BICYCLIC DERIVATIVE COMPOUNDS AS GABAA α5 RECEPTOR MODULATORS AND PHARMACEUTICAL COMPOSITION COMPRISING THEM

Abstract

Compounds of formula (1), salts, geometric isomers, stereoisomers, enantiomers, racemates, diastereomers, biologically active metabolites, prodrugs, solvates, hydrates and / or polymorphic forms thereof, which exhibit affinity and selectivity for the α5 subunit of the γ-aminobutyric acid receptor A and act as negative allosteric modulators of GABA A α5, therefore they are useful in the treatment or prevention of diseases related to the GABA receptor A α5, processes for preparing them, pharmaceutical compositions that contain them and their use as medicines.

Description

BICYCLIC DERIVATIVES AS RECEIVER MODULATORS GABAA A5 FIELD OF INVENTION The present invention provides compounds of formula (I) that exhibit affinity and selectivity for the alpha 5 subunit of the gamma-aminobutyric acid receptor A (GABAa α5) and act as negative allosteric modulators of GABAA α5 (NAM of GABAA α5), and are therefore useful in the treatment or prevention of diseases related to the GABAA α5 receptor, processes for preparing them, pharmaceutical compositions containing them, and their use as medicines. BACKGROUND OF THE INVENTION Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the central nervous system. GABA-sensitive receptors are divided into two main families: ligand-gated receptors (GABAA) and G protein-coupled receptors (GABAB). The ligand-gated GABAA receptor mediates most inhibitory neurotransmission in the mammalian brain. The receptor is composed of a pentameric array of multiple subunits (α1-6, β1-3, γ1-3, δ, ε, π, θ, ρ1-3) (Olsen and Sieghart, Pharmacol. Rev., 2008, 60:243-260), forming a ligand-gated chloride channel. The subunit distribution varies with development and brain region. This high variability results in a wide range of inhibitory neuronal mechanisms and provides the potential for targeted therapeutic interventions (Fritschy and Mohler, J. Comp. Neurol., 1995, 359:154-194). The physiological functions and pharmacological profiles of GABAA receptors CLARKE MODET & CO. (ARGENTINA) SA - 30540437455 Digitally signed by PORTALTRAMITES - INPI Date: 2019.09.27 08:48:42 -03:00 Reason: Digitally Signed by INPI 1 Location: Buenos Aires, Argentina depend largely on the constitution of the subunit. Through studies in genetically modified mice, it was found that the composition of the receptor subunits, especially in relation to the α subtypes, considerably determines the pharmacology of compounds that act on the benzodiazepine-sensitive allosteric modulator site (BDZ site) (Rudolph and Knoflach, Nat. Rev. Drug. Discov., 2011, 10:685-697). Widely distributed α1-containing receptors mediate sedative and amnesic effects, while α2- and α3-containing receptors are involved in anxiolytic, anticonvulsant, and muscle-relaxant effects (Sieghart and Sperk, Curr. Top. Med. Chem., 2002, 2:795-816; Whiting et al., Drug Discov. Today, 2003, 8:445-450).Receptors containing the α5 subunit (α5GABAAR) are preferentially expressed in the hippocampus in both rodents and primates, and are thought to be involved in cognitive functions (Wisden et al., J. Neurosci., 1992, 12:1040-1062; Quirck et al., Neuropharmacol., 1996, 35:1331-1335; Sur et al., Brain Res., 1999, 822:265-270). These α5-containing receptors are predominantly extrasynaptic and mediate tonic inhibition (Caraiscos et al., Proc. Natl. Acad. Sci. USA, 2004, 101:3662-3667). Their inhibitory effect on the excitability of principal neurons in the hippocampus and cortex may explain the significant effect of α5GABAAR on cognition, learning, and memory, and its potential therapeutic utility in various disorders, including stroke, cognitive impairment, schizophrenia, dementia-related conditions, and conditions involving social cognition impairment (Soh and Lynch, Curr. Drug Targets, 2015, 16:735-746). The first modulators acting on the BDZ site were non-selective compounds, either GABA enhancers, with anxiolytic, sedative, anesthetic, or anticonvulsant effects, or partial blockers, alternatively called inverse agonists or negative allosteric modulators (NAMs), with cognitive-enhancing effects. GABAA receptor agonists and enhancers have been characterized as effective drugs in clinical practice (Foster and Kemp, Curr. Opin. Pharmacol., 2006, 6:7-17), while NAMs have so far only been evaluated in animal behavioral experiments, with very few studies in humans (Soh and Lynch, Curr. Drug Targets, 2015, 16:735-746). Beneficial activity has been observed, but drugs that did not act selectively on various subtypes of the GABAA receptor caused undesirable side effects on the CNS, for example, sedation, amnesia, drug abuse, anxiety, agitation, or seizures.Therefore, in GABA research, there was a tendency to design new drugs selectively targeting specific subtypes of the GABAA receptor, including a5GABAAR (Mohler, Adv. Pharmacol., 2015, 72:1-36). By eliminating the α5 subunit, the involvement of the receptors containing it in neuronal plasticity (Martin et al., J. Neurosci., 2010, 30:5269-5282) and high-frequency oscillations in the neuronal network (Glykis et al., J. Neurosci., 2008, 28:1421-1426) was determined. These processes are fundamentally related to attention, information processing, and memory. Genetic or pharmacological reduction of α5 subunit function resulted in a significant improvement in cognitive performance in rodent models (Mohler and Rudolph, F1000). Research, 2017, 6[F1000 Faculty Rev.]:101). Through in vitro and in vivo experiments, it was found that the negative allosteric modulation of GABAaa5 is a promising strategy in the treatment or prevention of various pathological conditions or symptoms. As expected, the efficacy of various α5GABAAR-selective inverse agonists was proven, namely NGD 97-1 (Bednar et al., Clin. Pharmacol. Then, 75, 2004, 75:P30), α5ΙΑ (WO 02 / 06285 A1; Dawson et al., J. Pharmacol. Exp. Then, 2006, 316:1335-1345; 51:1023-102), a5IA-ll (WO 98 / 50385 A1; Collinson et al., Psychopharmacology, 2006, 188:619-628), MRK-016 (WO 99 / 67245 A1; Atack et al., J. Pharmacol. Exp. Then, 2009, 331:470-484), HT-2678 (Gupta et al., 241st ACS National Meeting, CA, March 27-31, 2011, MEDI 17), PWZ029 (WO 2007 / 018660 A2; Savic et al., Brain Res., 2008, 1208:150-159; Biawat, University of Wisconsin-Milwaukee Thesis, August 2014), TB21007 (Chambers et al., J. Med. Chern., 2003, 46:2227-2240), ONO-8590580 (Higashino et al., XXIV International Symposium on Medicinal Chemistry, Manchester, United Kingdom, August 29, 2016, Summary P280; Kawaharada et al., J. Pharm. Lett., 2009, 19:5940-5944), basmisanil (WO 2009 / 071476 A1; WO 2012 / 059482 A1; Hipp et al., Neuropsychiatric Electrophysiology, 2016, 2(suppl. 1):A20), and the selective competitive blocker of o5GABAaR S44819 (Gacsályi et al., Neuropharmacology, 2017, 125:30-38) in the relief of cognitive impairment in preclinical studies, without anxiogenic, proconvulsant, or motor side effects. The cognitive-enhancing effect of a5IA was demonstrated in healthy volunteers in an early pilot study (Nutt et al.Neuropharmacology, 2007, 53:810-820). In addition, basmisanil (coded as RG1662 or RO5186582), an α5-selective compound in clinical development to combat cognitive impairment associated with schizophrenia (NCT02953639), resulted in a significant increase in high-frequency gamma oscillations in EEG activity in patients with Down syndrome: an indication of a potential facilitative effect on cognitive functions (Bolognani et al., 67th Annual Meeting of the American Academy of Neurology, Washington, DC, April 23, 2015, Abstract P6273). To date, no CNS side effects have been reported for the clinically evaluated α5 blockers, a5IA, S44819 and basmisanil (Atack et al., Pharmacol. Therap., 2010, 125:11-26; Darmani et al., J. Neurosci., 2016, 36:12312-12320; Wandel et al., Eur. Neuropsychopharmacol., 2015, 25(suppl. 2):S259). Based on preclinical data and clinical findings, a favorable clinical profile can be predicted for selective negative modulators of the α5 subunit. After all, due to the specific function and expression profile of α5GABAAR in the CNS, a selective and mild intervention that negatively modulates its function could produce a therapeutic benefit compared to non-selective agents. Therefore, compounds that exhibit high affinity and selectivity for α5GABAAR and GABAa α5 NAMs can be used, alone or in combination with one or more additional active ingredients, in the treatment or prevention of central nervous system disorders characterized by one or more symptoms and / or syndromes related to the GABAa α5 receptor. These include, among others, neurocognitive disorders (Collinson et al., J. Neurosci., 2002, 22:5572-5580), for example, Alzheimer's disease (AD) (Kwakowsky et al., J. Neurochem., 2018, 145:374-392; Solas et al., Curr. Pharm. Des., 2015, 21:4960-4971; Wu et al., Nat. Commun., 2014, 4159), prodromal AD, mild cognitive impairment (Maubach, Curr. Drug Targets CNS Neurol. Disord., 2003, 2:233-239), vascular cognitive impairment, vascular dementia (Gacsályi et al., Eur. J. Pharmacol., 2018, 834:118-125), frontotemporal lobar degeneration, encompassing frontotemporal dementia, progressive supranuclear palsy, corticobasal syndrome (Murley and Rowe, Brain, 2018, 5:1263-1285), Lewy body dementia (Khundakar et al., Acta Neuropathol. Commun., 2016, 4:66), age-related memory impairment or cognitive decline (Koh et al., Neuropharmacology, 2013, 64:142-152), cognitive impairment associated with brain cancers, encompassing, without limitation, medulloblastomas (Sengupta et al., CNS Oncol., 2014, 3:245-247), postoperative dementia (Cheng et al., J. Neurosci., 2006, 26:3713-3720), inflammation-induced dementia (Wang et al., Cell Rep., 2012, 2:488-496), cognitive impairment associated with diseases including, but not limited to, migraine, tension headache (Russo et al., Am. J. Hum. Genet., 2005, 76:327-333), multiple sclerosis (Stefano and Giorgio, Brain, 2015, 138:2467-2468), Parkinson's disease (Blaszczyk, Front Neurosci., 2016, 10:269-277), epilepsy (Schipper et al., MolNeurobiol, 2016, 53:5252-5265), attention deficit hyperactivity disorder, adult attention deficit (Bollmann et al., Transl Psychiatry, 2015, 8:e589; Edden et al., Arch. Gen. Psychiatry, 2014, 69:750-753), other CNS diseases, e.g., post-traumatic stress disorder (Lu et al., Neuronal Plast., 2017, 2017:571-5816), schizophrenia (Guidotti et al., Psychopharmacology, 2005, 180:191-205), positive, negative, and / or cognitive symptoms of schizophrenia (Asai et al., Schizophrenia Res., 2008, 99:333-340; Gill et al., Neuropsychopharmacology, 2011, 36:1903-1911; Hauser et al., Mol. Psychiatry, 2005, 10:201-207; Redrobe et al., Psychopharmacology, 2012, 221:451-468), bipolar disorders (Otani et al., Neurosci. Lett., 2005, 381:108-113), autism spectrum disorders (ASD) (Mendez et al., Neuropharmacology, 2013, 68:195-201), fragile X disorder (Curia et al., Cereb.Cortex, 2009, 19:1515-1520), Prader-Willi syndrome (Bittel et al., J. Med. Genet., 2003, 40:568-574), Down syndrome (Braudeau et al., J. Psychopharmacol, 2011, 25:1030-1042; Martinez-Cue et al., J. Neurosci., 2013, 33:953-966), Huntington's disease (Du et al., Front Mol. Neurosci., 2017, 10:198), neurofibromatosis type I (Ribeiro et al., Cortex, 2015, 64:194-208), sleep disorders (Mesbah-Oskui et al., Neurotoxicol. Teratol., 2017, 61:115-122), alcoholism (Stephens et al., Eur. J. Pharmacol., 2005, 526:240-250), fetal alcohol syndrome (Toso et al., Am J. Obstet. Gynecol., 2006, 195:522-527), mood disorders (Carreno et al., Int J. Neuropsychopharmacol., 2017, 20:504-509; Choudary et al., Proc. Natl. Acad. Sci. USA, 2005, 102:15653-15658; Fischell et al., Neuropsychopharmacology, 2015, 40:2499-2509), psychotic disorders (Wearne et al., Neuropharmacology, 2016, 111:107-118), substance-induced psychotic disorders (Neugebauer et al., Behav.Brain Res., 2018, 342:11-18), anxiety disorders (Behlke et al., Neuropsychopharmacology, 2016, 41:2492-2501; Botta et al., Nat. Neuroscience, 2015, 18:1493-1500), fear-related disorders (Botta et al., Nat. Neuroscience, 2015, 18:1493-1500; Crestani et al., Proc. Natl. Acad. Sci. USA, 2002, 99:8980-8985), stress disorders (Fischell et al., Neuropsychopharmacology, 2015, 40:2499-2509), behavioral or drug addictions (Mick et al., Addict. Biol., 2017, 22:1601-1609), strokes (Clarkson et al., Nature, 2010, 468:305-309; Lake et al., J. Cereb. Blood Flow Metab., 2015, 35:1601-1609), neuropathic pain (Xiao et al., Proc. Natl. Acad. Sci., USA 2002, 99:8360-8365), inflammatory pain (BravoHernández et al., Eur. J. Pharmacol., 2014, 734:91-97; Munro et al., Neuropharmacology, 2011,61:121-132).Modulation of α5GABAAR may also be beneficial in the treatment of diseases and conditions including, but not limited to, bronchoconstrictor diseases such as asthma, chronic obstructive pulmonary disease, and bronchopulmonary dysplasia (Gallos et al., Am. J. Physiol. Lung Cell Mol. Physiol., 2015, 308:L931-942; Mizuta et al., Am. J. Physiol. Lung Cell Mol. Physiol., 2008, 294:L1206-1216). Compounds capable of modulating α5GABAAR are expected to be useful in the treatment of neurocognitive disorders, Alzheimer's disease, and schizophrenia. Numerous structurally different compounds that act on the α5 subunit of the GABAA receptor are known in the art (Guerrini et al., Expert Opin. Ther. Patents, 2013, 23 (7):843-866), including isoxazole derivatives (e.g., WO 2009 / 071464 A1, WO 2009 / 071477 A1, WO 2010 / 097368 A1, WO 2010 / 112475 A1, WO 2010 / 127978 A1) or triazole derivatives (e.g., WO 2012 / 062687 A1, WO 2014 / 001281 A1). Certain isoxazole or triazole derivatives are described as NR1 H4 receptor agonists (farnesoid X or FXR), for example, in WO 2017 / 133521 A1, WO 2013 / 007387 A1, WO 2008 / 157270 A1 or WO 2007 / 140174 A2. In addition, tetrahydroisoquinoline derivatives are described as modulators of LXR (hepatic X receptor), for example, in WO 2007 / 047991 A1. Despite numerous studies and modulators of the GABAA α5 receptor, there remains a need for compounds that are useful in the treatment or prevention of diseases related to the GABAA α5 receptor. SUMMARY OF THE INVENTION The present invention provides compounds of formula (I) where A is represented by a group N N N7 an 'r' group, or a group N'N N R1 is hydrogen or halogen, nym are independently of each other 1 or 2, R2 is hydrogen; C^alkyl optionally substituted independently with one or more halogens, C^alkoxy, -S(O)2-C1-4alkyl, or with R3; NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C^alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R3, R6 and R7 are optionally substituted carbocycles, heterocycles or heteroaryls and / or salts thereof and / or geometric isomers thereof and / or stereoisomers thereof and / or enantiomers thereof and / or racemates thereof and / or diastereomers thereof and / or biologically active metabolites thereof and / or prodrugs thereof and / or solvates thereof and / or hydrates thereof and / or polymorphs thereof. The present invention provides a compound of formula (I), as previously defined, for use in the treatment or prevention of diseases related to the GABAa α5 receptor. The present invention provides for the use of a compound of formula (I), as previously defined, in the manufacture of a drug for treating or preventing diseases related to the GABAA α5 receptor. The present invention provides a method for treating or preventing diseases related to the GABAA α5 receptor, comprising administering to the subject in need, for example, a human patient, an effective amount of at least one compound of formula (I), as previously defined. The present invention provides for the combined use of compounds of formula (I), as defined above, with one or more additional active ingredients, in the treatment or prevention of diseases related to the GABAA α5 receptor. The present invention provides pharmaceutical compositions containing a compound of formula (I), as previously defined, as an active ingredient. The present invention provides medicinal products (combined pharmaceutical compositions) comprising a combination of a compound of formula (I), as defined above, with one or more additional active ingredients. The present invention provides pharmaceutical compositions containing a compound of formula (I), as previously defined, as an active ingredient, alone or in combination with one or more additional active ingredients, for use in the treatment or prevention of diseases related to the GABAa α5 receptor. The present invention provides a process for preparing compounds of formula (I), as previously defined. The present invention also provides for the chemical or pharmaceutical preparation of pharmaceutical compositions containing compounds of formula (I), as defined above, alone or in combination with one or more additional active ingredients. DETAILED DESCRIPTION OF THE INVENTION The present invention provides compounds of formula (I) that exhibit affinity and selectivity for the gamma-aminobutyric acid receptor A containing the alpha 5 subunit (GABAA α5 receptor) and act as negative allosteric modulators of the GABAA α5 receptor, and are therefore useful in the treatment or prevention of diseases related to the GABAA α5 receptor, processes for preparing them, pharmaceutical compositions containing them, alone or in combination with one or more additional active ingredients, and their use as medicines. The present invention relates to compounds of formula (I) A is represented by O^ZN—Z N-nz Yes, a 'T' group, an r* group, or a *?* group R1 is hydrogen or halogen, nym are independently of each other 1 or 2, R2 is hydrogen; Z4 is optionally substituted alkyl independently with one or more halogens, C^alkoxy, -S(O)2-C1-4alkyl, or with R3; NR4R5 or R6, R4 and R5 are independently of each other hydrogen, Z4 alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R3, R6 and R7 are optionally substituted carbocycles, heterocycles or heteroaryls and / or salts thereof and / or geometric isomers thereof and / or stereoisomers thereof and / or enantiomers thereof and / or racemates thereof and / or diastereomers thereof and / or biologically active metabolites thereof and / or prodrugs thereof and / or solvates thereof and / or hydrates thereof and / or polymorphs thereof. Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly accepted by those skilled in the art to which this invention pertains. Although similar or equivalent methods and materials to those described herein may be used in the practice or evaluation of the invention, suitable methods and materials are described below. The nomenclature used is based on the IUPAC systematic nomenclature, unless otherwise indicated. Any open valency present on a carbon, oxygen, sulfur, or nitrogen atom in the structures presented indicates the presence of a hydrogen, unless otherwise stated. The following provides the definition of the general terms used herein, both individually and in combination with other groups. “Optional” or “optionally” means that the event or circumstance described below may occur, but does not necessarily, and that the description includes instances where the event or circumstance occurs and instances where it does not occur. The term “substituent” denotes an atom or group of atoms that replaces a hydrogen atom in the molecule. The term “substituted” denotes that a specified group has one or more substituents. When specifying the number of substituents, the term "one or more" refers to the range from one substituent to the maximum possible number, for example, replacing one hydrogen atom up to replacing all hydrogen atoms with substituents. One, two, or three substituents are preferred on a given atom, especially on a carbon atom. When a group can have multiple substituents and several possible substituents are provided, the substituents are selected independently and are not necessarily the same. The term “unsubstituted” means that the specified group has no substituents. The term “optionally substituted” means that any atom in the specified group is either unsubstituted or substituted with one or more substituents, independently selected from the pool of possible substituents. When the number of substituents is stated, “one or more” means from one substituent up to the maximum possible number of substituents, for example, from the replacement of one hydrogen to the replacement of all hydrogens by substituents. Possible substituents include, but are not limited to, C-alkyl, C-alkoxy, halogen, haloC-alkyl, haloC-alkoxy, hydroxyl, oxo, and the like. The term “C1-4 alkyl” refers, alone or in combination with other groups, to a linear or branched hydrocarbon radical, single or multiple branched, consisting of 1 to 4 carbon atoms. Examples include, but are not limited to, methyl, ethyl, propyl, i-propyl (isopropyl), n-butyl, 2-butyl (sec-butyl), or t-butyl (tert-butyl) groups. The preferred alkyl group is C3alkyl. The term “C1-4 alkoxy” refers, alone or in combination with other groups, to an -OC₂ alkyl group, where the C₂ alkyl is as defined above. Examples include, but are not limited to, methoxy, ethoxy, i-propoxy, n-propoxy, or t-butoxy. The preferred alkoxy group is C1-3 alkoxy. The term “-S(O)2-C1-4alkyl” refers, alone or in combination with other groups, to a C1-alkyl group substituted with -S(O)2-, where C1-alkyl is as defined above. Examples include, but are not limited to, methylsulfonyl, ethylsulfonyl, i-propylsulfonyl, n-propylsulfonyl, sec-butylsulfonyl, or t-butylsulfonyl. The preferred sulfonyl group is -S(O)2-C1-3alkyl. The term “halogen”, “halo”, or “halide” refers, alone or in combination with other groups, to fluoro (fluorine), chlorine (chlorine), bromo (bromine), or iodo (iodine), preferably fluoro (fluorine), chlorine (chlorine), or bromo (bromine). The preferred halogens are fluorine and chlorine. The term “C1-4 haloalkyl” refers, alone or in combination with other groups, to a C1-alkyl group as defined above substituted with one or more identical or different halogens on any carbon atom of said C1-alkyl group, including vicinal and germline halo-substitutions. The term “perhaloalkyl” refers to a C1-4 alkyl group in which all hydrogen atoms are replaced by identical or different halogen atoms. Examples include, but are not limited to, monohalo-, dihalo-, or trihalo-methyl, -ethyl, or -propyl, for example, 3,3,3-trifluoropropyl, 2-fluoroethyl, 2,2,2-trifluoroethyl, fluoromethyl, or trifluoromethyl. The preferred haloalkyl group is C1-3 haloalkyl. The term “carbocycle” refers, alone or in combination with other groups, to a monocyclic or bicyclic, fused or bridged, saturated, mono- or bi-unsaturated, or aromatic ring system comprising from 3 to 14 ring carbon atoms. The term “cycloalkyl” refers to a saturated, monocyclic or bicyclic, fused or bridged, monocyclic carbocyclic group comprising from 3 to 10 ring carbon atoms. Examples include cyclopropane, cyclobutane, cyclopentane, cyclohexane, cycloheptane, cyclooctane, bicyclo[2.2.1]heptane, bicyclo[2.2.2]octane, adamantane, and the like. The preferred cycloalkyl is monocyclic. The preferred monocyclic cycloalkyl has from 3 to 6 members. The term “cycloalkenyl” refers to a monocyclic or bicyclic, fused or bridged, mono- or bi-unsaturated monovalent carbocyclic group comprising between 3 and 10 ring carbon atoms.Examples include cyclobutene, cyclopentene, cyclopentadiene, cyclohexene, cyclohexadiene, cycloheptene, decalin, and the like. The preferred cycloalkenyl group is monocyclic. The preferred monocyclic cycloalkenyl group has between 4 and 6 members. The term “aryl” refers to a monocyclic, mono- or bicyclic aromatic carbocyclic group comprising between 6 and 14 ring carbon atoms. Bicyclic aryl groups comprise at least one aromatic carbocyclic group. Examples include phenyl, dihydroindene, indene, naphthyl, diallyl, tetralyl, anthril, azulenyl, indanyl, and the like. The preferred aryl group has between 6 and 10 members. The preferred aryl group is monocyclic. The preferred monocyclic aryl group is phenyl. The term “heterocycle” refers, alone or in combination with other groups, to a monocyclic, bicyclic, fused, bridged, or spiral saturated or partially unsaturated monovalent ring system of between 3 and 10 ring atoms comprising 1, 2, 3, or 4 ring heteroatoms independently selected from N, O, and S, the remaining ring atoms being carbon. The preferred heterocycle is monocyclic.Examples of monocyclic heterocycle are aziridine, 2H-azirine, oxirane, thiirane, azetidine, oxetane, thietane, azetidin-2-one, pyrrolidine, pyrrolidinone, pyrroline, pyrazolidine, imidazoline, pyrazoline, tetrahydrofuran, dihydrofuran, dioxolane, tetrahydrothiophene, oxazolidine, dihydro-oxazole, isoxazolidine, oxathiolane, sulfolane, thiazolidine, thiazolidinedione, succinimide, oxazolidone, hydantoin, piperidine, piperidinone, piperazine, tetrahydropyran, tetrahydrothiopyran, dihydropyran, tetrahydropyridine, dioxane, thiane, dithiane, 1,1-dioxo-thiane, morpholine, thiomorpholine, 1,1-dioxo-thiomorpholine, azepane, diazepane, homopiperazine, oxazepanyl and similar compounds. The preferred monocyclic heterocycle has between 4 and 6 members. The preferred monocyclic heterocycle is saturated.The examples of heterocyclo bicíclico, fusionado, en bridge or spiral son pyrrolizidine, dihidropyrrolopirrol, tetrahydropyrrolopirrol, furopirrol, tinopirrol, indolina, indole, isoindol, benzoisothiazolona, ​​decahidroisoquinolina, decahidroquinolina, tetrahydroquinolina, dihidroquinolina, dihidroisoquinolina, cromeno, isocromeno, benzoxazina, quinuclidina, azaadamantano, espiro[ciclobutan-1,3'-indol], 1-oxaespiro[4.5]decano, 1,6-oxaespiro[3.4]octano,. 8-aza-biciclo[3.2.1]octano, 8-oxa-3-aza-biciclo[3.2.1]octano, tetrahydroespiro[isobenzofuran-1,2'-pirano], 1-oxaespiro[4.4]nonan-2-ona, 2-oxa-7azaespiro[3.5]nonano, 1,4-dioxa-7-azaespiro[4.4]nonano, 1,3diazaespiro[4.4]non-2-en-4-ona, 9-aza-biciclo[3.3.1]nonano, 3-oxa-9azabiciclo[3.3.1]nonano, 3-tia-9-aza-biciclo[3.3.1]nonano, 1,4-ditia-7azaespiro[4.4]nonano, 8-azaespiro[4.5]decan-7,9-diona, 1,3,8triazaespiro[4.5]decan-4-ona y similares. The term “heteroaryl” refers, alone or in combination with other groups, to a monovalent, heterocyclic aromatic ring system, mono- or bicyclic, of between 5 and 12 ring atoms, comprising 1, 2, 3, or 4 heteroatoms independently selected from N, O, and S, the remaining ring atoms being carbon. The bicyclic heteroaryl group comprises at least one aromatic ring. Examples of heteroaryls include pyrrole, furan, thiophene, imidazole, oxazole, isoxazole, thiazole, isothiazole, triazole, tetrazole, oxadiazole, thiadiazole, tetrazole, pyridine, pyrazine, pyrazole, pyridazine, pyrimidine, triazine, azepine, diazepine, benzofuran, benzothiophene, indole, isoindole, isobenzofuran, benzimidazole, benzoxazole, benzoisoxazole, benzothiazole, benzoisothiazole, benzooxadiazole, benzothiadiazole, benzotriazole, purine, quinoline, isoquinoline, quinazoline, quinoxaline, carbazole, and acridine. The preferred heteroaryl has between 5 and 10 members. The preferred heteroaryl is monocyclic.The preferred monocyclic heteroaryl has 5 or 6 members. The terms “compound(s) of this invention,” “compound(s) of the present invention,” or “compounds of formula (I), as defined above” refer to compounds of formula (I) and / or salts thereof and / or geometric isomers thereof and / or stereoisomers thereof and / or enantiomers thereof and / or racemates thereof and / or diastereomers thereof and / or biologically active metabolites thereof and / or prodrugs thereof and / or solvates thereof and / or hydrates thereof and / or polymorphs thereof. Furthermore, any combination of embodiments A, R1-R7, and nym, as defined hereinafter, are preferred groups of compounds of formula (I). The term “salt” refers to pharmaceutically acceptable and / or pharmaceutically unacceptable salts. The term “pharmaceutically acceptable salt” refers to a conventional acid-addition or base-addition salt that preserves the efficacy and biological properties of compounds of formula (I) and that can be formed with suitable non-toxic organic or inorganic acids or bases.Examples of acid addition salts include salts derived from inorganic acids, such as, but not limited to, hydrochloric acid, hydrobromic acid, hydroiodic acid, sulfuric acid, sulfamic acid, phosphoric acid, nitric acid, and perchloric acid, and derived from various organic acids, such as, but not limited to, acetic acid, propionic acid, benzoic acid, glycolic acid, phenylacetic acid, salicylic acid, malonic acid, maleic acid, oleic acid, pamoic acid, palmitic acid, benzenesulfonic acid, toluenesulfonic acid, methanesulfonic acid, oxalic acid, tartaric acid, succinic acid, citric acid, malic acid, lactic acid, glutamic acid, fumaric acid, and the like. Examples of basic addition salts are salts derived from ammonium, potassium, sodium and quaternary ammonium hydroxides such as tetramethylammonium hydroxide.These salts usually exhibit more favorable solubility properties than the compounds used for their preparation and are therefore more suitable for use in the preparation of various pharmaceutical formulations. The use of “pharmaceutically unacceptable salts” may be preferred for the purification or isolation of compounds of formula (I) and are therefore also within the scope of the invention. The term “prodrug” refers to derivatives of compounds of formula (I) according to the invention that have no therapeutic effect of their own, but which contain groups that, after chemical or metabolic degradation in vivo (biotransformation), are converted into “biologically active metabolites” that are responsible for the therapeutic effect. Such decomposition groups associated with the compounds of formula (I) of the present invention, in particular those suitable for prodrugs, are known in the field and may also apply to the compounds of the present invention (Rautio et al., Nature Reviews - Drug Discovery 2008, 7:255-270). Compounds of formula (I) can exist in various geometric isomeric forms. In addition, certain compounds of formula (I) may contain one or more asymmetric centers, thus existing in stereoisomeric and diastereomeric forms. The term “stereoisomer” denotes a compound that has identical molecular connectivity and bond multiplicity but differs in the spatial arrangement of its atoms. All such compounds, such as cis isomers, trans isomers, diastereomeric mixtures, racemates, non-racemic mixtures of enantiomers, substantially pure enantiomers, and pure enantiomers, are within the scope of the invention. Substantially pure enantiomers contain up to 5 wt%, preferably 2 wt%, and preferably a maximum of 1 wt%, of the corresponding opposite enantiomer. Optical isomers can be prepared by resolving racemic mixtures using known methods, for example, by using an optically active acid or base to form diastereomeric salts or by forming covalent diastereomers. Suitable acids include, for example, tartaric acid, diacetyl tartaric acid, dibenzoyl tartaric acid, ditoluoyl tartaric acid, and camphorsulfonic acid. Iasteromeric mixtures can be separated into their individual diastereomers based on their physical and / or chemical differences by methods known to those skilled in the art, such as chromatography or fractional crystallization. Optically active acids or bases are then released from the separated diastereomeric salts. Various methods for separating optical isomers include chiral chromatography (e.g., chiral HPLC columns), optionally used with derivatization to maximize the separation of enantiomers.Chiral HPLC columns are Diacel columns, such as CHIRALPAK or CHIRALCEL columns, which can be routinely selected as needed. Where applicable, enzymatic separations by derivatization can also be performed. Optically active compounds of formula (I) can also be prepared using optically active starting materials via chiral synthesis without racemization reaction conditions. Compounds of formula (I) can exist in various polymorphic forms. As is well known in the field, polymorphism is the ability of a compound to crystallize in more than one crystalline form, for example, in polymorphic forms. The polymorphic forms of a particular compound can be defined as having an identical chemical formula or composition but differing in their chemical structure, such as the crystalline structures of two different chemical compounds. Compounds of formula (I) and salts thereof may also exist as solvates or hydrates, which are also within the scope of the invention. The term solvate refers to stoichiometric or non-stoichiometric non-covalent combinations of the solvent and the solute. The term hydrate refers to stoichiometric or non-stoichiometric non-covalent combinations of water and the solute. The present invention provides pharmaceutical compositions comprising at least one compound of formula (I), as previously defined, as the active ingredient. The present invention provides pharmaceutical compositions comprising a combination of a compound of formula (I), as defined above, with one or more additional active ingredients. A pharmaceutical composition may comprise at least one compound of the invention together with one or more additional active ingredients in the same dosage form or separately. The combined composition may be administered simultaneously, separately, or sequentially. The term “pharmaceutical composition” (or “composition”) refers to a mixture or solution comprising a therapeutically effective amount of an active ingredient, together with pharmaceutically acceptable excipients for administration to a subject in need, e.g., a human patient. The present invention is also related to the chemical and pharmaceutical preparation of pharmaceutical compositions. The pharmaceutical compositions of the present invention can be formulated in various pharmaceutical formulations, for example and without limitation, solid oral dosage forms such as tablets (e.g. buccal, sublingual, effervescent, chewable, orally dispersible), capsules, pills, coated tablets, orally dispersible films, granules or powders, liquid formulations such as solutions, emulsions, suspensions, syrups, elixirs or drops, parenteral dosage forms such as intravenous injections, intramuscular injections or subcutaneous injections, other medicinal forms such as eye drops, semisolid ophthalmic preparations, semisolid dermal preparations (e.g. ointments, creams, pastes), transdermal therapeutic systems, suppositories, rectal capsules, rectal solutions, emulsions, suspensions, etc. The pharmaceutical compositions of the present invention can be administered in various ways, for example and without limitation, orally, rectally, mucosally, transdermally or intestinally, parenterally, including intramuscular, subcutaneous, intravenous and intramedullary injections, by intra-articular, intrathecal, direct intraventricular, intraperitoneal, intranasal or intraocular injections or as eye drops. Alternatively, the compounds can be administered locally rather than systemically, for example, by direct injection into a kidney or heart, often in a modified-release formulation. Furthermore, the drug can be delivered via a targeted delivery system, such as a liposome encapsulated with tissue-specific antibodies. Liposomes selectively transfer the active agent to the target organ, where it is absorbed. A pharmaceutical composition can be administered in various ways and in various pharmaceutical forms. A compound of the invention can be administered alone or in combination with pharmaceutically acceptable excipients, in single or multiple doses. The dose required to obtain the desired therapeutic effect can vary widely and should always be tailored to individual needs, depending on the severity of the disease, the patient's condition and weight, sensitivity to the active ingredient, the dosage regimen, and the number of daily treatments. In simple administration, pharmaceutical compositions are preferably composed of individual dosage forms containing the desired amount of one or more active ingredients at once, or a portion such as half, a third, or a quarter. These individual dosage forms are, for example, tablets that may include scores to facilitate division into halves or quarters and provide the required amount of one or more active ingredients. Pharmaceutical compositions containing one or more active ingredients according to the invention generally comprise between 0.01 and 500 mg of these active ingredients per individual dosage form. It is also possible, of course, for the quantity of the active ingredients in each formulation to be lower or higher than the stated limits. The present invention is also related to pharmaceutical compositions for pediatric use, for example and without limitation, solutions, syrups, elixirs, suspensions, powders for the preparation of suspensions, dispersible or effervescent tablets, chewable tablets, orodispersible tablets, coated tablets, oral effervescent powders or granules, or capsules. The pharmaceutical compositions of the present invention can be prepared according to conventional methods, for example, mixing, dissolving, emulsifying, suspending, microencapsulating, lyophilizing, extruding and spheronizing, laminating, film coating, granulating, encapsulating, producing dragees or pressing. The pharmaceutical compositions of the present invention can be formulated in a conventional manner, using one or more physiologically (or pharmaceutically) acceptable excipients that promote the incorporation of the active ingredient into pharmaceutically acceptable dosage forms. The term “physiologically or pharmaceutically acceptable excipient” denotes any ingredient used in the formulation of pharmaceutical products that is neither therapeutically active nor toxic. The appropriate formulation depends on the selected route of administration. Various approaches and excipients known in the art may be used. The excipients applicable to the preparation may be selected from categories including, but not limited to, tablet or capsule fillers, tablet or capsule binders, modified drug release agents, disintegrants, glidants, lubricants, sweeteners, flavor maskers, flavoring agents, coating materials, surfactants, stabilizers, preservatives or antioxidants, buffering agents, complexing agents, wetting or emulsifying agents, salts for adjusting osmotic pressure, lyophilization excipients, microencapsulating agents, ointment materials, penetration enhancers, solubilizers, solvents, suppository materials, and suspending agents.Suitable pharmaceutical excipients may include, for example, starch, microcrystalline cellulose, talc, glucose, lactose, gelatin, silica, talc, magnesium stearate, sodium stearate, glycerol monostearate, cellulose derivatives, sodium chloride, glycerol, propylene glycol, water, ethanol, or similar. Another embodiment of the present invention relates to the use of special binders that can improve the solubility, dissolution, penetration, absorption, or bioavailability of the active ingredients, for example, and without limitation, hydrophilic polymers, hot-melt extrusion excipients, surfactants, buffering agents, complexing agents, emulsifying agents, freeze-drying excipients, disintegrants, microencapsulating agents, penetration promoters, solubilizers, cosolvents, or suspending agents. The excipients and preparation methods described above are provided for illustrative purposes only. Other materials and processing approaches known in the art may also be used. The term “additional active ingredient” refers to therapeutic agents including, but not limited to, acetylcholinesterase inhibitors (e.g., galantamine, rivastigmine, donepezil, tacrine, phenerin, ladostigil, or ABT-089), NMDA receptor agonists or antagonists (e.g., memantine, neramexane, EVT101, and AZD4282), anti-amyloid antibodies, including humanized anti-amyloid monoclonal antibodies (e.g., bapineuzumab, ACCOOl, CAD 106, AZD3102, H12A11V1), beta-secretase inhibitors or modulators (e.g., verubecestat or AZD3293) or gamma-secretase inhibitors or modulators (e.g., LY450139 or TAK 070), tau phosphorylation inhibitors, and ApoE4 conformation modulators. p25 / CDK5 inhibitors, NK1 / NK3 receptor antagonists, COX-2 inhibitors (e.g., celecoxib, rofecoxib, valdecoxib, 406381 or 644784), LRRK2 inhibitors, HMG-CoA reductase inhibitors, NSAIDs (e.g., ibuprofen), vitamin E,glycine transport inhibitors, glycine site antagonists (e.g., lacosamide), LXR β agonists, androgen receptor modulators, Aβ oligomer formation blockers, NR2B antagonists, anti-inflammatory compounds (e.g., (R)flurbiprofen, nitroflurbiprofen, ND-1251, VP-025, HT-0712, or EHT-202), PPAR gamma agonists (e.g., pioglitazone or rosiglitazone), CB-1 receptor antagonists or inverse agonists (e.g., AVE1625), CB-2 agonists (e.g., 842166 or SAB378), VR-1 antagonists (e.g., aMG517, 705498, 782443, PAC20030, VI 14380, or A425619), bradykinin B1 receptor antagonists (e.g., SSR240612 or NVPSAA164), sodium channel blockers or antagonists (e.g., VX409 or SPI860), NOS inhibitors (e.g., SD6010 or 274150), growth hormone secretagogue antibiotics (e.g., ibutamorene, ibutamorene mesylate, or capromorelin),potassium channel activators, AMPA agonists or modulators (e.g., CX-717, LY 451395, LY404187, or S-18986), GSK3 inhibitors (e.g., aZD1080, SAR502250, or CEP16805), neuronal nAChR α7 agonists or PAMs (e.g., aBT-126, aZD0328, EVP-6124, aVL-3288, or PNU-120596), MARK ligands, mAChR M1 or M4 agonists or PAMs, mGluR2 antagonists, NAMs, or PAMs, mGluR5 antagonists (e.g., aZD9272), alpha agonists, ADAM-10 ligands, sedatives, hypnotics, anxiolytics, antipsychotics, cyclopyrrolones, imidazopyridines, pyrazolopyrimidines, minor tranquilizers, melatonin agonists or antagonists, melatonergic agents, orexin antagonists or agonists, prokinetic agonists or antagonists, T-type calcium channel antagonists, triazolopyridines, benzodiazepines, barbiturates, 5-HT1A antagonists (e.g., lecozotan), 5-HT2 antagonists, 5-HT4 agonists (e.g., PRX-03140), 5-HT6 antagonists (e.g., GSK 742467, SGS-518,FK-962, SL-650155, SRA-333 or xaliprodene), histamine H3 receptor antagonists or inverse agonists (e.g., S38093, aBT-834, aBT 829, GSK 189254 or CEP16795), PDE4 inhibitors (e.g., HT0712), PDE9 inhibitors (e.g., BI40936), PDE10 inhibitors, HDAC inhibitors, KCNQ antagonists, GABAA signaling enhancers (e.g., L-838,417, TPA-023, alfaxalone, ganaxolone, gaboxadol, tiagabine, vigabatrin, bumetadine) or GABAA signaling blockers (e.g., S44819), GABAB signaling enhancers (e.g., baclofen), receptor antagonists V1a (e.g., balovaptan), MAO-B inhibitors, dopamine transporter inhibitors, norepinephrine transporter inhibitors, D2 agonists or partial agonists, anticholinergics (e.g., biperiden), COMT inhibitors (e.g., entacapone), adenosine A2a receptor antagonists, cholinergic agonists,compounds from the phenothiazine, thioxanthenes (e.g., chlorprothixene or thiothixene), heterocyclic dibenzazepines (e.g., clozapine), butyrophenones (e.g., haloperidol), diphenylbutylpiperidines (e.g., pimozide), or indolones (e.g., molindolone agents) classes, loxapine, sulpiride, atypical antipsychotics (e.g., aripiprazole, asenapine, brexpiprazole, cariprazine, iloperidone, lurasidone, olanzapine, paliperidone, quetiapine, risperidone, or ziprasidone), levodopa, calcium channel blockers (e.g., ziconotide or NMED160), MMP inhibitors, thrombolytic agents, opioid analgesics (e.g., codeine, fentanyl, hydromorphone, Levorphanol, meperidine, methadone, morphine, oxycodone, oxymorphone, pentazocine, propoxyphene), pramipexole, ropinirole, neutrophil inhibitory factor, SSRI or SSNRI, tricyclic antidepressant drugs, norepinephrine modulators, lithium, valproate, gabapentin, pregabalin, rizatriptan,zolmitriptan, naratriptan, sumatriptan, other drugs that affect receptors or enzymes that increase the efficacy, safety or convenience or reduce unwanted side effects or toxicity of the compounds of the present invention. In one embodiment, the additional active ingredient is an acetylcholinesterase inhibitor (e.g., galantamine, rivastigmine, donepezil, tacrine, phenerin, ladostigil, or ABT-089), an NMDA receptor agonist or antagonist (e.g., memantine, neramexane, EVT101, or AZD4282), an anti-amyloid antibody, such as a humanized anti-amyloid monoclonal antibody (e.g., bapineuzumab, ACCOOl, CAD 106, AZD3102, H12A11V1), a beta-secretase inhibitor or modulator (e.g., verubecestat or AZD3293) or a gamma-secretase inhibitor or modulator (e.g., LY450139 or TAK 070), a tau phosphorylation inhibitor, an ApoE4 conformation modulator, or an inhibitor of the transport of glycine, an AMPA agonist or modulator (e.g., CX-717, LY 451395, LY404187, or S18986), a neuronal α7 nAChR agonist or PAM (e.g., ABT-126, AZD0328, EVP-6124, AVL-3288, or PNU-120596), a 5-HT6 antagonist (e.g., GSK 742467, SGS-518, FK-962, SL-650155,SRA-333 or xaliprodene), a histamine H3 receptor antagonist or inverse agonist (e.g., S38093, ABT-834, ABT 829, GSK 189254 or CEP16795), a GABAa signaling enhancer (e.g., L-838,417, TPA-023, alfaxalone, ganaxolone, gaboxadol, tiagabine, vigabatrin, bumetadine) or a GABAA signaling blocker (e.g., S44819), a GABAB signaling enhancer (e.g., baclofen), a V1a receptor antagonist (such as balovaptan), a partial D2 agonist, a cholinergic agonist, a compound from the phenothiazine, thioxanthenes (e.g., chlorprothixene or thiothixene) classes, the heterocyclic dibenzazepines (e.g., clozapine), butyrophenones (e.g., haloperidol), diphenylbutylpiperidines (e.g., pimozide) or indolones (e.g., a molindolone agent), ioxapine, sulpiride or an atypical antipsychotic (e.g., aripiprazole, asenapine, brexpiprazole, cariprazine, iloperidone,lurasidone, olanzapine, paliperidone, quetiapine, risperidone or ziprasidone). The term “modulators” refers to molecules that interact with the target receptor, where the interaction can be, for example, agonist, antagonist, or inverse agonist. The term “inhibitors” refers to molecules that compete for the binding of a ligand to a particular receptor, reduce or prevent it, or that reduce or prevent the inhibition of the function of a particular protein. The term “agonists” refers to compounds that have an affinity for a receptor binding site and enhance the activity of the receptor-mediated response. “Full agonists” produce a full response, while “partial agonists” produce less than complete activation, even when they occupy the entire receptor population. The term “inverse agonists” refers to compounds that produce an effect opposite to that of an agonist by binding to the same binding site or that reduce the effect of an agonist by binding to a different allosteric binding site. The term “antagonists” refers to compounds that decrease or prevent the action of another compound or a site on a receptor, or that attenuate the effect of an agonist. “Competitive antagonists” bind to the same site as agonists but do not activate them, thus blocking their action. “Non-competitive antagonists” bind to an allosteric site on the receptor to prevent its activation. The binding of “reversible antagonists” to a receptor is non-covalent (it can be undone), while the binding of “irreversible antagonists” is covalent (it cannot be undone). The term “allosteric modulators” refers to compounds that bind to a receptor at a site other than the agonist binding site, that is, an allosteric site. This induces a change in the receptor's conformation and alters its affinity and / or activity with respect to endogenous ligands or agonists. “Positive allosteric modulators” (PAMs) increase affinity, while “negative allosteric modulators” (NAMs) decrease affinity, thus indirectly reducing receptor activity. The compounds of formula (I), as previously defined, are negative allosteric modulators that bind to the benzodiazepine binding site, exhibiting selective inverse agonist activity at the GABAa α5 receptor. The term “inhibition constant” (Ki) refers to the absolute binding affinity of a particular inhibitor for a receptor. It is determined through competitive binding studies and is equal to the concentration at which an inhibitor would occupy half of the receptors if no competing ligands were present. Ki values ​​can be logarithmically converted to pKi values ​​(-logKi), with higher values ​​representing exponentially greater powers. The term “submaximal effective concentration” refers to the concentration of a compound needed to obtain 10% of the maximum of a particular effect. The term “functional selectivity” refers to the varying degrees of modulation a particular compound exerts on different receptor subtypes. In this context, a compound exhibits functional selectivity when it acts as an inverse agonist of the GABAα receptor and reduces the effect of GABA by more than 20%, while its effect on other GABAα receptor subtypes is less than 10%. The terms “condition”, “defect”, “deficit”, “disability”, “disorder”, “disease” and “disease state” are used as synonyms to denote any disease, condition, symptom, syndrome, disorder or indication. The term “GABAA α5 receptor-related diseases” refers to diseases, conditions, or disorders of the central nervous system that present one or more symptoms and / or syndromes related to the GABAA α5 receptor. These diseases include, but are not limited to, neurodegenerative disorders, neurocognitive disorders, schizophrenia, mood disorders, pain disorders, substance-related or addiction disorders, and other diseases. The term “cognition” refers to the processes a subject, preferably a mammal, and more preferably a human, uses to organize information. This encompasses the acquisition (perception), selection (attention), representation (comprehension), and retention (memory) of information, as well as its use to guide behavior (reasoning and coordination of motor responses). Interventions to improve cognitive function can target any of these core abilities. In one embodiment, the compounds of formula (I), as previously defined, are useful as cognitive enhancers. The term “cognitive enhancer” refers to a compound that improves cognitive functions, particularly social cognition, complex attention, executive function, perceptual-motor function, language, learning, or memory. A cognitive enhancer is an intervention that improves a subsystem in some way that does not involve repairing a broken element or remediating a specific dysfunction. Diseases related to the GABAα5 receptor may present with concurrent morbidity. Concurrent morbidity is a medical condition that exists simultaneously with, but independently of, another condition in a patient, or a medical condition in a patient that causes, is caused by, or is otherwise related to another condition in the patient. However, in a psychiatric, psychological, or mental health illness, concurrent morbidity does not necessarily imply the presence of multiple diseases but may reflect the current inability to provide a single diagnosis that accounts for all symptoms. The term “neurodegenerative disorder” encompasses, without limitation, Alzheimer's disease (AD), Huntington's disease (HD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). The term “neurocognitive disorder” encompasses, without limitation, disorders of cognitive impairment, memory deficits, age-related memory impairment or cognitive decline, dementia (in various forms, e.g., dementia in Alzheimer's disease, Niemann-Pick disease, Parkinson's disease, Huntington's disease, dementia with Lewy bodies (DCCL), frontotemporal dementia, vascular dementia (DV), subcortical dementia, mixed or subcortical vascular dementia, dementia with multiple infarcts, postoperative dementia, or inflammation-induced dementia), mild cognitive impairment (MCI), vascular cognitive impairment (DCV), CNS conditions following stroke, cognitive impairment associated with brain cancers (including, without limitation, medulloblastomas), cognitive impairment in Down syndrome (DS), and cognitive dysfunction in major depressive disorder (MDD). The term “schizophrenia” encompasses, among others, various forms of schizophrenia, its positive, negative and / or cognitive symptoms, schizotypal disorders and delusions. The term “pain disorder” encompasses, without limitation, nociceptive, neuropathic, or inflammatory pain. The term “mood disorder” encompasses, among others, depression-related disorders (e.g., major depressive disorder (MDD), dysthymia, cyclothymic disorder, seasonal affective disorder / seasonal depression, post-traumatic brain injury (TBI) depression, postpartum depression, premenstrual dysphoric disorder, depressive symptoms associated with menopause, post-substance abuse / withdrawal depression, bipolar disorders, bipolar disorder in remission, depressive episodes of bipolar disorders), bipolar disorders, substance-induced disorders (alcohol or drugs), or other unspecified mood disorders (UE-NOS). The term “other disease” includes, among others, attention deficit hyperactivity disorder and adult attention deficit disorder, other stress-related conditions, stroke, neurofibromatosis type I, multiple sclerosis, acute meningitis, alcoholism, fetal alcohol syndrome, and bronchoconstrictor diseases (e.g., asthma, chronic obstructive pulmonary disease, or bronchopulmonary dysplasia). In one embodiment, GABAA α5 receptor-related disease encompasses Alzheimer's disease (AD), Huntington's disease (HD), Parkinson's disease, amyotrophic lateral sclerosis (ALS), cognitive impairment disorders, memory deficits, age-related memory impairment or cognitive decline, dementia or various variants thereof, e.g., dementia in Alzheimer's disease, Niemann-Pick disease, Parkinson's disease, Huntington's disease, dementia with Lewy bodies (DLCB), frontotemporal dementia, vascular dementia (VD), subcortical dementia, mixed or subcortical vascular dementia, dementia with multiple infarcts, postoperative dementia or inflammation-induced dementia), mild cognitive impairment (MCI), vascular cognitive impairment (VCI), CNS conditions following stroke, cognitive impairment associated with brain cancers (including, without limitation, medulloblastomas),cognitive impairment in Down syndrome (DS), cognitive dysfunction in major depressive disorder (MDD), various forms of schizophrenia, their positive, negative and / or cognitive symptoms, schizotypal disorders, delusions, nociceptive, neuropathic or inflammatory pain, depression-related disorders (e.g., major depressive disorder (MDD), dysthymia, cyclothymic disorder, seasonal affective disorder / seasonal depression, post-traumatic brain injury (TBI) depression, postpartum depression, premenstrual dysphoric disorder, depressive symptoms associated with menopause, post-substance abuse / withdrawal depression, bipolar disorders, bipolar disorder in remission, depressive episodes of bipolar disorders), bipolar disorders, substance-induced disorders (alcohol or drugs), other unspecified mood disorders (OT-NOE), attention deficit hyperactivity disorder and adult attention deficit,Other stress-related conditions, stroke, neurofibromatosis type I, multiple sclerosis, acute meningitis, alcoholism, fetal alcohol syndrome, or bronchoconstrictor diseases (e.g., asthma, chronic obstructive pulmonary disease, or bronchopulmonary dysplasia). In one embodiment, GABAa α5 receptor-related disease encompasses Alzheimer's disease (AD), cognitive impairment disorders, memory deficits, age-related memory impairment or cognitive decline, dementia, mild cognitive impairment (MCI), vascular cognitive impairment (VCI), post-stroke CNS conditions, cognitive impairment associated with brain cancers, cognitive impairment in Down syndrome (DS), cognitive dysfunction in major depressive disorder (MDD), or schizophrenia. The present invention provides a method for treating or preventing diseases related to the GABAa α5 receptor or for improving cognition, comprising administering to the subject in need, preferably a mammal, more preferably a human, a therapeutically effective amount of a compound of formula (I), as defined above, alone or in combination with at least one pharmaceutically acceptable excipient, in the form of a pharmaceutical formulation. The present invention provides a method for treating or preventing diseases related to the GABAa α5 receptor or for improving cognition, comprising administering to the subject in need, preferably a mammal, more preferably a human, a therapeutically effective amount of a compound of formula (I), as defined above, in combination with one or more additional active ingredients. The present invention provides a method for treating or preventing neurodegenerative disorders, neurocognitive disorders, schizophrenia, mood disorders, pain disorders, substance-related or addiction disorders, or other diseases, or at least one of their symptoms and / or syndromes, which may be related to the GABAa α5 receptor, in an affected subject, preferably a mammal, more preferably a human, or for improving cognition. This treatment method comprises administering to the subject in need, preferably a mammal, more preferably a human, a therapeutically effective amount of a compound of formula (I), as defined above.The treatment method may comprise administering to the subject in need, who is preferably a mammal, more preferably a human, a therapeutically effective amount of a pharmaceutical composition comprising a compound of formula (I), as previously defined. The present invention provides a method for treating or preventing Alzheimer's disease (AD), cognitive impairment disorders, memory deficits, age-related memory impairment or cognitive decline, dementia, mild cognitive impairment (MCI), vascular cognitive impairment (VCI), CNS conditions following stroke, cognitive impairment associated with brain cancers, cognitive impairment in Down syndrome (DS), cognitive dysfunction in major depressive disorder (MDD) or schizophrenia, or at least one of their symptoms and / or syndromes, in an affected subject, preferably a mammal, more preferably a human, or for improving cognition. The present invention provides a compound of formula (I), as previously defined, for use in the treatment or prevention of diseases related to the GABAa α5 receptor or as a cognition enhancer. The present invention provides a compound of formula (I), as previously defined, in combination with one or more additional active ingredients, for use in the treatment or prevention of diseases related to the GABAA α5 receptor or as a cognition enhancer. The present invention provides a compound of formula (I), as previously defined, for use in the treatment or prevention of neurodegenerative disorders, neurocognitive disorders, schizophrenia, mood disorders, pain disorders, substance-related or addiction disorders, or other diseases, or at least one of their symptoms and / or syndromes, or as a cognitive enhancer. The present invention provides a compound of formula (I), as defined above, for use in the treatment or prevention of Alzheimer's disease (AD), cognitive impairment disorders, memory deficits, age-related memory impairment or cognitive decline, dementia, mild cognitive impairment (MCI), vascular cognitive impairment (VCI), CNS conditions following stroke, cognitive impairment associated with brain cancers, cognitive impairment in Down syndrome (DS), cognitive dysfunction in major depressive disorder (MDD) or schizophrenia, or at least one of their symptoms and / or syndromes, or as a cognitive enhancer. The present invention provides for the use of a compound of formula (I), as previously defined, in the manufacture of a medicament for treating or preventing diseases related to the GABAa α5 receptor or for improving cognition. The present invention provides for the use of a compound of formula (I), as defined above, in combination with one or more additional active ingredients, in the manufacture of a medicament for treating or preventing diseases related to the GABAA α5 receptor or for improving cognition. The present invention provides for the use of a compound of formula (I), as previously defined, in the manufacture of a medicament to treat or prevent neurodegenerative disorders, neurocognitive disorders, schizophrenia, mood disorders, pain disorders, substance-related or addiction disorders, or other diseases, or at least one of their symptoms and / or syndromes, or to improve cognition. The present invention provides for the use of a compound of formula (I), as defined above, in the manufacture of a medicament for treating or preventing Alzheimer's disease (AD), cognitive impairment disorders, memory deficits, age-related memory impairment or cognitive decline, dementia, mild cognitive impairment (MCI), vascular cognitive impairment (VCI), CNS conditions following stroke, cognitive impairment associated with brain cancers, cognitive impairment in Down syndrome (DS), cognitive dysfunction in major depressive disorder (MDD) or schizophrenia, or at least one of their symptoms and / or syndromes, or for improving cognition. The present invention also relates to a pharmaceutical composition comprising a compound of formula (I), as previously defined, for use in the treatment or prevention of diseases related to the GABAa α5 receptor or for improving cognition. The present invention also relates to a pharmaceutical composition comprising a compound of formula (I), as defined above, in combination with one or more additional active ingredients, for use in the treatment or prevention of diseases related to the GABAA α5 receptor or for improving cognition. The term “treatment” refers to the relief of a specific pathological condition, the elimination or reduction of one or more of its symptoms, the slowing or suppression of its progression, or the prevention or delay of its recurrence in a patient or affected individual. “Prevention” (or prophylaxis or delay of disease action) is generally the result of administering the same or similar drug regimen to a patient already suffering from a disease or condition. The term “therapeutically effective amount” refers to the quantity of an active ingredient that results in the treatment, cure, prevention, or improvement of a disease, disease state, or side effect, or a reduction in its progression, compared to an untreated subject. The term also encompasses amounts effective in improving normal physiological function. In therapy, a compound of formula (I), as defined above, or a pharmaceutically acceptable salt thereof, may be administered in a therapeutically effective amount as a crude chemical. In addition, the active ingredient may be provided as a pharmaceutical formulation.The exact therapeutically effective amount of a compound of formula (I), as previously defined, depends on various factors, for example, the subject's (patient's) age or body weight, the precise type of disease to be treated, its severity, the nature of the drug, or the route of administration. The term “subject” refers to a vertebrate. In certain embodiments, the vertebrate is a mammal. Mammals include humans, non-human primates such as chimpanzees or other ape species, farm animals such as cows, horses, sheep, goats, or pigs, domestic animals such as rabbits, dogs, or cats, and laboratory animals, including rodents such as rats, mice, or guinea pigs. In certain embodiments, a mammal is a human being. The term “subject” does not denote a particular age or sex. In one embodiment, the present invention relates to compounds of formula (I') where R1 to R7, nym are as defined above for compounds of formula (I) A is represented by O^Z NyV·' b1 rnw a group ' a group >\ZN a1 b1 jww N or a group where site “a1” of any ring A is joined to site “a2” and where site “b1” of any ring A is joined to site “b2”. In one embodiment, the present invention relates to compounds of formula (Ia) where R1 is hydrogen or halogen, nym are independently of each other 1 or 2, R2 is hydrogen; C^alkyl optionally substituted independently with one or more halogens, C^alkoxy, -S(O)2-C1-4alkyl, or with R3; NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C^alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R3, R6 and R7 are optionally substituted carbocycles, heterocycles or heteroaryls, and / or salts thereof and / or geometric isomers thereof and / or stereoisomers thereof and / or enantiomers thereof and / or racemates thereof and / or diastereomers thereof and / or biologically active metabolites thereof and / or prodrugs thereof and / or solvates thereof and / or hydrates thereof and / or polymorphs thereof. In one embodiment, the present invention relates to compounds of formula (Ib) where R1 is hydrogen or halogen, nym are independently of each other 1 or 2, R2 is hydrogen; C^alkyl optionally substituted independently with one or more halogens, C^alkoxy, -S(O)2-C1-4alkyl, or with R3; NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C^alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R3, R6 and R7 are optionally substituted carbocycles, heterocycles or heteroaryls, and / or salts thereof and / or geometric isomers thereof and / or stereoisomers thereof and / or enantiomers thereof and / or racemates thereof and / or diastereomers thereof and / or biologically active metabolites thereof and / or prodrugs thereof and / or solvates thereof and / or hydrates thereof and / or polymorphs thereof. In one embodiment, the present invention relates to compounds of formula (Ic) 'm R where R1 is hydrogen or halogen, nym are independently of each other 1 or 2, R2 is hydrogen; Ci 4 alkyl optionally independently substituted with one or more halogens, Ci 4 alkoxy, -S(O)2-C1-4 alkyl, or with R3; NR4R5 or R6, R4 and R5 are independently hydrogen, C^alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R3, R6 and R7 are optionally substituted carbocycles, heterocycles or heteroaryls, and / or salts thereof and / or geometric isomers thereof and / or stereoisomers thereof and / or enantiomers thereof and / or racemates thereof and / or diastereomers thereof and / or biologically active metabolites thereof and / or prodrugs thereof and / or solvates thereof and / or hydrates thereof and / or polymorphs thereof. In one embodiment, the present invention relates to compounds of formula (I) where Ries is hydrogen. In one embodiment, the present invention relates to compounds of formula (I) where R1 is fluorine, chlorine, or bromine. In one embodiment, the present invention relates to compounds of formula (I) where R2 is hydrogen. In one embodiment, the present invention relates to compounds of formula (I) where R2 is C^alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is haloC^alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is C1-4 alkoxyC1-4 alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is methoxymethyl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is C1-4alkyl-S(O)2-C1-4alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is methylsulfonylmethane or ethylsulfonylmethane. In one embodiment, the present invention relates to compounds of formula (I) where R2 is C^alkyl substituted with optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5 and R4 and R5 are hydrogen. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5 and R4 and R5 are Ci .4 alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5 and R4 is hydrogen, R5 is Ci4alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5 and R4 is hydrogen, R5 is optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5 and R4 is C^alkyl, R5 is Ci4alkyl or optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5 and R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle. In one embodiment, the present invention relates to compounds of formula (I) where R2 is NR4R5 and R4 is hydrogen, R5 is an optionally substituted heterocycle, or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted monocyclic heterocycle. In one embodiment, the present invention relates to compounds of formula (I) where R2 are optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where R2 is C^cycloalkyl, C^waryl, C46heterocycle comprising 1 or 2 ring heteroatoms independently selected from N, O and S or C5-6heteroaryl comprising 1 or 2 ring heteroatoms independently selected from N and O optionally substituted. In one embodiment, the present invention relates to compounds of formula (I) where R2 is C^cycloalkyl, C^waryl, C46heterocycle comprising 1 or 2 ring heteroatoms independently selected from N, O and S or C5-6heteroaryl comprising 1 or 2 ring heteroatoms independently selected from N and O substituted with C^alkyl, C^alkoxy, halogen, haloC^alkyl, haloC^alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) wherein the optionally substituted carbocycle, heterocycle or heteroaryl is selected from the group comprising cyclopropyl, cyclobutane, cyclohexane, phenyl, oxethane, tetrahydrofuran, tetrahydropyran, thiane, pyrrolidine, piperidine, pyridine, isoxazole, pyrrole and morpholine. In one embodiment, the present invention relates to compounds of formula (I) where n is 1 and m is 2. In one embodiment, the present invention relates to compounds of formula (I) where n is 2 and m is 1. In one embodiment, the present invention relates to compounds of formula (I) where nym are 1. In one embodiment, the present invention relates to compounds of formula (I) where n is 2 and m is 2. In one embodiment, the present invention relates to compounds of formula (I) where R1 is halogen, nym are independently 1 or 2 and R2 is C14alkoxyC1-4alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R1 is halogen, nym are independently 1 or 2 and R2 is C14alkyl-S(O)2-C1-4alkyl. In one embodiment, the present invention relates to compounds of formula (I) where R1 is halogen, nym are independently of each other 1 or 2 and R2 is NR4R5. In one embodiment, the present invention relates to compounds of formula (I) where R1 is halogen, nym are independently 1 or 2 and R2 are optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where R1 is fluorine, bromine or chlorine, R2 is C1-3alkyl, C1-4alkoxyC1-3alkyl, C1-3alkyl-S(O)2-C1-3alkyl, NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C^alkyl or R7, and R6 and R7 are C^cycloalkyl, C^waryl, C^heterocycle comprising 1 or 2 ring heteroatoms independently selected from N, O and S or C5-6heteroaryl comprising 1 or 2 ring heteroatoms independently selected from N and O, optionally substituted with Ci 4alkyl, Ci4alkoxy, halogen, haloC^alkyl, haloC^alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where R1 is fluorine or chlorine, R2 is C1-4 alkoxy C1-3 alkyl, methylsulfonylmethane, ethylsulfonylmethane, NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C1-alkyl or R7, and R6 and R7 are carbocycle, heterocycle or heteroaryl selected from the group comprising cyclopropyl, cyclobutane, cyclohexane, phenyl, oxethane, tetrahydrofuran, tetrahydropyran, thiane, pyrrolidine, piperidine, pyridine, isoxazole, pyrrole and morpholine optionally substituted with C1-4 alkyl, C1-4 alkoxy, halogen, haloC1-4 alkyl, haloC1-4 alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where R1 is halogen, n is 1 and m is 2 R2 is Ci-4 alkyl optionally substituted independently with Ci4alkoxy, -S(O)2-C1-4 alkyl; NR4R5 or R6, R4 and R5 are independently hydrogen, C^alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R3, R6 and R7 are optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where Ries is fluorine, chlorine or bromine, n is iym is 2 R2 is C1-3alkyl, C1-4alkoxyC1-3alkyl, C1-3alkyl-S(O)2-C1-3alkyl, NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C1-alkyl or R7, and R6 and R7 are C3-6cycloalkyl, C3-6wadlo, C4-6heterocycle comprising 1 or 2 ring heteroatoms independently selected from N, O and S or C5-6heteroaryl comprising 1 or 2 ring heteroatoms independently selected from N and O, optionally substituted with C1-alkyl, C4alkoxy, halogen, haloC1-alkyl, haloC1-alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where Ries is fluorine or chlorine, n is iym is 2 R2 is C1-4 alkoxy C1-3 alkyl, methylsulfonylmethane, ethylsulfonylmethane, NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C1-alkyl or R7, and R6 and R7 are carbocycle, heterocycle or heteroaryl selected from the group comprising cyclopropyl, cyclobutane, cyclohexane, phenyl, oxethane, tetrahydrofuran, tetrahydropyran, thiane, pyrrolidine, piperidine, pyridine, isoxazole, pyrrole and morpholine optionally substituted with Ci-4 alkyl, Ci-4 alkoxy, halogen, haloCi-4 alkyl, haloC^alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where Ries is a halogen, n is 2 and m is 1 R2 is C^alkyl optionally substituted independently with Ci4alkoxy, -S(O)2-C1-4alkyl; NR4R5 or R6, R4 and R5 are independently hydrogen, C^alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R3, R6 and R7 are optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where R1 is fluorine, bromine or chlorine, n is 2 and m is 1 R2 is C1-3 alkyl, C1-4 alkoxyC1-3 alkyl, C1-3 alkyl-S(O)2-C1-3 alkyl, NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C^alkyl or R7, and R6 and R7 are C3-6cycloalkyl, C6-waryl, C4-6heterocycle comprising 1 or 2 ring heteroatoms independently selected from N, O and S or C5-6heteroaryl comprising 1 or 2 ring heteroatoms independently selected from N and O, optionally substituted with C1-alkyl, C14-alkoxy, halogen, haloC1-alkyl, haloC1-alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where R1 is fluorine or chlorine, n is 2 and m is 1 R2 is C1-4 alkoxy C1-3 alkyl, methylsulfonylmethane, ethylsulfonylmethane, NR4R5 or R6, R4 and R5 are independently of each other hydrogen, C1-alkyl or R7, and R6 and R7 are carbocycle, heterocycle or heteroaryl selected from the group comprising cyclopropyl, cyclobutane, cyclohexane, phenyl, oxethane, tetrahydrofuran, tetrahydropyran, thiane, pyrrolidine, piperidine, pyridine, isoxazole, pyrrole and morpholine optionally substituted with Ci 4alkyl, Z 4alkoxy, halogen, haloC1-4alkyl, haloZ 4alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where R1 is halogen, nym are 1, R2 is Z-4 alkyl optionally substituted independently with Ci4alkoxy, -S(O)2-C1—4 alkyl; NR4R5 or R6, R4 and R5 are independently of each other hydrogen, Z-4 alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R6 and R7 are optionally substituted carbocycle, heterocycle or heteroaryl. In one embodiment, the present invention relates to compounds of formula (I) where R1 is fluorine, chlorine or bromine, and nym are 1, R2 is Ci-3alkyl, Ci-4alkoxy Ci-3alkyl, Ci-3alkyl-S(Q)2-Ci-3alkyl, NR4R5 or R6, R4 and R5 are independently of each other hydrogen, Ci-4alkyl or R7, and R6 and R7 are C3-6Cycloalkyl, C6-ioaryl, C4-6heterocycle comprising io 2 ring heteroatoms independently selected from N, Q and S or C5-6heteroaryl comprising io 2 ring heteroatoms independently selected from N and Q, optionally substituted with Ci-4alkyl, Ci4alkoxy, halogen, haloCi-4alkyl, haloCi-4alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where Ries is fluorine or chlorine, nym are i, R2 is Ci-4-alkoxy Ci-3-alkyl, methylsulfonylmethane, ethylsulfonylmethane, NR4, R5, or R6, R4 and R5 are independently of each other hydrogen, Ci-3-alkyl or R7, and R6 and R7 are carbocycle, heterocycle or heteroaryl selected from the group comprising cyclopropyl, cyclobutane, cyclohexane, phenyl, oxethane, tetrahydrofuran, tetrahydropyran, thiane, pyrrolidine, piperidine, pyridine, isoxazole, pyrrole and morpholine optionally substituted with Ci-4-alkyl, Ci-4-alkoxy, halogen, haloCi-4-alkyl, haloCi-4-alkoxy, hydroxyl or oxo. In one embodiment, the present invention relates to compounds of formula (I) where Ries is a halogen, nym are 2, R2 is optionally independently substituted Ci-4 alkyl with Ci4alkoxy, -S(Q)2-Ci-4 alkyl; NR4R5 or R6, R4 and R5 are independently hydrogen, C^alkyl or R7; or R4 and R5 are taken together with the N to which they are attached to form an optionally substituted heterocycle, and R6 and R7 are optionally substituted carbocycle, heterocycle or heteroaryl. Any combination of the embodiments of A, R1-R7, nym as defined above are preferred groups of compounds of formula (I). In one embodiment, the present invention relates to compounds of formula (I), as defined above, selected from the group consisting of: -[2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-7,8-dihydro-1,6-naphthyridin6(5H)-yl]ethanone, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(oxolan-3-carbonyl)-5,6,7,8tetrahydro-1,6-naphthyridine, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(1,2-oxazol-5-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 6-cyclobutanecarbonyl-2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridine, 6-cyclopropanecarbonyl-2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridine, 4-(2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-carbonyl)-1lambda6-thiane-1,1-dione, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(oxolane-2-carbonyl)-5,6,7,8tetrahydro-1,6naphthyridin, -(2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)-2-methanesulfonylethan-1-one, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(oxan-4-carbonyl)-5,6,7,8tetrahydro-1,6-naphthyridine, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(5-methyl-1,2-oxazol-3carbonyl)-5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(1-methyl-1H-pyrrole-3carbonyl)-5,6,7,8-tetrahydro-1,6-naphthyridine, 2,2,2-trifluoro-1-(2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridin-6-yl)ethan-1-one, 4-(2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridine-6-carbonyl)-1-methylpyrrolidin-2-one, -(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)ethan-1-one, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(oxolane-2-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(oxolane-3-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-[(3R)-oxolane-3carbonyl]-5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-[(3S)-oxolane-3carbonyl]-5,6,7,8-tetrahydro-1,6-naphthyridine, 6-ciclopropancarbonyl-2-{[1 -(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5-yl]methoxy}5,6,7,8-tetrahydro-1,6-naphthiridina, 2-{[1 -(4-fluorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-6-(1,2-oxazol-5carbonyl)-5,6,7,8-tetrahydro-1,6-naphthyridine, 4-(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridine-6-carbonyl)-1-methylpyrrolidin-2-one, -(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)-2-methylpropan-1-one, 4-(2-{[1 -(4-fluorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridine-6-carbonyl)-1lambda6-thiane-1,1-dione, -(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)propan-1-one, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(pyridine-4-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(pyridine-2-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 6-(3-chlorobenzoyl)-2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(oxane-4-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1 -(4-chlorofenil)-4-metil-1 H-1,2,3-triazol-5-yl]methoxy}-6-(oxolan-3-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridina, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(oxane-3-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(3-methyloxolan-3carbonyl)-5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1 -(4-chlorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-6-(oxane-4-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1 -(4-chlorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-6-(pyridine-4-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, -(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,7naphthyridin-7-yl)ethan-1-one, 2-{[1 -(4-fluorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-6-(4methoxycyclohexanecarbonyl)-5,6,7,8-tetrahydro-1,6-naphthyridin, 1 -(2-{[1 -(4-chlorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)ethan-1-one, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-[6(trifluoromethyl)pyridine-3-carbonyl]-5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1 -(4-chlorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-[(3S)-oxolan-3carbonyl]-5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(pyridine-3-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, (5S)-5-(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridine-6-carbonyl)-1-methylpyrrolidin-2-one, (5R)-5-(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridine-6-carbonyl)-1-methylpyrrolidin-2-one, -(2-{[1-(4-chlorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)-2-methoxyethan-1-one, -ethyl-4-(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridin-6-carbonyl)pyrrolidin-2-one, 4-(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-carbonyl)-1-(propan-2-yl)pyrrolidin-2-one, -(2-{[1 -(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5-yl]methoxy}-5H,6H,7H-pyrrolo[3,4b]pyridin-6-yl)ethan-1-one, 5-(2-{[1 -(4-fluorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-carbonyl)-1-methylpiperidin-2-one, cyclopropyl(2-{[1 -(4-fluorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-5,7-dihydro6H-pyrrolo[3,4-b]pyridin-6-yl)methanone, -(2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)-3-methanesulfonylpropan-1-one, 1-(2-{[3-(4-fluorofenil)-5-metil-1,2-oxazol-4-yl]methoxy}-5H,6H,7H-pyrrolo[3,4b]pyridin-6-yl)-2-methanesulfonyletan-1-one, 1-(2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,7-dihydro-6H-pyrrolo[3,4b]pyridin-6-yl)ethanone, 2,2,2-trifluoro-1-(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,7dihydro-6H-pyrrolo[3,4-b]pyridin-6-yl)ethanone, -(2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,7-dihydro-6Hpyrrolo[3,4-b]pyridin-6-yl)propan-1-one, 2,2-difluoro-1 -(2-{[1 -(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5-il]metoxi}-5,7dihidro-6H-pirrolo[3,4-b]piridin-6-il)etanona, 2-fluoro-1-(2-{[1-(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5-il]metoxi}-5,7-dihidro6H-pirrolo[3,4-b]piridin-6-il)etanona, 1-(4-fluorofenil)-4-methyl-5-({[6-(oxan-4-carbonil)-5H,6H,7H-pirrolo[3,4-b]piridin-2il]oxi}methyl)-1H-1,2,3-triazol, -(2-{[1 -(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5-il]metoxi}-5H,6H,7H-pirrolo[3,4b]piridin-6-il)-3-metilbutan-1-ona, 5-[({6-ciclobutanecarbonil-5H,6H,7H-pirrolo[3,4-b]piridin-2-il}oxi)methyl]-1-(4fluorofenil)-4-methyl-1H-1,2,3-triazol, -(2-{[1 -(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5-il]metoxi}-5H,6H,7H-pirrolo[3,4b]piridin-6-il)-2-metilpropan-1-ona, -(2-{[1 -(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5-il]metoxi}-5H,6H,7H-pirrolo[3,4b]piridin-6-il)-2,2-dimetilpropan-1-ona, -(2-{[1 -(4-chlorofenil)-4-metil-1 H-1,2,3-triazol-5-il]metoxi}-5,7-dihidro-6Hpirrolo[3,4-b]piridin-6-il)etanona, 1-(4-fluorofenil)-4-methyl-5-({[6-(oxolan-2-carbonil)-5H,6H,7H-pirrolo[3,4-b]piridin2-il]oxi}methyl)-1H-1,2,3-triazol, 1-(4-fluorofenil)-4-methyl-5-({[6-(oxolan-3-carbonil)-5H,6H,7H-pirrolo[3,4-b]piridin2-il]oxi}methyl)-1H-1,2,3-triazol, 1-(4-fluorofenil)-4-methyl-5-({[6-(oxan-3-carbonil)-5H,6H,7H-pirrolo[3,4-b]piridin-2il]oxi}methyl)-1H-1,2,3-triazol, 4-(2-{[1-(4-fluorofenil)-4-methyl-1H-1,2,3-triazol-5-il]metoxi}-5H,6H,7H-pirrolo[3,4b]piridin-6-carbonil)piridina, 3-(2-{[1-(4-fluorofenil)-4-methyl-1H-1,2,3-triazol-5-il]metoxi}-5H,6H,7H-pirrolo[3,4b]piridin-6-carbonil)piridina, 2-(2-{[1-(4-fluorofenil)-4-methyl-1H-1,2,3-triazol-5-il]metoxi}-5H,6H,7H-pirrolo[3,4b]piridin-6-carbonil)piridina, -(2-{[4-(4-fluorophenyl)-1-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,7-dihydro-6Hpyrrolo[3,4-b]pyridin-6-yl)ethanone, -(2-{[4-(4-chlorophenyl)-1-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,7-dihydro-6Hpyrrolo[3,4-b]pyridin-6-yl)ethanone, -(2-{[4-(4-fluorophenyl)-1-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,7-dihydro-6Hpyrrolo[3,4-b]pyridin-6-yl)propan-1-one, 2-fluoro-1-(2-{[4-(4-fluorophenyl)-1-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,7-dihydro6H-pyrrolo[3,4-b]pyridin-6-yl)ethanone, 4-(4-fluorophenyl)-1-methyl-5-({[6-(oxolane-3-carbonyl)-5H,6H,7H-pyrrolo[3,4-b]pyridin2-yl]oxy}methyl)-1H-1,2,3-triazole, -(2-{[4-(4-fluorophenyl)-1-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5H,6H,7H-pyrrolo[3,4b]pyridin-6-yl)-2-methylpropan-1-one, 4-(4-fluorophenyl)-1-methyl-5-({[6-(oxolane-2-carbonyl)-5H,6H,7H-pyrrolo[3,4-b]pyridin2-yl]oxy}methyl)-1H-1,2,3-triazole, 4-(4-fluorofenil)-1-metil-5-({[6-(oxan-3-carbonyl)-5H,6H,7H-pyrrolo[3,4-b]pyridin-2yl]oxi}metil)-1 H-1,2,3-triazol,2-{[1 -(4-fluorofenil)-4-metil-1 H-1,2,3-triazol-5yl]methoxy}-N-(1-metil-5-oxopyrrolidin-3-yl)-5,6,7,8-tetrahydro-1,6-naphthyridin-6carboxamide, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-N,N-dimethyl-5,6,7,8tetrahydro-1,6-naphthyridine-6-carboxamide, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-6-(pyrrolidine-1-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-N-(oxolan-3-yl)-5,6,7,8tetrahydro-1,6-naphthyridine-6-carboxamide, N-(2-chlorophenyl)-2-{[1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridine-6-carboxamide, 2-{[1 -(4-fluorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-6-(morpholine-4-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, N-(4-chlorophenyl)-2-{[1 -(4-fluorophenyl)-4-methyl-1 H-1,2,3-triazol-5-yl]methoxy}-5,6,7,8tetrahydro-1,6-naphthyridine-6-carboxamide, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(morpholine-4-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-N,N-dimethyl-5,6,7,8-tetrahydro1,6-naphthyridine-6-carboxamide, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(pyrrolidin-1-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-6-(piperidin-1-carbonyl)5,6,7,8-tetrahydro-1,6-naphthyridine, and 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-N-(oxolan-3-yl)-5,6,7,8tetrahydro-1,6-naphthyridine-6-carboxamide. In the description of the general synthesis of compounds of formula (I), biological assays, intermediates, and examples, the following abbreviations are used: BOC = tert-butoxycarbonyl Boc2O = di-tert-butyl dicarbonate DCM = dichloromethane PBr3 = phosphorus tribromide TFA = trifluoroacetic acid DIPEA = N-ethyl-N-(propan-2-yl)propan-2-amine BzOH = benzyl alcohol 18-crown-6 = 1,4,7,10,13,16-hexaoxacyclooctadecane Pd / C = palladium on carbon AcCN = acetonitrile triphosgene = bis(trichloromethyl)carbonate Tris = 2-amino-2-(hydroxymethyl)propan-1,3-diol TLC = thin-layer chromatography; brine = high-concentration salt solution (usually sodium chloride). The present invention also relates to the synthesis of compounds of formula (I). Various methods for preparing the compounds of this invention are illustrated in the following Schemes and Examples. The starting materials are acquired or prepared according to procedures known in the field or as illustrated herein. The synthesis of intermediates of formula (III) is shown in Scheme 1, where A and R1 are as defined in any of the embodiments described above for formula (I). According to Scheme 1, the reaction of a compound of formula (II) in a suitable solvent, such as dichloromethane, with a brominating agent, such as PBr3, provides intermediates of formula (III). The hydroxy derivatives of formula (II) are known in the trade (e.g., WO 2013 / 057123 A1, WO 2012 / 062623 A1) or can be synthesized by conventional methods. VAJ^OH PBr3 / DCM vJ^Br Or RR1(II) rF (III) Scheme 1 The reagents and details of the process steps required for the preceding reactions are provided in the Intermediates. Compounds of formula (I) can be synthesized according to Scheme 2, where A, R1, R2, nym are as defined in any of the embodiments described above for formula (I). According to Scheme 2, the protection of commercially available bicyclic amine derivatives of formula (IV) yields N-BOC amines of formula (V). The reaction can be carried out in the presence of BOC anhydride in dichloromethane using a base such as triethylamine. Treatment of the chlorinated derivative of formula (V) with benzyl alcohol provides the benzyl ether intermediate of formula (VI), followed by a palladium-catalyzed separation of benzyl ether of formula (VI) to obtain the desired hydroxy derivatives of formula (VII). Etherification between alcohols of formula (VII) and intermediates of formula (III) can be carried out in the presence of K₂CO₃ in acetonitrile to form ether derivatives of formula (VIII). Deprotection of the ether derivative of formula (VIII) using an acid such as ethyl acetate saturated with hydrogen chloride or TFA in dichloromethane provides the final intermediate of formula (IX).Finally, the amine derivatives of formula (IX) can be acylated with R2COCl of formula (X) in the presence of a base (Et3N); or when R2 = NR4R5, the amine derivatives of formula (IX) can be reacted with HNR4R5 of formula (XI) using triphosgene in the presence of a base (DIPEA) to form compounds of formula (I). The acyl chlorides of formula (X) and the amines of formula (XI) can be obtained or prepared by conventional methods, where the definition of R2 is the same as that provided above for formula (I). (iv) Boc2O / Et3N DCM BzOH / KOH 18-crown-6, toluene hnr4re(XI) triphosgene DIPEA / DCM TFA Scheme 2 The reagents and details of the process steps required for the preceding reactions are provided in the Examples. The activity data for each of the compounds of formula (I) of the present invention are determined in vitro by means of the methods described below. Biological example 1. Junction study The ΘΑΒΑΑα5β3γ2 protein used in the receptor binding study was derived from membranes produced from HEK cells (Millipore CYL3073) expressing recombinant human ΘΑΒΑΑα5β3γ2 receptors. The cells were stored and cultured internally according to the supplier's (Millipore) instructions. The cell pellet was homogenized in a 10-fold modified Henseleit Krebs buffer (membrane preparation buffer): 20 mM Tris, 120 mM NaCl, 100 mM KCl, 25 mM CaCl₂, and 25 mM MgCl₂, pH 7.4, at 4°C, using the maximum speed of an Ultra Turrax device (Janke & Kunkel) for 15 seconds. The homogenate was centrifuged at 40,000 g for 30 minutes at 4°C. The supernatant was discarded, and the pellet was washed in the membrane preparation buffer. The pellet was resuspended in the membrane preparation buffer and stored in 1.4 mL aliquots in ampoules at -70°C until use. Receptor binding studies were performed in 96-well deep plates. For each 96-well plate, one ampoule of membrane homogenate was thawed, diluted in binding buffer (50 mM Tris, pH 7.4, 100 mM KCl), and 200 μL was applied to each cavity. The radioligand [3H]Ro151788 (Perkin Elmer: NET757250UC) was prepared in the binding buffer and applied to each cavity in a volume of 50 μL to provide a final concentration of 0.5 nM. The compounds to be evaluated were added at the appropriate concentrations in an additional 50 μL. The final volume in the study was 300 lp. The plates were incubated at 4°C for 60 minutes. For nonspecific binding, 10 pM unlabeled diazepam was used. After incubation, the samples were filtered onto UniFilter® GF / B™ using a Filtermate Harvester device (Perkin Elmer) and washed 5 times with 1 ml of the bonding buffer.The plate was dried at 40°C for one hour and 40 pl / cavity of the Microscint scintillation cocktail (Perkin Elmer) was added. The plate was read on a Microbeta device (Perkin Elmer). Specific radioligand binding (SB) was defined as the difference between total binding (Tot) and non-specific binding (NSB). Results were expressed as the percentage of inhibition of specific binding in the presence of the compound of interest. To determine IC50 and Ki, a minimum of six concentrations of each drug were used in triplicate. IC50 values ​​(the concentration of each compound at which 50% inhibition of the specific binding was obtained) were calculated from concentration-deviation curves using a sigmoidal fit with Origin 7.5 software. Ki values ​​(the inhibition constant) were calculated using the Cheng-Prusoff equation: Ki = IC50 / [1+(L / Kd)], where [L] is the concentration of the radioligand and Kd is the affinity of the labeled ligand for the receptor, where Kd was determined by saturation analysis. When evaluating various compounds of the present invention as indicated, it was determined that all exhibited a high affinity for the GABAAa5 receptor (Ki<200 nM). Compounds with Ki<50 nM are preferred. Table 1. Representative K¡ results in a study with hGABAA α5 as described Example Ki for hGABAA α5 (nM) Example Ki for hGABAA α5 (nM) Example Ki for hGABAA α5 (nM) 1 2.8 31 44 61 4.8 2 7.0 32 22 62 5.7 3 5.0 33 14 63 9.5 4 16 34 112 64 25 5 7.8 35 71 65 28 6 2.7 36 9.8 66 59 7 6.8 37 69 67 20 8 3.7 38 18 68 7.5 9 6.2 39 24 69 25 10 21 40 56 70 9.2 11 11 41 67 71 56 12 14 42 13 72 29 13 4.3 43 30 73 18 14 28 44 54 74 46 15 42 45 3.2 75 38 16 42 46 84 76 30 17 69 47 7.2 77 66 18 50 48 33 78 28 19 49 49 1.2 79 108 20 24 50 0.8 80 38 21 35 51 31 81 37 22 57 52 37 82 5.2 23 45 53 11 83 3.8 24 46 54 5.3 84 8.9 25 29 55 13 85 36 26 80 56 17 86 6.5 27 137 57 14 28 43 58 13 29 18 59 31 30 82 60 1.2 Biological example 2. Functional study In functional studies, human HEK293 cell lines expressing GABAAa1e3Y2 and GABAAa5e3Y2 receptors were used in an automated QPatch patch clamp system. HEK293 cell lines stably expressed recombinant human GABAAa1e3Y2 receptor subunits (Millipore, CYL3073) or recombinant human GABAAa5e3Y2 receptor subunits (Millipore, CYL3053) in DMEM plus 10% FBS (Gibco), were cultured twice a week and placed in Petri dishes previously coated with poly-d-lysine. Automated patch-clamp recordings were performed with whole cells 2-4 days after seeding. Cells were separated using trypsin / EDTA treatment (Sigma) (2 minutes in 0.25% trypsin at 37°C), centrifuged (125 G, 3 minutes, 2x) and resuspended in a serum-free medium (Gibco, CHO-S-SFM-II) containing 12.5 mM HEPES, 1x penicillin-streptomycin-amphotericin (SigmaMix) and a soybean trypsin inhibitor (Sigma, 0.04 mg / ml). The cell suspensions, the extracellular solution (NaCl 130 mM, KCl 5 mM, HEPES 5.1 mM, HEPES-Na 4.9 mM, CaCl2 10 mM, MgCl2 2 mM, glucose 10 mM and 0.1% DMSO, pH 7.35-7.4) and the intracellular solution (KCl 80 mM, KF 50 mM, KOH 36 mM, EGTA 10 mM, HEPES 10 mM, MgCl2 1.75 mM, CaCl20.5 mM, Na2ATP 4 mM, phosphocreatine 14 mM, 50 U / ml creatine phosphokinase, GTP 0.3 mM, pH 7.25-7.3) were placed in an automated patch clamp system QPatch-HTX (Sophion), in single cell mode at room temperature. Internal currents were evoked with a holding potential of -80 mV by applying the control GABAa agonist for 3 seconds at a submaximal effective concentration (1 μM) at 2-4 minute intervals, first five times in a control solution with DMSO at an identical concentration (0.1% or 0.3%), then four times in the presence of the compound to be evaluated, and finally three times in the control solution (wash).At the end of the experiment, 100 μM GABA was applied to saturate the GABA response and evaluate the effectiveness of the GABA control application. The current signals were filtered through a 100 Hz low-pass filter and recorded at a sampling frequency of 1 kHz. The modulation percentage was calculated by comparing the amplitudes of the maximum GABA-evoked currents in the presence and absence of the evaluated compound. In this study, compounds of the present invention were evaluated at 10 μM, and it was found that all of them exhibited negative allosteric modulating activity on GABAa α5 and selectivity for the α5 subtype over α1. The preferred compounds have a functional efficiency on the α5 subtype of less than -20%. Table 2. Representative results in a functional study with hGABAA α5 and HGABAa α1 as described Example Efficacy on hGABAA α5 (%) Efficacy on hGABAA α1 (%) 2 -40 -14 6 -38 -10 8 -39 -2 9 -37 -9 13 -34 -3 14 -36 0 15 -43 -8 16 -39 -7 17 -37 -6 18 -45 -5 23 -47 -4 25 -40 -9 28 -40 -6 29 -25 -2 32 -32 -7 40 -42 -12 41 -40 -7 43 -37 -9 44 -44 -5 45 -30 -7 47 -34 -10 49 -26 -4 53 -39 -1 54 -37 -5 55 -45 -15 56 -40 -14 58 -40 -21 60 -27 -8 61 -41 -20 62 -34 -23 63 -34 -16 64 -39 -12 65 -41 -22 75 -35 -3 78 -34 -3 The present invention will be illustrated in greater detail by the following intermediaries and examples, without limiting its scope. From the preceding description, intermediaries, and examples, those skilled in the art should be able to determine the essential features of the invention and, without departing from its essence or scope, should be able to make changes and modifications to adapt it to various applications and conditions. Therefore, the invention is not limited to the illustrative examples, and its scope is defined only by the appended claims. In general, compounds of formula (I) can be prepared based on the common knowledge of those skilled in the art and / or according to the methods described in the working examples and / or intermediates. Those skilled in the art should be able to readily select the solvents, temperatures, pressures, and other reaction conditions. The starting materials are commercially available and / or can be readily prepared by those skilled in the art according to procedures in the literature. During the preparation of the compounds, combined approaches may be used, for example, when the intermediates are appropriate for use in the described methods. 4.98 g (24.0 mmol) of [3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methanol (WO 2013 / 057123 A1, Hoffmann-La Roche) was dissolved in 80 mL of anhydrous dichloromethane, and 9.76 g (3.39 mL, 36.1 mmol) of phosphorus tribromide was added dropwise to the stirred solution. The reaction mixture was stirred for 1 hour at room temperature and then poured onto 50 mL of saturated sodium bicarbonate solution. The mixture was stirred for another 10 minutes, and the phases separated. The organic phase was washed with water, dried over anhydrous sodium sulfate, and evaporated to give 5.89 g (97%) of the title compound as a yellowish-brown solid. MS (ESI) m / z: 269.9 [M+H]+. Intermediary 2 Analogously to Intermediate 1, [1-(4-fluorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methanol (WO 2012 / 062623 A1, Hoffmann-La Roche) was converted into the title compound (114 mg, 87%), which was obtained as a translucent oil. The compound is unstable and decomposes slowly upon standing; therefore, it was generated in situ during the etherification reaction step. Analogously to Intermediate 1, [1-(4-chlorophenyl)-4-methyl-1H-1,2,3-triazol-5-yl]methanol (WO 2012 / 062623 A1, Hoffmann-La Roche) was converted into the title compound (210 mg, 81.7%), which was obtained as a translucent oil. The compound is unstable and decomposes slowly upon standing; therefore, it was generated in situ during the etherification reaction step. Analogously to Intermediate 1, [4-(4-fluorophenyl)-1-methyl-1H-1,2,3-triazol-5-yl]methanol (WO 2012 / 062623 A1, Hoffmann-La Roche) was converted into the title compound (55 mg, 73%), which was obtained as a translucent oil. The compound is unstable and decomposes slowly upon standing; therefore, it was generated in situ during the etherification reaction step. Analogously to Intermediate 1, [4-(4-chlorophenyl)-1-methyl-1H-1,2,3-triazol-5-yl]methanol (WO 2012 / 062623 A1, Hoffmann-La Roche) was converted into the title compound (120 mg, 85%), which was obtained as a translucent oil. The compound is unstable and decomposes slowly upon standing; therefore, it was generated in situ during the etherification reaction step. Example 1 1-f2-{f3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-7,8-dihydro-1,6- a.: tert-butyl 2-chloro-7,8-dihydro-1,6-naphthiridin-6(5H)-carboxylate (WO 2013 / 079452 A1, Hoffmann-La Roche) A suspension of 10.0 g (59.3 mmol) of commercially available 2-chloro5,6,7,8-tetrahydro-1,6-naphthyridine hydrochloride and 6.6 g (9.0 mL, 65.0 mmol of triethylamine in 150 mL of DCM was added dropwise to a solution of 14.2 g (65.0 mmol) of di-tert-butyl dicarbonate in 10 mL of DCM using an addition funnel over 15 min. The resulting solution was stirred at room temperature for 2 hours and monitored using TLC (cyclohexane-ethyl acetate 1:1 as eluent). Upon completion, the reaction mixture was concentrated. The residue was dissolved in 50 mL of ethyl acetate and washed three times with 30 mL of water and 30 mL of brine, then dried over MgSO4. The solvent was evaporated under reduced pressure to give the title compound as an opaque white solid. Yield: 15.4 g (97%). MS (ESI) m / z: 269.1 [M+H]+. b.: tert-butyl 2-(benzyloxy)-7,8-dihydro-1,6-naphthyridine-6(5H)-carboxylate (WO 2016 / 107832 A1, Hoffmann-La Roche) To an ice-cooled solution of 15.0 g (55.8 mmol) of tert-butyl 2-chloro-7,8-dihydro-1,6-naphthyridin-6(5H)-carboxylate in 150 mL of toluene, 9.4 g (167.4 mmol) of solid potassium hydroxide was added, followed by 30 minutes of stirring and then dropwise addition of a solution of 8.7 mL (83.7 mmol) of benzyl alcohol in 150 mL of toluene. Then, 1.5 g (5.58 mmol) of solid 18-crown-6 was added, and the reaction mixture was stirred at 130 °C overnight. After cooling, filtration of the inorganic materials and concentration of the filtrate under reduced pressure yielded the residue, which was purified by flash chromatography on silica gel (cyclohexane-ethyl acetate, 10:1 as eluent). The title compound was obtained as a white solid. Yield: 10.5 g (55.4%). MS (ESI) m / z: 341.1 [M+H]+. c.: tert-butyl 2-oxo-1,5,7,8-tetrahydro-1,6-naphthyridin-6(2 H)-carboxylate (WO 2016 / 107832 A1, Hoffmann-La Roche) A solution of 4.0 g (11.7 mmol) of tert-butyl 2-(benzyloxy)-7,8-dihydro-1,6-naphthyridin-6(5H)-carboxylate in 500 mL of ethyl acetate and 150 mL of methanol was stirred under a nitrogen atmosphere until the mixture became a clear solution. Pd / C catalyst (10% w / w, 200 mg) was added, and hydrogen gas was bubbled through the reaction mixture for 3.5 hours. Once the reaction was complete, as monitored by TLC (chloroform-methanol 10:1 as eluent), the catalyst was removed by filtration, and the filtrate was concentrated under reduced pressure to give the crude product. After recrystallization from diethyl ether, the title compound was isolated as a white solid. Yield: 2.6 g (89.0%). MS (ESI) m / z: 251,1[M+H]+. d.: tert-butyl 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridine-6-carboxylate 9.10 g (33.7 mmol) of 4-(bromomethyl)-3-(4-fluorophenyl)-5-methyl-1,2-oxazole and 8.43 g (33.7 mmol) of tert-butyl 2-oxo-1,5,7,8-tetrahydro-1,6-naphthiridin6(2H)-carboxylate were dissolved in 100 mL of anhydrous acetonitrile. Then, 9.31 g (67.4 mmol) of anhydrous potassium carbonate were added to the solution, and the suspension was stirred under reflux for 5 hours. After conversion, it was subjected to TLC (DCM:MeOH=20:1 as eluent, silica plate). Once the reaction was complete, the mixture was filtered and evaporated to yield 15.6 g of crude oily product, which was further purified by flash column chromatography (silica gel, eluent: DCM:MeOH, gradient 0–5%). Yield: 11.6 g (77%) of glassy solid. MS (ESI) m / z: 440.3 [M+H]+. e.: 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6-naphthyridin 11.5 g (26.2 mmol) of tert-butyl 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6-naphthiridin-6-carboxylate were dissolved in 200 mL of ethyl acetate. 180 mL of ethyl acetate saturated with hydrogen chloride were added dropwise to the solution. The reaction mixture was stirred for 15 minutes at room temperature. The white precipitate formed was separated by filtration, washed with a small amount of ethyl acetate, and dried in a vacuum desiccator, yielding 10.2 g of a white crystalline solid. MS (ESI) m / z: 340.2 [M+H]+. The crude compound was used without purification. f.: 1-[2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-7,8-dihydro-1,6naphthyridin-6(5 H)-yl]ethanone 7.63 g (22.5 mmol) of 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6-naphthyridine were dissolved in 100 mL of anhydrous dichloromethane. 6.83 g (9.4 mL, 67.4 mmol) of anhydrous triethylamine were added in one portion to the solution, and the reaction mixture was cooled in an ice-water bath. A solution of 1.60 mL (1.76 g, 22.5 mmol) of acetyl chloride in 20 mL of anhydrous dichloromethane was added dropwise to the reaction mixture while stirring for 10 minutes. The ice bath was removed, and the mixture was allowed to warm to room temperature. The conversion was verified by TLC (DCM:MeOH=10:1 or cyclohexane:EtOAc=1:3 as eluent, silica plate). The reaction mixture was washed with saturated sodium bicarbonate solution and water, dried over anhydrous sodium sulfate, and evaporated. 10.4 g of residue were obtained, which was purified by flash column chromatography (silica gel, eluent: cyclohexane:EtOAc gradient 40-80%). Yield: 6.28 g (64 %), white amorphous solid identical to the title compound. MS (ESI) m / z: 404.1 [M+Na]+. Table 3 exhibits compounds synthesized according to Scheme 2: For example. MS structure m / z Name 2 'í O o <\ ~Z- A / / ~Z.—' o=¿ Ό 438.2 [M+H]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(oxolan-3carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 3 ° or Ά / / z—' or=¿ or Λ ~z. 435.1 [M+H]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4- yl]methoxy}-6-(1,2-oxazol-5-carbonyl)- 5,6,7,8-tetrahydro-1,6- naphthyridine 4 No. 1 η m JrOtü^ AxJ / OF 422.1 [M+H]+ 6-cyclobutanecarbonyl2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-5,6,7,8tetrahydro-1,6naphthyridine 5 ° o ~Ζ- Ά / / Ζ—' 408.1 [M+H]+ 6-cyclopropanecarbonyl2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-5,6,7,8tetrahydro-1,6naphthyridine 6 ν·'·.'.:· ^Ρο AW ο F 522.1 [M+Na]+ 4-(2-{[3-(4-fluorophenyl)5-methyl-1,2-oxazol-4yl]methoxy}-5,6,7,8- tetrahydro-1,6naphthyridin-6-carbonyl)1lambda6-thian-1,1- dione 7 A ° A° / —Z zy O z 460.2 [M+Na]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(oxolan-2carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 8 o ^COs. £ !—Z zyo °' z 460.1 [M+H]+ 1-(2-{[3-(4-fluorophenyl)- 5-methyl-1,2-oxazol-4- yl]methoxy}-5,6,7,8- tetrahydro-1,6- naphthyridin-6-yl)-2- methanesulfonylethane-1- . ona 9 OAW o F 474.1 [M+Na]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(oxane-4carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 10 ___,O ri zyo „—ΑΛ z 471.1 [M+Na]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(5-methyl- 1,2-oxazol-3-carbonyl)5,6,7,8-tetrahydro-1,6naphthyridine 11 Α-Α / Ο N^ / - ζΑ Mx?NyCN' F 447.2 [M+H]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(1-methyl- 1 H-pyrrol-3-carbonyl)5,6,7,8-tetrahydro-1,6naphthyridine 12 z° o (\ ~Z. Ά / / z—' “Π X “Π 436.3 [M+H]+ 2,2,2-trifluoro-1-(2-{[3(4-fluorophenyl)-5-methyl- 1,2-oxazol-4-yl]methoxy}- 5,6,7,8-tetrahydro-1,6- naphthyridin-6-yl)ethan-1- ona 13 \^z—° o Ά / / z—' ο=ζ \,Z^ O 465,1 [M+H]+ 4-(2-{[3-(4-fluorofenil)- 5-metil-1,2-oxazol-4- il]metoxi}-5,6,7,8- tetrahidro-1,6- naftiridin-6-carbonyl)-1- metilpirrolidin-2-ona 14 N-~y nvC°yn^ / \ 9 wr F 382,2 [M+H]+ 1-(2-{[1-(4-fluorofenil)- 4-metil-1H-1,2,3triazol-5-il]metoxi}5,6,7,8-tetrahidro-1,6naftiridin-6-il)etan-1- on 15 N^Z NUCoy^ / X 0 W / °> F 438,1 [M+H]+ 2-{[1-(4-fluorofenil)-4methyl-1 H-1,2,3-triazol5-il]metoxi}-6-(oxolan2-carbonil)-5,6,7,8tetrahydro-1,6naftiridine 16 NN jf 0 N 0 w> F 438,1 [M+H]+ 2-{[1-(4-fluorofenil)-4methyl-1 H-1,2,3-triazol5-il]metoxi}-6-(oxolan3-carbonil)-5,6,7,8tetrahydro-1,6naftiridine 17 N^Z NX< p W,OF 438,1 [M+H]+ 2-{[1-(4-fluorofenil)-4metil-1 H-1,2,3-triazol5-il]metoxi}-6-[(3R)oxolan-3-carbonil]- 5,6,7,8-tetrahydro-1,6-naftiridina 18 o ¿ z W / / -Z.—' 438,1 [M+H]+ 2-{[1-(4-fluorofenil)-4metil-1 H-1,2,3-triazol5-il]metoxi}-6-[(3S)oxolan-3-carbonil]5,6,7,8-tetrahydro-1,6naftiridina 19 ^O o ~Z- Ά / / z—' O=<^ 408,1 [M+H]+ 6-ciclopropancarbonil2-{[1-(4-fluorofenil)-4metil-1 H-1,2,3-triazol5-il]metoxi}-5,6,7,8tetrahidro-1,6naftiridina 20 nN Y 0 Wn F 435,1 [M+H]+ 2-{[1-(4-fluorofenil)-4metil-1 H-1,2,3-triazol5-il]metoxi}-6-(1,2oxazol-5-carbonyl)5,6,7,8-tetrahidro-1,6naftiridina 21 o / o=¿ 1 465.1 [M+H]+ 4-(2-{[1-(4-fluorophenyl)- 4-methyl-1 H-1,2,3triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-carbonyl)-1methylpyrrolidin-2-one 22 N— / Nf^OY^ 0 TO / . F 410.1 [M+H]+ 1-(2-{[1-(4-fluorofenil)- 4-metil-1H-1,2,3triazol-5-yl]methoxy}5,6,7,8-tetrahydro-1,6- naphthiridin-6-yl)-2metilpropan-1-ona 23 Ny 1 η NOF 500.1 [M+H]+ 4-(2-{[1-(4-fluorofenil)-4-methyl-1H-1,2,3triazol-5-yl]methoxy}5,6,7,8-tetrahydro-1,6- naphthiridin-6-yl)-2 4-metil-1H-1,2,3triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6naphthyridin-6-carbonyl)1lambda6-thian-1,1-dione 24 N^ZN^K.-OYNY'··. <1 wr F 396.3 [M+H]+ 1-(2-{[1-(4-fluorophenyl)- 4-methyl-1H-1,2,3- triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6- naphthyridin-6-yl)propan-1- one 25 o ¿ ~Z- W / / z—' O=¿ \=z 445.4 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(pyridine-4carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 26 o ¿ ~Z- W / / Z—' O=¿ \— z 445.3 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(pyridine-2carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 27 N^-X NüCOyvw 0 WAT, F 478.3 [M+H]+ 6-(3-chlorobenzoyl)-2{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol- 5-yl]methoxy}-5,6,7,8tetrahydro-1,6naphthyridina 28 o ¿ z Ά / / z—' o=¿ 452.1 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(oxan-4carbonyl)-5,6,7,8tetrahydro-1,6naphthyridina 29 o Ά / / -Ζ.—' % 438.1 [M+H]+ 2-{[1-(4-chlorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(oxolan3-carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 30 ,—Ό / ^° ο 452.2 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(oxane-3carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 31 Ν—- / Ν'Ν^'''-'Ογ%ί'χ\] . / °D ^X^n^St-^ o F 452.1 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(3methyloxolan-3carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 32 ΩΌ~ΰζ o ¿ ~Z. Ά / / z—' ο=ζ O 468.2 [M+H]+ 2-{[1-(4-chlorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(oxane-4carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 33 ΩΌ~Ο o ó ~ZW / / z—' O=¿ \=z 461.2 [M+H]+ 2-{[1-(4-chlorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(pyridin-4carbonyl)-5,6,7,8,8-trachydidyne-1,64-naphthyl N— / o ^Co^^QnA F 382,2 [M+H]+ 1-(2-{[1-(4-fluorophenyl)- 4-methyl-1H-1,2,3- triazol-5-yl]methoxy}- 5,6,7,8-tetrahydro-1,7- naphthyridine-7-yl ethanol-35) NOC. / Ox.N, / -^ / ^AN 0 W / Ú F 480.3 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6-(4methoxycyclohexanocarb onyl)-5,6,7,8,3,8,3-trahydro-napht N^Z Nn-.on:. 0 wr Cl 398.1 [M+H]+ 1-(2-{[1-(4-chlorophenyl)4-methyl-1 H-1,2,3triazol-5-yl]methoxy}5,6,7,8-tetrahydro-1,6naphthyridin-6-yl)ethane-1one 37 N^ F NVCoYN ^<F F 513,2 [M+H]+ 2-{[1-(4-fluorofenil)-4metil-1 H-1,2,3-triazol5-il]metoxi}-6-[6- (trifluorometil)piridin-3carbonil]-5,6,7,8tetrahidro-1,6- naftiridina 38 o ¿ z y / / Z—' A 454,1 [M+H]+ 2-{[1-(4-clorofenil)-4metil-1 H-1,2,3-triazol5-il]metoxi}-6-[(3S)oxolan-3-carbonil]5,6,7,8-tetrahidro-1,6naftiridina 39 nNY o n WyO F 445,2 [M+H]+ 2-{[1-(4-fluorofenil)-4metil-1 H-1,2,3-triazol5-il]metoxi}-6-(piridin-3carbonil)-5,6,7,8tetrahidro-1,6naftiridina 40 O Ó,—z z y O 465,2 [M+H]+ (5S)-5-(2-{[1-(4fluorofenil)-4-metil-1 H- 1,2,3-triazol-5il]metoxi}-5,6,7,8- tetrahidro-1,6- naftiridin-6-carbonil)-1- methylpyrrolidin-2-one 41 o <Λ zw / / z—' ο=ζ ^z \ o 465.2 [M+H]+ (5R)-5-(2-{[1-(4fluorophenyl)-4-methyl-1 H- 1,2,3-triazol-5yl]methoxy}-5,6,7,8- tetrahydro-1,6- naphthyridin-6-carbonyl)-1- methylpyrrolidin-2-one 42 N^Z ^^0.^^ Cl 428.1 [M+H]+ 1-(2-{[1-(4-chlorophenyl)- 4-methyl-1H-1,2,3- triazol-5-yl]methoxy}- 5,6,7,8-tetrahydro-1,6- naphthyridin-6-yl)-2- methoxyethan-1-one 43 N^ZN fl o AaAzs, Λ F 479.2 [M+H]+ 1-ethyl-4-(2-{[1-(4-fluorophenyl)-4-methyl-1H- 1,2,3-triazol-5-yl]methoxy}-5,6,7,8-tetrahydro-1,6-naphthyridin-6-carbonyl)pyrrolidin-2-one 44 N^ZN ¢) W / N^ F 493.2 [M+H]+ 4-(2-{[1-(4-fluorofenil)- 4-methyl-1H-1,2,3triazol-5-il]metoxi}- 5,6,7,8-tetrahydro-1,6naftiridin-6-carbonil)-1(propan-2-il)pirrolidin- 2-ona 45 NN^n NAF 368.2 [M+H]+ 1-(2-{[1-(4-fluorofenil)- 4-methyl-1H-1,2,3-triazol-5-il]metoxi}5H,6H,7H-pirrolo[3,4b]piridin-6-il)etan-1-ona 46 NCC^O^N,.^ ^-^0 N II ίΓ I 1 0 ΙΑγ^ F 479,1 [M+H]+ 5-(2-{[1-(4-fluorofenil)- 4-metil-1 H-1,2,3triazol-5-il]metoxi}- 5,6,7,8-tetrahidro-1,6naftiridin-6-carbonil)-1metilpiperidin-2-ona 47 N—Z NOCo-YNyA J> NN 0 U..., 0 F 394,1 [M+H]+ ciclopropil(2-{[1-(4fluorofenil)-4-metil-1 H- 1,2,3-triazol-5il]metoxi}-5,7-dihidro6H-pirrolo[3,4-b]piridin- 6-il)metanona 48 \=== / ~<\ ° o ¿ ~z. Α / / z—' \ zO ,(Z>' O' \ 474.2 [M+H]+ 1-(2-{[3-(4-fluorophenyl)- 5-methyl-1,2-oxazol-4- yl]methoxy}-5,6,7,8- tetrahydro-1,6- naphthyridin-6-yl)-3- methanesulfonylpropan-1- ona 49 ° o ñ z oíS o=«^ o 446.1 [M+H]+ 1-(2-{[3-(4-fluorophenyl)5-methyl-1,2-oxazol-4-yl]methoxy}-5H,6H,7Hpyrrolo[3,4-b]pyridin-6yl)-2-methanesulfonylethane1-one 50 N\jC ON T' ych F 390.1 [M+Na]+ 1-(2-{[3-(4-fluorophenyl)- 5-metil-1,2-oxazol-4-yl]methoxy}-5,7-dihydro- 6H-pyrrolo[3,4-b]pyridin-6-yl)ethanona 51 ou 1 π f ΙΙ ΙΙ 410.1 [M+H]+ 2,2,2-trifluoro-1-(2-{[1(4-fluorofenil)-4-metil1H-1,2,3-triazol-5yl]methoxy}-5,7-dihydro6H-pyrrolo[3,4-b]pyridin6-yl)ethanone 52 o •ί °^Ί 382.1 [M+H]+ 1-(2-{[1-(4-fluorophenyl)4-methyl-1 H-1,2,3- triazol-5-yl]methoxy}-5,7dihydro-6H-pyrrolo[3,4b]pyridin-6-yl)propan-1one 53 N^Z _; ΝΝ'^χ / ΟγΝγ^ >~F 0 F 404.1 [M+H]+ 2,2-difluoro-1-(2-{[1-(4fluorophenyl)-4-methyl-1 H- 1,2,3-triazol-5yl]methoxy}-5,7-dihydro6H-pyrrolo[3,4-b]pyridine- . 6-yl)ethanone 54 o $ ζ Ο^ τι 386.1 [M+H]+ 2-fluoro-1-(2-{[1-(4fluorophenyl)-4-methyl-1 H- 1,2,3-triazol-5yl]methoxy}-5,7-dihydro6H-pyrrolo[3,4-b]pyridine- . 6-yl)ethanone 55 o'''''-) k / L^O ü o 438.1 [M+H]+ 1-(4-fluorophenyl)-4methyl-5-({[6-(oxane-4carbonyl)-5H,6H,7Hpyrrolo[3,4-b]pyridin-2yl]oxy}methyl)-1H-1,2,3triazole 56 N^ZF 410,1 [M+H]+ 1-(2-{[1-(4-fluorophenyl)4-methyl-1 H-1,2,3triazol-5-yl]methoxy}5H,6H,7H-pyrrolo[3,4b]pyridin-6-yl)-3methylbutan-1-one NZ-5-ZO—ZO 408,1 [M+H]+ 5-[({6- cyclobutanecarbonyl5H,6H,7H-pyrrolo[3,4b]pyridin-2-yl}oxy)methyl]1-(4-fluorophenyl)-4- methyl-1 H-1,2,3-triazole 58 N^Z NÑ Z-Z-0 Z-ZOF-0 396,1 [M+H]+ 1-(2-{[1-(4-fluorophenyl)4-methyl-1 H-1,2,3triazol-5-yl]methoxy}5H,6H,7H-pyrrolo[3,4b]pyridin-6-yl)-2methylpropan-1-one 59 N^Z ^Z 40-1 M+H 1-(2-{[1-(4-fluorophenyl)4-methyl-1 H-1,2,3triazol-5-yl]methoxy}5H,6H,7H-pyrrolo[3,4b]pyridin-6-yl)-2,2dimethylpropan-1-one 60 rffY o NA w Cl 384,1 [M+H]+ 1-(2-{[1-(4-chlorofenil)-4-methyl-1 H-1,2,3triazol-5-il]metoxi}-5,7dihydro-6H-pirrolo[3,4b]piridin-6-il)etanona 61 ^NA,,α,-ν^ CO j jlH 0 0 F 424,2 [M+H]+ 1-(4-fluorofenil)-4metil-5-({[6-(oxolan-2carbonil)-5H,6H,7Hpirrolo[3,4-b]piridin-2il]oxi}metil)-1H-1,2,3triazol 62 V\zO o 424,2 [M+H]+ 1-(4-fluorofenil)-4-methyl-5-({[6-(oxolan-3carbonil)-5H,6H,7Hpirrolo[3,4-b]piridin-2il]oxi}metil)-1H-1,2,3triazol 63 Ο-Λ o ft ΟίίγΧΧ0 ^cx 438,2 [M+H]+ 1-(4-fluorofenil)-4-methyl-5-({[6-(oxan-3carbonil)-5H,6H,7Hpirrolo[3,4-b]piridin-2il]oxi}metil)-1H-1,2,3triazol 64 o ñ z 431.2 [M+H]+ 4-(2-{[1-(4-fluorophenyl)4-methyl-1 H-1,2,3triazol-5-yl]methoxy}5H,6H,7H-pyrrolo[3,4b]pyridin-6carbonyl)pyridine 65 oz An xzx 431.2 [M+H]+ 3-(2-{[1-(4-fluorophenyl)4-methyl-1H-1,2,3- triazol-5-yl]methoxy}5H,6H,7H-pyrrolo[3,4b]pyridin-6carbonyl)pyridine 66 ^AA^° ü o 431.2 [M+H]+ 2-(2-{[1-(4-fluorophenyl)4-methyl-1 H-1,2,3triazol-5-yl]methoxy}5H,6H,7H-pyrrolo[3,4b]pyridin-6carbonyl)pyridine 67 .,·-' / Τ' OCos F 368.2 [M+H]+ 1-(2-{[4-(4-fluorophenyl)1-methyl-1 H-1,2,3- triazol-5-yl]methoxy}-5,7dihydro-6H-pyrrolo[3,4b]pyridin-6-yl)ethanone 68 n-nz ZXch Cl 384.1 [M+H]+ 1-(2-{[4-(4-chlorophenyl)- 1-methyl-1 H-1,2,3triazol-5-yl]methoxy}-5,7dihydro-6H-pyrrolo[3,4b]pyridin-6-yl)ethanone 69 o •Í °^Ί 382.1 [M+H]+ 1-(2-{[4-(4-fluorophenyl)1-methyl-1H-1,2,3- triazol-5-yl]methoxy}-5,7dihydro-6H-pyrrolo[3,4b]pyridin-6-yl)propan-1one 70 ll zo JC®, 386.1 [M+H]+ 2-fluoro-1-(2-{[4-(4fluorophenyl)-1-methyl-1 H- 1,2,3-triazol-5yl]methoxy}-5,7-dihydro6H-pyrrolo[3,4-b]pyridin- 6-yl)ethanone 71 ,N~NZ Z'xO XA^O^T, )—1 Λ IA / X ó 0 F 424.2 [M+H]+ 4-(4-fluorophenyl)-1methyl-5-({[6-(oxolan-3carbonyl)-5H,6H,7Hpyrrolo[3,4-b]pyridin-2yl]oxy}methyl)-1H-1,2,3triazole 72 oz 396.1 [M+H]+ 1-(2-{[4-(4-fluorofenil)1-methyl-1 H-1,2,3triazol-5-il]metoxy}5H,6H,7H-pirrolo[3,4-b]piridin-6-il)-2methylpropan-1-ona 73 TOO V / X^O z $ o 'z 'Z± 424.2 [M+H]+ 4-(4-fluorofenil)-1metil-5-({[6-(oxolan-2carbonil)-5H,6H,7Hpirrolo[3,4-b]piridin-2il]oxi}metyl)-1H-1,2,3triazol 74 oz οίίγχχ> 438.2 [M+H]+ 4-(4-fluorofenil)-1methyl-5-({[6-(oxan-3carbonil)-5H,6H,7Hpirrolo[3,4-b]piridin-2il]oxi}methyl)-1H-1,2,3triazol Ejemplo 75 2-{f1-(4-fluorofenil)-4-metil-1H-1,2,3-triazol-5-il]metoxi}-N-(1-metil-5oxopyrrolidin-3-il)-5,6,7,8-tetrahidro-1,6-naftiridin-6-carboxamida To a solution of 284 mg (2.49 mmol) of 4-amino-1-methylpyrrolidine-2-one in 30 mL of anhydrous dichloromethane, 704 mg (0.95 mL, 5.45 mmol) of N,N-diisopropylethylamine were added in one portion, and the reaction mixture was cooled with an ice-water bath, then 296 mg (0.998 mmol) of bis(trichloromethyl)carbonate was added in one portion. The solution thus obtained was stirred for 30 minutes, then 757 mg (2.23 mmol) of 2-{[3-(4-fluorophenyl)-5-methyl-1,2-oxazol-4-yl]methoxy}-5,6,7,8-tetrahydro-1,6-naphthyridine in 10 mL of anhydrous dichloromethane was added dropwise to the reaction mixture while stirring for 5 minutes. The cold bath was removed, and the mixture was allowed to warm to room temperature and stirred for 8 hours. The reaction mixture was washed with saturated sodium bicarbonate solution and water, dried over anhydrous sodium sulfate, and evaporated.The residue obtained was purified by flash column chromatography (silica gel, eluent: 100% DCM ^ 80% DCM: 20% MeOH (35 min)). Yield: 338 mg (32%), white amorphous solid identical to the title compound. MS (ESI) m / z: 480.2 [M+H]+. Table 4 displays compounds synthesized according to Example 75: Ex. MS Structure m / z Name 76 ° ) < o 8 °=( z— / 411.2 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-N,Ndimethyl-5,6,7,8tetrahydro-1,6naphthyridine-6carboxamide 77 N^Z v'Ov 0 F 437.2 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6- (pyrrolidin-1-carbonyl)5,6,7,8-tetrahydro-1,6naphthyridine N^Z ΙΧγΗθ F 453,2 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-N-(oxolan3-yl)-5,6,7,8-tetrahydro1,6-naphthyridine-6carboxamide 79 ! / %» ° \ / ~rz >° / —Z zyo 492.9 [M+H]+ N-(2-chlorophenyl)-2-{[1(4-fluorophenyl)-4-methyl1 H-1,2,3-triazol-5yl]methoxy}-5,6,7,8tetrahydro-1,6naphthyridine-80carboxamide NZ N'N^OYNYX ^oa F 453,2 [M+H]+ 2-{[1-(4-fluorophenyl)-4methyl-1 H-1,2,3-triazol5-yl]methoxy}-6- (morpholine-4-carbonyl)5,6,7,8-tetrahydro-1,6naphthyridine 81 N^Z AON ό ^Ζί-κχ F 492,9 [M+H]+ N-(4-chlorophenyl)-2-{[1(4-fluorophenyl)-4-methyl1 H-1,2,3-triazol-5yl]methoxy}-5,6,7,8tetrahydro-1,6naphthitridine-62amide VK / OvN^ / X zx. N^ ΧτΧ^ΝγΝ^ F 453,1 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(morpholine4-carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 83 / —z CL > 23 oz [M+Na]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-N,N-dimethyl5,6,7,8-tetrahydro-1,6naphthyridine-6carboxamide 84 n0Ca^n.í / -xn\ U^JN n 4Q VΟ, FΟ π [M+H]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(pyrrolidine1-carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 85 OZ—Z ° o ¿ ~Z. Ά / / °=(zo 473.3 [M+H]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-6-(piperidine1-carbonyl)-5,6,7,8tetrahydro-1,6naphthyridine 86 NyjC. yo o F 453,2 [M+H]+ 2-{[3-(4-fluorophenyl)-5methyl-1,2-oxazol-4yl]methoxy}-N-(oxolan-3yl)-5,6,7,8-tetrahydro1,6-naphthyridine-6carboxamide Examples of pharmaceutical preparations The following formulation examples illustrate representative pharmaceutical compositions of this invention. However, the present invention is not limited to these pharmaceutical compositions. (A) Solid oral dosage forms I. Tablets Active ingredients 0.01-90% Filler 1-99.9% Binder 0-20% Disintegrant 0-20% Lubricant 0-10% Other specific excipients 0-50% 100 101 buffering agent qs (D) Other dosage forms VI. Suppositories Active ingredients 0.01-50% Suppository base 1-99.9% Surfactants 0-20% Lubricant 0-20% Preservatives qs VII. Eye Drops Active ingredients 0.01-50% Water 0-99.9% Solvent 0-99.9% Osmotic agent 0-20% Viscosity enhancer 0-20% Buffering agent qs Preservatives qs VIII. Nasal drops or sprays Active ingredients 0.01-50% Water 0-99.9% Solvent 0-99.9% Osmotic agent 0-20% Viscosity enhancer 0-20% Cosolvent qs Buffering agent qs Preservatives qs

Claims

1. A compound of formula (I) FORMULA 1 characterized in that A is represented by a group FORMULA 2, a group FORMULA 3, or a group FORMULA 4, R 1 is hydrogen or halogen, n and m are independently of each other 1 or 2, R 2 is hydrogen; C1-4 alkyl optionally substituted independently with one or more halogen, C1-4 alkoxy, -S(O)2-C1-4 alkyl, or with R 3 ; NR 4 R 5 or R 6 , R 4 and R 5 are independently of each other hydrogen, C1-4 alkyl or R 7 ;or R4 and R5 are taken together with the N to which they are attached to form a saturated or partially unsaturated, monocyclic, bicyclic, fused, bridged or spiral monovalent ring system of 3 to 10 ring atoms, comprising 1, 2, 3 or 4 ring heteroatoms independently selected from N, O and S, the remaining ring atoms being carbon, and R3, R6 and R7 is a (i) optionally substituted monocyclic or bicyclic, fused or bridged monovalent ring system comprising from 3 to 14 ring carbon atoms; (ii) optionally substituted monocyclic, bicyclic, fused, bridged or spiro saturated or partially unsaturated monovalent ring system of between 3 and 10 ring atoms comprising 1, 2, 3 or 4 ring heteroatoms independently selected from N, O and S, the remaining ring atoms being carbon;or (iii) a monovalent, aromatic heterocyclic, optionally substituted mono- or bicyclic ring system of between 5 and 12 ring atoms, comprising 1, 2, 3, or 4 heteroatoms independently selected from N, O, and S, the remaining ring atoms being carbon; and / or salts thereof and / or geometric isomers thereof and / or stereoisomers thereof and / or enantiomers thereof and / or racemates thereof and / or diastereomers thereof and / or solvates thereof and / or hydrates thereof and / or polymorphs thereof. 12 Claims follow;