H NMR (400 MHz, Chloroform-d) δ 7.97 (s, 1H), 7.55 – 7.45 (m, 3H), 7.18 – 7.10 (m, 1H), 5.20 (s, 1H), 4.47 (d, J = 6.1 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 293.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (75% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.21 (s, 1H), 7.57 – 7.44 (m, 3H), 7.18 – 7.10 (m, 1H), 5.84 (s, 1H), 4.68 (d, J = 5.3 Hz, 2H), 1.98 (tt, J = 7.9, 5.5 Hz, 1H), 1.05 – 0.96 (m, 4H). LC / MS (m / z): 301.0 [M+H]+Example 6 Synthesis of 5-cyclopropyl-N-((1-(4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: was with the procedure described in Step 1 of Example 3 as a white solid (71% yield).1H NMR (400 MHz, Chloroform-d) δ 7.92 (s, 1H), 7.69 (dd, J = 9.1, 4.6 Hz, 2H), 7.24 – 7.17 (m, 2H), 5.16 (s, 1H), 4.47 (d, J = 6.7 Hz, 2H), 1.42 (s, 9H). LC / MS (m / z): 293.2 [M+H]+Stap 2: described in Step 3 of Example 1 as a white solid (74% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.13 (s, 1H), 7.75 – 7.62 (m, 2H), 7.23 – 7.16 (m, 2H), 5.67 (s, 1H), 4.67 (d, J = 5.9 Hz, 2H), 2.02 – 1.93 (m, 1H), 1.05 – 0.96 (m, 4H). LC / MS (m / z): 301.0 [M+H]+Example 7 Synthesis of 5-cyclopropyl-N-((1-(m-tolyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine Step 1: with the procedure described in Step 1 of Example 3 as a white solid (66% yield).1H NMR (400 MHz, Chloroform-d) δ 7.94 (s, 1H), 7.55 (s, 1H), 7.51 – 7.46 (m, 1H), 7.41 – 7.36 (m, 1H), 7.26 – 7.22 (m, 1H), 5.17 (s, 1H), 4.47 (d, J = 6.0 Hz, 2H), 2.44 (s, 3H), 1.45 (s, 9H). LC / MS (m / z): 289.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (78% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.14 (s, 1H), 7.54 (s, 1H), 7.49 (d, J = 8.1 Hz, 1H), 7.38 (t, J = 7.8 Hz, 1H), 7.24 (d, J = 7.7 Hz, 1H), 5.61 (s, 1H), 4.67 (d, J = 6.2 Hz, 2H), 2.43 (s, 3H), 2.02 – 1.93 (m, 1H), 1.03 – 0.97 (m, 4H). LC / MS (m / z): 297.1 [M+H]+Example 8 Synthesis of 5-cyclopropyl-N-((1-(p-tolyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine with the procedure described in Step 1 of Example 3 as a white solid (69% yield).1H NMR (400 MHz, Chloroform-d) δ 7.92 (s, 1H), 7.59 (d, J = 8.4 Hz, 2H), 7.31 (d, J = 8.2 Hz, 2H), 5.16 (s, 1H), 4.47 (d, J = 6.0 Hz, 2H), 2.42 (s, 3H), 1.45 (s, 9H). LC / MS (m / z): 289.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (72% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.10 (s, 1H), 7.58 (d, J = 8.0 Hz, 2H), 7.30 (d, J = 8.1 Hz, 2H), 5.48 (s, 1H), 4.67 (d, J = 5.8 Hz, 2H), 2.41 (s, 3H), 2.02 – 1.93 (m, 1H), 1.04 – 0.95 (m, 4H). LC / MS (m / z): 297.0 [M+H]+Example 9 Synthesis of N-((1-(4-chlorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4- oxadiazol-2-amine Step 1: in accordance with the procedure described in Step 1 of Example 3 as a white solid (66% yield). 1H NMR (400 MHz, Chloroform-d) δ 7.95 (s, 1H), 7.67 (d, J = 8.8 Hz, 2H), 7.50 (d, J = 8.8 Hz, 2H), 5.18 (s, 1H), 4.47 (d, J = 6.1 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 309.2 [M+H]+Step 2: Starting from compound 9a, example 9 in accordance with the procedure described in Step 3 of Example 1 as a white solid (71% yield).1H NMR (400 MHz, Chloroform- d) δ 8.14 (s, 1H), 7.67 (d, J = 8.6 Hz, 2H), 7.49 (d, J = 8.6 Hz, 2H), 5.37 (s, 1H), 4.67 (d, J = 3.2 Hz, 2H), 2.02 – 1.92 (m, 1H), 1.07 – 0.96 (m, 4H). LC / MS (m / z): 317.2 [M+H]+Example 10 Synthesis of 5-cyclopropyl-N-((1-(4-(trifluoromethyl)phenyl)-1H-1,2,3-triazol-4-yl)methyl)- 1,3,4-oxadiazol-2-amine Step 1: in accordance with the procedure described in Step 1 of Example 3 as a white solid (54% yield).1H NMR (400 MHz, Chloroform-d) δ 8.04 (s, 1H), 7.93 – 7.85 (m, 2H), 7.83 – 7.76 (m, 2H), 5.18 (s, 1H), 4.49 (d, J = 6.2 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 343.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (77% yield).1H NMR (400 MHz, Chloroform- d) δ 8.25 (s, 1H), 7.89 (d, J = 8.3 Hz, 2H), 7.79 (d, J = 8.4 Hz, 2H), 5.46 (s, 1H), 4.69 (s, 2H), 2.03 – 1.93 (m, 1H), 1.05 – 0.97 (m, 4H). LC / MS (m / z): 351.2 [M+H]+Example 11 Synthesis of 4-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1- yl)benzonitrile Step 1: Starting from (4-cyanophenyl)boronic title compound 11a was synthesized in accordance with the procedure described in Step 1 of Example 3 as a white solid (64% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.05 (s, 1H), 7.91 (d, J = 8.8 Hz, 2H), 7.84 (d, J = 8.8 Hz, 2H), 5.17 (s, 1H), 4.48 (d, J = 6.1 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 322.2 [M+Na]+Step 2: described in Step 3 of Example 1 as a white solid (62% yield).1H NMR (400 MHz, Chloroform- d) δ 8.26 (s, 1H), 7.91 (d, J = 8.8 Hz, 2H), 7.83 (d, J = 8.8 Hz, 2H), 5.23 (s, 1H), 4.69 (d, J = 5.9 Hz, 2H), 2.02 – 1.93 (m, 1H), 1.04 – 0.97 (m, 4H). LC / MS (m / z): 308.2 [M+H]+Example 12 Synthesis of (3-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1- yl)phenyl)methanol Step 1: was synthesized in accordance with the procedure described in Step 1 of Example 3 as a white solid (70% yield).1H NMR (400 MHz, Chloroform-d) δ 8.34 (s, 1H), 8.11 (d, J = 6.4 Hz, 1H), 8.06 – 7.98 (m, 2H), 7.62 (t, J = 7.9 Hz, 1H), 5.17 (s, 1H), 4.49 (d, J = 6.0 Hz, 2H), 3.97 (s, 3H), 1.46 (s, 9H). LC / MS (m / z): 333.2 [M+H]+Step 2: with the procedure described in Step 3 of Example 1 as a white solid (48% yield).1H NMR (400 MHz, Chloroform-d) δ 8.34 (s, 1H), 8.22 (s, 1H), 8.11 (d, J = 7.8 Hz, 1H), 7.99 (dd, J = 8.6, 2.9 Hz, 1H), 7.61 (t, J = 8.0 Hz, 1H), 5.32 (s, 1H), 4.69 (d, J = 6.2 Hz, 2H), 3.97 (s, 3H), 2.01 – 1.94 (m, 1H), 1.04 – 0.98 (m, 4H). LC / MS (m / z): 341.2 [M+H]+ in anhydrous THF (5 mo L) at 0 C, LiAlH4(0.15 mL, 1M in THF) was added. The mixture was stirred for 2 hours at 0oC. Then, the reaction was poured into saturated potassium sodium tartrate ice water solution (30 mL) and extracted with EtOAc (10 mL). The EtOAc layer was separated, and the aqueous layer extracted with EtOAc (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 12 as white solid (13 mg, 42%). 1H NMR (400 MHz,Chloroform-d) δ 8.16 (s, 1H), 7.74 (s, 1H), 7.66 – 7.60 (m, 1H), 7.52 – 7.46 (m, 1H), 7.44 – 7.39 (m, 1H), 5.47 (s, 1H), 4.79 (s, 2H), 4.66 (d, J = 5.6 Hz, 2H), 2.01 – 1.93 (m, 1H), 1.05 – 0.95 (m, 4H). LC / MS (m / z): 313.2 [M+H]+Example 13 Synthesis of 2-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1- yl)benzonitrile Step 1: in accordance with the procedure described in Step 1 of Example 3 as white solid (67% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.17 (s, 1H), 7.89 – 7.76 (m, 3H), 7.64 – 7.57 (m, 1H), 5.18 (s, 1H), 4.52 (d, J = 6.0 Hz, 2H), 1.46 (s, 9H). LC / MS (m / z): 300.2 [M+H] Step 2: described in Step 3 of Example 1 as a white solid (53% yield).1H NMR (400 MHz, Chloroform- d) δ 8.30 (s, 1H), 7.89 – 7.84 (m, 1H), 7.83 – 7.77 (m, 2H), 7.67 – 7.58 (m, 1H), 5.45 (s, 1H), 4.72 (d, J = 5.5 Hz, 2H), 2.03 – 1.92 (m, 1H), 1.05 – 0.96 (m, 4H). LC / MS (m / z): 308.2 [M+H]+ Example 14 Synthesis of N-((1-(2-chlorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4- oxadiazol-2-amine Step 1: in accordance with the procedure described in Step 1 of Example 3 as a white solid (66% yield). 1H NMR (400 MHz, Chloroform-d) δ 7.96 (s, 1H), 7.64 – 7.54 (m, 2H), 7.49 – 7.41 (m, 2H), 5.18 (s, 1H), 4.50 (d, J = 6.0 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 309.2 [M+H] Step 2: described in Step 3 of Example 1 as a white solid (61% yield).1H NMR (400 MHz, DMSO- d6).1H NMR (400 MHz, Chloroform-d) δ 8.10 (s, 1H), 7.62 – 7.53 (m, 2H), 7.49 – 7.40 (m, 2H), 5.61 (s, 1H), 4.71 (d, J = 5.3 Hz, 2H), 2.05 – 1.92 (m, 1H), 1.06 – 0.97 (m, 4H). LC / MS (m / z): 317.1 [M+H]+Example 15 Synthesis of 5-cyclopropyl-N-((1-(4-methoxyphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: in accordance with the procedure described in Step 1 of Example 3 as a white solid (45% yield). 1H NMR (400 MHz, Chloroform-d) δ 7.87 (s, 1H), 7.61 (d, J = 9.0 Hz, 2H), 7.01 (d, J = 9.0 Hz, 2H), 5.17 (s, 1H), 4.47 (d, J = 6.1 Hz, 2H), 3.87 (s, 3H), 1.45 (s, 9H). LC / MS (m / z): 305.2 [M+H] described in Step 3 of Example 1 as a white solid (81% yield).1H NMR (400 MHz, Chloroform- d) δ 8.10 (s, 1H), 7.58 (d, J = 9.0 Hz, 2H), 6.96 (d, J = 9.0 Hz, 2H), 6.30 (s, 1H), 4.65 (d, J = 4.5 Hz, 2H), 3.83 (s, 3H), 2.00 – 1.90 (m, 1H), 1.03 – 0.93 (m, 4H). LC / MS (m / z): 313.2 [M+H]+Example 16 Synthesis of 5-cyclopropyl-N-((1-(phenyl-d5)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine Step 1: with the procedure described in Step 1 of Example 3 as a white solid (65% yield).1H NMR (400 MHz, Chloroform-d) δ 7.96 (s, 1H), 5.18 (s, 1H), 4.48 (d, J = 6.0 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 280.2 [M+H] Step 2: described in Step 3 of Example 1 as a white solid (78% yield).1H NMR (400 MHz, Chloroform- d) δ 8.16 (s, 1H), 5.59 (s, 1H), 4.68 (d, J = 6.0 Hz, 2H), 2.00 – 1.93 (m, 1H), 1.04 – 0.98 (m, 4H). LC / MS (m / z): 288.0 [M+H]+Example 17 Synthesis of 5-cyclopropyl-N-((1-(furan-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine Step 1: with the procedure described in Step 1 of Example 3 as a white solid (54% yield).1H NMR (400 MHz, Chloroform-d) δ 7.92 – 7.90 (m, 1H), 7.77 (s, 1H), 7.50 (t, J = 1.9 Hz, 1H), 6.80 (d, J = 2.9 Hz, 1H), 5.18 (s, 1H), 4.44 (d, J = 6.1 Hz, 2H), 1.44 (s, 9H). LC / MS (m / z): 265.2 [M+H] Step 2: described in Step 3 of Example 1 a white solid (43% yield).1H NMR (400 MHz, Chloroform- d) δ 8.01 (s, 1H), 7.91 (d, J = 1.7 Hz, 1H), 7.48 (t, J = 2.0 Hz, 1H), 6.79 (d, J = 2.1 Hz, 1H), 6.19 (s, 1H), 4.63 (s, 2H), 2.01 – 1.91 (m, 1H), 1.03 – 0.93 (m, 4H). LC / MS (m / z): 273.2 [M+H]+Example 18 Synthesis of 5-cyclopropyl-N-((1-(thiophen-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: in accordance with the procedure described in Step 1 of Example 3 as a white solid (51% yield). 1H NMR (400 MHz, Chloroform-d) δ 7.88 (s, 1H), 7.56 – 7.53 (m, 1H), 7.46 – 7.43 (m, 2H), 5.17 (s, 1H), 4.46 (d, J = 6.1 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 281.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (58% yield).1H NMR (400 MHz, Chloroform- d) δ 8.09 (s, 1H), 7.55 (t, J = 2.4 Hz, 1H), (d, J = 2.3 Hz, 2H), 5.71 (s, 1H), 4.66 (d, J = 5.6 Hz, 2H), 2.02 – 1.92 (m, 1H), 1.04 – 0.94 (m, 4H). LC / MS (m / z): 289.0 [M+H]+Example 19 Synthesis of N-((1-(5-chlorothiophen-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4- oxadiazol-2-amine Step 1: in accordance with the procedure described in Step 1 of Example 3 as a white solid (65% yield). 1H NMR (400 MHz, Chloroform-d) δ 8.13 (s, 1H), 7.38 (d, J = 6.0 Hz, 1H), 7.27 (d, J = 3.4 Hz, 1H), 5.17 (s, 1H), 4.49 (d, J = 6.0 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 315.1 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (59% yield).1H NMR (400 MHz, Chloroform- d) δ 8.27 (s, 1H), 7.35 (d, J = 6.0 Hz, 1H), 7.26 (d, J = 6.0 Hz, 1H), 5.40 (s, 1H), 4.69 (d, J = 5.1 Hz, 2H), 2.02 – 1.93 (m, 1H), 1.04 – 0.97 (m, 4H). LC / MS (m / z): 322.8 [M+H]+Example 20 Synthesis of 5-cyclopropyl-N-((1-(pyridin-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol- 2-amine Step 1: with the procedure described in Step 1 of Example 3 as a white solid (71% yield).1H NMR (400 MHz, Chloroform-d) δ 9.01 (s, 1H), 8.71 (s, 1H), 8.12 (d, J = 6.5 Hz, 1H), 8.03 (s, 1H), 7.50 (dd, J = 8.4, 4.9 Hz, 1H), 5.20 (s, (d, J = 6.1 Hz, 2H), 1.45 (s, 9H). LC / MS (m / z): 276.2 [M+H] Step 2: described in Step 3 of Example 1 as a white solid (77% yield).1H NMR (400 MHz, Chloroform- d) δ 9.02 (d, J = 2.6 Hz, 1H), 8.70 (dd, J = 4.8, 1.5 Hz, 1H), 8.25 (s, 1H), 8.10 (ddd, J = 8.2, 2.6, 1.5 Hz, 1H), 7.49 (dd, J = 8.3, 4.8 Hz, 1H), 5.60 (s, 1H), 4.70 (d, J = 5.9 Hz, 2H), 1.98 (tt, J = 8.6, 5.2 Hz, 1H), 1.04 – 0.96 (m, 4H). LC / MS (m / z): 284.2 [M+H]+Example 21 Synthesis of 5-cyclopropyl-N-((1-ferrocenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine Step 1: with the procedure described in Step 1 of Example 3 as a yellow solid (25% yield).1H NMR (400 MHz, Chloroform-d) δ 7.77 (s, 1H), 5.14 (s, 1H), 4.82 (t, J = 2.0 Hz, 2H), 4.42 (d, J = 6.0 Hz, 2H), 4.26 (t, J = 2.0 Hz, 2H), 4.20 (s, 5H), 1.45 (s, 9H). LC / MS (m / z): 382.2 [M+H]+Step 2: described in Step 3 of Example 1 as a yellow solid (37% yield).1H NMR (400 MHz, Chloroform-d) δ 7.93 (s, 1H), 5.74 (s, 1H), 4.81 (t, J = 2.0 Hz, 2H), 4.63 (d, J = 5.4 Hz, 2H), 4.31 – 4.23 (m, 2H), 4.19 (s, 5H), 2.02 – 1.93 (m, 1H), 1.06 – 0.93 (m, 4H). LC / MS (m / z): 391.2 [M+H]+Example 22 Synthesis of 5- (1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: NN HN Boc N N C SH 1) HCl / 1,4-dioxaneNNN NH N N NH NH H O NHN were added and the mixture was stirred at room temperature for 2 hours, the mixture was concentrated under vacuo to dryness. Then, 50 mL CHCl3and 50 mL saturated NaHCO3were added. After the reaction was vigorously stirred, SCCl2 (thiophosgene, 115 mg, 1 mmol) was added dropwise and the reaction was kept at room temperature for 18 hours. The mixture was separated and the aqueous layer was extracted three times with CH2Cl2 (20 mL × 3). The combined organic phase was washed with saturated brine (30 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was dissolved in CHCl3(30 mL) and NH2NH2.H2O (65 mg, 1.1 mmol, 85% aqueous solution) was added. The reaction was stirred at rt. for another 18 hours and concentrated under vacuo to dryness. The product 22a was obtained as a white solid and further used without purification (236 mg, 95%).1H NMR (400 MHz, DMSO-d6) δ 8.85 (s, 1H), 8.62 (s, 1H), 8.24 (s, 1H), 7.88 (d, J = 7.4 Hz, 2H), 7.59 (t, J = 7.9 Hz, 2H), 7.51 – 7.45 (m, 1H), 4.83 (d, J = 5.0 Hz, 2H), 4.52 (s, 2H). LC / MS (m / z): 249.2 [M+H] Step 2: 0.6 mmol) in CH2Cl2(10 mL) at room temperature, EDCI (288 mg, 1.5 mmol) was added. The mixture was stirred at room temperature for 18 hours diluted with CH2Cl2(30 mL) and water (10 mL). The aqueous layer was further extracted with CH2Cl2(10 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. The crude residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to provide the desired product 22 as white solid (83 mg, 51%).1H NMR (400 MHz, Chloroform-d) δ 8.17 (s, 1H), 7.79 – 7.66 (m, 2H), 7.56 – 7.49 (m, 2H), 7.48 – 7.39 (m, 1H), 5.79 (s, 1H), 4.70 (d, J = 4.5 Hz, 2H), 2.67 (d, J = 7.5 Hz, 2H), 2.29 – 2.15 (m, 1H), 1.82 – 1.76 (m, 2H), 1.66 – 1.52 (m, 4H), 1.32 – 1.25 (m, 2H). LC / MS (m / z): 325.1 [M+H]+ Example 23 Synthesis of 5-(cyclopropylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine acid, example 23 was synthesized in accordance with the procedure described in Example 22 as a white solid (56% yield).1H NMR (400 MHz, Chloroform-d) δ 8.18 (s, 1H), 7.76 – 7.68 (m, 2H), 7.54 – 7.47 (m, 2H), 7.46 – 7.40 (m, 1H), 5.85 (s, 1H), 4.71 (d, J = 5.7 Hz, 2H), 2.59 (d, J = 7.1 Hz, 2H), 1.12 – 0.97 (m, 1H), 0.60 – 0.48 (m, 2H), 0.33 – 0.22 (m, 2H). LC / MS (m / z): 297.1 [M+H]+Example 24 Synthesis of 5-(1-cyclopropylethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine acid, example 24 was synthesized in accordance with the procedure described in Example 22 as a white solid (61% yield).1H NMR (600 MHz, Chloroform-d) δ 8.19 (s, 1H), 7.72 (d, J = 7.9 Hz, 2H), 7.51 (t, J = 7.7 Hz, 2H), 7.43 (t, J = 7.4 Hz, 1H), 5.73 (s, 1H), 4.76 – 4.66 (m, 2H), 2.21 – 2.12 (m, 1H), 1.38 (d, J = 7.1 Hz, 3H), 1.00 – 0.91 (m, 1H), 0.60 – 0.46 (m, 2H), 0.36 – 0.16 (m, 2H). LC / MS (m / z): 311.2 [M+H]+Example 25 Synthesis of 2-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2- yl)propan-2-ol 2-methylpropanoic acid, example 25 was synthesized in accordance with the procedure described in Example 22 as a white solid (43% yield).1H NMR (400 MHz, Chloroform-d) δ 8.15 (s, 1H), 7.72 (d, J = 2H), 7.57 – 7.40 (m, 3H), 5.56 (s, 1H), 4.71 (d, J = 5.4 Hz, 2H), 2.68 (s, 1H), 1.63 (s, 6H). LC / MS (m / z): 301.2 [M+H]+Example 26 Synthesis of 1-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2- yl)cyclopropan-1-ol 1-carboxylic acid, example 26 was synthesized in accordance with the procedure described in Example 22 as a white solid (23% yield).1H NMR (400 MHz, Chloroform-d) δ 8.18 (s, 1H), 7.70 (d, J = 8.7 Hz, 2H), 7.52 – 7.41 (m, 3H), 6.31 (s, 1H), 4.67 (s, 2H), 1.34 – 1.24 (m, 4H). LC / MS (m / z): 299.2 [M+H]+Example 27 Synthesis of 5-phenyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine acid, example 27 was synthesized in accordance with the procedure described in Example 22 as a white solid (61% yield).1H NMR (400 MHz, DMSO-d6) δ 8.78 (s, 1H), 8.44 (t, J = 5.9 Hz, 1H), 7.90 (d, J = 8.0 Hz, 2H), 7.86 – 7.78 (m, 2H), 7.61 – 7.47 (m, 6H), 4.60 (d, J = 5.8 Hz, 2H). LC / MS (m / z): 319.0 [M+H]+Example 28 Synthesis of 5-cyclobutyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine acid, example 28 was synthesized in accordance with the procedure described in Example 22 as a white solid (58% yield).1H NMR (400 MHz, Chloroform-d) δ 8.18 (s, 1H), 7.78 – 7.66 , 7.55 – 7.38 (m, 3H), 5.72 (s, 1H), 4.71 (s, 2H), 3.63 – 3.48 (m, 1H), 2.42 – 2.26 (m, 4H), 2.10 – 1.89 (m, 2H). LC / MS (m / z): 297.1 [M+H]+Example 29 Synthesis of 5-methyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine acid, example 29 was synthesized in accordance with the procedure described in Example 22 as a white solid (38% yield).1H NMR (400 MHz, Chloroform-d) δ 8.17 (s, 1H), 7.80 – 7.65 (m, 2H), 7.50 (t, J = 7.8 Hz, 2H), 7.47 – 7.40 (m, 1H), 6.01 – 5.85 (m, 1H), 4.70 (d, J = 5.8 Hz, 2H), 2.36 (s, 3H). LC / MS (m / z): 257.1 [M+H]+Example 30 Synthesis of N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(thiazol-5-yl)-1,3,4-oxadiazol-2- amine 5-carboxylic acid, example 30 was synthesized in accordance with the procedure described in Example 22 as a white solid (37% yield).1H NMR (400 MHz, DMSO- d6) δ 9.27 (s, 1H), 8.78 (s, 1H), 8.60 (t, J = 5.9 Hz, 1H), 8.35 (s, 1H), 8.06 – 7.82 (m, 2H), 7.65 – 7.55 (m, 2H), 7.55 – 7.44 (m, 1H), 4.59 (d, J = 5.9 Hz, 2H). LC / MS (m / z): 326.0 [M+H]+Example 31 Synthesis of N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(2-azaspiro[3.3]heptan-6-yl)-1,3,4- oxadiazol-2-amine N NN HNNNN HNN N HCl / 1,4NO -dioxane acid, compound 31a was synthesized in accordance with the procedure described in Example 22 as a white solid (55% yield).1H NMR (400 MHz, d) δ 8.17 (s, 1H), 7.70 (d, J = 7.7 Hz, 2H), 7.54 – 7.39 (m, 3H), 6.16 (s, 1H), 4.69 (d, J = 5.3 Hz, 2H), 3.96 (s, 2H), 3.87 (s, 2H), 3.40 (p, J = 8.2 Hz, 1H), 2.59 – 2.45 (m, 4H), 1.41 (s, 9H). LC / MS (m / z): 438.3 [M+H]+The example 31 was obtained as a yellow solid by the de-protection of 31a in HCl / 1,4-dioxane solution and basification.1H NMR (400 MHz, Chloroform-d) δ 8.16 (s, 1H), 7.71 (d, J = 7.8 Hz, 2H), 7.51 (t, J = 7.7 Hz, 2H), 7.43 (t, J = 7.4 Hz, 1H), 4.68 (s, 2H), 3.71 (s, 2H), 3.62 (s, 2H), 3.40 (p, J = 8.4 Hz, 1H), 2.57 (t, J = 10.5 Hz, 2H), 2.48 (t, J = 10.4 Hz, 2H). LC / MS (m / z): 338.1 [M+H]+Example 32 Synthesis of 5-isopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine acid, example 32 was synthesized in accordance with the procedure described in Example 22 as a white solid (55% yield).1H NMR (400 MHz, Chloroform-d) δ 8.19 (s, 1H), 7.72 (dd, J = 7.6, 1.7 Hz, 2H), 7.55 – 7.47 (m, 2H), 7.47 – 7.34 (m, 1H), 5.88 (s, 1H), 4.70 (d, J = 4.8 Hz, 2H), 3.01 (p, J = 7.0 Hz, 1H), 1.31 (d, J = 6.9 Hz, 6H). LC / MS (m / z): 285.1 [M+H]+Example 33 Synthesis of N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(pyridin-4-yl)-1,3,4-oxadiazol-2- amine acid, example 33 was synthesized in accordance with the procedure described in Example 22 as a white solid (41% yield).1H NMR (400 MHz, DMSO-d6) δ 8.80 (s, 1H), 8.77 – 8.67 (m, 3H), 7.90 (dd, J = 7.6, 1.7 Hz, 2H), 7.77 – 7.69 (m, 2H), 7.59 (t, J = 7.7 Hz, 2H), 7.48 (t, J = 7.4 Hz, 1H), 4.63 (d, J = 5.9 Hz, 2H). LC / MS (m / z): 320.0 [M+H]+Example 34 Synthesis of 5-(tert-butyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine in accordance with the procedure described in Example 22 as a white solid (61% yield).1H NMR (400 MHz, Chloroform-d) δ 8.21 (s, 1H), 7.72 (d, J = 7.8 Hz, 2H), 7.58 – 7.39 (m, 3H), 5.90 (s, 1H), 4.70 (d, J = 4.2 Hz, 2H), 1.33 (s, 9H). LC / MS (m / z): 299.1 [M+H]+Example 35 Synthesis of 5-(methoxymethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol- 2-amine acid, example 35 was synthesized in accordance with the procedure described in Example 22 as a white solid (41% yield).1H NMR (400 MHz, Chloroform-d) δ 8.14 (s, 1H), 7.72 (d, J = 7.8 Hz, 2H), 7.52 (t, J = 7.7 Hz, 2H), 7.44 (t, J = 7.4 Hz, 1H), 5.60 (s, 1H), 4.74 (d, J = 5.3 Hz, 2H), 4.48 (s, 2H), 3.41 (s, 3H). LC / MS (m / z): 287.0 [M+H]+Example 36 Synthesis of 5-benzyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine acid, example 36 was synthesized in accordance with the procedure described in Example 22 as a white solid (58% yield).1H NMR (400 MHz, Chloroform-d) δ 8.10 (s, 1H), 7.68 (d, J = 7.3 Hz, 2H), 7.50 (t, J = 7.6 Hz, 2H), 7.46 – 7.40 (m, 1H), 7.35 – 7.23 (m, 5H), 5.83 (s, 1H), 4.67 (s, 2H), 4.03 (s, 2H). LC / MS (m / z): 333.2 [M+H]+Example 37 Synthesis of 5-(2-fluoropropan-2- (1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine 2-methylpropanoic acid, example 37 was synthesized in accordance with the procedure described in Example 22 as a white solid (28% yield).1H NMR (400 MHz, Chloroform-d) δ 8.16 (s, 1H), 7.72 (d, J = 8.2 Hz, 2H), 7.51 (t, J = 7.6 Hz, 2H), 7.48 – 7.40 (m, 1H), 5.90 (s, 1H), 4.74 (d, J = 5.9 Hz, 2H), 1.79 (d, J = 21.1 Hz, 6H). LC / MS (m / z): 303.2 [M+H]+Example 38 Synthesis of 5-(oxetan-3-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2- amine 3-carboxylic acid, example 38 was synthesized in accordance with the procedure described in Example 22 as a white solid (33% yield).1H NMR (400 MHz, Chloroform-d) δ 8.17 (s, 1H), 7.71 (d, J = 8.2 Hz, 2H), 7.51 (t, J = 7.6 Hz, 2H), 7.44 (t, J = 7.4 Hz, 1H), 5.90 (s, 1H), 4.98 – 4.87 (m, 4H), 4.74 (d, J = 6.0 Hz, 2H), 4.41 – 4.31 (m, 1H). LC / MS (m / z): 299.2 [M+H]+Example 39 Synthesis of 5-(3,3-difluorocyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine 1-carboxylic acid, example 39 was synthesized in accordance with the procedure described in Example 22 as a white solid (47% yield).1H NMR (400 MHz, Chloroform-d) δ 8.15 (s, 1H), 7.71 (d, J = 8.2 Hz, 2H), 7.52 (t, J = 7.6 Hz, 2H), 7.48 – 7.41 (m, 1H), 5.75 (s, 1H), 4.72 (d, J = 2H), 3.48 – 3.37 (m, 1H), 3.02 – 2.89 (m, 4H). LC / MS (m / z): 333.2 [M+H]+Example 40 Synthesis of 5-(3-methoxycyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine 1-carboxylic acid, example 40 was synthesized in accordance with the procedure described in Example 22 as a white solid (55% yield).1H NMR (400 MHz, Chloroform-d) δ 8.15 (s, 1H), 7.72 (d, J = 7.3 Hz, 2H), 7.51 (t, J = 7.6 Hz, 2H), 7.47 – 7.39 (m, 1H), 5.47 (s, 1H), 4.71 (d, J = 6.1 Hz, 2H), 3.92 – 3.83 (m, 1H), 3.25 (s, 3H), 3.17 – 3.06 (m, 1H), 2.70 – 2.59 (m, 2H), 2.31 – 2.20 (m, 2H). LC / MS (m / z): 327.2 [M+H]+Example 41 Synthesis of 5-(3,3-dimethylcyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine 1-carboxylic acid, example 41 was synthesized in accordance with the procedure described in Example 22 as a white solid (59% yield).1H NMR (400 MHz, Chloroform-d) δ 8.18 (s, 1H), 7.71 (d, J = 7.8 Hz, 2H), 7.50 (t, J = 7.8 Hz, 2H), 7.46 – 7.40 (m, 1H), 5.79 (s, 1H), 4.71 (d, J = 5.5 Hz, 2H), 3.56 – 3.42 (m, 1H), 2.19 – 2.03 (m, 4H), 1.20 (s, 3H), 1.12 (s, 3H). LC / MS (m / z): 325.0 [M+H]+Example 42 Synthesis of 5-(bicyclo[1.1.1]pentan-1-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Starting from bicyclo[1.1.1]pentane-1- acid, example 42 was synthesized in accordance with the procedure described in Example 22 as a white solid (49% yield).1H NMR (400 MHz, Chloroform-d) δ 8.18 (s, 1H), 7.71 (d, J = 8.2 Hz, 2H), 7.50 (t, J = 7.6 Hz, 2H), 7.45 – 7.39 (m, 1H), 5.88 (s, 1H), 4.70 (d, J = 6.0 Hz, 2H), 2.52 (s, 1H), 2.21 (s, 6H). LC / MS (m / z): 309.2 [M+H]+Example 43 Synthesis of 5-(bicyclo[3.1.0]hexan-3-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine hexane-3-carboxylic acid, example 43 was synthesized in accordance with the procedure described in Example 22 as a white solid (44% yield).1H NMR (400 MHz, Chloroform-d) δ 8.16 (s, 1H), 7.72 (d, J = 8.0 Hz, 2H), 7.51 (t, J = 7.8 Hz, 2H), 7.47 – 7.39 (m, 1H), 5.55 (s, 1H), 4.69 (d, J = 5.7 Hz, 2H), 3.44 – 3.31 (m, 1H), 2.33 – 2.01 (m, 4H), 1.40 – 1.30 (m, 2H), 0.52 – 0.41 (m, 1H), 0.17 (q, J = 4.1 Hz, 1H). LC / MS (m / z): 323.2 [M+H]+Example 44 Synthesis of ethyl 5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazole-2- carboxylate 44 was synthesized in accordance with the procedure described in Step 3 of Example 1 as a white solid (72% yield).1H NMR (400 MHz, DMSO-d6) δ 8.94 (t, J = 5.8 Hz, 1H), 8.77 (s, 1H), 7.92 – 7.86 (m, 2H), 7.63 – 7.55 (m, 2H), 7.53 – 7.45 (m, 1H), 4.61 (d, J = 5.9 Hz, 2H), 4.34 (q, J = 7.1 Hz, 2H), 1.30 (t, J = 7.1 Hz, 3H). LC / MS (m / z): 315.0 [M+H]+Example 45 Synthesis of (5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2- yl)methanol mL) at 0oC, NaBH4 (7 mg, 0.2 mmol) was added. The mixture was stirred for 2 hours at room temperature. Then, water (15 mL) was added and extracted with EtOAc (10 mL). The EtOAc layer was separated, and the aqueous layer extracted with EtOAc (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4 and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 45 as white solid (17 mg, 64%).1H NMR (400 MHz, DMSO-d6) δ 8.73 (s, 1H), 8.18 (t, J = 5.9 Hz, 1H), 7.89 (d, J = 7.9 Hz, 2H), 7.59 (t, J = 7.7 Hz, 2H), 7.48 (t, J = 7.4 Hz, 1H), 5.67 (t, J = 6.1 Hz, 1H), 4.51 (d, J = 5.9 Hz, 2H), 4.42 (d, J = 6.1 Hz, 2H). LC / MS (m / z): 273.0 [M+H]+Example 46 Synthesis of 5-(difluoromethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine Step 1: (10 mL), DMP (233 mg, 0.55 mmol) was added. The mixture was stirred for 2 hours at room temperature. Then, saturated Na2S2O3 aqueous solution (15 mL) was added. The CH2Cl2 layer was separated, and the aqueous layer was extracted with CH2Cl2(10 mL × 2). The combined organic layers were washed with saturated NaHCO3aqueous solution and dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 46a as white solid (69 mg, 51%). 1H NMR (400 MHz, Chloroform-d) δ 9.71 (s, 1H),8.17 (s, 1H), 7.71 (d, J = 8.1 Hz, 2H), 7.52 (t, J = 7.5 Hz, 2H), 7.48 – 7.41 (m, 1H), 4.84 (s, 2H). LC / MS (m / z): 303.2 [M+CH3OH+H]+Step 2: To a solution of compound 46a (27 mg, in CH2Cl2(3 mL), DAST (80 mg, 0.5 mmol) was added. The mixture was stirred for 16 hours at room temperature. Then, H2O (15 mL) was added and extracted with CH2Cl2 (10 mL). The CH2Cl2 layer was separated, and the aqueous layer was extracted with CH2Cl2 (10 mL × 2). The combined organic layers were washed with saturated NaCl aqueous solution and dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 25 / 1 v / v) to give 46 as white solid (13 mg, 45%).1H NMR (400 MHz, Chloroform-d) δ 8.15 (s, 1H), 7.71(d, J = 7.7 Hz, 2H), 7.58 – 7.41 (m, 3H), 6.67 (t, J = 51.7 Hz, 1H), 6.42 (s, 1H), 4.78 (d, J = 5.4 Hz, 2H). LC / MS (m / z): 293.2 [M+H]+Example 47 Synthesis of 5-ethynyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine (138 mg, 1 mmol) was added followed by a solution of (1-diazo-2-oxo-propyl)-phosphonic acid dimethyl ester (115 mg, 0.6 mmol) in dry MeOH (5 mL) at room temperature and the resulting mixture was stirred for 2 h. Then, the mixture was poured into H2O (30 mL) and extracted with EtOAc (10 mL). The EtOAc layer was separated, and the aqueous layer was extracted with EtOAc (10 mL × 2). The combined organic layers were washed with saturated NaCl aqueous solution and dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 47 as white solid (75 mg, 56%).1H NMR(400 MHz, Chloroform-d) δ 8.14 (s, 1H), 7.72 (d, J = 8.2 Hz, 2H), 7.52 (t, J = 8.1 Hz, 2H), 7.48 – 7.42 (m, 1H), 5.95 (s, 1H), 4.76 (d, J = 5.9 Hz, 2H), 3.43 (s, 1H). LC / MS (m / z): 267.2 [M+H]+Example 48 Synthesis of N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(phenylethynyl)-1,3,4-oxadiazol-2- amine To a solution of 47 (80 mg, 0.3 mmol) (61 mg, 0.3 mmol) in THF (10 mL), Pd(PPh3)4 (21 mg, 0.03 mmol), CuI (6 mg, 0.03 mmol), PPh3 (16 mg, 0.06mmol) and TEA (303 mg, 3 mmol) were added. The resulting mixture was stirred at 28oC for 16 hours under argon atmosphere. Then, H2O (60 mL) was added and extracted with EtOAc (15 mL). The EtOAc layer was separated, and the aqueous layer was extracted with EtOAc (15 mL × 2). The combined organic layer was washed with saturated NaCl aqueous solution and dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 15 / 1 v / v) to give 48 as white solid (55 mg, 42%). 1H NMR (400 MHz,Chloroform-d) δ 8.20 (s, 1H), 7.73 (d, J = 7.3 Hz, 2H), 7.59 – 7.54 (m, 2H), 7.54 – 7.48 (m, 2H), 7.48 – 7.39 (m, 2H), 7.40 – 7.34 (m, 2H), 6.43 (s, 1H), 4.79 (s, 2H). LC / MS (m / z): 343.1 [M+H]+Example 49 Synthesis of 1-((5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2- yl)methyl)imidazolidin-2-one Step 1: (96 mg, 0.6 mmol) and NaBH(OAc)3 (318 mg, 1.5 mmol) were added. The mixture was stirred for 16 hours at rt. Then, it was diluted with DCM (10 mL) and water (30 mL). The aqueous layer was further extracted with DCM (10 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. The crude residue was purified by flash chromatography (DCM / CH3OH, 10 / 1 v / v) to provide compound 49a as a light yellow solid (95 mg, 46%).1H NMR (600 MHz, Chloroform-d) δ 8.15 (s, 1H), 7.73 – 7.69 (m, 2H), 7.54 – 7.49 (m, 2H), 7.46 – 7.42 (m, 1H), 5.00 (s, 1H), 4.71 (s, 2H), 3.86 (s, 2H), 3.26 – 3.20 (m, 2H), 2.78 (t, J = 5.9 Hz, 2H), 1.42 (s, 11H). LC / MS (m / z): 415.3 [M+H]+Step 2: solution were added and the mixture was stirred at room temperature for 2 hours. After the mixture was concentrated under vacuo to DCM, CDI (20 mg, 0.125 mmol) and TEA (126 mg, 1.25 mmol) were added. The mixture was stirred for 16 hours at rt., then it was diluted with DCM (10 mL) and water (30 mL). The aqueous layer was further extracted with DCM (10 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. The crude residue was purified by flash chromatography (DCM / CH3OH, 15 / 1 v / v) to provide compound 49 as a white solid (14 mg, 33%).1H NMR (600 MHz, DMSO-d6) δ 8.72 (s, 1H), 8.19 (t, J = 5.9 Hz, 1H), 7.89 (d, J = 8.0 Hz, 2H), 7.59 (t, J = 7.8 Hz, 2H), 7.48 (t, J = 7.4 Hz, 1H), 6.59 (s, 1H), 4.50 (d, J = 5.9 Hz, 2H), 4.31 (s, 2H), 3.36 – 3.30 (m, 2H), 3.26 – 3.20 (m, 2H). LC / MS (m / z): 341.2 [M+H]+Example 50 Synthesis of 5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazole-2- carboxamide in methanol (3 mL) was stirred in a sealed tube at rt. for 16 hours. Then, the mixture was concentrated to give 50 as a whitesolid (27 mg, 95%).1H NMR (400 MHz, DMSO-d6) δ 8.75 (s, 1H), 8.64 (t, J = 6.0 Hz, 1H), 8.21 (s, 1H), 7.93 – 7.81 (m, 3H), 7.59 (t, J = 7.9 Hz, 2H), 7.48 (t, J = 7.4 Hz, 1H), 4.59 (d, J = 5.8 Hz, 2H). LC / MS (m / z): 286.2 [M+H]+Example 51 Synthesis of 1-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)ethan- 1-one in Example 22 above using 2-hydroxypropanoic acid. LC / MS (m / z): 286.2 [M+H].+Without purification, crude compound 51a (29 mg, 0.1 mmol) was solved in CH2Cl2(10 mL) and DMP (47 mg, 0.11 mmol) was added. The mixture was stirred for 2 hours at room temperature. Then, saturated Na2S2O3 aqueous solution (10 mL) was added. The CH2Cl2 layer was separated, and the aqueous layer was extracted with CH2Cl2(10 mL × combined organic layers were washed with saturated NaHCO3 aqueous solution and dried over anhydrous Na2SO4 and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 51 as white solid (8 mg, 28%).1H NMR (400 MHz, DMSO-d6) δ 8.99 (t, J = 6.0 Hz, 1H), 8.76 (s, 1H), 7.92 – 7.86 (m, 2H), 7.63 – 7.56 (m, 2H), 7.52 – 7.46 (m, 1H), 4.63 (d, J = 5.9 Hz, 2H), 2.52 (s, 3H). LC / MS (m / z): 285.2 [M+H]+Example 52 Synthesis of 5-(cyclopentylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- thiadiazol-2-amine Step 1: 5 mmol) in CH3OH (10 mL), 0.5 mL NH2NH2.H2O aqueous solution (85 %) was added. The reaction was heated to reflux for 16 hours and concentrated in vacuo to dryness. Compound 52a was further used without purification.1H NMR (400 MHz, Chloroform-d) δ 6.79 (s, 1H), 3.89 (s, 2H), 2.29 – 2.18 (m, 1H), 2.16 (s, 1H), 2.14 (d, J = 1.1 Hz, 1H), 1.88 – 1.76 (m, 2H), 1.68 – 1.48 (m, 4H), 1.19 – 1.07 (m, 2H). LC / MS (m / z): 143.2 [M+H]+Step 2: To a round-bottom flask, 137 mg 3a (0.5 mmol) and 5 mL 4M HCl / 1,4-dioxane solution were added and the mixture was stirred at room temperature. After the reaction was complete after about 2 hours (determined by TLC analysis), the mixture was concentrated under vacuo to dryness. Then, TCDI (107 mg, 0.6 mmol), DIPEA (5 mL) and THF (10 mL) were added and the mixture was stirred at rt. for 1 hour. After that, 52a (71 mg, 0.5 mmol) was added and the reaction was heated to reflux for 2 hours. After the reaction was cooled to room temperature, 30 mL of water was added. The aqueous layer was extracted three times with ethyl acetate (10 mL × 3). The combined organic phase was washed with saturated brine (15 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was purified by flash chromatography (DCM / MeOH, 20 / 1 v / v) to give 52b as light yellow solid (149 mg, 83%).1H (30 mg, 0.3 mmol) were added. The reaction was stirred at rt. for 2 hours and 30 mL of water was added. The aqueous layer was extracted three times with ethyl acetate (15 mL × 3). The combined organic phase was washed with saturated brine (15 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was purified by flash chromatography (DCM / MeOH, 20 / 1 v / v) to give 52 as white solid (26 mg, 77%).1H NMR (400 MHz, Chloroform-d) δ 8.21 (s, 1H), 7.72 (d, J = 7.7 Hz, 2H), 7.50 (t, J = 7.6 Hz, 2H), 7.42 (t, J = 7.4 Hz, 1H), 6.66 (s, 1H), 4.76 (s, 2H), 2.87 (d, J = 7.5 Hz, 2H), 2.22 – 2.09 (m, 1H), 1.86 – 1.72 (m, 2H), 1.64 – 1.49 (m, 4H), 1.35 – 1.26 (m, 2H). LC / MS (m / z): 341.1 [M+H]+Example 53 Synthesis of N-((1-cyclohexyl-1H-1,2,3-triazol-4-yl)methyl)-5-(cyclopentylmethyl)-1,3,4- oxadiazol-2-amine Step 1: with the procedure described in Step 1 of Example 1 as a white solid (56% yield).1H NMR (400 MHz, Chloroform-d) δ 7.49 (s, 1H), 5.08 (s, 1H), 4.47 – 4.40 (m, 1H), 4.39 (d, J = 6.0 Hz, 2H), 2.23 – 2.14 (m, 2H), 1.96 – 1.88 (m, 2H), 1.80 – 1.67 (m, 3H), 1.51 – 1.46 (m, 2H), 1.44 (s, 9H), 1.29 (tt, J = 12.7, 3.5 Hz, 1H). LC / MS (m / z): 281.3 [M+H]+Step 2: Starting from compound 53a, compound 53b was synthesized in accordance with the procedure described in Example 52 as a light yellow solid (79% yield).1H NMR (400 MHz, DMSO-d6) δ 9.65 (s, 1H), 9.29 (s, 1H), 8.23 (s, 1H), 7.90 (s, 1H), 4.84 – 4.59 (m, 2H), 4.53 – 4.31 (m, 1H), 2.28 – 1.92 (m, 5H), 1.91 – 1.63 (m, 7H), 1.63 – 1.36 (m, 6H), 1.30 – 0.96 (m, 3H). LC / MS (m / z): 365.3 [M+H]+Step 3: mmol) and pyridine (24 mg, 0.3 mmol) were added. The reaction was heated to reflux for 16 hours and 30 mL of water was added after it was cooled to room temperature. The aqueous layer was extracted three times with ethyl acetate (15 mL × 3). The combined organic phase was washed with saturated brine (15 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was purified by flash chromatography (DCM / MeOH, 20 / 1 v / v) to give 53 as white solid (25 mg, 76%).1H NMR (400 MHz, Chloroform-d) δ 7.66 (s, 1H), 5.54 (t, J = 6.2 Hz, 1H), 4.60 (d, J = 5.8 Hz, 2H), 4.41 (tt, J = 11.8, 3.8 Hz, 1H), 2.67 (d, J = 7.4 Hz, 2H), 2.27 – 2.14 (m, 3H), 1.95 – 1.86 (m, 2H), 1.82 – 1.71 (m, 5H), 1.67 – 1.52 (m, 4H), 1.50 – 1.38 (m, 2H), 1.31 – 1.19 (m, 3H). LC / MS (m / z): 331.1 [M+H]+Example 54 Synthesis of (R)-5-cyclopropyl-N-(1-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2-amine Step 1: methanol (175 mg, 1 mmol) in CH2Cl2 (10 mL), DMP (466 mg, 1.1 mmol) was added. The mixture was stirred for 2 hours at room temperature. Then, saturated Na2S2O3 aqueous solution (30 mL) was added. The CH2Cl2 layer was separated, and the aqueous layer extracted with CH2Cl2 (15 mL × 2). The combined organic layers were washed with NaHCO3aqueous solution and dried over anhydrous Na2SO4 and concentrated. The residue was purified by flash chromatography (PE / EtOAc, 2 / 1 v / v) to give 54a as white solid (107 mg, 62%).1H NMR (400 MHz, Chloroform-d) δ 10.23 (s, 1H), 8.53 (s, 1H), 7.80 – 7.75 (m, 2H), 7.62 – 7.50 (m, 3H). LC / MS (m / z): 174.2 [M+H]+Step 2: (67 mg, 0.55 mmol) and anhydrous CuSO4 (399 mg, 2.5 mmol) were added. The reaction was stirred at rt. for 16 hours, filtrated and washed with 10 mL CH2Cl2. The organic solventwas concentrated in vacuo to dryness and 10 mL THF was added at 0oC. Then, CH3MgBr (1 mL, 1M CH3MgBr / THF) was added dropwise to the reaction and it was stirred for additional 2 hours at 0oC. The mixture was poured into saturated NH4Cl aqueous solution (30 mL) and extracted three times with ethyl acetate (15 mL × 3). The combined organic phase was washed with saturated brine (15 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was purified by flash chromatography (DCM / MeOH, 30 / 1 v / v) to give mixture 54b as a white solid (129 mg, 88%). LC / MS (m / z): 293.2 [M+H]+Step 3: were added and the mixture was stirred at room temperature. After the reaction was complete as determined by TLC analysis (about 4 hours), the mixture was concentrated under vacuo to dryness. The crude product was used without further purification. Then, 1b (95 mg, 0.5 mmol), K2CO3 (138 mg, 1 mmol) and DMF (5 mL) were added and the mixture was heated to 120 °C for 2 hours. After the reaction was cooled to room temperature, 50 mL of water was added. The aqueous layer was extracted three times with ethyl acetate (15 mL × 3). The combined organic phase was washed with saturated brine (15 mL), dried over anhydrous Na2SO4, and concentrated in vacuo. The residue was purified by flash chromatography (DCM / MeOH, 20 / 1 v / v) to give 54c as white solid (105 mg, 71%).1H NMR (400 MHz, Chloroform-d) δ 8.06 (s, 1H), 7.75 – 7.69 (m, 2H), 7.50 (dd, J = 8.4, 7.0 Hz, 2H), 7.46 – 7.39 (m, 1H), 5.72 (d, J = 8.1 Hz, 1H), 5.08 (p, J = 7.1 Hz, 1H), 2.02 – 1H), 1.76 (d, J = 7.1 Hz, 3H), 1.02 – 0.94 (m, 4H). LC / MS (m / z): 297.2 [M+H]+Step 4: 54was obtained as a white solid (peak 1, 46% yield, 98% ee., retention time= 3.76 min). The absolute configuration of 54 was determined by X-ray crystallography (crystallized from ethyl acetate).1H NMR (400 MHz, Chloroform-d) δ 8.02 (s, 1H), 7.74 – 7.69 (m, 2H), 7.51 (t, J = 7.6 Hz, 2H), 7.47 – 7.41 (m, 1H), 5.33 (d, J = 8.2 Hz, 1H), 5.13 – 5.05 (m, 1H), 2.01 – 1.94 (m, 1H), 1.77 (d, J = 6.9 Hz, 3H), 1.03 – 0.97 (m, 4H). LC / MS (m / z): 297.2 [M+H]+Example 55 Synthesis of (S)-5-cyclopropyl-N-(1-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2- amine 54c gave example 55 as a white solid (peak 2, 42% yield, 98% ee, retention time= 4.92 min). 1H NMR (400 MHz, Chloroform-d) δ 8.03 (s, 1H), 7.74 – 7.69 (m, 2H), 7.51 (t, J = 7.6 Hz, 2H), 7.46 – 7.41 (m, 1H), 5.40 (d, J = 8.0 Hz, 1H), 5.13 – 5.04 (m, 1H), 2.02 – 1.93 (m, 1H), 1.77 (d, J = 6.9 Hz, 3H), 1.03 – 0.96 (m, 4H). LC / MS (m / z): 297.2 [M+H]+Example 56 Synthesis of 5-cyclopropyl-N-((5-fluoro-1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: To a solution of iodobenzene (816 mg, 4 in DMF (15 mL) with a two-neck bottle, CuI (762 mg, 4 mmol), NaN3 (390 mg, 6 mmol) and DBU (608 mg, 4 mmol) were added at room temperature. The resulting mixture was heated to 90 °C for 2 hours under argon atmosphere protection. After it was cooled to room temperature, tert-butyldimethyl(prop-2-yn-1- yloxy)silane (681 mg, 4 mmol) and NIS (990 mg, 4.4 mmol) in DMF (15 mL) solution was added by a syringe. The mixture was stirred at rt. for 16 hours and diluted with EtOAc (60 mL) and water (100 mL). The aqueous layer was further extracted with EtOAc (30 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. The crude residue was purified by flash chromatography (petroleum ether / EtOAc, 8 / 1 v / v) to provide compound 56a as a yellow solid (570 mg, 34%). LC / MS (m / z): 416.1 [M+H]+Step 2: mg, 0.5 mmol) in THF (10 mL) at 0oC, tetrabutylammonium fluoride (TBAF) in THF (1 mL, 1 M) was added. The mixture was stirred for 1 hours at room temperature. Then, saturated NH4Cl solution (25 mL) was added and extracted with EtOAc (10 mL). The EtOAc layer was separated, and the aqueous layer extracted with EtOAc (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4 and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 30 / 1 v / v) to give 56b as brown solid (83 mg, 55%). 1H NMR (400 MHz,Chloroform-d) δ 7.61 – 7.50 (m, 5H), 4.84 (d, J = 5.8 Hz, 2H), 4.35 (d, J = 5.3 Hz, 1H). LC / MS (m / z): 302.0 [M+H]+Step 3: To a solution of 56b (343 mg, 1 mmol) in anhydrous toluene (10 mL), AgF (349 mg, 3 mmol) and N,N,N',N'-tetramethylethylenediamine (58 mg, 0.5 mmol) were added at room temperature. The resulting mixture was heated to reflux for 16 hours under argon atmosphere protection. After it was cooled to room temperature, the mixture was concentrated under vacuo to dryness. The crude residue was purified by flash chromatography (CH2Cl2 / CH3OH, 30 / 1 v / v) to provide the desired product 56c as a white solid (99 mg, 51%).1H NMR (400 To a solution of 5-cyclopropyl-1,3,4-oxadiazol-2-amine (118 mg, 2 mmol) in DCM (10 mL) at rt., (Boc)2O (480 mg, 2.2 mmol) and TEA (607 mg, 6 mmol) were added. The mixture was stirred for 16 hours at room temperature. Then, water (30 mL) was added and extracted with DCM (10 mL). The DCM layer was separated, and the aqueous layer extracted with DCM (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (petroleum ether / EtOAc, 1 / 1 v / v) to give 56d as white solid (74 mg, 40%). 1H NMR (600 MHz, Chloroform-d) δ 8.39 (s, 1H), 2.11 –2.05 (m, 1H), 1.52 (s, 9H), 1.13 – 1.08 (m, 4H). LC / MS (m / z): 473.3 [2M+Na]+Step 5: was added. The mixture was stirred for 4 hours at rt. Then, the reaction was concentrated in vacuo to dryness for further use. To another round-bottom bottle, DMF (5 mL), 56d (113 mg, 0.5 mmol) and NaH (24 mg, 0.6 mmol, 60% in mineral oil) was added at 0oC. This reaction was stirred at rt. for 15 minutes. Then, the prepared crude chlorinated product was solved in DMF (1 mL) and added to the previous reaction at 0oC. The reaction was warmed to rt. and reacted for 16 hours, then it was diluted with EtOAc (10 mL) and water (30 mL). The aqueous layer was further extracted with EtOAc (10 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. Then, 5 mL 4M HCl / 1,4-dioxane solution were added and the mixture was stirred at room temperature for 2 hours and concentrated under vacuo to dryness. The crude residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to provide compound 56 as a white solid (22 mg, 15%).1H NMR (600 MHz, Chloroform-d) δ 7.68 – 7.63 (m, 2H), (m, 3H), 4.70 (s, 2H), 2.03 – 1.99 (m, 1H), 1.13 – 1.10 (m, 4H). LC / MS (m / z): 301.2 [M+H]+Example 57 Synthesis of 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl-d2)-1,3,4-oxadiazol-2- amine Step 1: 4-carboxylate (217 mg, 1 mmol) in anhydrous THF (15 mL) at 0oC, LiAlD4(84 mg, 2 mmol) was added. The mixture was stirred for 1 hour at rt. Then, the reaction was poured into saturated potassium sodium tartrate ice water solution (30 mL) and extracted with CH2Cl2(10 mL). The CH2Cl2layer was separated, and the aqueous layer was extracted with CH2Cl2 (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4 and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 30 / 1 v / v) to give 57a as white solid (122 mg, 69%).1H NMR(400 MHz, Chloroform-d) δ 7.98 (s, 1H), 7.75 – 7.70 (m, 2H), 7.56 – 7.50 (m, 2H), 7.48 – 7.42 (m, 1H), 2.42 (s, 1H). LC / MS (m / z): 178.2 [M+H]+Step 2: was added. The mixture was stirred for 4 hours at rt. Then, the reaction was concentrated in vacuo to dryness. DMF (10 mL), K2CO3 (104 mg, 0.75 mmol) and Di-tert-butyl iminodicarboxylate (217 mg, 1 mmol) were added. The reaction was stirred at 70oC for 16 hours and diluted with EtOAc (10 mL) and water (30 mL). The aqueous layer was further extracted with EtOAc (10 mL × 2). The combined organic layer was washed with brine, dried (anhydrous Na2SO4) and concentrated. The crude residue was purified by flash chromatography (petroleum ether / EtOAc, 3 / 1 v / v) to provide compound 57b as a white solid (136 mg, 72%).1H NMR (400 MHz, Chloroform-d) δ 7.93 (s, 1H), 7.74 – 7.69 (m, 2H), 7.54 – 7.49 (m, 2H), 7.46 – 7.40 (m, 1H), 1.51 (s, 18H). LC / MS (m / z): 377.3 [M+H]+ described in Step 3 of Example 1 as a white solid (83% yield).1H NMR (400 MHz, DMSO-d6) δ 8.70 (s, 1H), 7.94 (s, 1H), 7.89 (d, J = 7.4 Hz, 2H), 7.59 (t, J = 7.9 Hz, 2H), 7.52 – 7.45 (m, 1H), 2.05 – 1.97 (m, 1H), 1.02 – 0.95 (m, 2H), 0.87 – 0.81 (m, 2H). LC / MS (m / z): 285.2 [M+H]+Example 58 Synthesis of 5-cyclopropyl-N-methyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine 0oC, NaH (24 mg, 0.6 mmol, 60% in mineral oil) was added. The reaction was stirred for 15 minutes at 0oC, CH3I (85 mg, 0.6 mmol) was added and the reaction was warmed to rt. and stirred for 12 hours. The mixture was extracted with EtOAc (10 mL) and H2O (30 mL). The EtOAc layer was separated, and the aqueous layer was extracted with EtOAc (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4 and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 58 as a white solid (56 mg, 38%).1H NMR(400 MHz, Chloroform-d) δ 8.12 (s, 1H), 7.70 (d, J = 8.2 Hz, 2H), 7.53 – 7.46 (m, 2H), 7.45 – 7.37 (m, 1H), 4.70 (s, 2H), 3.11 (s, 3H), 2.01 – 1.92 (m, 1H), 1.03 – 0.97 (m, 4H). LC / MS (m / z): 297.2 [M+H]+Example 59 Synthesis of 2-cyclopropyl-5-(2-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazole in accordance with the procedure described in Step 1 of Example 3 as a white solid (62% yield).1H NMR (400 MHz, Chloroform-d) δ 7.80 (s, 1H), 7.71 (d, J = 7.3 Hz, 2H), 7.51 (t, J = 8.1 Hz, 2H), 7.45 – 7.39 (m, 1H), 3.70 (s, 3H), 3.13 (t, J = 7.2 Hz, 2H), 2.81 (t, J = 7.2 Hz, 2H). LC / MS (m / z): 232.2 [M+H]+Step 2: monohydrate (168 mg, 4 mmol) was added. The reaction was stirred for 12 hours and then, water (15 mL) was added and 2N HCl was used to adjust pH between 2~3. The mixture was extracted with EtOAc (10 mL). The EtOAc layer was separated, and the aqueous layer was extracted with EtOAc (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4 and concentrated. Then, DMF (10 mL), cyclopropanecarbohydrazide (80 mg, 0.8 mmol), HATU (304 mg, 0.8 mmol) and TEA (242 mg, 2.4 mmol) were added to this reaction. The mixture was stirred for 12 hours at rt. and water (30 mL) was added. The mixture was extracted with EtOAc (10 mL× 3). The combined organic layers were dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to provide the title compound 59b as a white solid (72% yield).1H NMR (400 MHz, DMSO-d6) δ 9.99 (s, 1H), 9.85 (s, 1H), 8.61 (s, 1H), 7.88 (d, J = 8.8 Hz, 2H), 7.62 – 7.55 (m, 2H), 7.51 – 7.44 (m, 1H), 2.97 (t, J = 7.3 Hz, 2H), 2.54 (t, J = 7.3 Hz, 2H), 1.65 – 1.56 (m, 1H), 0.77 – 0.69 (m, 4H). LC / MS (m / z): 300.2 [M+H]+Step 3: mg, 1 mmol) and TEA (152 mg, 1.5 mmol) were added. The reaction was stirred for 12 hours under reflux and cooled to room temperature. Water (30 mL) was added and the CH2Cl2layer was separated. The aqueous layer was extracted with CH2Cl2(10 mL × 2) and the combined organic layers were dried over anhydrous Na2SO4and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give the title compound 59 as a white solid (67% yield).1H NMR (400 MHz, DMSO-d6) δ 8.63 (s, 1H), 7.85 (d, J = 7.4 Hz, 2H), 7.59 (t, J = 7.9 Hz, 2H), 7.48 (t, J = 7.4 Hz, 1H), 3.25 – 3.18 (m, 2H), 3.18 – 3.11 (m, 2H), 2.22 – 2.14 (m, 1H), 1.13 – 1.05 (m, 2H), 0.98 – 0.91 (m, 2H). LC / MS (m / z): 282.2 [M+H]+Example 60 Synthesis of 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-4H-1,2,4-triazol-3- amine To a solution of 54a (87 mg, 0.5 mmol) in DCE (15 mL) at rt., 5-cyclopropyl-4H-1,2,4-triazol- 3-amine (62 mg, 0.5 mmol) and TFA (68 mg, 0.6 mmol) were added. The reaction was stirred for 12 hours under reflux and cooled to room temperature. NaBH(OAc)3(318 mg, 1.5 mmol) was added to the reaction and the reaction was stirred for 6 hours at rt. Then, H2O (30 mL) was added and the DCE layer was separated. The aqueous layer was extracted with CH2Cl2 (10 mL × 2) and the combined organic layers were dried over anhydrous Na2SO4 and concentrated. The residue was purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 60 as white solid (62 mg, 44%). 1H NMR (400 MHz, DMSO-d6) δ 8.57 (s, 1H), 7.90 –7.84 (m, 2H), 7.63 – 7.55 (m, 2H), 7.51 – 7.44 (m, 1H), 6.87 (s, 1H), 6.05 (s, 1H), 4.39 (s, 2H), 1.88 – 1.71 (m, 1H), 0.93 – 0.67 (m, 4H). LC / MS (m / z): 282.2 [M+H]+Example 61 Synthesis of 5-cyclopropyl-N-(2-(1- 1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2- amine Step 1: synthesized in accordance with the procedure described in Step 1 of Example 3 as a white solid (69% yield).1H NMR (400 MHz, Chloroform-d) δ 7.81 (s, 1H), 7.71 (d, J = 8.4 Hz, 2H), 7.56 – 7.49 (m, 2H), 7.46 – 7.37 (m, 1H), 5.02 (s, 1H), 3.54 (d, J = 6.5 Hz, 2H), 3.00 (t, J = 6.7 Hz, 2H), 1.43 (s, 9H). LC / MS (m / z): 289.2 [M+H]+Step 2: described in Step 3 of Example 1 as a white solid (68% yield).1H NMR (400 MHz, Chloroform- d) δ 7.83 (s, 1H), 7.74 – 7.69 (m, 2H), 7.53 (t, J = 7.7 Hz, 2H), 7.47 – 7.42 (m, 1H), 5.29 (s, 1H), 3.80 – 3.73 (m, 2H), 3.13 (t, J = 6.2 Hz, 2H), 2.02 – 1.94 (m, 1H), 1.02 – 0.97 (m, 4H). LC / MS (m / z): 297.0 [M+H]+Example 62 Synthesis of 5-cyclopropyl-N-((5-methyl-1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: Starting from ethyl 5-methyl-1-phenyl- triazole-4-carboxylate, compound 62a was synthesized in accordance with the procedure described in Step 1 of Example 57 as a white solid (77% yield).1H NMR (400 MHz, Chloroform-d) δ 7.59 – 7.50 (m, 3H), 7.48 – 7.43 (m, 2H), 4.82 (d, J = 6.0 Hz, 2H), 2.49 (t, J = 6.1 Hz, 1H), 2.37 (s, 3H). LC / MS (m / z): 190.2 [M+H]+Step 2: with the procedure described in Step 2 of Example 57 as a white solid (56% yield).1H NMR (400 MHz, Chloroform-d) δ 7.57 – 7.48 (m, 3H), 7.46 – 7.40 (m, 2H), 4.96 (s, 2H), 2.32 (s, 3H), 1.50 (s, 18H). LC / MS (m / z): 389.3 [M+H]+Step 3: described in Step 3 of Example 57 as a white solid (73% yield).1H NMR (400 MHz, Chloroform-d) δ 7.61 – 7.51 (m, 3H), 7.51 – 7.42 (m, 2H), 5.46 (s, 1H), 4.62 (d, J = 4.2 Hz, 2H), 2.40 (s, 3H), 2.02 – 1.95 (m, 1H), 1.09 – 0.97 (m, 4H). LC / MS (m / z): 297.2 [M+H]+Example 63 Synthesis of 1-(4-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1- yl)phenyl)ethan-1-one Step 1: Starting from (4-acetylphenyl)boronic 63a was synthesized in accordance with the procedure described in Step 1 of Example 3 as a white solid (62% yield).1H NMR (400 MHz, Chloroform-d) δ 8.12 (d, J = 8.7 Hz, 2H), 8.05 (s, 1H), 7.86 (d, J = 8.7 Hz, 2H), 5.18 (s, 1H), 4.49 (d, J = 6.1 Hz, 2H), 2.66 (s, 3H), 1.45 (s, 9H). LC / MS (m / z): 317.3 [M+H]+Step 2: procedure described in Step 2 of Example 52 as a white solid (42% yield).1H NMR (400 MHz, DMSO-d6) δ 9.98 (s, 1H), 9.35 (s, 1H), 8.66 (s, 1H), 8.53 (s, 1H), 8.17 (d, J = 8.7 Hz, 2H), 8.04 (d, J = 8.7 Hz, 2H), 4.82 (d, J = 5.7 Hz, 2H), 2.64 (s, 3H), 2.03 – 1.95 (m, 1H), 0.80 – 0.70 (m, 4H). LC / MS (m / z): 359.2 [M+H]+Step 3: procedure described in Step 3 of Example 53 as a white solid (39% yield).1H NMR (400 MHz, Chloroform-d) δ 8.29 (s, 1H), 8.09 (d, J = 8.3 Hz, 2H), 7.86 (d, J = 8.3 Hz, 2H), 5.89 (s, 1H), 4.69 (s, 2H), 2.64 (s, 3H), 2.05 – 1.92 (m, 1H), 1.06 – 0.93 (m, 4H). LC / MS (m / z): 325.2 [M+H]+Example 64 Synthesis of 5-cyclopropyl-N-((1-(4-ethynylphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4- oxadiazol-2-amine Step 1: with the procedure described in Step 1 of Example 3 as a white solid (69% yield).1H NMR (400 MHz, Chloroform-d) δ 7.95 (s, 1H), 7.74 – 7.53 (m, 4H), 5.22 (s, 1H), 4.45 (d, J = 4.9 Hz, 2H), 1.44 (s, 9H). LC / MS (m / z): 354.2 [M+H]+Stap 2: procedure described in Step 2 of Example 52 as a white solid (62% yield).1H NMR (400 MHz, DMSO-d6) δ 9.96 (s, 1H), 9.34 (s, 1H), 8.59 – 8.46 (m, 1H), 7.94 – 7.77 (m, 4H), 7.14 (s, 1H), 4.79 (d, J = 5.6 Hz, 2H), 1.65 – 1.54 (m, 1H), 0.78 – 0.69 (m, 4H). LC / MS (m / z): 396.1 [M+H]+Step 3: with the procedure described in Step 3 of Example 53 as a white solid (69% yield).1H NMR (400 MHz, DMSO-d6) δ 8.74 (s, 1H), 7.97 (t, J = 6.0 Hz, 1H), 7.88 (d, J = 8.9 Hz, 2H), 7.79 (d, J = 8.9 Hz, 2H), 4.46 (d, J = 5.9 Hz, 2H), 2.05 – 1.96 (m, 1H), 1.01 – 0.95 (m, 2H), 0.87 – 0.81 (m, 2H). LC / MS (m / z): 362.1 [M+H]+Step 4: (707 mg, 7 mmol) in THF (5 mL), Pd(PPh3)2Cl2(49 mg, 0.07 mmol), CuI (13 mg, 0.07 mmol) and PPh3(37 mg, 0.14 mmol) were added. The reaction was heated to reflux for 16 hours under argon atmosphere. After the reaction was cooled to rt., water (45 mL) was added and the mixture was extracted with EtOAc (15 mL). The EtOAc layer was separated, and the aqueous layer was extracted with EtOAc (10 mL × 2). The combined organic layers were dried over anhydrous Na2SO4 and concentrated. Then, K2CO3 (276 mg, 2 mmol) and CH3OH (15 mL) were added and the reaction was stirred at rt. for 2 hours. The mixture was concentrated and purified by flash chromatography (CH2Cl2 / CH3OH, 20 / 1 v / v) to give 64 as awhite solid (175 mg, 83%).1H NMR (400 MHz, Chloroform-d) δ 8.17 (s, 1H), 7.71 (d, J = 8.7 Hz, 2H), 7.62 (d, J = 8.7 Hz, 2H), 5.46 (s, 1H), 4.68 (d, J = 5.9 Hz, 2H), 3.18 (s, 1H), 2.03 – 1.93 (m, 1H), 1.05 – 0.96 (m, 4H). LC / MS (m / z): 307.2 [M+H]+Example 65 Synthesis of 5-(1,3-dithiolan-2-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol- 2-amine acid monohydrate (10 mg, 0.05 mmol) and ethane-1,2-dithiol (47 mg, 0.5 mmol) was added. The reaction was heated to reflux for 16 hours and concentrated in vacuo to dryness. The residue was purified by flash chromatography (DCM / MeOH, 20 / 1 v / v) to give 65 as a light yellow solid (76 mg, 44%).1H NMR (400 MHz, Chloroform-d) δ 8.14 (s, 1H), 7.72 (d, J = 8.2 Hz, 2H), 7.52 (t, J = 8.2 Hz, 2H), 7.48 – 7.42 (m, 1H), 5.67 (s, 1H), 5.59 (s, 1H), 4.72 (d, J = 5.8 Hz, 2H), 3.53 – 3.44 (m, 2H), 3.41 – 3.31 (m, 2H). LC / MS (m / z): 347.1 [M+H]+ Example 66 Synthesis of 5-(1,3-dioxolan-2-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol- 2-amine with the procedure described in Example 65 as a white solid (18% yield).1H NMR (600 MHz, Chloroform-d) δ 8.14 (s, 1H), 7.74 – 7.69 (m, 2H), 7.52 (t, J = 7.9 Hz, 2H), 7.47 – 7.42 (m, 1H), 6.02 (s, 1H), 5.74 (s, 1H), 4.74 (d, J = 5.9 Hz, 2H), 4.19 – 4.13 (m, 2H), 4.09 – 4.02 (m, 2H). LC / MS (m / z): 315.2 [M+H]+II. BIOLOGICAL ASSAYS The hIL4i1 enzymatic activity assay: is an oxidase that degrades L-phenylalanine into phenylpyruvate acid (PPA), hydrogen peroxide (H2O2), and ammonia (NH3). The product H2O2 can be detected by the Amplex Red reagent, which is a highly sensitive and stable fluorescent probe and an ideal fluorogenic substrate for peroxidase. In the presence of horseradish peroxidase (HRP), the Amplex Red reagent reacts in a 1:1 stoichiometry with H2O2 to produce highly fluorescent, strongly absorbing resorufin. The fluorescent signal represents IL4i1 enzymatic activity and the reactions in which the production of H2O2is inhibited show a low fluorescence. Protocol of hIL4i1 enzymatic assay The assay was performed in a black 384-well plate with a volume of 10 µL 1 x assay buffer (50 mM phosphate buffer pH 7 + 0.01% Tween-20, pH 7.0). The recombinant protein hIL4i1 (R&D Systems, #5684-AO) and a serial dilution of compounds were pre-incubated for 10 min at room temperature. Then, a mix containing 500 µM L-phenylalanine (Sigma, #78019), 0.1 U / mL HRP (Sigma, #P2088) and 50 µM Amplex Red (Invitrogen, #A22177) was added and incubated at room temperature for 60 min. The fluorescence intensity was measured by Tecan Spark®Multimode Microplate Reader at Ex 544 nm / Em 590 nm. Curve fitting for dose response IC50was analyzed using Prism. IC50values are given as mean ± standard deviation from two independent experiments. Table 1. IL4I1 enzymatic activity IC50. Compound IL4I1 IC50 CompoundIL4I1 IC50(nM) (nM) 1 1921 ± 368 34 183 ± 14 2 1525 ± 264 35 399 ± 78 3 61 ± 6 36 104 ± 5 4 341 ± 0 37 302 ± 6 5 150 ± 11 38 27 ± 4 6 118 ± 1 39 287 ± 9 7 758 ± 20 40 304 ± 31 8 106 ± 1 41 65 ± 0 9 136 ± 19.2 42 39 ± 14 10 2243 ± 342 43 83 ± 17 11 458 ± 41 44 2283 ± 520 12 3879 ± 1105 45 1353 ± 120 13 1053 ± 11 46 1949 ± 45 14 613 ± 11 47 61 ± 0 15 2007± 219 48 2843 ± 209 16 58 ± 5 49 2535 ± 54 17 216 ± 14 50 2960 ± 271 18 38 ± 7 51 2277 ± 401 19 216 ± 25 52 244 ± 7 20 1098± 64 53 395 ± 7 21 993± 118 54 88 ± 2 22 21 ± 0 55 273 ± 17 23 16 ± 0 56 85 ± 8 24 119 ± 17 57 28 ± 5 25 1374 ± 11 58 382 ± 29 26 945 ± 44 59 209 ± 15 27 301 ± 12 60 1430 ± 115 35 ± 1 61 77 ± 9 570 ± 24 62 207 ± 13 417 ± 24 63 4287 ± 204 3961 ± 4 64 149 ± 18 86 ± 2 65 151 ± 26 356 ± 23 66 104 ± 2

Claims

Claims 1. A compound of Formula (I)wherein A represents -CH2-; -N(RA)-, wherein RArepresents hydrogen or (C1-4)alkyl; or -CH2-NH-*, wherein the asterisk indicates the bond which is linked to the heteroaromatic carbon atom; X represents -O-, -S-, or -NH-; R1represents (C1-6)alkyl; (C2-4)alkenyl; (C2-4)alkynyl which is independently unsubstituted or mono-substituted with aryl; (C1-4)fluoroalkyl; (C1-4)hydroxyalkyl; (C1-4)alkoxy-(C1-4)alkyl; (C1- 4)alkyl-carbonyl; (C1-4)alkoxy-carbonyl; amino-carbonyl; (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1-4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; (C3-8)heterocyclyl; (2-oxoimidazolidin-1-yl)methyl; aryl; aryl-(C1-4)alkyl; or heteroaryl; R2represents (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted with halogen; ferrocenyl; aryl which is independently unsubstituted or substituted with 1 to 5 substituents independently selected from the group consisting of deuterium, (C1-4)alkyl, (C2- 4)alkynyl, (C1-4)alkoxy, (C1-4)alkyl-carbonyl, cyano, halogen, (C1-4)fluoroalkyl, and (C1- 4)hydroxyalkyl; or heteroaryl which is independently unsubstituted or mono- or di-substituted with halogen; R3represents hydrogen, (C1-4)alkyl, or halogen; R4represents hydrogen, deuterium, (C1-4)alkyl, or (C1-4)fluoroalkyl; and R5represents hydrogen, or deuterium; or a salt thereof; with the proviso that the compound is not: N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-propyl-1,3,4-oxadiazol-2- amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-ethyl-1,3,4-thiadiazol-2- amine;N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3- 4-yl)methyl)-5-(cyclopropylmethyl)-1,3,4- oxadiazol-2-amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-(tetrahydrofuran-2-yl)-1,3,4- oxadiazol-2-amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-(difluoromethyl)-1,3,4- thiadiazol-2-amine; N-((1-(3-chloro-4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-isopropyl-1,3,4-thiadiazol-2- amine; 5-methyl-N-(1-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-thiadiazol-2-amine; 5-(difluoromethyl)-N-((1-(4-methoxyphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-thiadiazol-2- amine; and N-((1-(3-methoxyphenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-methyl-1,3,4-oxadiazol-2-amine.

2. A compound according to claim 1, wherein A represents -N(RA)-, wherein RArepresents hydrogen or (C1-4)alkyl; or a salt thereof.

3. A compound according to any one of claims 1 or 2, wherein X represents -O-, or -S-; or a salt thereof.

4. A compound according to any one of claims 1 to 3, wherein R1represents (C1-6)alkyl; (C3-8)cycloalkyl which is independently unsubstituted or mono- or di-substituted, wherein the substituents are independently selected from the group consisting of (C1-4)alkyl, hydroxy, (C1- 4)alkoxy, and halogen; (C3-8)cycloalkyl-(C1-4)alkyl; or (C3-8)heterocyclyl; or a salt thereof.

5. A compound according to any one of claims 1 to 3, wherein R1represents aryl; aryl-(C1-4)alkyl; or heteroaryl; or a salt thereof.

6. A compound according to any one of claims 1 to 5, wherein R2represents aryl which is independently unsubstituted or substituted with 1 or 2 substituents independently selected from the group consisting of (C1-4)alkyl, (C2-4)alkynyl, cyano, and halogen; pentadeutero- phenyl; or heteroaryl which is independently unsubstituted or mono- or di-substituted with halogen; or a salt thereof.

7. A compound according to any one of claims 1 to 5, wherein R2represents phenyl or pentadeutero-phenyl; or a salt thereof.

8. A compound according to any one of 1 to 7, wherein R3represents hydrogen or fluoro; or a salt thereof.

9. A compound according to any one of claims 1 to 8, wherein R4represents hydrogen, deuterium, or methyl; or a salt thereof.

10. A compound according to claim 1 selected from the group consisting of: 5-cyclopropyl-N-((1-(4,4-difluorocyclohexyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-(bicyclo[1.1.1]pentan-1-yl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(2-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(3-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(4-fluorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(m-tolyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(p-tolyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-(4-chlorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(4-(trifluoromethyl)phenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 4-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1-yl)benzonitrile; (3-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1-yl)phenyl)methanol; 2-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1-yl)benzonitrile; N-((1-(2-chlorophenyl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(4-methoxyphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(phenyl-d5)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(furan-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(thiophen-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-(5-chlorothiophen-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-5-cyclopropyl-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-(pyridin-3-yl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-ferrocenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(cyclopentylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(cyclopropylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(1-cyclopropylethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 2-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)propan-2-ol; 1-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)cyclopropan-1-ol; 5-phenyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclobutyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine;5-methyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl) 2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(thiazol-5-yl)-1,3,4-oxadiazol-2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(2-azaspiro[3.3]heptan-6-yl)-1,3,4-oxadiazol-2-amine; 5-isopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(pyridin-4-yl)-1,3,4-oxadiazol-2-amine; 5-(tert-butyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(methoxymethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-benzyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(2-fluoropropan-2-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(oxetan-3-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(3,3-difluorocyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(3-methoxycyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(3,3-dimethylcyclobutyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(bicyclo[1.1.1]pentan-1-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-(bicyclo[3.1.0]hexan-3-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; ethyl 5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazole-2-carboxylate; (5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)methanol; 5-(difluoromethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-ethynyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-5-(phenylethynyl)-1,3,4-oxadiazol-2-amine; 1-((5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)methyl)imidazolidin-2-one; 5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazole-2-carboxamide; 1-(5-(((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)amino)-1,3,4-oxadiazol-2-yl)ethan-1-one; 5-(cyclopentylmethyl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-thiadiazol-2-amine; N-((1-cyclohexyl-1H-1,2,3-triazol-4-yl)methyl)-5-(cyclopentylmethyl)-1,3,4-oxadiazol-2-amine; (R)-5-cyclopropyl-N-(1-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2-amine; (S)-5-cyclopropyl-N-(1-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((5-fluoro-1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl-d2)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-methyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 2-cyclopropyl-5-(2-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazole; 5-cyclopropyl-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-4H-1,2,4-triazol-3-amine; 5-cyclopropyl-N-(2-(1-phenyl-1H-1,2,3-triazol-4-yl)ethyl)-1,3,4-oxadiazol-2-amine; 5-cyclopropyl-N-((5-methyl-1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; 1-(4-(4-(((5-cyclopropyl-1,3,4-oxadiazol-2-yl)amino)methyl)-1H-1,2,3-triazol-1-yl)phenyl)ethan-1-one; 5-cyclopropyl-N-((1-(4-ethynylphenyl)-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine;5-(1,3-dithiolan-2-yl)-N-((1-phenyl-1H-1,2,3- -1,3,4-oxadiazol-2-amine; and 5-(1,3-dioxolan-2-yl)-N-((1-phenyl-1H-1,2,3-triazol-4-yl)methyl)-1,3,4-oxadiazol-2-amine; or a salt thereof.

11. A pharmaceutical composition comprising, as active principle, a compound according to any one of claims 1 to 10, or a pharmaceutically acceptable salt thereof, and at least one therapeutically inert excipient.

12. A compound according to any one of claims 1 to 10, or a pharmaceutically acceptable salt thereof, for use as a medicament.

13. A compound according to any one of claims 1 to 10, or a pharmaceutically acceptable salt thereof, for use in the prevention or treatment of cancer.

14. Use of a compound according to any one of claims 1 to 10, or a pharmaceutically acceptable salt thereof, for the preparation of a medicament for the prevention or treatment of cancer.

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