MXPA06009894A - Sulphonylpyrroles as hdac inhibitors - Google Patents

Abstract

Compounds of a certain formula (l), in which R1, R2, R3, R4, R5, R6 and R7 have the meanings indicated in the description, are novel effective HDAC inhibitors.

Description

SULFONYL PYROLROLES AS INHIBITORS OF DEACETILEASE HISTONES (HDAC) Field of the Invention The invention relates to N-sulfonylpyrrole derivatives, which are used in the pharmaceutical industry for the production of pharmaceutical compositions. Background of the Invention Transcriptional regulation in cells is a complete biological process. A basic principle is the regulation by post-translational modification of histone proteins, that is, histone proteins H2NB, H3 and H4 that form the central complex of histone octameric. These complex N-terminal modifications in the lysine residues by acetylation or methylation and serine residues by phosphorylation are part of the so-called "histone code" (Strahl &Ellis, Nature 403, 41 -45, 2000). In a simple model, the acetylation of positively charged lysine residues reduces the affinity with negatively charged DNA, which now becomes accessible for the input of transcription factors. Acetylation and deacetylation of histone is catalyzed by histone acetyltransferases (HAT) and histone deacetylases (HDAC). HDACs are associated with transcriptional repressor complexes, converting chromatin into a silent, transcriptionally inactive structure (Marks et al., Nature Cancer Rey 1, 194-202, 2001). The opposite is repeated for HATs that are associated with transcriptional activating complexes. So far three classes have been described of HDAC, ie class 1 (HDAC 1 -3, 8) with Mr 42-55 kDa mainly in the nucleus and sensitive with respect to inhibition by Trichostatin A (TSA), class II (HDAC 4-7 9, 1 0) with Mr = 120-130 kDa and sensitivity with respect to TSA and class III (Sir2 homologs) that are quite different due to their dependence on NAD + and no sensitivity to TSA (Ruijter et al., Biochem. J. 370, 737-749, 2003; Khochbin et al., Curr Opin Gen Dey 1 1, 162-166, 2001 Verdin et al., Trends Gen 19, 286-293, 2003). HDAC 1 1 with Mr 39 kDa was recently cloned and showed homology with class I and I I and family members (Gao et al., J Sol Chem 277, 25748-25755, 2002). The HAT and HDAC exist in broad complexes together with the transcription factor and platform proteins in the cells (Fischle et al., Mol Cell 9, 45-47, 2002). Surprisingly, only about 2% of all genes are regulated by histone acetylation (von Lint et al., Gene Expression 5, 245-253, 1 996). New studies with SAHA (suberoylanilide hydroxamic acid) in multiple myeloma cells revealed that these transcriptional changes can be grouped into different classes of functional genes important for the regulation of apoptosis or proliferation (Mitsiades et al., Proc Nati Acad Sci 101, pp 540, 2004). There are substrates other than histone proteins. For HDACs such different substrates include transcription factors such as p53 and TFI I E / or chaperones such as Hsp9O (Johnstone &Licht, Cancer Cell 4, 1 3-18, 2003). Therefore, the correct name for the HDAC would be lysine-specific deacetylase proteins. As a consequence of these findings, HDAC inhibitors effect not only the chromatin structure and genetic transcription but also the stability and function of the protein in regulating the acetylation of the protein in general. This function of HDACs in protein acetylation could also be important to understand the immediate genetic repression by treatment with HDl (von Lint et al., Gene Expression 5, 245-253, 1 996). In this regard, the proteins involved in the oncogenic transformation and the growth of malignant cells are of particular importance. Different publications highlight the importance of histone acetylation for the development of cancer (review by Kramer et al, Trends Endocrin Metabol 12, 294-300, 2001, Marks et al, Nature Cancer Rev 1, 1 94-202, 2001). These diseases include (i) mutations of the binding protein of the response element of the binding protein to the HAT cAMP response element (CBP) associated with the Rubinstein-Taybi syndrome, a carcinogenic predisposition (Murata et al., Hum Mol Genet 10 , 1 071 -1076, 2001); (ii) aberrant recruitment of HDAC 1 activity by transcription factors in acute promyelocytic leukemia (APL) by the fusion gene of the PML-retinoic acid receptor (He et al., Nat. genet. 8, 126-1 35, 1 998 ); (iii) aberrant recruitment of HDAC activity by the protein over-expressed BCL6 in non-Hodgkins lymphoma (Dhordain et al., Nucleic Acid Res 26, 4645-4651, 1998); and, finally, (iv) aberrant recruitment of HDAC activity by the AML-ETO fusion protein in acute myelogenous leukemia (AML subtype M2, Wang et al, Proc Nati Acad Sci USA 95, 0860-1 0865, 1998).

In this subtype AML, the recruitment of HDAC1 activity causally leads to genetic silencing, a block of differentiation and oncogenic transformation. (v) An HDAC1 knockout gene in a mouse revealed that HDAC1 has a profound role in the proliferation of embryonic stem cells by repressing cyclin-dependent kinase inhibitors p21 wafi and p 27k'Pi (Lagger et al., Embo J. 21, 2672-2681, 2002). As p21 waf1 is induced by HDl in many cancer cell lines, HDAC1 could be a crucial component also in the proliferation of cancer cells. SiRNA experiments based on a knock down gene in HeLa cells support this hypothesis (Glaser et al., 31 0, 529-536, 2003). (vi) HDAC2 is overexpressed in colon carcinoma by the constitutive activation of the wnt / β-catenin / TCF signaling pathway due to the loss of the functional protein of adenomatous polyposis colposis (APC) as recently indicated by Zhu et al., (Cancer Cell, 5, 455-463, 2004). At the molecular level, a large number of published data with several HDAC inhibitors such as Trichostatin A (TSA) revealed that many cancer-relevant genes are up-regulated or down-regulated, including p21 CIP 1, Cyclin E, transforming growth factor (TGFβ), p53 or tumor suppressor genes von Hippel-Lindau (VHL) that are up-regulated, whereas Bcl-XL, bcl2, hypoxia-inducible factor ( HI F) 1 a, vascular endothelial growth factor (VEGF) and cyclin A / D are down regulated by inhibition of HDAC (reviewed by Kramer et al., Trends Endocrin Metabol 12, 294-300, 2001). HDAC inhibitors arrest G 1 and G 2 / M cells in the cell cycle and reduce S-phase cells, as indicated for the depsipeptide as an example (Sandor et al., British J Cancer 83, 817-825, 2000) . The inhibitory compounds of HDAC induce independent apoptosis p53 and caspase 3/8 and have broad antitumor activity. Anti-angiogenic activity was also described, which may be related to up-regulation of VEGF and HIF1 a. In summary, the inhibition of HDAC effects tumor cells at different molecular levels and multiple cellular proteins serve as targets. Interestingly, it has been found that HDAC inhibitors induce cell differentiation and this pharmacological activity could also contribute to their anticancer activity. For example, it has recently been shown that suberoylanilide hydroxamic acid (SAHA) induces the differentiation of breast cancer cell lines, exemplified by resynthesis of the milk fat membrane globule protein (MFMG), lipid and milk fat globule protein (Munstery collaborators, Cancer Res. 61, 8492, 2001). There is a growing interest in the synergism of inhibitors HDAC with chemotherapeutics as well as specific drugs for cancer to treat. For example, synergism was shown for SAHA with the kinase / cdk inhibitor flavopiridol (Alemenara et al., Leukemia 1 6, 1 331 -1 343, 2002), for LAQ-824 with the bcr-abl kinase inhibitor Glivec in cells CML (Nimmanapalli et al., Cancer Res. 63, 5126-5135, 2003) and for SAHA and Trichostatin A (TSA) with etoposide (VP16), cisplatin and doxorubicin (Kim et al., Cancer Res. 63, 7291-7300, 2003) and LBH589 with the inhibitor of hsp90 1 7-allyl-amino-demethoxy-geldanamycin (17-AAG; George et al., Blood online, Oct.28, 2004). It was also shown that inhibition of HDAC causes the re-expression of androgen or estrogen receptors in prostate and breast cancer cells with the potential to re-sensitize these tumors for antihormonal therapy (Yang et al., Cancer Res. 60, 6890-6894, 2000; Nakayama et al., Lab Invest 80, 1789-1 796, 2000). HDAC inhibitors of various chemical classes have been described in four major classes, namely (i) hydroxamic acid analogues, (ii) benzamide analogs, (iii) peptolides / cyclic peptides, and (iv) acid analogs fatty. A comprehensive summary of the known HDAC inhibitors was recently published (Miller et al., J Med Chem 46, 5097-51 1 6, 2003). There are only limited published data regarding the specificity of these histone deacetylase inhibitors. In general, most hydroxamate-based HDl are not specific for HDAC class I and I I enzymes. For example, TSA inhibits HDACs 1, 3, 4, 6 and 1 0 with values IC50 of approximately 20 nM, while HDAC8 was inhibited with IC50 = 0.49 μM (Tatamiya et al., AACR Annual Meeting 2004, Abstract # 2451). But these are exceptions such as HDl experimental Tubacin, selective for enzyme H DAC 6 class I I (Haggarty et al., Proc natl Acad Sci USA 1 00, 4389-4394, 2003).

Also, data on the class I selectivity of HDIs of benzamide are emerging. HDAC1 class I and 3 inhibited in MS-275 with IC50 = 0.51 μM and 1.7 μM, respectively. In contrast, HDAC 4, 6, 8 and 10 of class I I were inhibited with IC50 values of > 100 μM, > 1 00 μM, 82.5 μM and 94.7 μM, respectively (Tatamiya et al., AACR Annual Meeting 2004, Summary # 2451). Until now it is not clear if the specificity with respect to the HDAC enzymes of class I or I I or a defined simple isoenzyme should be higher in relation to the index and the therapeutic efficacy. Clinical trials of cancer with HDAC inhibitors are still ongoing, ie with SAHA (Merck Inc.), valproic acid, FK228 / depsipeptide (Gloucester Pharmaceuticals / NCI), MS275 (Berlex-Schering), NVP LBH-589 (Novartis) , PXD-1 01 (Topotarget / Curagen), MGCDO1 03 (Methylgene Inc.) and Pivaloyloxymethylbutyrate / Pivanex (Titan Pharmaceuticals). These studies showed; the first evidence of clinical efficacy, recently highlighted by complete and partial responses with FK228 / depsipeptide in patients with peripheral T-cell lymphoma (Plekarz et al., Blood, 98, 2865-2868, 2001). Recent publications also showed medical use possible of H DAC inhibitors in diseases other than cancer. These diseases include systemic lupus erythematosus (Mishra et al., J Clin Invest 1 1 1, 539-552, 2003, Reilly et al., J. Immunol. 1 73, 4171 -4178, 2004), rheumatoid arthritis (Chung et al., Mol. Therapy 8, 707-717, 2003; Nishida et al.

Arthritis & Rheumatology 50, 3365-3376, 2004), inflammatory diseases (Leoni et al., Proc Nati Acad Sci USA 99, 2995-3000, 2002) and neurodegenerative diseases such as Huntington's disease (Steffan et al., Nature 413, 739-743, 2001 , Hockly et al., Proc NatiAcad Sci USA 1 00 (4): 2041 -6, 2003). Chemotherapy for cancer was established on the basis of the concept that uncontrolled proliferating cancer cells and a high proportion of cells in mitosis are preferably eliminated. Standard chemotherapeutic drugs eventually kill cancer cells under the induction of programmed cell death ("apoptosis") by focusing on basic cellular molecules and processes, ie, RNA / DNA (carbamylation and alkylation agents, platinum analogs and topoisomerase inhibitors), metabolism (drugs of this class are called anti-metabolites) as well as well as the mitotic spindle apparatus (stabilizing and destabilizing the tubulin inhibitors). Histone deacetylase (HDI) inhibitors constitute , a new class of anti-cancer drug with apoptosis-inducing and differentiating activity. By focusing histone deacetylases, the HDl effect acetylation of (protein) histone and chromatin structure, inducing a complex transcriptional reprogramming, exemplified by reactivation of tumor suppressor genes and repression of oncogenes. In addition to acetylation of N-terminal lysine residues in central histone proteins, there are targets not directed to histone that are important for the biology of cancer cells such as heat shock protein 90 (Hsp9O) or tumor suppressor protein p53 . The medical use of HDl may not be restricted to cancer therapy, since the efficacy in models for inflammatory diseases, rheumatoid arthritis and neurodegeneration was revealed. Prior Art The pyrrolylpropenamides substituted by acetyl or benzoyl have been described as HDAC inhibitors, while the connectivity of the acyl group is in the 2 or 3 position of the pyrrole structure. (Mai et al., Journal Med. Chem. 2004, Vol. 47, No. 5, 1 098-1 109). Other hydroxamic acid derivatives substituted by pyrrolyl are described in US 4,960,787 as lipoxygenase inhibitors or in the US 6,432,999 as cyclo-oxygenase inhibitors. Several compounds, which are established as HDAC inhibitors, are described in WO 01/38322; Journal Med. Chem. 2003, Vol. 46, No. 24, 5097-51 16; Journal Med. Chem. 2003, Vol. 46, No. 4, 512-524; Journal Med. Chem. 2003, Vol, 46, No. 5, 820-830; and in Current Opinion Drug Discovery 2002, Vol. 5, 487-499. In the art, the need for new and more efficient HDAC inhibitors continues. Description of the Invention It has been found that the N-sulfonylpyrrole derivatives, which are described in detail below, differ profoundly from the compounds of the prior art and are effective inhibitors of histone deacetylases and have surprising and particularly advantageous properties. Therefore, the invention is related, in a first aspect (aspect 1), with the compounds of formula 1 wherein R 1 is hydrogen, C 1-4 alkyl, halogen, or C 1-4 alkoxy, R 2 is hydrogen or C 1-4 alkyl, R 3 is hydrogen or C 1-4 alkyl, R 4 is hydrogen, C 1-4 alkyl, halogen, or alkoxy C1-4, R5 is hydrogen, C1-4alkyl halogen, or C1-4alkoxy, R6 is -T1-Q1, wherein T1 is a bond, or C1-4alkylene, Q1 is Ar1, Aa1, Hh1, or there wherein Ar1 is phenyl, or phenyl substituted by R61 and / or R62, wherein R61 is C1-4 alkyl, or -T2-N (R611) R612, wherein either T2 is a bond, and R611 is hydrogen, alkyl C1-4, C2-4 hydroxyalkyl, C1-4 alkyl alkoxy C2-4, phenylalkyl C1-4, or Har1-C1-4alkyl, wherein Har1 is optionally substituted by R6111 and / or R6112, and is a 5 to 10 membered unsaturated monocyclic or bicyclic unsaturated heteroaromatic ring comprising one to three heteroatoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, wherein R6111 is halogen, or C1-4alkyl, R6112 is C1-4alkyl, and R612 is hydrogen, C1-4alkyl, C1alkoxy -4alkylC2-4 or C2-4 hydroxyalkyl, or R611 and R612 together or with the inclusion of the nitrogen atom, to which they are linked form a heterocyclic ring Het1, wherein Het1 is morpholino, thiomorpholino, S-oxo-iiomorpholino, S, S-dioxo-fiomorpholino, piperidino, pyrrolidino, piperazino, or 4N- (C 1-4 alkyl) -piperazino, or T 2 is C 1-4 alkylene, or C 2-4 alkylene interrupted by oxygen, and R 61-1 is hydrogen, C 1-4 alkyl, C 2-4 hydroxyalkyl, C 1-4 alkyloxy C 2-4 alkyl, phenylalkyl C 1-4, or C 1-4 alkyl, wherein C 1-4 optionally is susíiido by R6111 and / or R6112, and is a ring 5 to 10 members monocyclic or fused bicyclic heieroaromatic inssare comprising one to heferoatomos, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, where R61 1 1 is halogen, or C 1-4 alkyl, R61 12 is C 1-4 alkyl, and R 612 is hydrogen, C 1-4 alkyl, C 1-4 alkyloxyC 2-4 alkyl or C 2-4 hydroxyalkyl, 5 or R61 1 and R 612 in conjugated form or with the inclusion of the nihologen atom, to which they are linked they form a heterocyclic ring He1, wherein He1 is morpholino, iomorpholino, S-oxo-iiomorpholino, S, S-dioxo-iiomorpholino, piperidino, pyrrolidino, piperazino, 4N- ( C 1-4 alkyl) -10 piperazino, imidazole, pyrrolo or pyrazolo, R 62 is C 1-4 alkyl, C 1-4 alkoxy, halogen, cyano, C 1-4 alkyloxy C 1-4 alkyl, C 1-4 alkylcarbonylamino, or alkylsulfonylamino C1-4, Aa1 is a bisaryl radical formed by two aryl groups, which are independently selected from a group consisting of phenyl and Naphtyl, and which are linked by a single bond, Hh 1 is a bis-hepheraloyl radical formed by two hepheroaryl groups, which are independently selected from a group consisting of 5 or 6 monocyclic heteroaryl radicals comprising one or two heteroarylanes , each of which is selected from the group which consists of nitrogen, oxygen and sulfur, and which are joined by a single bond, Ah i is a heteroaryl radical or aryl-heteroaryl radical formed by a heteroaryl group selected from the group consisting of 5 or 6 monocyclic monoaryl radicals which they comprise one or two . heir workers, each of whom is selected from the group consists of nitrogen, oxygen and sulfur, and an aryl group selected from the group consisting of phenyl and naphthyl, wherein such aryl and heteroaryl groups are attached via a single bond, R7 is hydroxyl, or Cyc1, wherein Cyc1 is a formula ring wherein A is C (carbon), B is C (carbon), R71 is hydrogen, halogen, C 1-4 alkyl, or C 1-4 alkoxy, R 72 is hydrogen, halogen, C 1-4 alkyl, or C 1-4 alkoxy , M including A and B is either an Ar2 ring or a Har2 ring, where Ar2 is a benzene ring, Har2 is a monocyclic 5 or 6 membered unsaturated heieroaromatic ring comprising one to three heteroatoms, each of which is selected from the group consisting of nifrogen, oxygen and sulfur, and the salts of compound esimos. The invention relates, in a second aspect (aspect 2), to the compounds of the formula I, wherein R 1 is hydrogen, C 1 -4 alkoxy, halogen, or C 1 -4 alkoxy, R 2 is hydrogen or C 1-4 alkyl, R 3 is hydrogen or C 1-4 alkyl, R 4 is hydrogen, C 1-4 alkyl, halogen, or C 1-4 alkoxy, R 5 is. hydrogen, C1-4alkyl, halogen, or C1-4alkoxy, R6 is -T1-Q1, wherein T1 is a bond, or C1-4alkylene, Q1 is Ar1, Aa1, Hh1, or Ahi, where Ar1 is phenyl, or phenyl substituted by R61 and / or R62, wherein R61 is C1-4alkyl, or -T2-N (R611) R612, wherein T2 is a bond, C1-4alkylene, or C2-4alkylene uninterrupted by oxygen, R611 is hydrogen, C1-4 alkyl, C2-4 hydroxyalkyl, C1-4 alkyl alkoxy C2-4, phenylalkyl C1-4, or Har1-C1-4alkyl, wherein Har1 is optionally substituted with R6111 and / or R6112, and is a 5 to 10 membered monocyclic or bicyclic fused ring comprising one to three Each of which is selected from the group consisting of nitrogen, oxygen and sulfur, wherein R6111 is halogen, or C1-4 alkyl, R6112 is C1-4 alkyl, R612 is hydrogen, C1-4 alkyl, C1-6 alkoxy, 4C2-4alkyl or hydroxyalkyl C2-4, R62 is C1-4 alkyl, C1-4 alkoxy, halogen, cyano, C1-4 alkyloxy C1-4, C1-4 alkylcarbonylamino, or C1-4 alkylsulfonylamino, Aa1 is a bisaryl radical formed by two aryl groups, which independently selected from the group consisting of phenyl and naphtyl, and which are linked by a single bond, Hh 1 is a bis-heeroaryl radical consisting of two heteroaryl groups, which are independently selected from a group consisting of monocyclic 5-arylaryl radicals; 6 members comprising one or two heyerogens, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, and which are joined by a single bond, is a heteroaryl-aryl radical or an aryl-heteroaryl radical. formed by a heteroaryl group selected from a group consisting of 5- or 6-membered monocyclic heyeroaryl radicals comprising one or two heteroaryne, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, and an aryl group which is selected from the group selected from a group consisting of phenyl and naphthyl, wherein such aryl and heeroaryl groups are linked by a bond if mple, R7 is hydroxyl, or C and d, wherein Cyc1 is a ring system of the formula wherein A is C (carbon), B is C (carbon), R71 is hydrogen, halogen, C 1-4 alkyl, or C 1-4 alkoxy, R 72 is hydrogen, halogen, C 1-4 alkyl, or C 1-4 alkoxy, M including A and B is either an Ar 2 ring or a Har 2 ring, where Ar 2 is a benzene ring, Har 2 is a ring A monoecyclic 5 or 6 member monoecyclic heyeroaromatic comprising one of two heteroaryl groups, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, and the salts of compound compounds. The C 1-4 alkyl represents a straight or branched chain alkyl radical having 1 to 4 carbon atoms. Examples are the buíilo, isobuilo, sec-buíilo, íerc-buíilo, propilo, isopropilo and preferably radicals éíilo and meíilo. The C2-4 alkyl represented a straight or branched chain alkyl radical having 2 to 4 carbon atoms. Examples which may be mentioned are bufyl, isobuyl, sec-buyl, urea-buyl, propyl, isopropyl and preferably ethylene and me yl radicals. The C1-4 alkylene is a branched or straight chain alkylene radical having from 1 to 4 carbon atoms. Examples that may be mentioned are the methylene radical (-CH2-), ethylene (-CH2- CH2-), trimeyylene (-CH2-CH2-CH2-) and the tetramethylene (-CH2-CH2-CH2-CH2-). The C2-4 alkylene interrupted by oxygen represented a straight chain alkylene radical having 1 to 4 carbon atoms which is suitably interrupted by an oxygen atom such as example, the radical [-CH2-CH2-O-CH2-CH2-]. C 1 -4 alkoxy represents radicals which, in addition to the oxygen atom, contain a straight or branched chain alkyl radical having from 1 to 4 carbon atoms. Examples which may be mentioned are buioxy, isobutoxy, sec-butoxy, tert-buzoxy, propoxy, iopropoxy and preferably the ethoxy and methoxy radicals. The C 1-4 alkoxy C 1-4 alkyl represents one of the aforementioned C 1-4 alkyl radicals, which are substituted by one of the aforementioned C 1-4 alkoxy radicals. Examples which may be mentioned are the methoxymethyl, methoxy-yl and isopropoxy-yl radicals, particularly the 2-methoxy-yl and 2-isopropoxy-yl radicals. C 1-4 alkoxy C 2-4 alkyl represented one of the abovementioned C 2-4 alkyl radicals which are substituted by the abovementioned C 1-4 alkoxy radicals. Examples which may be mentioned are the radicals meioxieíilo, eioxieíilo and isopropoxieíilo, pariicularmente the radicals 2-meioxieiilo, 2-eioxieíilo and 2-isopropoxieíilo. The C2-4 hydroxyalkyl represented one of the aforementioned C2-4 alkyl radicals, which are substituted by C2-4 alkyl radicals, which is substituted by a hydroxy radical. An example that can be mentioned is the 2-hydroxyethyl or 3-hydroxypropyl radical. The phenyl C 1-4 alkyl represented one of the aforementioned C 1-4 alkyl radicals, which is supported by a radical phenyl radical. Examples that can be mentioned are benzyl radicals and phenethyl. The halogen within the meaning of the invention is bromine or, in particular, chlorine or fluorine. The C 1 -4 alkylcarbonyl represented a radical which, in June with the carbonyl group, contains one of the abovementioned C 1-4 alkyl radicals. An example that can be mentioned is the acetyl radical. The C 1-4 alkylcarbonylamino represented an amino radical which is supported by one of the C 1-4 alkylcarbonyl radicals. An example that can be mentioned is the radical aceiamide [CH3C (O) -NH-]. The C1-4 alkylsulfonylamino is, for example, the propylsulfonylamino radical [C3H7S (O) 2NH-], the alkylsulfonylamino [C2H5S (O) 2NH-] and the methylsulfonylamino [CH3S (O) 2NH-]. Aa1 is a bisaryl radical formed by two aryl groups, which are independently selected from the group consisting of phenyl and naphtyl, and which are linked by a single bond. Aa1 may include the biphenyl radical, for example the radical 1, 1 '-bifen-4-yl or 1,1' -bifen-3-yl, without being limited thereto. Hh 1 is a bis-heeroaryl radical formed by two heteroaryl groups, which are independently selected from a group consisting of monocyclic 5-or 6-membered heteroaryl radicals comprising 1 or 2 heteroaryne moieties, each of which is selected from the group consisting of in niírógeno, oxygen and sulfur, and that are united by a simple bond. Hh 1 can include biphenyl, bipyridyl, pyrazolyl-pyridinyl radical (particularly pyrazol-1-pyridinyl), imidazo I-pyridinyl (particularly imidazol-1-pyridinyl) or pyridinyl-iiophenyl, for example, the 5- (pyridin-2-yl) -iiophen-2-yl radical, without being limited thereto. In particular, exemplified Hh 1 radicals may include pyridinyl-phenyl phenyl, for example 5- (pyridin-2-yl) -iiophen-2-yl. There is a heteroarylaryl radical or an aryl heteroaryl radical formed by a heteroaryl group selected from the group consisting of 5 or 6 membered monocyclic heyeroaryl radicals comprising one or two heteroaryne, each of which is selected from the group consisting of nihinogen , oxygen and sulfur, and an aryl group selected from the group consisting of phenyl and naphtyl, wherein the heteroaryl and aryl groups are attached by a single bond. The Ahl radical can be linked either through the heyaroaryl medians or through the aryl fraction to the parental molecular group. A particular modality of radical fales Ah se refers to free radicals, for example, 3- (heieroaryl) -phenyl or 4- (heeroaryl) -phenyl radicals. It may include phenyl-phenyl or phenyl-pyridyl radicals, without being limited thereto. Alternatively, it may include the furanylphenyl, pyrazolyl-phenyl radicals (for example pyrazol-1-phenyl-phenyl or 1 H-pyrazol-4-ylphenyl), imidazolyl-phenyl (e.g. imidazol-1-pyl) phenyl) or pyridinyl phenyl, without being limited thereto. In particular, exemplified Ah radicals may include 3- (pyrazol-1-yl) -phenyl, 4- (pyrazolyl) -phenyl, 4- (pyridinyl) -phenyl or 3- (pyridinyl) -phenyl. In particular, exemplified Ah radicals can include 3- (pyrazol-1-yl) -phenyl, 4- (p-razol-1-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, - (pyridin-4-yl) -phenyl, 4- (pyridin-3-yl) -phenyl, 3- (pyridin-3-yl) -phenyl, 3- (1 H -pyrazol-4-yl) -phenyl or 4- (1 H-pyrazol-4-yl) -phenyl. It should be clarified that each of the radicals Hh 1 and Ah 1 are preferably linked by a ring of carbon atom to the Ti moiety. Har1 is optionally substituted by R61 1 1 and / or R61 12, and is a 5- to 10-membered monocyclic or bicyclic unsaturated heteroaryl (heteroaromatic) radical comprising one to three hetero-atoms, each of which is selected from the group consisting of It consists of niigogen, oxygen and sulfur. The following should be mentioned fused hephenoaryl radicals, in particular bicyclic 9- or 10-membered benzo-fused members comprising one to three, in particular one or two, hetero-axons, each of which is selected from the group consisting of nihorogen, oxygen and sulfur. Examples of Har1 include thiophenyl, furanyl, pyrrolyl, oxazolyl, isoxazolyl, pyrazolyl, imidazolyl, thiazolyl, isothiazolyl, triazolyl, oxadiazolyl, thiadiazolyl, pyridinyl, pyrimidinyl, pyrazinyl or pyridazinyl; and, in particular, the stable benzo-fused derivatives thereof, such as, for example, benzothiophenyl, benzofuraryl, indolyl, benzoxazolyl, benzothiazolyl, indazolyl, benzimidazolyl, benzisoxazolyl, benzisothiazolyl, benzofurazaryl, quinolinyl, isoquinolinyl, quinazolinyl, quinoxalinyl, phthalazinyl or cinolinyl; and purinyl, indolizinyl, naphthyridinyl or pteridinyl, without limiting oneself to the same. In particular, the exemplified Har1 radicals may include pyridinyl, benzimidazolyl, benzoxazolyl, benzofuraryl, benzofiofenyl and indolyl, eg, as pyridin-2-yl, pyridin-3-yl, pyridin-4-yl, benzimidazol-2-yl. , benzoxazol-2-yl, benzofuran-2-yl, benzofuran-3-yl, benzothiophen-2-yl, benzoyiophen-3-yl, indole-2-yl, indole-3-yl or indole-5-yl. In still more special detail, an exemplified Har1 radical can be indolyl, such as, for example, indole-2-yl, indole-3-yl or indole-5-yl. In still more special detail, an exemplified Har1 radical can be pyridinyl, eg as pyridin-2-yl, pyridin-3-yl, or pyridin-4-yl. As further examples of Har1, there may be mentioned the R61 1 1 - and / or R61 12 -substituted derivatives of the aforementioned exemplified Har1 radicals. The Har1-C1-4alkyl represented one of the above-mentioned C1-4alkyl radicals, such as, for example, methyl, ethyl or propyl, suspended by one of the aforementioned Har1 radicals, such as imidazolyl, benzimidazolyl, indolyl or pyrrolyl and the like or derivative thereof thereof. As examples, there may be mentioned pyridinylmethyl (for example pyridin-3-yl-metyl), midazolylmeiyl, pyrrolylmefyl, 2-imidazolyleryl (for example, 2-imidazol-5-yl-efyl), 2-pyridinylelyl, 3- (benzofuran-Q) -yl) propyl, 3- (benzimidazol-2-yl) propyl, 2-indolylelyl (for example, 2-indol-2-yl-eyl or 2-indol-3-yl-yl), indolylmelyl (for example, indole -2-il-meityl, indol-3-yl-meityl or indole-5-yl- methyl), 2-benzimidazoylylyl (for example 2-benzimidazol-2-yl-eyl), benzimidazolylmelyl (for example benzimidazol-2-yl-metyl) and the like. In particular, the Har1-C 1 -4 -alkyl radicals exemplified may include pyridinylmethyl (for example pyridin-3-yl-meiyl, pyridin-4-ylmethyl or pyridin-4-yl-meityl), 2-pyridinylelyl ( example 2-pyridyl-3-yl-ethyl), indolylmephyl (for example indole-2-ylmethyl, indole-3-ylmethyl or indole-5-ylmethyl) or 2-indolenyl (eg 2- indolyl-2-yl-eyl or 2-indolyl-3-yl-eyl). In still more special detail, the exemplified Har1-C1-4 alkyl radicals may include pyridin-3-yl-methyl, pyridin-4-yl-methyl, 2-pyridin-3-yl-ethyl, indol-2-yl-methyl indol-3-yl-methyl, indol-5-yl-methyl, 2-indolyl-2-yl-eyl or 2-indolyl-3-yl-ylyl. In the context of the Har1-C1-4 alkyl radical, it should be mentioned that the Har1 portion is preferably linked by a carbon atom ring to the C1-4 alkyl moiety. One embodiment of the radicals Har1-C1-4alkyl, wherein the fraction of Har1 is a fused bicyclic ring containing a benzene ring, refers to those radicals, wherein the fraction of Har1 is preferably linked to the fraction of C1-4 alkyl by a ring of ring carbon atom comprising one or more heteroatoms. Another embodiment of the Har1-C 1-4 alkyl radicals, wherein the Har 1 moiety is a fused bicyclic ring containing a benzene ring, refers to the radicals wherein the Har 1 moiety is preferably linked to the C-alkyl moiety. 1-4 for a ring carbon atom of the benzene ring. Har2 represents a 5 or 6 membered monocyclic unsaturated heteroaromatic ring comprising one to three heteroatoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur. Har2 may include thiophene, oxazole, isoxazole, thiazole, isothiazole, imidazole, pyrazole, iazole, fiadiazole, oxadiazole, pyridine, pyrimidine, pyrazine or pyridazine, without being limited thereto. In particular, an exemplified Har2 radical can be pyridine. C and d represents a ring system of formula la, which is linked to the nihologen atom of the carboxamide group by fraction A. C and d can include 2-aminophenyl suspended by R71 and / or R72, without being limited thereto. as part of a group, it includes naphthalene-1-yl and nafialen-2-yl. In the meaning of the present invention it should be understood that when two structural portions of the compounds according to this invention are joined by a constituent which has the meaning "link", then the two parts are directly linked to each other by a simple link. In general, unless the conirare is indicated, the heyerocyclic groups mentioned in the present report refer to all possible isomeric forms. The heyerocyclic groups mentioned in the present reference, unless otherwise indicated, in particular to all Possible positional isomers of it. Thus, for example, the term "pyridyl" or "pyridinyl", alone or as part of another group, includes pyridin-2-yl, pyridin-3-yl and pyridin-4-yl. The constituents that are optionally substituted as set forth in the present may be suspended, unless otherwise indicated, in any possible position. The carbocyclic groups, alone or as part of other groups, mentioned herein may be replaced by their parent or substituted molecular groups, unless otherwise indicated, in any ring of carbon atom that is susíituible. The heterocyclic groups, alone or as part of other groups, mentioned herein, may be substituted by their given subsides or parental molecular groups, unless otherwise indicated, in any possible position, such as, for example, any ring. carbon atom or ring of niígeno atom susíifuible. The rings conforming ring of nickel atoms of the magnetizable (-N =) type may be preferably not quaternized in these rings of the nihinogen shaft of the imino type by the mentioned parent or silicon molecular groups. It is assumed that any heyeroatome of a heyerocyclic ring with unsubstantiated valencies mentioned in the present has the hydrogen atom (s) to satisfy the valences. When a variable occurs more than once in any case, each definition is independent.

Suitable salts for the compounds of the formula I - depending on the substitution - are all acid addition salts or salts with bases. Particular mention should be made of the pharmacologically and inorganic organic acids that can be used and bases usually used in pharmacy. Suitable are the acid addition salts, on the one hand, insoluble in water, and, in particular, soluble in water, with natural acids such as, for example, hydrochloric acid, hydrobromic acid, phosphoric acid, nitric acid, sulfuric acid, acetic acid, citric acid, D-gluconic acid, benzoic acid, 2- (4-hydroxybenzoyl) benzoic acid, bufiric acid, sulfosalicylic acid, maleic acid, lauric acid, malic acid, fumaric acid, succinic acid, oxalic acid, taric acid , embonic acid, esophalic acid, foluenesulfonic acid, methane sulphonic acid, or 3-hydroxy-2-naphioic acid. Such acids are used in the preparation of the salt, depending on whether a mono- or polybasic acid is used and, depending on the desired salt, in an equimolar quantity or difference. On the other side, the salts with bases, according to the susíiíución, are also suitable. Examples of salts with bases are the salts of lithium, sodium, potassium, calcium, aluminum, magnesium, typhonium, ammonium, meglumine or guanidinium, here also the bases are used in the preparation of the salt in equimolar quantitative proportion or difference . The pharmacologically undesirable salts, which can be obtained, for example, as process products during the preparation of the compounds according to the invention on an industrial scale, are converted into pharmacologically tolerable salts by means of. processes known to the person skilled in the art. According to the knowledge of the person skilled in the art, the compounds of the invention as well as their salts may contain, for example, when they are isolated in crystalline form, different amounts of solvents. All the solvates and, in particular, all the hydraions of the compounds of formula 1 as well as all the solvates and in particular all the hydraions of the salts of the compounds of formula I are included within the scope of the invention. . Substitutes R61 and R62 of the compounds of formula 1 can be attached in the ortho, me, or para position with respect to the linkage position in which the phenyl ring is bound to T1, where preference is given to binding in position meía, paríicularmenie, in the position for. In another mode, Ar1 is phenyl which is mono-substituted by R61, wherein preference is given to the binding of R6I in the meta or para position with respect to the bonding position in which the phenyl ring is linked to T1. In yet another embodiment, Ar1 is phenyl which is mono-substituted by R61, where preference is given to the binding of R61 in the para position with respect to the linking position where the phenyl ring is linked to T1. In yet another embodiment, Ar1 is phenyl which is mono-substituted by R61, where preference is given to the binding of R61 in the meta position with respect to the linking position where the phenyl ring is linked to T1. Compounds according to the aspect 1 of the present invention which is important to mention are the compounds of formula 1 wherein R 1 is hydrogen, or C 1-4 alkyl, R 2 is hydrogen, or C 1-4 alkyl, R 3 is hydrogen, or alkyl C1-4, R4 is hydrogen, or C1-4 alkyl, R5 is hydrogen, or C1-4 alkyl, R6 is -T1-Q1, wherein • T1 is a bond, or C1-4 alkylene, Q1 is Ar1, Aa1 , Hh1, or there, wherein Ar1 is phenyl, or R61-substituted phenyl, wherein R61 is C1-4 alkyl, or -T2-N (R611) R612, wherein either T2 is a bond, R611 is hydrogen, C1-4alkyl, phenylalkyl C1-4, or Har1-C1-4alkyl, wherein Har1 is either a 5-membered monocyclic monocyclic ring comprising one, two or more heteroaryne atoms, each of which is selected from the group which consists of niógeno, oxygen and sulfur, or a 6-membered monocyclic monocyclic iron ring comprising one or two nitrogen atoms, or a heyeroaromatic ring or 9-member merged bicyclic inssauri comprising one, two or more heteroatoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, or a fused bicyclic heyeroaromatic ring of 1 0 members comprising one or two heteroerobes, each of which it is selected from the group consisting of nitrogen, oxygen and sulfur, and R612 is hydrogen, C1-4 alkyl, or C2-4 hydroxyalkyl, or R61 1 and R612 together and including the nihologen atom to which they are bonded, form a heterocyclic ring Het1, wherein He1 is morpholino, T2 is C1-4alkylene, R611 is hydrogen, C1-4alkyl, phenylalkyl C1-4, or Har1-C1-4alkyl, wherein Har1 is either a 5-membered monocyclic monocyclic iron ring comprising one, two or Heteropathogens, each of which is selected from the group consisting of nihologen, oxygen, and sulfur, or a monocyclic 6-membered unsaturated monocyclic ring comprising one or two nitrogen atoms, or a 9-membered unsaturated bicyclic unsaturated heteroaromatic ring it comprises one, two or three hetero-atoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, or an unsaturated, bisected, bicyclic, 1-membered ring comprising one or two heteroaryne, each of which is selects from the group consisting of niógeno, oxygen and sulfur, and R612 is hydrogen, C1-4 alkyl, or C2-4 hydroxyalkyl, or R611 and R612 together or with the nitrogen atom, to which they are linked, form a heterocyclic ring Het1, where Het1 is morpholino, Aa1 is a biphenyl radical , Hh1 is a bipyridyl, pyrazolyl-pyridinyl, imidazolyl-pyridinyl or pyridinyl-thiophenyl radical, there is a pyridinyl-phenyl, pyrazolyl-phenyl, or imidazolyl-phenyl radical, R7 is hydroxyl, or 2-aminophenyl, and the salts of compound esters. Compounds according to the aspect 2 of the present invention which is more important to mention are the compounds of formula I wherein R 1 is hydrogen, or C 1-4 alkyl, R 2 is hydrogen, or C 1-4 alkyl, R 3 is hydrogen, or C1-4 alkyl, R4 is hydrogen, or C1-4 alkyl, R5 is hydrogen, or C1-4 alkyl, R6 is -T1-Q1, where T1 is a bond, or C1-4 alkylene, Q1 is Ar1, or Aa1, wherein Ar1 is phenyl, or R61-substituted phenyl, wherein R61 is C1-4alkyl, or -T2-N (R611) R612, wherein T2 is a bond, or C1-4alkylene, R611 is hydrogen, C1-4alkyl, or Har1-C1-4alkyl, wherein Har1 is imidazolyl, benzimidazolyl, indolyl or pyrrolyl, R612 is hydrogen, or C1-4alkyl, Aa1 is a biphenyl radical, R7 is hydroxyl, or 2-aminophenyl, and the salts of compounds. The compounds according to aspect 1 of the present invention which are particularly important to mention are the compounds of formula I wherein R 1 is hydrogen, R 2 is hydrogen, R 3 is hydrogen, R 4 is hydrogen, R 5 is hydrogen, R 6 is-T 1 -Q!, Aa1, Hh1, or A, where T1 is a bond, or alkylene C1-2, Q1 is Ar1, where Ar1 is phenyl, or phenyl R61-susitute; wherein R61 is C1-4alkyl, or -T2-N (R611) R612, wherein either T2 is a bond, R611 is hydrogen, C1-4alkyl, phenylalkyl C1-2, or Har1-C1-2alkyl, wherein Har1 is pyridinyl, benzimidazolyl, benzoxazolyl, benzofuraryl, benzoyl phenyl or indolyl, and R612 is hydrogen, C1-4 alkyl, or C2-3 hydroxyalkyl, or R61 1 and R612 together and including nitrogen atom, to which they are bonded, form a heterocyclic ring He1, wherein He1 is morpholino or T2 is C1-2alkylene, R611 is hydrogen, C1-4alkyl, phenylalkyl C1-2, or Har1-C1-2alkyl, wherein Har1 is pyridinyl, benzimidazolyl, benzoxazolyl, benzofuranyl benzoyiophenyl or indolyl, and R612 is hydrogen, C1-4alkyl, or C2-3 hydroxyalkyl, or R61 1 and R612 together and including the nihologen atom to which they are bonded form a heterocyclic ring He1, wherein He1 is morpholino, Aa1 is a biphenyl radical, Hh1 is a bipyridyl, pyrazolyl-pyridinyl, imidazolyl-pyridinyl or pyridinyl-iiophenyl radical, there is a pyridinyl-phenyl radical, pyrazolyl-phenyl, or imidazolyl-phenyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of compound compounds . The compounds according to aspect 2 of the present invention which deserve to be mentioned in particular are the compounds of formula I wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1-Q1, or biphenyl, where T1 is a bond, or C1-2 alkylene, Q1 is Ar1, wherein Ar1 is phenyl, or phenyl R61-susiiuuide, wherein R61 is C1-4 alkyl, or -T2-N (R611) R612, wherein T2 is a bond, or C1-2 alkylene, R611 is C1-4 alkyl, or Har1-1-C1-2alkyl, wherein Har1 is benzimidazolyl or ndolyl, R612 is C1-4alkyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of compound esters. Compounds according to the aspect 1 of the present invention which are more particularly indestructible of desfacar are the compounds of formula I wherein R 1 is hydrogen, R 2 is hydrogen, R 3 is hydrogen, R 4 is hydrogen, R 5 is hydrogen, R6 is -T1-Q1, Aa1, Hh1, Ahi, or benzyl, wherein T1 is a bond, Q1 is Ar1, where Ar1 is phenyl, or phenyl R61-substituted, wherein R61 is C1-4 alkyl, or - T2-N (R611) R612, wherein either T2 is a bond, R611 is C1-4alkyl, and R612 is C1-4alkyl, or T2 is C1-2alkylene, R611 is hydrogen, C1-4alkyl, phenylalkyl C1-2, or Har1-C1-2 alkyl, wherein Har1 is pyridinyl, or indolyl, and R612 is hydrogen, C1-4alkyl, or C2-3 hydroxyalkyl, or R611 and R612 together and including the nitrogen atom at which are linked, form a hei-cyclic ring Hei1, where Het1 is morpholino, Aa1 is 1,1'-bfen-4-yl or 1, 1 '-bifen-3-yl, Hh1 is a pyridinyl-thiophenyl radical, There it is a 3- (pyridinyl) -phenyl, 3- (pyrazolyl) -phenyl, 4- (pyridinyl) -phenyl or 4- (pyrazolyl) -phenyl radical, R 7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. The compounds according to aspect 2 of this invention which are more particularly interesting to note are the compounds of formula I wherein R 1 is hydrogen, R 2 is hydrogen, R 3 is hydrogen, R 4 is hydrogen, R 5 is hydrogen, R 6 is-T 1 -Q 1, biphenyl, or benzyl, wherein T1 is a bond, Q1 is Ar1, where Ar1 is phenyl R61 -substituted, in parficular 4- (R61) -phenyl where R61 is methyl, dimethylamino, o-T2-N (R61 1) R612, wherein T2 is methylene, R61 1 is methyl or 2- (indol-2-yl) etyl, R612 is methyl, R7 is hydroxyl, or 2- aminophenyl, and the salts of these compounds. The compounds according to the aspect 1 of the present invention more particularly important to emphasize are the compounds of formula 1 wherein, R 1 is hydrogen, R 2 is hydrogen, R 3 is hydrogen, 3 R4 is hydrogen, R5 is hydrogen, R6 is -T1-Q1, Aa1, Hh1, Ahy, or benzyl, where T1 is a bond, Q1 is Ar1, where Ar1 is phenyl, 3- (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is methyl, or -T2-N (R611) R612, wherein either T2 is a bond, R611 is methyl, and R612 is methyl, or T2 is methylene, R611 is hydrogen , meiyl, isobuyl, benzyl, Har1-methyl, or 2 (Har1) -yloyl wherein Har1 is pyridinyl or indolyl, and R612 is hydrogen, meiyl, or 2-hydroxy-ethyl, or R611 and R612 together and including the atom of nihologen, to which they are bonded, form a heterocyclic ring He1, where Het1 is morpholino, A1a is 1, 1'-bifen-4-yl or 1,1'-bifen-3-yl, Hhl is a pyridinyl radical iiophenyl, there is a 3- (pyridinyl) -phenyl, 3- (pyrazolyl) -phenyl, 4- (pyridinyl) -phenyl or 4- (pyrazolyl) -phenyl radical, R 7 is hydroxyl, or 2-aminophenyl, and the salts of compose esíos. Compounds according to aspect 1 of the present invention even more particularly noteworthy are the compounds of formula I wherein R 1 is hydrogen, R 2 is hydrogen, R 3 is hydrogen, R 4 is hydrogen, R 5 is hydrogen, R 6 is -T 1 - Q1, Aa1, Hh1, Ah1, or benzyl, where T1 is a bond, Q1 is Ar1, where Ar1 is phenyl, 3- (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is metyl, or -T2-N (R61 1) R612, where either T2 is a bond, R61 1 is metyl, and R612 is metyl, or T2 is methyleneo, R61 1 is hydrogen, me yl, isobuyl, benzyl, Har1 -methyl, or 2- (Har1) -yloyl wherein Har1 is pyridin-3-yl, pyridin-4-yl, indol-2-yl, indole-3-yl or indole-5-yl, and R612 is hydrogen , melyo, or 2-hydroxy-yl, or R61 1 and R612 together and including the nitrogen atom, to which they are linked form a heterocyclic ring Het1, wherein He1 is morpholino, Aa1 is 1.1 '-bifen-4-yl or 1, 1'-bifen- 3-yl, Hh 1 is 5- (pyridin-2-yl) -iiophen-2-yl, there is 3- (pyridin-3-yl) -phenyl, 3- (pyridin-4-yl) -phenyl, - (pyrazol-1-yl) -phenyl, 3- (1 H -pyrazol-4-yl) -phenyl, 4- (pyridin-3-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, 4- (pyrazol-1-yl) -phenyl or 4- (1H-pyrazol-4-yl) -phenyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. The compounds according to the aspect 1 of the present invention which deserve to be mentioned in particular are the compounds of formula I wherein R 1 is hydrogen, R 2 is hydrogen, R 3 is hydrogen, R 4 is hydrogen, R 5 is hydrogen, R 6 is -T 1 - Q 1, Aa1, Hh 1, Ahi, or benzyl, where T1 is a bond, Q 1 is Ar1, where Ar1 is phenyl, 3- (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is methyl, or -T2-N (R61 1) R612, where either T2 is a bond, R61 1 is metyl, and R612 is metyl, or T2 is methylene, R61 1 is hydrogen, isobutyl, benzyl, Har1 -methyl, or 2- (Har1) -ephyl, wherein Har1 is pyridin-3- ilo, pyridin-4-yl, indole-2-yl, indol-3-yl or indole-5-yl, and R612 is hydrogen, or T2 is methyleneo, R61 1 is methylo, or 2- (Har1) -yleno, wherein Har1 is indole-2-yl, and R612 is methylo, or T2 is methylene, R61 1 is 2- (Har1) ) -ethyl, wherein Har1 is indole-2-yl, and R612 is 2-hydroxy-efyl, or T2 is meleylene, and R61 1 and R612 together with the nitrogen atom, to which they are linked form a Het1 of the heterocyclic ring, wherein Het1 is morpholino, Aa1 is 1, 1'-bifen-4-? lo or 1, 1'-bifen-3-yl, Hh 1 is 5- (pyridin-2-yl) -thiophen-2 -ilo, Ah is 3- (pyridin-3-yl) -phenyl, 3- (pyridin-4-yl) -phenyl, 3- (pyrazol-1-yl) -phenyl, 3- (1 H -pyrazol-4-yl) -phenyl, 4- (pyridin-3-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, 4- (pyrazol-1-yl) -phenyl or 4- (1H-pyrazol-4-yl) -phenyl, R7 is hydroxyl, and the salts of these compounds. Still the compounds according to aspect 1 of the present invention which deserve to be mentioned in particular are the compounds of formula I wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1 -Q1, Aa1, Hh1, Ah1, or benzyl, where T1 is a bond, Q1 is Ar1, where Ar1 is phenyl, 3- (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is methyl, or -T2-N (R61 1) R612, where either T2 is a bond, R61 1 is methyl, and R612 is methyl, or T2 is methylene, R61 1 is hydrogen, butyl, benzyl, Har1-methyl, or 2- (Har1) -ethyl, wherein Har1 is pyridin-3-yl, pyridin-4-yl, indole-3-yl or indole-5-yl , and R612 is hydrogen, or T2 is meyylene, R61 1 is meylyl, or 2- (HAr1) -ylenyl, wherein Har1 is ndol-2-yl, and R612 is meylyl, or T2 is methyleneo, R61 1 is 2 - (HAr1) -ylenyl, where Har1 is indole-2-yl, and R612 is 2-hydroxy-ylyl, or T2 is meleylene, and R61 1 and R612 are together and including the nifrogen atom, to which they are bound they form a Het 1 of the heterocyclic ring, wherein Het 1 is morpholino, Aa 1 is 1,1 '-bifen-4-yl or 1,1' -bifen-3-yl, Hh 1 is 5- (pyridin-2-yl) -thiophen -2-yl, Ah i is 3- (pyridin-3-yl) -phenyl, 3- (pyridin-4-yl) -phenyl, 3- (pyrazol-1-yl) -phenyl, 3- (1 H- pyrazol-4-yl) -phenyl, 4- (pyridin-3-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, 4- (pyrazol-1-yl) -phenyl or 4- (1 H -pyrazol-4-yl) -phenium, R7 is 2-aminophenyl, and the salts of these compounds. 1 A special interest in the compounds according to the present invention refers to the compounds of this invention which are included -within the scope of this invention- by one or, when possible, a combination of more of the following modalities: of the compounds according to the present invention relates to compounds of formula I, wherein R 1, R 2, R 3, R 4 and R 5 are all hydrogen. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R7 is hydroxyl. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R7 is Cyc1, wherein in a sub-modality thereof C and C is 2-phenyl. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R 7 is 2-aminophenyl. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R6 is Aa1. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R6 is Ar1 or -CH2-AR1. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein Ar 1 is phenyl substituted with R61. Listen to the modality of the compues according to the present invention relates to compounds of formula I, wherein Ar1 is monosubstituted phenyl? by R61 in the meta position with respect to the bonding position in which the phenyl ring is bound to T1. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein Ar1 is phenyl monosubstituted by R61 in the para position with respect to the linking position wherein the phenyl ring is linked to T1. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R6 is Hh1. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R6 is Ah1. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein T2 is a bond. Another embodiment of compound coughs according to the present invention relates to compounds of formula I, wherein T 2 is C 1-4 alkylene, such as for example methylene. Ofra embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R6 is Ar1, wherein Ar1 is phenyl substituted with R61, wherein R61 is -T2-N (R61 1) R612, wherein T2 is a link. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R6 is Ar1, where Ar1 is phenyl substituted with R61, wherein R61 is -T2-N (R61 1) R612, wherein T2 is C1-4 alkylene, such as for example meyylene. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R 1, R 2, R 3, R 4 and R 5 are all hydrogen, and R 6 is Ar 1, wherein Ar 1 is selected from the group consisting of 3-methyl-phenyl, 4-meityl-phenyl, 3-dimethylamin-o-phenyl, 4-dimethylamino-phenyl, 3-aminomethy-phenyl, 4-aminomethyl-phenyl, 3- (morpholin-4-yl-meityl) -phenyl 4- (morpholin-4-yl-meiyl) -phenyl, 3- (N-benzylamino-methyl) -phenyl-3- (N-isobuylamino-meityl) -phenyl, 4- (N-benzylamino-methyl) -phenyl 4- (N-isobutylamino-meityl) -phenyl, 3- [N- (pyridinylmethyl) amino-meiyl] -phenyl, 3- [N- (indolylmethyl) amino-methylenyl-phenyl] 4- [N- ( pyridinylmethyl) aminomethyl] -phenyl, 4- [N- (indolylmeityl) aminomethyl-phenyl, 3- (N, N-dimethylamino-methyl) -phenyl, 4- (N, N-dimethylamino-methyl) - ' phenyl, 3- [N, N- (2-indolyleryl) -methylamino-methyl] -phenyl, 4- [N, N- (2-indolyleryl) -methyl-amino-methyl] -phenyl, 3- [N, N- (2-indolylethyl) - (2-hydroxyethyl) -amino-methyl] -phenyl, and 4- [N, N - (2-indolylethyl) - (2-hydroxyethyl) -amino-methyl] -phenyl.

Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Aa1, wherein Aa1 is a biphenyl radical, Another embodiment of the compounds according to the present invention refers to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Ha1, wherein Ha1 is a pyridinyl-thiophenyl radical. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Ah1, where A is a 3- (pyrazolyl) radical ) -phenyl, 4- (pyrazolyl) -phenyl, 4- (pyridinyl) -phenyl, or 3- (pyridinyl) -phenyl. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R7 is hydroxyl. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R 1, R 2, R 3, R 4 and R 5 are iodos hydrogen, and R 7 is Cyd. Another embodiment of the compounds according to the invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R7 is 2-aminophenyl.

Another embodiment of the compounds according to the present The invention relates to compounds of formula I, wherein R 1, R 2, R 3, R4 and R5 are all hydrogen, and R7 is aminopyridyl. A special embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Ar1, wherein Ar1 is selected from the group consisting of 3-mephyl-phenyl, 4-methyl-phenyl, 3-dimethylamino-phenyl, 4-dimethylamino- phenyl, 3-aminomethyl-phenyl, 4-aminomethyl-phenyl, 3- (morpholin-4-yl-methyl) -phenyl, 4- (morpholin-4-yl-meityl) -phenyl 3- (N-benzylamino-methyl) -phenyl, 3- (N-isobuylamino-mephyl) -phenyl 4- (N-benzylamino-meitylyl) -phenyl, 4- (N-isobuylamino-meityl) -phenyl, 3-EN- (pyridin-3-yl-methyl) ) amino-meityl] -phenyl, 3- [N- (pyridin-4-yl-methyl) amino-meityl] -phenyl, 3- [N- (indol-5-yl-meityl) amino-meityl] phenyl, - [N- (indoI-3-yl-meiyl) amino-methyl] -phenyl, 4- [N- (pyridin-3-yl-methyl) amino-methyl] phenyl, 4- [N- (pyridine-4- il-methyl) amino-meityl] -phenyl, 4- [N- (indol-5-yl-methyl) amino-methyl] -fyl, 4- [N- (indol-3-yl-methyl) amino-methyl] phenyl, 3- (N, N-dimethylamino-meityl) -phenyl 4- (N, N-di-ethylamino-meityl) -phenyl, 3-. { N, N- [2- (indol-2-yl) -ethyl] -methylamino-methyl] -phenyl 4-. { N, N- [2- (indol-2-yl) -ethyl] -methylamino-meityl} -phenyl, 3-. { N-N- [2- (indol-2-yl) -ethyl] - (2-hydroxy-yl) -amino-methyl} -phenyl and 4-. { N, N- [2- (indol-2-yl) -ethyl] - (2-hydroxy-yl) -amino-methyl} phenyl, and R7 is hydroxyl, and the salts thereof. Ofra special embodiment of the compounds according to the present invention relates to the compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Aa 1, wherein Aa1 is 1, 1 '-bifen-4-yl or 1, 1' -bifen-3-yl, and R7 is hydroxyl, and the salts thereof. Another special embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Hai, where Ha1 is 5- (pyridin-2-yl) -thiophen-2-yl, and R7 is hydroxyl, and the salts of the same. Another special embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Ah1, where Ah1 is 3- (pyrazol-1-yl) -phenyl, 4- (pyrazol-1-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, 3- (pyridin-4-yl) -phenyl, 4- (pyridin-3-yl) -phenyl, 3- (pyridin-3-yl) -phenyl, 3- ( 1 H-pyrazol-4-yl) -phenyl or 4- (1 H -pyrazol-4-yl) -phenyl, R7 is hydroxyl, and salts thereof. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are all hydrogen, and R6 is Ar1, wherein Ar1 is selected from the group consisting of -methyl-phenyl, 4-methyl-phenyl, 3-di-methylmethyl o-phenyl, 4-dimethylamino-phenyl, 3-aminomethyl-phenyl, 4-aminomethyl-phenyl, 3- (morpholin-4-yl-methyl) - phenyl, 4- (morpholin-4-yl-mephyl) -phenyl, 3- (N-benzylamino-methyl) -phenyl, 3- (N-isobutylamino-meityl) -f-enyl, 4- (N-benzylamino-meityl) -phenyl, 4- (N-isobuylamino-meityl) -phenyl, 3- [N- (pyridin-3-yl-meityl) amino-meityl] -phenyl, 3- [N- (pyridin-4-yl-methyl) amino-methyl} -phenyl, 3- [N- (indol-5-yl-methyl) amino-meityl] -phenyl, 3- [N- (indol-3-yl-methyl) amino-methyl} phenyl, 4- [N- (pyridin-3-yl-methyl) amino-methyl] -phenyl], 4- [N- (pyridin-4-yl-methyl) amino-methyl] -phenyl, 4- [ N- (indol-5-yl-methyl) amino-meitylphenyl, 4- [N- (indol-3-yl-methyl) amino-methyl] -phenyl, 3- (N, N-dimethylamino-methyl) - phenyl, 4- (N, N-dimethylamino-methyl) -phenyl, 3-. { N, N- [2- (indol-2-yl) -ethyl] -methylamino-mephile} -phenyl, 4-. { N, N- [2- (indol-2-yl) -yl] -methylamino-meityl} -phenyl, 3-. { N, N- [2- (indol-2-yl) -yl] - (2-hydroxyethyl) -aminomethyl} -phenyl and 4-. { N, N- [2- (indol-2-yl) -ethyl] - (2-hydroxyethyl) -amino-meityl} phenyl, and R7 is 2-aminophenyl, and the salts thereof. Another special embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R 1, R 2, R 3, R 4 and R 5 are iodos hydrogen, and R 6 is Aa 1, wherein Aa 1 is 1, 1 '-bifen -4-yl or 1, 1 '-bifen-3-yl, and R7 is 2-aminophenyl, and the salts thereof. Another special embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R 1, R 2, R 3, R 4 and R 5 are all hydrogen, and R 6 is Hal, wherein Ha 1 is 5- (pyridin-2 -yl) -thiophen-2-yl, and R7 is 2-aminophenyl, and the salts thereof. Another embodiment of the compounds according to the present invention relates to compounds of formula I, wherein R1, R2, R3, R4 and R5 are hydrogen ions, and R6 is Ah1, where Ah1 is 3- (pyrazole- 1 -yl) -phenyl, 4- (pyrazol-1-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, 3- (pyridin-4-yl) -phenyl, 4- (pyridin-3- il) -phenyl, 3- (pyridin-3-yl) -phenyl, 3- (1 H -pyrazol-4-yl) -phenyl or 4- (1 H -pyrazol-4-yl) -phenyl, R7 is 2-aminophenyl, and the salts thereof. The compounds according to this invention may include any selected from 1. (E) -N-hydroxy-3- [1- (loluen-4-sulfonyl) -1-H-pyrrol-3-yl] -acrylamide 2. N-hydroxy-3- (1-phenylmenesulfonyl-1H-pyrrol-3-yl) -acrylamide 3. (E) -3- [1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl] -N -hydroxy-acrylamide 4. (E) -3- [1- (4-dim eti lam-inobenzenesulfonyl) -1 H-pi-rrol-3-yl] -Nh id roxy-acrylamide 5. (E) -N- (2-amino- phenyl) -3- [1- (toluene-4-sulfonyl] -1 H -pyrrol-3-yl] -acrylamide 6. (E) -N- (2-amino-phenyl) -3 (1-phenylmetanesulfonyl-1H -pyrrol-3-yl) -acrylamide 7. (E) -N- (2-amino-phenyl) -3- [1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl] -acrylamide 8. (E) -N- (2-amino-phenyl) 3- [1- (4-dimethylamino-benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide 9. (E) -N-hydroxy-3- (1 - [4 - (([2- (1H-indol-2-yl) -ethyl] -methyl-amino) -methyl) -benzenesulfonyl] -1H-pyrrol-3-yl) -acrylamide 10. (E) -3 - [1- (4-dimethylaminomeleyl-benzenesulfonyl) -1H-pyrrol-3-yl] -N-hydroxy-acrylamide 11. (E) -N-hydroxy-3- [1- (4- { [( pyridin-3-yl-methyl) -amino] -methyl] -benzenesulfonyl) -1H-pyrrol-3-yl.} - acrylamide 12. (E) -N-hydroxy-3- [1- (4- { [(1H-indol-3-yl-methyl) -amino] -methyl] -benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide 13. (E) -3-. { 1- [4- (benzylamino-methyl) -benzenesulfonyl] -1H-pyrrol-3-yl} -N-hydroxy-acrylamide 14. (E) -N-hydroxy-3-. { 1- [4- (isobutylami non-methyl) -benzenesulfonyl] -1H-pyrrol-3-yl} -Acrylamide 15. (E) -N-hydroxy-3-. { 1- (4-. {[[(1H-indol-5-yl-methyl) -amino] -methyl] -benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide 16. (E) -N- hydroxy-3- [1- (4-. {[[(pyridin-4-yl-meiyl) -amino] -mefl] -benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide (E) -3- [1- (4-aminomeylyl-benzenesulfonyl.) -1 H -pyrrol-3-yl] -N-hydroxy-acrylamide 18. (E) -Nh-droxy-3- [1- ( 4-pyridin-4-yl-benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide 19. (E) -N-hydroxy-3-. { 1- [4- (1H-pyrazol-4-yl) -benzenesulfonyl] -1H-pyrrol-3-yl-acrylamide 20. (E) -N- (2-amino-phenyl) -3- [1- (4 -pyridin-4-yl-benzenesulfonyl) -1H-pyrrolidone 3-yl] -acrylamide 21. (E) -N- (2-amino-phenyl) -3- [1- (4-pyridin-3-yl-benzenesulfonyl) -1H-pyrrole-3-yl] -acrylamide 22. (E) -N- (2-amino-phenyl) -3-. { 1- [4- (1H-pyrazol-4-yl) -benzenesulfonyl] -1H-pyrrol-3-yl} -acrylamide 23. (E) -3- [1- (biphenyl-3-sulfonyl) -1H-pyrrol-3-yl] -N-hydroxy-acrylamide 24. (E) -N-hydroxy-3- [1- (5-pyridin-2-yl-iiophen-2-sulfonyl) -1H-pyrrol-3-yl] -acrylamide 25. (E) -N-hydroxy- 3-yl- (4-pyrazol-1-yl-benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide 26. (E) -N- (2-amino-phenyl) -3- [1 - (5-pyridin-2-yl-thiophen-2-sulfonyl) -1 H -pyrrol-3-yl] -acrylamide 27. (E ) -N-hydroxy-3- [1 - (4-morpholin-4-yl-methyl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 28. (E) -N-hydroxy-3-. { 1 - [4- ( { (2-hydroxy-ethyl) - [2- (1 H -indole-2-yl) -ilel] -amino} -methyl) -benzenesulfonyl] -1 H-pyrrole -3-il} Acrylamide 29. (E) -N-hydroxy-3- [1- (3-pyridin-4-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 30. (E) -N- (2 -amino-f eni l) -3- [1 - (3-pyridin-4-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 31. (E) -N- (2-ami no-f en il) -3- [1 - (3-pyridin-3-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 32. (E) -N-hydroxy-3-. { l- [3- (1 H -pyrazol-4-yl) -benzenesulfonyl-1 H-pyrrol-3-yl} Acrylamide and 33. (E) -N- (2-amino-phenyl) -3-. { 1 - [3- (1 H -pyrazol-4-yl) -benzenesulfonyl] -1 H -pyrrol-3-yl) -acrylamide, and the salts thereof. The compounds according to the present invention may be prepared, for example, as shown in the following reaction scheme and in accordance with the reaction steps specified below, or, particularly, in a manner as described by way of example. example in the following examples, or analogously or similarly thereto using preparation procedures and synthesis strategies known to the person skilled in the art. In Reaction Scheme 1, the carbon chain of the compounds of formula V, wherein R.sup.1, R.sup.2, R.sup.4 and R.sup.5 have the meanings mentioned above, is extended, for example, by a condensation reaction (with a malonic acid derivative) or by a Wittig or Julia reaction or, in particular, in the case where R 2 is hydrogen, mediates a Homer-Wadsworth-Emmons reaction (with a dialkyl ester of β- (alkoxycarbonyl) -phosphonic acid) to obtain compounds of formula IV, wherein R 1, R 2, R 3, R 4 and R 5 have the meanings mentioned above and PG 1 represents a temporary proiective group suitable for the carboxyl group, for example tertbutyl or one of the protecting groups known in the art mentioned in "Proiecíivo Groups in Organic Syníhesis" by T. Greene and P. Wuts ( John Wiley &Sons, Inc. 1999 3rd Ed.) Or in "Protective Groups (Thieme Foundations Organics Chemistry Series. N Group" by P. Kocienski (Thieme Medical Publishers, 2000).

Reaction Scheme 1 Compounds of formula V, wherein R 1, R 2, R 4 and R 5 have the meanings mentioned above, are known, or can be prepared according to procedures, or can be obtained as described in the following examples for the case where R2 is hydrogen of the compounds of formula VI. The compounds of formula VI are known or accessible in a known manner or as described in the following examples. The compounds of formula IV, wherein R 1, R 2, R 3, R 4 and R 5 have the meanings mentioned above and PG 1 represents the appropriate protecting group, they can be reacted with the compounds of formula R6-SO2-X, wherein R6 has the abovementioned meanings and X is a suitable starting group, such as, for example, chlorine, to form the corresponding compounds of formula 11 . In the next reaction step, the protecting group PG 1 of the compounds of formula I can be removed in the manner as described in the following examples or according to a manner known in the art to obtain the compounds of formula I I. Compounds of formula R6-SO2-X are known or can be prepared in a known manner. The compounds of formula II, wherein R.sup.1, R.sup.2, R.sup.3, R.sup.4, R.sup.5 and R.sup.6 have the meanings mentioned above, may be linked with the compounds of formulas H 2 N-O-PG.sub.2, wherein PG.sub.2 is a suitable pro-cycfor oxygen group. It is, for example, a suitable prophylactic group of silyl or pheirahydropyran-2-yl, where PG 3 represents a suitable nihinogen protecting group, such as, for example, the tert-butyloxycarbonyl group, by reaction with reactants. of amide linkage optionally in the presence of binding additives known to the person skilled in the art. By way of example, the amide bond binding reagents known to the person skilled in the art which can be mentioned are, for example, carbodiimides (for example dicyclohexylcarbodiimide or, preferably, 1-ethyl-3- (3-dimethylaminopropyl) carbodiimide hydrochloride) azodicarboxylic acid derivatives (for example, diethylazodicarboxylase), uronium salts [for example O- (benzoyriazole-1-yl) -N, N, N ', N'-tetramethyluronium or O- (benzofriazol-1-yl) -etrafluoroborate -N, N, N ', N'-teframeyyl-uronium-hexafluorophosphate] and N, N'-carbonylimidazole. Alternatively, the compounds of formula I I can be acylated prior to the binding reaction by forming an acid or anhydrous acid halide optionally in an in-situ procedure without isolating the acid halide or acid anhydride. Compounds of formulas H2N-Q-PG2 or l ia are known or can be prepared according to procedures known in the art. The removal of the pro-segmental groups PG2 or PG3 can be obtained in a manner known to the person skilled in the art or as described in the following examples to give the com ponents of formula I, wherein R1, R2, R3, R4, R5 , R6 and R7 have the aforementioned meanings. The compounds of formula I, where T2 is. C 1-4 alkylene, particularly methylene, can be prepared as outlined in the following reaction schemes 2 to 5, and specified as follows, or as described by way of example in the following examples or analogously or similarly to m isms.

As illustrated in reaction scheme 2, the compounds of formula VII, wherein T 2 is C 1-4 alkylene, particularly methylene, and Y 1 is a suitable starting group, such as, for example, iodine, chlorine or, particularly, bromine, and PG4 represented a suitable temporary group for the carboxyl group, for example tertiary-buíyl, can be reacted with the compounds of formula HN (R61 1) R612 to form in a nucleophilic substitution reaction known in the art amino compounds corresponding, which are disproved through the removal of PG4 to give corresponding free acids of formula VI II, which can be bound with the compounds of formulas H2N-O-PG2 or lia as described above to form, after elimination of PG2 and PG3, the corresponding compounds of formula la. Reaction scheme 2: Alternatively, as illustrated in reaction scheme 3, the compounds of formula VII, wherein T2 is alkylene C1-4, para-finely methylene, and Y1 is a suitable starting group, such as, for example, iodine, chlorine or, particularly, bromine, and PG4 represented a suitable temporal group for the carboxyl group, for example urea-butyl, can be reacted with a temporarily protected amine (a primary, or particularly, a secondary), such as, for example, phthalimide, to give in a reaction nucleophilic substitution known in the art, corresponding amino compounds, which are deprotected by the removal of PG4 to give corresponding free acids of formula IX, which can be linked with the compounds of formulas H2N-O-PG2 or as described above to give the corresponding compounds of formula X. Reaction Scheme 3: The amino moiety of the compounds of formula X can be deprotected in a manner known in the art to give the corresponding compounds of formula XI, such as for example when the phthalimide protecting group is used, it can be removed per se by custom. the person skilled in the art, for example with the aid of hydrazine. Compounds of formula XI can be deprotected to form the corresponding compounds of formula Ib. Alternatively, as illustrated in reaction scheme 4, the compounds of formula XI can be reacted with compounds of formula R61 1 -Y1 and / or R612-Y2, wherein R61 1 and R612 have the meanings mentioned above and they are different from hydrogen and Y1 and Y2 are suitable starting groups, such as, for example, a chlorine, bromine, iodine or sulfonate starting group (for example triflate), to give a known nucleophilic substitution reaction in the corresponding compound technique of formula XI I or XIG. The compounds of formula XI I or XI I 'can be deprotected to give corresponding compounds of formula Ie or Id, respectively.

Reaction scheme 4: Still in an aligning manner, as illustrated in reaction scheme 5, the compounds of formula XI can be reacted with aldehydes or ceiones in a reduction reaction, as, for example, the compounds of formula XI can be reacted with benzaldehyde, or compounds of formulas alkyl-C1 -3-CHO or Har1-CHO, wherein Har1 has the meanings given above, to form, in a reductive amination reaction known in the art, corresponding compounds of formula X11.

The compounds of formula X1 can be deprotected to form the corresponding compounds of formula I.

Reaction scheme 5: R ": benzyl or -CH2-Harl or alkyl-Cl-4 The compounds of formula Vll can be obtained according to the illusory synthesis route in the reaction scheme 1 and described above. The compounds of formulas HN (R61 1) R612, R61 1 -Y1, R612-Y2, alkyl-C 1 -3-CHO or Har1-CHO mentioned above are known or can be obtained according to methods known in the art. The compounds of formula I, wherein R6 is Aa1 or A, can be prepared as outlined in the following reaction scheme 6, and specified above, or as described by way of example in the following examples, or analogously or analogously to the same.

Reaction scheme 6: As illustrated in reaction scheme 6, the compounds of formula XIV, wherein Y 3 is a suitable starting group, such as, for example, iodine or bromine, and PG 5 represents a suitable temporary protecting group for the carboxyl group, for example, eerc-buíilo, the boronic acids of the formula R'-B (OH) 2 may be reacted, wherein R 'is the heteroaryl or aryl terminal fraction of the above-mentioned radicals Aa1 or Ha1, or the esters of the boronic acid (for example the pinacol esters) thereof, to give in a Suzuki reaction known in the art the corresponding CC-bound compounds, which are deprotonated by removal of PG5 to give the corresponding free acids of formula XV, which can be join with the compounds of formulas H2N-O-PG2 or as described above to form, after elimination of PG2 and PG3, corresponding compounds of formula If. Aliernaiivamenie, as shown in the compounds of reaction scheme 7 of formula XIV, wherein Y3 is a suitable leaving group, eg as iodine or bromine, and PG5 represented a suitable femporary proiector group for the group carboxyl, for example urea-butyl, can be deprotected by the removal of PG5, and the free carboxylic acid can then be linked with the compounds of formula H2N-O-PG2 or as described above to give the corresponding compounds of formula XVI . The compounds of formula XVI are reacted with boronic acids of formula R'-B (OH) 2, wherein R 'is the terminal aryl or heteroaryl portion of the above-mentioned radicals Aa 1 or Ha 1, or of the acid esters boronic (for example, pinacol esters) thereof, to give in a Suzuki reaction known in the art the corresponding CC joined compounds, which are deprotected by the elimination of PG2 or PG3 to give the corresponding compounds of For formula. Reaction scheme 7: The Suzuki reaction can be carried out customarily per se by the skill in the art or as described in the following examples, or analogously or similarly thereto. The compounds of formula XIV can be obtained according to the synthesis cycle shown in reaction scheme 1 and described below. The aforementioned compounds with formula R'B (OH) 2 are known or can be obtained according to methods known in the art. The above-mentioned reactions can be carried out easily in a manner analogous to the methods known to those skilled in the art or as described by way of example in the following examples. The person skilled in the art also knows that if there are a number of reactive centers in an initial or intermediate compoundIt may be necessary to block one or more reagents temporarily by protective groups to enable a reaction that is specifically achieved in the desired reaction site. A detailed description for the use of a large number of protective groups can be found, for example, in "Proiecíive Groups in Organic Syníhesis" by T. Greene and P. Wuis (Yohn Wiley &Sons, Inc. 1999, 3rd Ed.) Or in "Protecting Groups (Thieme Foundations Organic Chemistry and Series N Group" by P. Kocienski (Thieme Medical Publishers, 2000). and purification of the substrates according to the invention is carried out in a manner known per se, for example by fi the solvent under vacuum and recrystallizing the resulting residue from a suitable solvent or by submitting it to one of the usual purification methods, such as, for example, column chromatography on suitable support material Optionally, the compounds of formula I can be converted in their salts, or, optionally, the salts of the compounds of formula I can be converted into free compounds. The salts are obtained by dissolving the free compound in a suitable solvent (for example a cation, such as acetone, methylethylacetylene, or methyliso-isobutyl ether, an ether, such as diethyl ether, hydro-hydrofuran, or dioxane, a crystal hydrocarbon, such as methylene chloride or chloroform. , or a low molecular weight aliphatic alcohol such as ethanol or isopropanol) containing the desired base or acid, to which the desired base or acid is then added. The salts are obtained by filtration, reprecipitation, precipitation with a non-solvent for the addition salt or by evaporation of the solvent. The salts obtained can be converted by alkalization or by acidification into the free compounds, which, in turn, can be converted into salts. In this way, pharmaceutically intolerable salts can be converted into pharmacologically tolerable salts. Suitably, the conversions mentioned in this invention can be carried out analogously or similarly to the methods that are familiar per se to the person skilled in the art. The person skilled in the art knows, thanks to his experience and on the basis of these syn- thesis routes, that the way of finding possible syn- thesis rumors for the compounds of formula I is illusi- ated and described in the description of this invention. All other possible synthesis routes are also part of this invention. Having described the invention in detail, the scope of the present invention was not limited only to the characteristics or modalities descriptions. As will be apparent to those skilled in the art, analogies, variations, derivations, homologations and adaptations can be made to the invention described on the basis of prior art knowledge and / or, particularly, on the basis of the description (e.g. the explicit, implicit, or inherent description) of the present invention without apparition of the spirit and scope of this invention as defined in the scope of the appended claims. The following examples serve to illustrate the invention additionally, without limiting it. Also, other compounds of formula I can be prepared, the preparation of which is not explicitly described, analogously or in a manner familiar per se by the experience in the art using conventional processing techniques. The compounds that are mentioned as final products in the following examples as well as their salts are a preferred objection of the present invention. In the examples, MS must be listed as mass spectral, M as molecular ion, TSP by ionization by thermo-spray, ESI as electrospray ionization, E as electronic ionization, h as hours, min as minutes. Other abbreviations used herein have the usual meanings per se for the expert in the art. Examples Final products 1. (E) -N-hydroxy-3- [1 - (toluene-4-sulfonyl) -1H-pyrrol-3-yl] -acrylamide 0.23 1 g of (E) -3- [1] acid are dissolved. - (íoluen-4-sulfonyl) -1 H -pyrrol-3-yl] -acrylic (compound A1) in 8 ml of dichloromethane a ambience ambience. Then add 50 μl of N, N-dimethylformamide (DMF), add 0.275 g of oxalic acid chloride dissolved in 2 ml of dichloromethane and stir for 1.5 hours. To the solution 0.439 g of O- (dimethyl) hydroxylamine are added and stirred for 15 minutes. Then add 20 ml of aqueous hydrochloric acid (strength 1 M) and extracted with ethyl acetate. The combined organic phase is dried over sodium sulfate. Subsequently, it is filtered and evaporated under vacuum. The crude product is purified by flash chromatography on silica gel using a gradient of dichloromean and methanol from 98: 2 to 6: 4 to obtain 0.050 g of the title compound as a white solid. MS (TSP): 307.0 (MH +, 100%) 1 H-NMR (DMSO-d 6): 1 H-NMR (DMSO-d 6): 2.37 (s, 3H); 6.12 (d, J = 15.9 Hz, 1 H); 6.54 (m, 1 H); 7.25 (m, J = 16.1 Hz, 2H); 7.42 (d, J = 8.1 Hz, 2H); 7.79 (m, 1 H); 7.85 (d, J = 8.2 Hz, 2H); 8.96 (broad, níercambiable, 1 H); 10.61 (broad, irrelevant, 1 H). 2. N-hydroxy-3- (1-phenylmethanesulfonyl-1H-pyrrol-3-yl) -acrylamide 0.189 g of (E) -3- (1-phenylmetanesulfonyl-1H-pyrrol-3-yl) - is dissolved. N- (tetrahydropyran-2-yloxy) -acrylamide (compound A2) in 50 ml of a methanol / water solution (312). Subsequently, 0.102 g of amberlysi IR15 ionic resin was added and the mixture was stirred for a long time. 91 hours in ambient atmosphere. The mixture is filtered. The filtrate evaporates. The residue is crystallized from methanol to form 0.144 g of the title compound as white chrysolics. MS (TSP): 307.0 (MH +, 100%) 1 H-NMR (DMSO-d 6): 5.00 (s, 2H); 6.1 1 (d, J = 15.7 Hz, 1 H); 6.50 (m, 1 HOUR); 6.96 (m, 1H); 7.11 (m, 2H); 7.32 (m, J = 17 Hz, 5H); 8.90 (s, interchangeable, 1H); 10.60 (s, interchangeable, 1H). 3. (E) -3- (1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl] -N-hydroxy-acrylamide The method used for the preparation of this compound is analogous to the method described for the compound 2. Start materials: (E) -3- (1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl) -N- (teirahydro-pyran-2-yloxy) -acrylamide (Compound A3) (0.150 g), meianol / water 3/2 (50 ml), amberlysí IR15 (0.300 g). Reaction conditions: room temperature, 34 hours. Yield: 0.041 g, pale gray crystals EM (ESI): 381.1 (MH + -CH3NO2, 100%) 1 H-NMR (DMSO-d6): 6.14 (d, J = 15.8 Hz, 1H); 6.58 (m, 1H); 7.31 (d, J = 15.7 Hz, 1H); 7.43 (m, J = 6.9 Hz, 4H); 7.70 (m, J = 6.6 Hz, 3H); 7.91 (d, J = 8.0 Hz, 2H); 8.02 (d, J = 8.1 Hz, 2H); 8.92 (s, interchangeable, 1H); 10.60 (s, interchangeable, 1H). 4. (E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1H-pyrrol-3-yl] -N-hydroxy-acrylamide The method used for the preparation of this compound is analogous to the method described for the compound 2. Starting materials: (E) ~ 3- [1- (4-dimethylamino-benzenesulfonyl) -1 H -pyrrol-3-yl] -N (ephehydro-pyran-2-yloxy) -acrylamide (compound A4) (0.200 g), meianol / water 3/2 (50 ml), amberlyst IR15 (0.402 g). Reaction conditions: ambient temperature, 34 hours. Yield: 0.098 g, pale red chrysotile EM (ESI): 336.0 (MH +, 100%) 1 H NMR (DMSO-d 6): 6.10 (m, J = 16.5 Hz 1 H); 6.49 (m, 1 H); 6.75 (d, J = 9.2 Hz, 2H); 7.24 (m, 2H); 7.64 (m, J, = 8.6 Hz, J2 = 17.7 Hz, 3H); 8.89 (broad, irrelevant, 1 H), 10.59 (broad, infercambiable, 1 H). 5. (E) -N- (2-amino-4-phenyl) -3- [1 - (toluene-4-sulfonyl) -1 H -pyrrol-3-yl] -acrylamide Dissolve 0. 1 16 g tert. (2- ({(E) -3- [1 - (toluene-4-sulfonyl) -1H-pyrrol-3-yl] -arylamino} -phenyl) -carbamic acid ester (compound A5) ) in 20 ml of dichloromethane at room temperature. 2 ml of trifluoroacetic acid (TFA) are added and the solution is stirred for 93 hours. The solvent is evaporated to dryness and 25 ml of water are added to the residue. The water phase is extracted exhaustively with ethyl acetate. Subsequently, the combined organic phases are dried in sodium sulfate and filtered. The filtrate is evaporated in vacuo. Subsequently, the residue is crystallized from meianol to form 0.050 g of the title compound as white crystals. MS (ESI): 382.0 (MH +, 1 00%) 1 H-NMR (DMSO-d 6): 2.38 (s, 3H); 4.48 (s, irrelevant, 2H); 6.55 (m, 3H); 6.71 (m, 1 H); 6.90 (m, 1 H); 7.40 (m, J = 8.1 Hz, 5H); 7.70 (m, 1 H); 7, 89 (d, J = 8.3 Hz, 2H); 9.20 (s, unchanged, 1 H). 6. (E) -N- (2-Amino-phenyl) -3- (1-phenylmethanesulfonyl-1 H-pyrrol-3-yl) -acrylamide The method used for the preparation of this compound is analogous to the method described for the preparation. compound 5 except that the product is purified by flash chromatography on silica gel using a dichloromethane / meianol gradient of 99: 1 to 95: 5.

Starting materials: acid tertiary builders. { 2 - [(E) -3- [1 - (phenylmenesulfonyl-1H-pyrrol-3-yl) -arylamino] -phenyl} -carbamic (compound A6) (0.146 g), CH2Cl2 (20 ml), TEA (2 ml). Reaction conditions: room temperature, 65 hours. Yield: 0.037 g, white crystals MS (ESI): 382.0 (MH +) 1 H-NMR (DMSO-d6): 4.90 (s, 2H); 5.01 (s, irrelevant, 1 H); 6.58 (m, J = 5.7 Hz, 3H); 6.74 (m, J = 6.7 Hz, 2H); 6.90 (m, 1 H); 7.01 (m, 1 H); 7. 1 1 (m, J = 5.6, 2H); 7.34 (m, J1 = 5.7 Hz, J2 = 6.7 Hz, 5H); 9.25 (s, interchangeable, 1 H). 7. (E) -N- (2-amino-phenyl) -3- [1 - (biphenyl-4-sulfonyl) -1 H -pyrrol-3-yl] -acrylamide The method used for the preparation of this compound is analogous to the method described for compound 5. Starting materials: (2 { (E) -3- [1 - (biphenyl-4-sulf onyl) -1H-pyrrole-3-yl) tert-butylester ] -alanylamino.}. -phenyl) -carbamic (compound A7) (0.460 mmol), CH2Cl2 (50 mL), TFA (5 mL). Reaction conditions: ambient temperature, 18 hours. Yield: 0.061 g, white chrysotile MS (ESI): 444.0 (MH +) 1 H-NMR (DMSO-d6): 4.90 (broad, irrelevant, 2H); 6.58 (m, J1 = 51.4 Hz, J2 = 7.5 Hz, 3H); 6.71 (m, J1 = 1 .4 Hz, J2 = 6.6 Hz, 1 H); 6.90 (m, J1 = 1 .4 Hz, J2 = 6.6 Hz, 1 H); 7.40 (m, J = 7.5 Hz, J2 = 7.7 Hz, 6H); 7. 78 (m, J = 7.7 Hz, 3H); 7.95 (d, J = 8.6 Hz, 2H); 8.08 (d, J = 8.8 Hz, 2H); 9.23 (s, irrelevant, 1 H). 8. '(E) -N- (2-amino-phenyl) -3- [1- (4-dimethylamino-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide, The method used for the preparation of this compound is analogous to the method described for compound 5 with the exception that the product is purified by crystallization of ethyl acetate.

Starting materials: (2- {(E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1 H -pyrrol-3-yl] -alanylamino} -phenyl} -carbamic acid eerc-buylester (compound A8) (0.141 g), CH2Cl2 (10 ml), TFA (1 ml).

Reaction conditions: room temperature, 20 hours. Yield: 0.1 09 g, pale red chrysanthemum MS (ESI): 41 1.0 (MH +, 1.00%) 1 H-NMR (DMSO-d6): 3.00 (s, 6H); 3.97 (s, irreversible, 2H); 6.79 (m, J = 15.4 Hz, 2H); 6.79 (d, J = 9.2 Hz, 2H); 7.04 (m, J, = 2.7 Hz, J2 = 8.7 Hz, J3 = 15.5 Hz, 3H); 7.40 (m, J-, = 15.6 Hz, J2 = 8.6 Hz, 3H) 7.70 (m, J, = 2.9 Hz, J2 = 9.2 Hz, 3H) 9.74 (s, unchanging, 1 H). 9. (E) -N-hydroxy-3- (1 - [4 - (([2- (1 H -indol-2-yl) -ethyl] -methyl-amino) -methyl) -benzenesulfonyl] -1 H -pyrrol-3-yl) -acrylamide 81 mg of (E) -3- (1 - [4 - (([2- (1 H -indol-2-yl) -yl] -methyl-amino) are dissolved benzenesulfonyl] -1H-pyrrol-3-yl) -N- (iorahydropyran-2-yloxy) acrylamide (Compound A9) in 5 ml of melanol. ml of 0.1 N hydrochloric acid, the mixture was stirred for 21 hours. Then the reaction mixture is evaporated. The residue is washed with ethyl acetate and dried under vacuum at -50 ° C. Yield: 55 mg, pale yellow solid. 10. (E) -3- [1- (4-Dimethylaminomefil-benzenesulfonyl) -1 H -pyrrol-3-yl] -N- The hydroxy acrylamide ET method used for the preparation of this compound is analogous to the method described for the compound 9. Starting material: (E) -3- [1- (4-dimethylaminomefil-benzenesulfonyl) ~ 1 H-pyrrole-3- il] -N-y-ehydro-pyran-2-yloxy) -acrylamide (compound A1 0) 1 1. (E) -N-hydroxy-3- [1 - (4. {[[(Pyridin-3-yl-mephyl) -amino] -methyl]} - benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide Starting from the compound A1 1, the method that can be used for the preparation is analogous to the method described for compound 9. The crude product is sufficiently pure for its biological evaluation.

MH + = 413.0 12. (E) -N-hydroxy-3- [1 - (4. {[[(1 H -indol-3-ylmethylamino] -methyl] -benzenesulfonyl) -1 H- pyrrol-3-yl] -acrylamide Starting from the compound A12, the method that can be used for the preparation is analogous to the method described for compound 9. The crude product is sufficiently pure for its biological evaluation. MH + = 449.0 13. (E) -3-. { 1 - [4- (benzylamino-meiyl) -benzenes ulf onyl] - 1 H-pyrrole-3-l} -N-hydroxy-acrylamide Starting from the compound A13, the amount that can be used for the preparation is analogous to the method described for compound 9. MH + = 412.1 14. (E) -N-h idroxy-3-. { 1 - [4- (isobutylam-ino-methyl) -benzenesulfonyl] -1H-pyrrol-3-yl} -acrylamide Starting from compound A14, the method that can be used for Preparation is analogous to the method described for compound 9. MH + = 378.1 15. (E) -N-hydroxy-3- [1 - (4. {[[(1 H -indol-5-ylmethyl) -amino] - mephyl] -benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide Starting from compound A15, the method that can be used for the preparation is analogous to the method described for compound 9. MH + = 449.1 16. (E) -N-hydroxy-3- (1 - (4. {[[(Pyridin-4-yl-meityl) -amino] -methyl} - benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide Starting of compound A16, the method that can be used for the preparation is analogous to the method described, for compound 9. MH + = 41 3. 1 17. (E) -3- [1- (4-aminomethyl-benzene ulf onyl ) - 1 H-pyrrol-3-yl] -N-hydroxy-acrylamide Starting from compound B6, the method that can be used for the preparation is analogous to the method described for compound 9. The crude product is purified by washing with methanol A solid of 69% yield is obtained Melting point: 227.0-228.6 ° C 18. (E) -N-hydroxy-3- [1 - (4-pi Ridin-4-yl-benzenesulfonyl) -1H-pyrrol-3-yl] -acrylamide Starting from compound A17, the method that can be used for the preparation is analogous to the method described for compound 9. The mixture of The reaction is partially evaporated and the resulting suspension is filtered. The product is isolated as a colorless solid.

Melting point: 21 9.3-221 .4 ° C 19. (E) -N-hydroxy-3. { 1 - [4- (1 H -pyrazol-4-yl) -benzenesulfonyl] -1 H -pyrrol-3-yl} acrylamide Starting with compound A18, the method that can be used for the preparation is analogous to the method described for compound 9. Melting point: 203.8-21 1 .9 ° C 20. (E) -N- (2-a) my non-phenyl) -3- [1 - (4-pyridin-4-I-benzenesulfonyl) -1H-pyrroi-3-yl] -acrylamide Starting from compound A19, the method that can be used for the preparation is analogous to the method described for the compound Melting point: 244.2-246.5 ° C 21. (E) -N- (2-Amino-phenyl) -3- [1- (4-pyridin-3-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide The compound is prepared by ferrous ionization. (2- ({(E) -3- [1- (4-pyridin-3-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -arylamino) -phenyl) -carbamic acid ester (compound) A20) in dioxane with HCl. Once the reaction is stopped, the production is precipitated from the reaction mixture. Melting point: 199.7-202.3 ° C 22. (E) -N- (2-amino-phenyl) -3-. { 1 - [4- (1 H -pyrazol-4-yl) -benzenesulfonyl] -1 H -pyrrol-3-yl} Acrylamide Starting from compound A21, the method that can be used for the preparation is analogous to the method described for compound 21. Melting point: 232.3-240.9 ° C 23. (E) -3- [1 - (biphenyl-3-sulfonyl) -1 H -pyrrol-3-yl] -N-hydroxy-acrylamide Starting from compound A22, the method that can be used for the preparation is analogous to the method described for compound 9. Melting point: 1 14-1 59.4 ° C, Sintering at 83 ° C 24. (E) -N-hydroxy -3- [1 - (5-pyridin-2-yl-thiophen-2-suiofonyl) -1H-pyrrol-3-yl] -acrylamide Starting from compound A23, the amount that can be used for the preparation is analogous to the time description for the compound 9. The product is crystallized from the reaction mixture. Melting point: 181 .3-1 82 ° C 25. (E) -N-hydroxy-3- [1- (4-pyrazol-1-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide Starting from compound A24, the method that can be used for the preparation is analogous to the method described for compound 9. The crude product is purified by washing with dichloromethane. Melting point: 160.7-1 66.6 ° C 26. (E) -N- (2-amino-phenyl) -3- [1- (5-pyridin-2-yl-thiophene-2-sulfonyl) -1 H- pyrrol-3-yl] -acrylamide Starting from compound A25, the method that can be used for the preparation is analogous to the method described for compound 21. The product is purified by washing the crude product with ethyl acetate. Melting point: 171 .3-1 74.7 ° C 27. (E) -Nh id roxy-3- [1 - (4-m orf olí-4-yl-methyl-benzenesulfonyl) - 1 H-pyrrole -3-yl] -acrylamide Starting from compound A26, the method that can be used for the preparation is analogous to the method described for compound 9. The Compound of title is isolated by freeze drying methods. Melting point: 168-170 ° C 28. (E) -N-hydroxy-3-. { 1 - (4- ( { (2-hydroxy-ethyl) - [2- (1 H -indole-2-yl) -ei] -amino} - methyl) -benzenesulfonyl] -1 H -pyrrol-3-il.}. -acrilamida Beginning of the compound A27, the method that can be used for the preparation is analogous to the method described for compound 9. The reaction mixture is evaporated and the thioule compound is isolated as an oil. MH + = 509.1 Starting from compound D6, the following compounds can be prepared by synthetic routes that are analogous to the synthetic routes resulting from Examples 1 to 22. 29. (E) -N-hydroxy-3- [1 - (3-pyridin-4-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 30. (E) -N- (2-amino-phenyl) -3- [1- (3-pyridin-4 -yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 31. (E) -N- (2-amino-phenyl) -3- (1- (3-pyridin-3-yl-benzenesulfonyl) - 1 H ~ pyrrol-3-yl] -acrylamide 32. (E) -N-hydroxy-3- { 1 - [3- (1 H -pyr.azol-4-yl) -benzenesulfonyl] -1 H-pyrrol-3-yl.} - acrylamide 33. (E) -N- (2-amino-phenyl) -3- { 1- [3- (1 H -pyrazol-4-yl) -benzenesulfonyl ] -1 H-pyrrol-3-yl.} - acrylamide Starting materials A1 (E) -3- [1 - (Ioluen-4-sulfonyl) -1 H -pyrrol-3-yl] -acrylic acid 1.60 g of (E) -3- [1- (toluene-4-sulfonyl) -1H-pyrrol-3-yl] -acrylic acid tert-butylester (compound C1) are dissolved in 70 ml of dichloromethane room temperature. Subsequently, 7 ml of trifluoroacetic acid (TFA) are added and stirred for 4 hours. The solvent is evaporated to dryness and 30 ml of water are added to the residue. The water phase is exhaustively extracted with ethyl acetate. Then, the organic phase is dried in sodium sulfate. The filtrate is evaporated and dried under vacuum to give 0.951 g of the compound of the product as a pale gray solid. MS (TSP): 290.0 (M-H +, 100%) 1 H-NMR (DMSO-d 6): 2.36 (s, 3H); 6.20 (d, J = 1 5.9 Hz, 1 H); 6.74 (m, J = 3.1 Hz, 1 H); 7.41 (m, J, = 3.1 Hz, J2 = 8.2 Hz, J3 = 16.1 Hz, 4H); 7.78 (m, 1 H), 7.87 (d, J = 8.4 Hz, 2H); 1 1 .80 (broad, irrelevant, 1 H). A2 (E) -3- (1-phenylmenessulfonyl-1 H -pyrrol-3-yl) '- N- (tephrahydropyran-2-yloxy) -acrylamide 0.295 g of (E) -3- (1-phenylmethanesulfonyl) acid are dissolved. -1 H-pyrrol-3-yl) -acrylic (compound B1), 0.152 g of N-hydroxybenzoyriazole hydrate (HOBt-H2O) and 561 μl of triethylamine in 20 ml of N, N-dimethylarformamide (DMF) at room temperature . Subsequently, 0.601 g of N- (3-dimethylaminopropyl) -N'-ethylcarbodiimide hydrochloride (EDC-HCl) is added and stirred for 1 hour at room temperature. Then 0.152 g of O- (teirahydro-2H-pyran-2-yl) -hydroxylamine is added and stirred for 2 hours. The DMF is evaporated in high vacuum. Water is added and the mixture is extracted with acetyl ether. The organic phase is dried over sodium sulfafo. Then it is filtered and evaporated under empty. The crude product is purified by flash chromatography on silica gel using a dichloromethane / methanol gradient of 99: 1 to 98: 2 to give 0.189 g of the title compound as a pale gray solid. MS (ESI): 390.9 (MH +, 100%) 1 H-NMR (DMSO-d 6): 1.60 (m, 6H); 3.51 (m, 1H); 3.91 (m, 1H); 4.89 (m, 1 HOUR); 5.00 (s, 2H); 6.18 (d, J = 15.3 Hz, 1H); 6.50 (s, 1H); 6.96 (m, J = 5.2 Hz, 1H); 7.10 (m, Ji = 7.3 Hz, J2 = 7.9 Hz, 2H); 7.30 (m, J1 = 5.1 Hz, J2 = 7.3 Hz, J3 = 8.1 Hz, J4 = 8.1 Hz, J5 = 15.2 Hz, 5H); 10.60 (s, interchangeable, 1H); 11.08 (broad, interchangeable, 1H). A3 (E) -3- (1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl) -N- (tetrahydropyran-2-yloxy) -acrylamide The method used for the preparation of this compound is analogous to Described method for the A2 component with the exception that the production is purified by crystallization of water and methanol. Starting materials: (E) -3- [1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl] -acrylic acid (compound B2) (0.300 g), HOBi-H2O (0.130 g), eryrylamine (668 μl), DMF (20 ml), EDC-HCl (0.508 g), O- (terahydro-2H-pyranyl) hydroxylamine (0.089 g). Reaction conditions: ambient temperature, 1 hour; room temperature, 18 hours. Yield: 0.345 g, pale gray solid EM (ESI): 452.8 (MH +); 369.0 (MH + -C5H9O, 100%) 1 H-NMR (DMSO-d6): 1.61 (m, 6); 3.50 (m, 1H); 3.92 (m, 1H); 4.87 (m, 1H); 6.21 (d, J = 14.7 Hz, 1H); 6.60 (s, 1H); 7.48 (m, J = 6.9 Hz, 5H); 7.72 (m, J-i = 7.0 Hz, J2 = 14.7 Hz, 3H); 7.98 (d, J = 8.5 Hz, 2H); 8.06 (d, J = 8.6 Hz, 2H); 11.06 (broad, interchangeable, 1H).

A4 (E) -3- [1- (4-Dimethylamino-benzenesulfonyl) -1H-pyrrol-3-yl] -N- (tetrahydro-pyran-2-yloxy) -acrylamide The method used for the preparation of this compound is analogous to the method described for compound A2 with the exception that the product is purified by silica gel flash chromatography using a gradient of dichloromean and methanol of 99: 1 to 98: 2.

Starting maferials: (E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1H-pyrrol-3-yl) -acrylic acid (compound B3) (0.150 g), HOBt-H2O (0.072 g), ithylamine (259 μl), DMF (10 ml), EDC-HCl (0.269 g), O- (1-hydroxy-2H-pyran-2-yl) hydroxylamine (0.049 g). Reaction conditions: ambient temperature, 1 hour; ambient ambience, 17 hours. Yield: 0.187 g, pale red solid EM (ESI): 419.2 (MH +); 336.0 (MH + -C5H9O, 100%) 1 H-NMR (DMSO-d6): 1.61 (m, 6); 3.02 (s, 6H); 3.50 (m, 1H); 3.92 (m, 1H); 4.85 (m, 1H); 6.19 (m, 1H); 6.50 (m, 1H); 6.75 (m, J = 9.2 Hz, 2H); 7. 31 (m, 2H); 7.64 (m, J = 9.2 Hz, 3H); 11.01 (broad, unchangeable, 1 HOUR). A5 (2- ({(E) -3- [1- (toluene-4-sulfonyl) -1-H-pyrrol-3-yl] -alanylamino} -phenyl) -carbamic acid fer-butyl ester The method used for the preparation of this compound is analogous to the method described for compound A2 with the exception that the product is purified by flash chromatography on silica gel using a gradient of dichloromethane and methanol of 99: 1 to 98: 1.

Starting materials: (E) -3- [1- (toluene-4-sulfonyl) -1H-pyrroyl-3-yl] -acrylic acid (compound Al) (0.400 g), HOBtH2O (0.285 g), triethylamine (652) μl), DMF (25 ml), EDC-HCI (0.698 g), N-BOC-1, 2-phenylenediamine (0.286 g). Reaction conditions: ambient femperairy, 1 hour; ambience temperaíura, 2 hours. Yield: 0.609 g, pale gray solid EM (ESI): 481.7 (MH +, 100%) 1 H-NMR (DMSO-d6): 1.40 (m, 9H); 2.39 (s, 3H); 6.61 (m, J1 = 1 .7 Hz, J2 = 2.2 Hz, J3 = 5.0 Hz, 2H); 7.09 (, = 1 .8 Hz, J2 = 2.3 Hz, 2H); 7.37 (m, J-, = 2.0 Hz, J2 = 5.0 Hz, J3 = 8.0 Hz, 4H); 7.64 (m, 1 H); 7.88 (d, J = 8.4 Hz, 2H); 8.41 (s, interchangeable, 1 H); 9.57 (s, interchangeable, 1 H) A6 urea-butyl ester of the acid. { 2 - [(E) -3- [1 - (Phenylmethanesulfonyl-1H-pyrrol-3-yl) -arylamino] -phenyl} -carbamic The method used for the preparation of this compound is analogous to the method described for compound A2 with the exception that the product is purified by silica gel chromatography using a gradient of dichloromethane and methanol of 99: 1 to 95: 5.

Starting materials: (E) -3- (1-phenylmethanesulfonyl-1H-pyrrol-3-yl) -acrylic acid (compound B1) (0.180 g), HOBiH2O (0.090 g), triethylamine (295 μl), DMF ( 10 ml), EDC-HCl (0.315 g), N-BOC-1,2, phenylenediamine (0.081 g). Reaction conditions: ambient temperature, 1 hour; Ambient temperature, 1 7 hours. Yield: 0.218 g, pale gray solid EM (ESI): 504.0 (MNa +, 100%); 481.8 (MH +) 1 H-NMR (DEMO-d6): 1.42 (m, 9H); 5.04 (s, 2H); 6.56 (m, J., = 2.2 Hz, J2 = . 2 Hz, 2H); 7.14 (m, J., = 2.2 Hz, J2 = 5.5 Hz, J3 10.1 Hz, 4H); 7.36 (m, J-, = 5.5 Hz, J2 = 7.2 Hz, 4H); 7.52 (m, J1 = 2.2 Hz, J2 = 7.2 Hz, 2H); 8.49 (s, inferchangeable 1 H); 9.67 (s, unchanged, 1 H). A7 (2- ({(E) -3- [1 - (biphenyl-4-sulfonyl) -1 H -pyrrol-3-yl.} - alanylamino) -phenyl) -carbamic acid fer-butyl ester The method used for the preparation of this compound is analogous to the method described for compound A2 with the exception that the product is purified by instantaneous silica gel chromatography using a toluene / ethyl acetate gradient of 99: 1 to 9: 1. . Starting materials: (E) -3- [1 - (biphenyl-4-sulfonyl) -1 H -pyrrol-3-yl) -acrylic acid (compound B2) (0.300 g), HOBt-H2O (0.130 g), idyllamine (668 μl), DMF (20 ml), EDC-HCl (0.508 g), NBOC-1, 2-phenylenediamine (0.176 g). Reaction conditions: ambient temperature, 1 hour; room temperature, 17 hours. Yield: 0.285 g, pale gray solid EM (ESI): 543.8 (MH +); 487.9 (MH + -C4H8); 336.1 (MH + -C1 1 H14N2O2, 100%) 1 H-NMR (DMSO-d6): 1.47 (m, 9H); 6.50 (m, J = 5.4 Hz, 1 H); 6.64 (m, J = 7.7 Hz, 2H); 7.10 (m, J-, = 5.4 Hz, J2 = 7.7 Hz, 3H); 7.51 (m, J ^ = J2 = J3 = 3.6 Hz, 5H); 7.73 (m, 2H); 7.81 (m, 1 H); 7.96 (d, J = 8.6 Hz, 2H); 8.08 (d, J = 8.6 Hz, 2H); 8.41 (s, interchangeable, 1 H); 8.59 (s, interchangeable, 1 H). A8 tert-builder (2 { (E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1 H -pyrrol-3-yl] -arylamino} -phenyl) -carbamic acid The method used for the preparation of this compound is analogous to the method described for compound A2 with the exception that the product is purified by crystallization of ethyl acetate.

Starting materials: (E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1H-pyrrol-3-yl) -acrylic acid (compound B3) (0.150 g), HOBi-H2O (0.072 g), iaryrylamine (259 μl), DMF (10 ml), EDC-HCl (0.269 g), N-BOC-1, 2-phenylenediamine (0.049 g). Reaction conditions: ambient temperature, 1 hour; Ambient temperature, 21 hours. Yield: 0.142 g, pale red solid EM (ESI): 510.9 (MH +, 1 00%) H-NMR (DMSO-d6): 1.42 (m, 9H); 3.00 (s, 6H); 6.51 (m, 2H) 6.79 (d, J = 9.2 Hz, 2H); 7.09 (m, J = 5.5 Hz, 2H); 7.36 (m, 2H); 7.50 (m, J = 5.5 Hz, 2H); 7.70 (m, J = 9.2 Hz, 2H); 8.41 (s, interchangeable, 1 H); 9.55 (s, interchangeable, 1 H). A9 (E) -3- (1 - [4 - (([2- (1 H -indol-2-yl) -ethyl] -methylamino) -benzenesulfonyl] -1 H -pyrrol-3-yl) - N- (teirahydropyran-2-yloxy) -acrylamide 825 mg of (E) -3- (1 - [4 - (([2- (1 H -indol-2-yl) -ethyl] -methyl- acid is dissolved. amino) -benzenesulfonyl] -1H-pyrrol-3-yl) -acrylic acid (compound B4), 165 mg of HOBtH2O and 1.24 ml of erytylamine in 70 ml of DMF at ambient temperature, then add 726 mg of EDCHCl The mixture is stirred for 1 hour, then 140 mg of O- (terahydro-2H-pyran-2-yl) -hydroxylamine is added and the mixture is stirred for 18 hours.The DMF is evaporated in an empty vessel, then water is added to the residue and The organic phase is dried over sodium sulfate and evaporated in vacuo, then the mixture is evaporated and the crude product is purified by flash chromatography on silica gel using a gradient of 98: 2 dichloromethane and mefanol. - 9: 1 Yield: 289 mg, pale red solid A10 (E) -3- [1 - (4-dim eti lam inomefil-ben cens ulf onyl) - 1 H -pyrrol-3-yl] -N-teirahydro-pyran-2-yloxy) -acrylamide The method used for The preparation of the thioule compound is analogous to the method described for compound A9. Starting materials: (E) -3- [1- (4-dimethylaminomefil-benzenesulfonyl) -1H-pyrrol-yl] -acrylic acid (compound B5) (1.78 g), HOBtH2O (366 mg), triethylamine ( 2.1 ml), DMF (80 ml), EDC-HCl (1.54 g), O- (feirahydro-2H-pyran-2-yl) -hydroxylamine (306 mg). Reaction condition: ambient temperature, 1 hour; room temperature, 48 hours. Yield: 835 mg, pale yellow solid A1 1 (E) -3- [1 - (4-. {[[(Pyridin-3-ylmethyl) -amino] -methyl] -benzenesulfonyl) -1 H-pyrrole -3-yl] -N- (tephrahydro-pyran-2-yloxy) -acrylamide A mixture of the compound B6, sodium idioceroxyborohydride, meianol and 3-pyridinecarboxaldehyde was stirred at ambient temperature overnight. The reaction mixture is evaporated and separated in dies between dichloromethane and water. The crude product is purified by flash chromatography on silica gel. Obtain an almost colorless oil. Starting with the compound B6 and the appropriate aldehyde, the following compounds A12 to A16 can be obfuscated according to the compound A1 1. A12 (E) -3- [1 - (4-. {((1 H-indol-3-yl-methyl) -amino] -methyl} - benzenesulfonyl) -1 H -pyrrol-3-yl] -N- (5-ylhydro-pyran-2-yloxy) -acrylamide A13 (E) -3- { 1 - [4- (benzylamino-mephyl) -benzenesulfonyl] -1 H -pyrrol-3-yl}. N- (tetrahydro-pyran-2-yloxy) -acrylamide A14 (E) -3-. { 1 - (4- (isobutylamino-meityl) -benzenesulfonyl] -1 H -pyrrol-3-yl) -N- (1-eryhydro-pyran-2-yloxy) -acrylamide A1 (E) -3- [1 - (4 - { [(1 H-indol-5-ii-meityl) -amino] -methyl] -benzenesulfonyl) -1 H- pyrrol-3-yl] -N- (teirahydro-pyran-2-yloxy) -acrylamide A1 6 (E) -3- [1 -. { [(pyridin-4-ylmethyl) -amino] -methyl} -benzenesulfonyl) -1 H-pyrrol-3-yl] -N- (teirahydro-pyran-2-yloxy) -acrylamide A17 (E) -3- [1- (4-pyridin-4-ylphenylsulfonyl) -1 H- pyrrol-3-yl] -N- (ε-tetrahydro-pyran-2-yloxy) -acrylamide Starting with compound B7, the thioule compound can be obtained according to the compound A2. A18 (E) -3-. { 1 - [4- (1 H -pyrazol-4-yl) -phenylsulfonyl] -1 H -pyrrol-3-yl} -N- (ieiraf? Idropyran-2-yloxy) -acrylamide Starting with the compound B8, the title compound can be obtained according to the compound A2. A19 tert-butyl ester of the acid [2 - ((E) -3- { 1 - [4-pyridin-4-yl-benzenesulfonyl] -1 H -pyrrol-3-yl} - alanylamino) -phenyl ] -Carbamic Beginning with compound B7, the compound of the tíulo can obíener according to the compound A5. A20 Ferric-butyl ester of [2 - ((E) -3-. {1 - [4-pyridin-3-yl-benzenesulfonyl] -1 H -pyrrol-3-yl.} - ~ alanoylamino) -phenyl ester ] -carbamic Beginning with the compound B9, the compilation of the title can be obtained according to the compound A5. A21 acid-2-builder acid [2 - ((E) -3-. {1 - [4- (1 H -pyrazol-4-yl) -benzenesulfonyl] -1 H -pyrrol-3-yl}. -alanoylamino) -phenyl] -carbamic Beginning with the compound B8, the compound of the can obíener according to the compound A5. A22 (E) -3- (1 - (biphenyl-3-sulfonyl) -1 H -pyrrol-3-yl) -N- (eeryhydro-pyran-2-yloxy) -acrylamide Starting with the compound B 10, the compound of the product can be obtained according to compound A2. A23 (E) -3- (1 - (5-pyridin-2-yl-thiophen-2-sulfonyl) -1 H -pyrrol-3-yl) -N- (teirahydro-pyran-2-yloxy) -acrylamide Starting by the compound B 1 1, the compound of the tíulo can obíener according to the compound A2. A24 (E) -3- (1- (4-pyrazol-1-yl-benzenesulfonyl) -1 H -pyrrol-3-yl) -N- (teirahydro-pyran-2-yloxy) -acrylamide. Starting with compound B12, the title compound can be obtained according to the compound A2. A25 (2 { (E) -3- [1 - (5-pyridin-2-yl-thiophen-2-ylsulphonyl) -1 H -pyrrol-3-yl] - (2. alanoylamino.).-phenyl) -carbamic Starting from compound B1 1, the title compound can be obtained according to compound A5. A26 (E) -3-. { 1 - [4- (Morpholin-4-yl-methyl) -benzenesulfonyl] -1 H -pyrrol-3-yl} -N-eryhydro-pyran-2-yloxy) -arylamide Starting with the compound B 13, the compound of the title can be obtained according to the compound A2. A27 (E) -3-. { 1 - [4- ( { [2-hydroxy-eiii] - [2 (1 H-indol-3-yl) -yl] -amino} -methyl) -benzenesulfonyl] -1 H-pyrrole -3-il} -N- (tephrahydro-pyran-2-yloxy) -acrylamide Dissolves (E) -3-. { 1 - [4- ( { [2- (tert-butyl-dimethylsilanyloxy) -efyl.} - [2- (1 H -indol-3-yl) -ethyl] -amino}. ) -benzenesulfonyl] -1 H-pyrrol-3-yl} -N- (1-tetrahydro-pyran-2-yloxy) -acrylamide (compound B 14) (120 mg, 0.169 mmol) in THF (20 ml). Then tetrabufilamonium fluoride is added (203 μl, 0.203 ml, 1 M in THF) and isopylamine (47 μl, 0.338 mmol) and the mixture is stirred for 17 hours. After the addition of water (50 ml) and extraction with ethyl acetate, the organic phase is dried over sodium sulfate, filtered and evaporated. The crude product is purified by flash chromatography on silica gel using eluent of dichloromethane-methanol. B1 (E) -3- (1-phenylmethanesulfonyl-1H-pyrrol-3-yl) -acrylic acid The method used for the preparation of this compound is analogous to the described method for compound A1 with the exception that the product is isolates by chilling a mixture of acefone (29.7 g), water (10.8 g) and HCl (C (Hc?) = 1 mol / l, 5.3 g). Starting materials: (E) -3- (1-phenylmethanesulfonyl-1H-pyrrol-3-yl) -acrylic acid tert-buylester (compound C2) (1.45 g), CH2CI2 (80 ml), TFA (8 ml). Reaction conditions: ambient temperature, 2 hours. Performance; 0.660 g, pale gray crystals EM (TSP): 289.9 (M-H +, 100%) 1 H-NMR (DMSO-d 6): 5.00 (s, 2H); 6.21 (d, J = 15.9 Hz, 1 H); 6.72 (m, J-, = 1 .9 Hz, J2 = 3.4 Hz, 1 H); 7.01 (m, J = 5.3, 1 H); 7. 1 0 (m, J = 1 .6 Hz, 2H); 7. 31 (m, 7.41 (m, J, = 1 .6 Hz, J2 = 1 .9 Hz, J3 = 3.4 Hz, J4 = 5.3 Hz, J5 = 16. 1-Hz, 4H). B2 acid (E) -3- [1 - (biphenyl-4-sulfonyl) -1 H -pyrrol-3-yl] -acrylic The method used for the preparation of this compound is analogous to the method described for compound A1. Starting materials: (E) -3- [1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl) -acrylic acid tert-butyl ester (.05.05 g), CH2Cl2 (100) ml), TFA (10 ml). Reaction conditions: ambient temperature, 21 hours. Yield: 0.710 g, pale yellow solid EM (ESI): 728.7 (2MNa +, 100%); 354.1 (MH +) 1 H-NMR (DMSO-d 6): 6.29 (d, J = 16.0 Hz, 1H); 6.81 (m, J-, = 1.2 Hz, J2 = 1.8 Hz, J3 = 3.0 Hz, 1H); 7.49 (m, J-¡= 3 Hz, J2 = 7.7 Hz, J0 = 16.0 Hz, 5H); 7.75 (m, Ji = 1.3 Hz, J2 = 1.8 Hz, J3 = 7.7 Hz, 2H); 7.85 (s, 1H); 7.95 (d, J = 8.6 Hz, 2H); 8.09 (d, J = 8.6 Hz, 2H); 12.17 (broad, interchangeable, 1H). B3 (E) -3- [1- (4-dimethylamino-benzenesulphonyl) - 1H-pyrrol-3-yl) -acrylic acid The method used for the preparation of this compound is analogous to the method described for the compound A1. Starting materials: (E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1H-pyrrol-3-yl) -acrylic acid (tert-C4) (0.801 g), CH2Cl2 (100 ml) acid tert-buíilésfer , TFA (10 ml). Reaction conditions: ambient temperature, 16 hours. Yield: 0.550 g, pale red solid EM (ESI): 662.7 (2MNa \ 100%); 321.0 (MH +) 1 H-NMR (DMSO-d 6): 2.98 (s, 6H); 6.16 (d, J = 15.8 Hz, 1H); 6.68 (m, J = 3.2 Hz, 1H); 6.75 (m, J = 9.2 Hz, 2H); 7.29 (m, J = 2.9 Hz, 1H); 7.43 (d, J = 15.9 Hz, 1H); 7.70 (m, J = 9.1 Hz, 3H); 12.11 (broad, iníercambiabie, 1H) B4 (E) -3- (1 - [4 - (([2- (1 H -indol-2-yl) -ethyl] -methyl-amino) -benzenesulfonyl] -1 H -pyrrol-3-yl) acid -Acrylic 1.01 g of (E) -3- (1- [4 - (([2- (1H-indol-2-yl) -efil] -methylamino) -carboxylic acid is dissolved. benzenesulfonyl] -H-pyrrol-3-yl) -acrylic acid (Compound C5) in 100 ml of dichloromethane and stir for 5 min., Add 10 ml of TFA and the mixture is agitated for 1 9 hours. vacuum is then added to the residue (small amount to purify the TFA salt) and evaporated in vacuo Yield: 1.32 g, pale brown solid B5 (E) -3- [1- (4-dimethylaminomethyl) acid -benzenesulfonyl) -1 H-pyrrol-yl] -acrylic The method used for the preparation of this compound is analogous to the method described for compound B4. Starting materials: tertiary-builder-acid (E) -3- [1] (4-dimethylaminomethyl-benzenesulfonyl) -1 H -pyrrol-yl] -acrylic (compound C6) (2.13 g), TFA (10 mL); 24 hours. Yield: 3.21 g (with salts of TFA 3), pale brown solid. B6 (E) -3- [1 - (4-aminomethyl-benzenesulfonyl) -1 H -pyrrol-3-yl] -N- (teirahydro-pyran-2-yloxy) -acrylamide To a mixture of 1 g of C7 compound and 50 ml ethanol are added 0. 57 ml of hydrazine hydrate (80%). The mixture is refluxed for 2.5 hours. Subsequently, the reaction mixture is cooled in an ambient atmosphere and the white suspension is filtered off. The filtering product is purified by chromaffin instantaneous gel of silica. B7 (E) -3- [1- (4-Pyridin-4-ylphenylsulfonyl) -1 H -pyrrol-3-yl] -acrylic acid Starting from the compound C8 the thiulo compound can be obtained according to the compound A1 . B8 acid (E) -3-. { 1 - [4- (1 H -pyrazol-4-yl) -4-phenylsulfonyl-1 H -pyrrol-3-yl} - acrylic Starting with compound C9, the title compound can be obtained according to compound A1. B9 acid (E) -3-. { 1- (4-pyridin-3-ylphenylsulfonyl) -1 H -pyrrol-3-yl} - acrylic Starting with compound C 10, the title compound can be obtained according to compound A1. B1 0 (E) -3- (1 - (biphenyl-3-sulfonyl) -1 H -pyrrol-3-yl) -acrylic acid Starting from the compound C1 1, the title compound can be obtained according to the compound A1. B 1 1 (E) -3- (1 - (5-pyridin-2-yl-thiophene-2-sulfonyl) -1 H -pyrrol-3-yl) -acrylic acid Starting with compound C 12, the. Title compound can be obtained according to compound A1. B 12 (E) -3- (1- (4-pyrazol-1-yl-benzenesulfonyl) -1 H -pyrrol-3-yl) -acrylic acid Starting from the compound C13, the title compound can be obtained according to with the compound A1. B13 acid (E) -3-. { 1 - [4- (Morpholin-4-yl-methyl) -benzenesulfonyl] -1 H -pyrrol-3-yl} -acrylic Starting with compound C14, the compound of formula can be obtained according to the compound A1. B14 (E) -3-. { 1 - [4- ( { [2- (eerc-buyyl-dimethylsilanyloxy) -ethyl] - [2- (1 H -indol-3-yl) - ethyl] -amino} -methyl) -benzenesulfonyl] -1 H-pyrrol-3-yl} -N- (tetrahydro-pyran-2-yloxy) -acrylamide. (E) -3- acid is dissolved. { 1 - [4- ( { [2- (tert-Butyl-dimethyl-silanyloxy) -ethyl] - [2- (1 H -indol-3-yl) -ethyl] -amino} -methyl) - benzenesulfonyl] -1 H-pyrrol-3-yl} - acrylic (compound C15) (1.15 g, 1.16 mmol), HOBt-H2O (171 mg, 1.16 mmol) and eryrylamine (2 ml) in DMF (100 ml) at ambient temperature.

After the addition of EDCHCl (786 mg, 3.48 mmol) the mixture was stirred for 1.5 hours. Then O- (1-tetrahydro-2H-pyran-2-yl) -hydroxylamine (136 mg, 1.16 mmol) was added and stirred for 17 hours. After evaporation and addition of 200 ml of water, the mixture is extracted with ethyl acetate. The organic phase is dried over sodium sulfate. Then it is filtered and evaporated. The crude product is purified by flash chromatography on silica gel using eluent dichloromethane-methanol.

C1 ferric-builder of (E) -3- [1 - (toluene-4-sulfonyl) -1H-pyrrol-3-yl] -acrylic acid. 0.230 g of sodium hydride (60%) are suspended in 6 ml of Hydrofuran under nitrogen at -30 ° C. 1.01 g of (E) -3- (1 H-pyrrol-3-yl) acrylic acid tert-bufilésfer (compound D1) is added to the suspension and slowly warmed to room temperature and agitated for 30 minutes. Subsequently, it is re-cooled to -30 ° C and 1.1 g of p-toluenesulfonylchloride are added and stirred for 2.5 hours.

The suspension is heated slowly to room temperature and 40 ml of aqueous sodium chloride solution is added. The mixture is extracted with acellum of effilo. The combined organic phase is added in sodium sulfate (Na2SO). Subsequently, it is filtered and evaporated under vacuum. The crude product is purified by flash chromatography on silica gel using a gradient of hexane-ethyl acetate from 9: 1 to 1: 1 to give 1.6 g of the title compound as a pale yellow solid. MS (ESI): 347.6 (MW): 291.9 (MH + -C4H9, 100%). 1 H NMR (DMSO-d 6): 1.43 (s, 9H); 2.37 (s, 3H); 6.21 (d, J = 15.9 Hz, 1 H); 6.74 (m, J = 3.1 Hz, 1 H); 7.40 (m, J, = 1 5.9 Hz, J2 = 12.7 Hz, J3 = 3.2 Hz, 4H); 7.82 (m, J = 12.6 Hz, 3H). C2 tert-butylester of (E) -3- (1-phenylmethanesulfonyl-1H-pyrroI-3-yl) -acrylic acid The method used for the preparation of this compound is analogous to the method described for compound C1 with the exception of The product is purified by flash chromatography on silica gel using hexane / ethyl acetate gradient from 8: 1 to 5: 1. Starting materials: 60% sodium hydride (0.240 g), (E) -3- (1 H -pyrrol-3-yl) -acrylic acid (compound D1) (1 .01) 9), α-lyonuenesulfonylchloride (1 .19 g). Reaction conditions: -30 ° C, 30 min; 30 ° C, 2.5 hours. Yield: 1.45 g, pale yellow solid MS (TSP): 346.3 (M-H +, 100%) 1 H-NMR (DMSO-d6): 1.47 (s, 9H); 5.00 (s, 2H); 6.21 (d, J = 15.8 Hz, 1 H); 6.72 (m, J, = 1.8 Hz, J2 = 3.3 Hz, 1 H); 6.98 (m, J = 5.3, 1 H); 7.09 (m, J-, = 2.1 Hz, J2 = 7.8 Hz, 2H); 7.31 (m, J, = 1 .9 Hz, J2 = 3.5 Hz, J3 = 5.4 Hz, J4 = 7.7 Hz, J5 = 15.7 Hz, 5H).

C3 tert-builder of (E) -3- [1 - (biphenyl-4-sulfonyl) -1 H -pyrrol-3-yl] -acrylic acid The method used for the preparation of this compound is analogous to the method described for Compound C1 with the exception that the product is purified by silica gel flash chromatography using petroleum ether / diethyl ether gradient from 7: 1 to 1: 1. Starting materials: 60% sodium hydride (0.207 g), (E) -3- (1 H -pyrrol-3-yl) -acrylic acid (D 1) ester (0.531 g), 4-biphenylsulphonylchloride (0.834 g). Reaction conditions: -30 ° C, 1 0 min; -30 ° C, 30 min. Yield: 1.05 g, pale yellow solid MS (ESI): 354.0 (MH + -C4H9, 100%) 1 H-NMR (DMSO-de): 1.45 (s, 9H); 6.26 (d, J = 15.9 Hz, 1 H); 6.80 (m, J = 1 .7 Hz, 1 H); 7.47 (m, J = 15.7 Hz, 5H); 7.72 (m, J = 1.8 Hz, 2H); 7.87 (m, i H), 7.92 (d, J = 8.7 Hz, 2H); 8.09 (d, J = 8.6 Hz, 2H). C4 tert-builder of (E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylic acid The method used for the preparation of this compound is analogous to the method described for Compound C1 with the exception that the product is purified by flash chromatography on silica gel using petroleum ether / diethyl ether gradient of 7: 1 to 1: 1. Starting materials: 60% sodium hydride (0.031 g), (E) -3- (1 H -pyrrol-3-yl) -acrylic acid tert-bufilyester (D1 compound) (0.100 g), -dimethylamino-benzenesulfonyl (0.145 g). Reaction conditions: -30 ° C, 45 min; -30 ° C, 2.5 hours.

Yield: 0.160 g, pale red solid EM (ESI): 376.8 (MH +); 321.0 (MH + -C4H9, 100%). 1 H NMR (DMSO-d 6): 1.42 (s, 9H); 3.00 (s, 6H); 6.1 9 (d, J = 1 5.8 Hz, 1 H); 6.72 (m, J = 9.2 Hz, 3H); 7.25 (m, 1 H); 7.37 (d, J = 15.8 Hz, 1 H); 7.69 (m, J = 9.1 Hz, 3H). C5 (E) -3- (1 - [4 - (([2- (1 H -indodo-2-yl) -ethyl) -methylamino) -benzenesulfonyl] -1 H -pyrrole 3-yl) -acrylic 1.50 g of (E) -3- [1 - (4-bromomethyl-benzenesulfonyl) -1H-pyrrol-3-yl] -acrylic acid (-3- [4-yl] -acrylates are dissolved. Compound D2) in 70 ml of ethanol at ambient temperature After the addition of 0.486 ml of ithylamine and 696 mg of omega-methyltriptamine, the mixture is stirred for 21 hours, then the solution is evaporated under vacuum and the crude product is purified by flash chromatography. of silica gel using a gradient of hexane and efflux acetyl of 5: 1 -2: 1. Replenishment: 1.08 g, pale yellow solid C6 eerc-butyl ester of (E) -3- (1 - ( 4-dimethylaminometyl-benzenesulfonyl) -1H-pyrrol-yl] -acrylic The method used for the preparation of this compound is analogous to the method described for compound C5 with the exception that the product was crystallized from ethanol. ferc-butilé of (E) -3- [1- (4-bromomethyl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylic acid (compound D2) (3.94 g), ethanol (150 ml), dimethylamine ( 1.89 g) Yield: 2.1 9 g, pale yellow solid. C7 acid (E) -3-. { 1 - [4- (1, 3-dioxo-1,3-dihydro-isoindol-2-ylmethyl) - benzenesulfonyl] -1 H-pirphol-3-yl} acrylic Starting with compound D3, the method that can be used for this preparation is analogous to the method described for compound B4. The tífulo compound is purified by washing with toluene. Starting with (E) -3- [1- (4-bromo-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylic acid tert-builder (compound D4) and the appropriate boronic acid derivative, the following compounds C8 and C9 can be obtained according to compound C10. C8 tert-butylester of (E) -3- [1- (4-pyridin-4-yl-phenylsulfonyl) -1 acid H-pyrrole-3-ii] -acrylic acid C 9 eerc-builder of (E) -3- acid. { 1 - [4- (1 H -pyrazol-4-yl) -phenylsulfonyl] -1 H -pyrrol-3-yl} C10-acrylic acid tert-buiyl ester of (E) -3- [1- (4-pyridin-3-phenylsulfonyl) -1H-pyrrol-3-yl] -acrylic acid 0.18 g of tert-builder of (E) -3- [1- (4-Bromo-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylic acid (compound D4) and 62 mg of 3-pyridylboronic acid in 10 ml of DME. A catalytic amount of bis (triphenylphosphine palladium (IL) chloride and 0.6 ml of an aqueous sodium carbonate solution are added and the mixture is heated to reflux temperature overnight, and the compound of the isolate is isolated by means of chromatography. C1 1-tert-butylester of (E) -3- (1 - (biphenyl-3-sulfonyl) -1 H -pyrrol-3-yl] -acrylic acid Starting with tert-buylester of (E) -3- ( 1 H-pyrrol-3-yl) -acrylic (compound D1) and 3-biphenylsulfonylchloride known in the art, the title compound can be obtained analogously or similar to that described for compound C1. C12 tert-butyl ester of (E) -3- [1 - (5-pyridin-2-yl-thiophene-2-sulfonyl) -1 H- pyrrol-3-yl-acrylic acid ester Starting from tert-bufilic acid ester ( E) -3- (1 H -pyrrol-3-yl) -acrylic (compound D1) and 5-pyridin-2-yl-thiophen-2-sulfonylchloride known in the art, the title compound can be obtained analogously or similar to that described for the C1 compound. C 13 (E) -3- [1- (4-pyrazol-1-yl-benzenesulfonyl) -1 H -pyrrol-3-yl) -acrylic acid e-butyl ester starting with (E) - acid e-buleylester 3- (1H-pyrrol-3-yl) -acrylic (compound D1) and 4-pyrazol-1-yl-benzenesulfonylchloride known in the art, the title compound can be obtained analogously or similar to that described for the compound C 1. C14 tert-buylester of (E) -3- acid. { 1 - [4- (Morpholin-4-yl-meityl) -benzenesulfonyl] -1 H-pyrrole-3M} -acrylic Starting from the compound D2 and morpholine, the title compound can be obtained in a manner analogous to that described for compound C5. C15 acid (E) -3-. { 1 - (4- ( { [2- (tert-Butyl-dimethyl-silanyloxy) -yryl] - [2- (1 H -indol-3-yl) -ethyl] -amino} -methyl) - benzenesulfonyl] -1 H -pyrrol-3-yl.} - acrylic Terc-buíiiésíer of (E) -3-. {3- [4- ( { [2- (ert-buil-dimethyl -silyloxy) -efil] - [2- (1 H -indol-3-yl) -ethyl] -amino.} - methyl) -benzenesulfonyl] -1 H -pyrrol-3-yl.} - acrylic (compound D5) in dichloromethane (50 ml), then TFA is added and the mixture is stirred for 26 hours.

After evaporation, the residue is washed with íoluene. D 1 (E) -3- (1 H -pyrrol-3-yl) -acrylic acid ether (buffers) 5.29 g of 60% sodium hydride are suspended in 100 ml of tetrahydrofuran under nitrogen at -30 ° C. 27.81 g of tert-butyl diphosphone acetate are added to the suspension and warmed slowly to room temperature - and stirred for 30 minutes. Subsequently, the mixture is re-cooled to -30 ° C and 5.24 g of 1 H-pyrrole-3-carbaldehyde (El compound) are added and stirred at -30 ° C for 30 minutes. The suspension is warmed slowly at ambient temperature and 200 ml of aqueous ammonia solution are added. Then it is exhausted with oil from the air. The combined organic phase is dried over Na 2 SO 4, filtered and evaporated under vacuum. The crude product is purified by flash chromatography on silica gel using a gradient of n-hexanoethyl acetate from 2: 1 to 1: 1 to give 9.68 g of the title compound as a pale yellow solid. MS (El): 193.1 (M +); 137.1 (M + -C 4 H 8, 100%). 1 H NMR (DMSO-d 6): 1.45 (s, 9H); 5.96 (d, J = 15.7 Hz, 1 H); 6.40 (m, 1 H); 6.78 (m, 1 H); 7.19 (m, 1 H); 7.47 (d, J = 15.7 Hz, 1 H); 1 1 .1 1 (broad, irrelevant, 1 H). D2 (E) -3- [1 - (4-Bromomeiyl-benzenesulfonyl) -1H-pyrrol-3-yl] -acrylic acid-2-butyl ester of sodium. 4.25 g of sodium hydride (60% purity) are suspended in 300 g. ml of THF under nitrogen at -30 ° C. 9.78 g of (E) -3- (1 H-pyrrol-3-yl) -acrylic acid (E) -3- (1 H-pyrrol-3-yl) -acrylic acid (compound D1) are added to the suspension and slowly warmed at room temperature for 55 min. With Thereafter, it is re-cooled to -30 ° C and 13.98 g of 4- (bromomethyl) -benzenesulfonylchloride are added and stirred for 45 min. Then warm to room temperature and stir for 2 hours. After cooling to 0-5 ° C water is added. The mixture is then extracted with ethyl acetate and the organic phase is dried over sodium sulfate. The organic phase is evaporated under vacuum. The crude product is purified by flash chromatography on silica gel using a gradient of hexane and ethyl acetate of 9: 1 -7: 1. Yield: 1 7.21 g, pale yellow solid. D3 urea-butyl ester of (E) -3- acid. { 1 - [4- (1, 3-dioxo-1,3-dihydro-isoindol-2-ylmethyl) -benzenesulfonyl] -1 H -pyrrol-3-yl} -acrylic 10 g of (E) -3- [1- (4-bromomethy-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylic acid (D2) alkyl ester are dissolved in acetone and added. 6.5 g of potassium phthalimide and the mixture was stirred for 17.5 hours. The suspension is filtered and the product is purified by chilling. D4 (E) -3- [1 - (4-bromo-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylic acid ether D-starter and starting with compound D1 and 4-bromo-benzenesulfonyl chloride, the title compilation can be obtained analogously to the one described for the compound D2. D5 ferric-butyl ester of (E) -3- acid. { 1 - [4- ( { [2- (tert -buyldimethylsilanyloxy) -yryl] - [2- (1 H -indol-3-yl) -yl] -amino} -methyl ) -benzenesulfonyl] -1 H -pyrrol-3-yl} - acrylic Dissolve [2- (tert-butyl-dimethylsilanyloxy) -ethyl] - [2- (1 H-indol-3-yl) - efil] -amine (compound E2) (830 mg, 2.60 mmol) in ethanol (200 ml). (E) -3- [1- (4-Bromomethyl-benzenesulfonyl) -1H-pyrrol-3-yl] -acrylic acid ether (butadiene D4) (1.01 g, 2.37 mmol) is added and the mixture is added. stir for 43 hours, and evaporate. The residue is purified by an instantaneous chromatograph of silica gel which is used as eluyenie éer-éir of peiróleo. D6 (E) -3- (1 - (3-bromobenzenesulfonyl) -1 H -pyrrol-3-yl] -acrylic acid ether-buylester Starting from compounds D1 and 3-bromo-benzenesulfonyl chloride, the title compound can be obtained in a manner analogous to that described for compound D4 E1 1 H-pyrrole-3-carbaldehyde 4.70 g of dimethyl- (1 H -pyrrol-3-ylmeiylene) -ammonium chloride (compound F1) is dissolved in 500 g. ml of 5.0% aqueous sodium hydroxide solution and agitated for 4 hours at room temperature Subsequently, the reaction mixture is exhaustively extracted into CH 2 Cl 2 The combined organic phase is dried over Na 2 SO 4. filter and evaporate in vacuo The crude product is purified by flash chromatography on silica gel using as eluyenie peirolol ether / diethyl ether 1: 1 to give 3.01 g of the title compound as a pale yellow solid. El): 95.1 (M +, 1 00%) 1 H-NMR (DMSO-de): 6.42 (dd, J-, = 1.5 Hz, J2 = 6.5 Hz , 1 H), 6.90 (m, 1 H), 7.69 (dd, J ^ = 1.5 Hz, J2 = 6.4 Hz, 1 H); 9.68 (s, 1 H); 1 1 .59 (wide, interchangeable, 1 H).

E2 [2- (tert -buyldimethylsilanyloxy) -yryl] - (2- (1H-indol-3-yl) -ethyl] -amine Triptamine (3.34 g, 20.85 mmol) and t-buffyldimethylsilyloxylacetaldehyde (2.44 g) 13.99 mmol) are dissolved in dichloromethane (200 ml) for 10 minutes.The mixture is cooled to 0 ° C and sodium triaceioxyborohydride (5.38 g, 25.38 mmol) is added.The mixture is slowly enyylated at room temperature and stirred Water is added and the mixture is extracted with dichloromethane The organic phase is dried over sodium sulphate, filtered and evaporated The crude product is purified by flash chromatography on silica gel using dichloromethane-meianol as eluent. F1 Dimethyl (1 H-pyrrol-3-ylmeiylene) ammonium chloride 1 0.60 g of (chloromethylene) dimethylammonium chloride and 6.25 g of N- (triisopropylsilyl) -pyrrole in 200 ml of CH 2 Cl 2 are suspended under nitrogen at 0 ° C. 5 ° C. The suspension is warmed to 60 ° C. and stirred for 30 minutes, after which the mixture is cooled to room temperature. The suspension is filtered and washed with diethylether to give 5.67 g of the title compound as a gray-colored solid. MS (ESI): 123.3 (MH +, 100%). 1 H NMR (DMSO-de): 3.55 (s, 3H); 3.63 (s, 3H); 6.82 (m, J ^ 1 .4 Hz, J2 = 1 .5Hz, J3 = J4 = 4.8 Hz, 1 H); 7.22 (dd, J1 = 4.7 Hz, J2 = 4.9, 1 H), 8. 00 (dd, J! = 1 .6 Hz, J2 = 1 .7 Hz, 1 H); 8.78 (s, 1 H); 12.94 (broad, interchangeable, 1 H). Commercial utility The N-sulfonylpyrrole derivatives of formula I or salts of these compounds have pharmacological properties, of value to inhibit the activity and function of histone deacetylase. Histone deacetylase (HDAC) represented an enzyme with activity towards the e-acetyl group of lysine residues in a substrate protein. The HDACs are histone H2A, H2B, H3 or H4 proteins and isoforms but there are substrate proteins other than histones such as, but not limited to, heat shock protein 90 (Hsp9O), tubulin or tumor suppressor protein p53 . In particular, the deacetylase hisphones catalyze the hydrolysis of the α-acetyl group of lysine residues in these substrate proteins, forming the lysine-free amino group. The inhibition of histone deacetylase by the compounds according to this invention means the inhibition of the activity and function of one or more HDAC isoenzymes, in particular isoenzymes selected from histone deacetylases hitherto known, ie, H DAC 1 , 2, 3 and 8 (class 1) and HDAC 4, 5, 6, 7, 1 0 (class IL), HDAC 1 1 as well as the ILI class dependent on NAD + (Sir2 homologs). In a preferred modality, this inhibition is at least about 50%, more preferably at least 75% and even more preferably over 90%. Preferably, this inhibition is specific to a specific class of histone deacetylase (for example, HDAC class I enzymes), a selection of isoenzymes of greater pathophysiological relevance (for example, HDAC enzymes 1, 2, 3) or a simple isoenzyme (for example, HDAC enzyme example 1). The term histone deacetylase inhibitor is used to identify a compound capable of interacting with a histone deacetylase and inhibiting its activity, in Particularly its enzymatic activity. In this context, the "major group" defines the residues in a hisyone deacetylase inhibitor responsible for infecting the active site of the enzyme, eg, Zn2 + ion. The inhibition of histone deacetylases is determined in biochemical assays of various formats and sources of enzymatic activity. The activity of HDAC is used either derived from cellular or nuclear exarcises or by heirogymous expression of isoenzymes of a HDAC defined in E. coli, inseccal cells or mammalian cells. Since HDACs are active in muliprotein complexes and form homo- and heterodimers, nuclear extractions derived from human cancer cells are preferred, for example the HeLa human cervical carcinoma cell line. These nuclear exfracts contain class I and class I enzymes, but are enriched in class 1 enzymes. For expression of recombinant HDAC isoenzymes, mammalian expression systems such as HEK293 cells are preferred. The HDAC isoenzyme is expressed as a fusion protein with an affinity tag, as a FLAG epitope. By affinity chromatography, the tagged protein is purified alone or in complex with endogenous proteins (e.g., HDAC isoenzymes and codactivators / platform proteins). Biochemical tests are described and well known by experts in the field. As susíratos, the histone proteins, peptides derived from histone proteins or other HDAC substrates are used as well as acetylated lysine mimetics. A preferred HDAC promiscuous substrate is the tripeptide Ac-NH-GGK (Ac), linked with fluorophore 7- aminomethylcoumarin (AMC). The invention also relates to the use of the compounds according to this invention to inhibit the activity of histone deacetylase in cells and tissues, causing hyperacetylation of prophets of subsidence and as a functional consequence, for example the induction or repression of gene expression. , induction of proiein degradation, arrest of the cell cycle, induction of differentiation and / or induction of apoptosis. The cellular activity of a histone deacetylase inhibitor means any cellular effect related to the inhibition of histone deacetylase, in particular protein hyperaceilation, activation and transcriptional repression, induction of apoptosis, differentiation and / or cytoxicity. The term "apoptosis induction" and similar terms are used to idenify a compound that performed programmed cell death in cells in conjunction with the compound. Apoptosis is defined by complex biochemical events in contacting cells, such as activation of specific cisine proteinase ("caspases") and chromatin fragmentation. The induction of apoptosis in cells in contact with the compound may not necessarily bind to the inhibition of cell proliferation or cell differentiation. Preferably, the inhibition of proliferation, induction of differentiation and / or induction of apoptosis is specific to cells with aberrant cell growth. "Cyto-toxicity" in general means stopping proliferation and / or Induction of apoptotic cell death in vitro in mammalian cells, in particular, human cancer cells. "Induction of differentiation" is defined as a process of cellular reprogramming that generates a reversible or irreversible cell cycle arrest in GO and re-expression of a typical subset of genes for a certain specific normal cell or cell type (for example, expression of milk fat and fat proteins in breast carcinoma cells). The assays for the quantification of cell proliferation, apoptosis or differentiation are well known to the experts and to the state of the art. For example, the metabolic activity that is linked to cell proliferation is quantified using the Alamar Blue / Resazurin assay (O'Brian et al., Eur. Biochem 267, 5421-5426, 2000) and the induction of apoptosis is quantified by measurement of chromatin fragmentation with ELISA cell death detection marketed by Roche. Examples of cellular assays for the determination of hyperacetylation of HDAC substrates are obtained by measuring the histone central acetylation using specific antibodies by Western blotting, report genetic assays using respective response promoters or promoter elements (for example, the p21 promoter or siRNA). sp1 as a response element) or finally by image analysis again using acetylation-specific antibodies for central histopic proffers. The compounds according to this invention can be applied commercially due to their HDAC inhibitory activity. antiproliferative and / or induction of apoptosis that may be beneficial in the therapy of diseases that respond to it, such as for example any of the diseases mentioned herein. The invention also relates to a method for inhibiting or bringing about cellular neoplasia by administering an effective amount of a compound according to this invention to a mammal, in particular a human in need of fai-tration. A "neoplasia" is defined by cells that show aberrant cell proliferation and / or survival and / or a block in differentiation. The term neoplasia includes "benign neoplasia" that is described by the hyperproliferation of cells, unable to form an aggressive metastatic tumor in vivo, and, conversely, "malignancy" that is described by cells with multiple cellular and biochemical abnormalities, capable of form a systemic disease, for example form metastatic tumor in distant organs. The N-sulfonylpyrrole derivatives of the present invention are preferably used for the treatment of malignancy, also described as cancer, characterized by tumor cells that are ultimately metastasized to different organs or tissues. Examples of malignancy brought with N-sulfonylpyrrole derivatives of the present invention include solid and hematological tumors. Solid tumors are exemplified by tumors of the breast, bladder, bone, brain, nervous system, central and peripheral, colon, endocrine glands (eg adrenal and thyroid cortex), esophagus, endometrium, germ cells, head and neck, kidney, liver , lung, larynx, and hypopharynx, mesothelioma, ovary, pancreas, prósíata, strong, thin mest, light, stomach, íesíis, skin, urethra, vagina and vulva. Malignant neoplasm includes hereditary cancers exemplified by Retinoblastoma and Wilms tumor. Likewise, malignancy includes primary tumors in the organs and corresponding secondary tumors in diseased organs ("tumorous meystasta"). Hematological tumors are exemplified by aggressive and indolent forms of leukemia and lymphoma, ie, non-Hodgkins disease, acute and chronic myeloid leukemia (CML / AML), acute lymphoblastic leukemia (ALL), Hodgkins disease, multiple myeloma and cell lymphoma. T. Also included are myelodysplastic syndrome, plasma cell neoplasia, paraneoplastic syndromes, cancers of unknown primary site as well as ailments related to SI DA. Neoplastic cell proliferation could also effect normal cellular behavior and organ function. For example, the formation of new blood vessels, a process described as neovascularization, is included by tumor or tumor metastasis. The N-sulfonylpyrrole derivatives as described herein may be commercially applicable for the treatment of pathophysiological relapse processes caused by benign or neoplastic cell proliferation, such as but not limited to neovascularization by non-physiological proliferation of vascular endothelial cells, without . Drug resistance is of particular importance because of the frequent failure of standard therapeutic agents for cancer. This resistance The drug is caused by several cellular and molecular mechanisms such as over-expression of drug efflux pumps, mutation in the cellular protein sought or fusion proteins formed by chromosomal translocations. The commercial applicability of N-sulfonylpyrrole derivatives according to the present invention is not limited to the first-line treatment of patients. Patients with resistance to specific cancer chemotherapies or targeted anticancer drugs are also favorable for treatment with these compounds for, for example, second- and long-term line cycles.A prominent example is given by patients with promyelocytic leukemia. Acute with the PML-RARα fusion protein, resists standard retinoid therapy These patients can be re-sensitized with respect to retinoids by treatment with HDAC inhibitor drugs such as N-sulfonylpyrrole derivatives according to the present invention. The invention also comprises a method for treating a mammal, in particular a human, suffering from a disease different from cellular neoplasia, sensitive to histone deacetylase inhibitor therapy, which comprises administering to said mammal a pharmacologically active and therapeutically effective amount and tolerable of a compound according to These non-malignant diseases include (i) arthropairies and osfeopalliogenic conditions such as rheumatoid arthritis, osteoariritis, gout, polyarthritis and psoriatic arthritis, (l) systemic lupus erythematosus, (ili) light muscle cell proliferation including vascular proliferative disorders, atherosclerosis and restenosis (iv) inflammatory conditions and dermal conditions such as ulcerative coliitis, Chron's disease, allergic rhinitis, allergic dermatitis, cystic fibrosis, chronic bronchitis and asthma (v) endometriosis , uterine fibroids, endometrial hyperplasia and benign prostate hyperplasia (vi) cardiac dysfunction (vile) immunosuppressive conditions of inhibition such as VI H infections (vili) neuropathological disorders such as Parkinson's disease, Alzheimer's disease or disorders related to polyglutamine (ix) favorable pathological conditions for the trava- lization of the endogenous gene expression as well as for the improvement of transgene expression in gene therapy. The present invention also includes a method for the irradiation of mammals, including humans, who suffer from one of the above-mentioned conditions, ailments, fraternities or diseases. The method is characterized in that the pharmacologically active and therapeutically effective and tolerable cannity of one or more of the N-sulfonylpyrrole derivatives mentioned above, or a salt of such compounds of formula I, which function by inhibiting histone deacetylases and by modulating the acetylation of proteins, induce several cellular effects in parficular induction or repression of gene expression, arresting cell proliferation and / or inducing apoptosis, is administered to a subject who needs the rape. The invention also includes a method for treating diseases and / or disorders responsive to or responsive to the inhibition of deacetylase histories, particularly the diseases mentioned above, such as, for example, cell neoplasia or diseases other than cell neoplasia as indicated above, in mammals, including humans, that suffer from them, comprising administering to such mammals in need thereof a pharmacologically active and therapeutically effective and tolerable amount of one or more of the compounds according to the present invention. The present invention also includes a therapeutic method to modulate prophylactic acetylation, gene expression, cell proliferation, cell differentiation and / or apoptosis in vivo in the diseases mentioned above, in particular cancer, which comprises administering to a subject in need of therapy. a pharmacologically active and therapeutically effective and tolerable substance of one or more of the N-sulfonylpyrrole derivatives mentioned above, or a salt of such compounds of formula I, which function to inhibit histone deacetylases. The present invention also comprises a method for regulating the endogenous or heterologous promoter activity by contacting a cell with a compound of formula I as mentioned aníeriormenfé. The invention also includes a method for bringing diseases, particularly the aforementioned diseases, into mammals, including humans, which suffer from them comprising administering to such mammals in need thereof a therapeutically effective and tolerable amount of one or more of the compounds according to the present invention, optionally, simultaneously, sequentially or separately with one or more other pharmacological agents, such as, for example, those mentioned above. The invention also relates to the use of the compounds according to the present invention for the production of pharmaceutical compositions that are used for the treatment and / or prophylaxis of diseases, disorders, conditions and / or conditions as mentioned in I presented. The invention also relates to the use of the compounds according to the present invention for the production of pharmaceutical compositions that are used for the treatment and / or prophylaxis of diseases, and / or disorders that respond or are sensitive to histone inhibition. deacetylases, particularly the diseases mentioned above, such as, for example, cell neoplasia or diseases other than cell neoplasia as indicated above. The invention also relates to the use of the compounds according to the present invention for the production of pharmaceutical compositions having histone inhibitory activity. deacetylases. The invention also relates to the use of the compounds according to the present invention for the production of pharmaceutical compositions for inhibiting or treating cellular neoplasia, such as for example benign or malignant neoplasm, for example, cancer. The invention also relates to the use of the compounds according to the present invention for the production of pharmaceutical compositions for the treatment of a disease other than cellular neoplasia and sensitive to histone deacetylase inhibitor therapy, such as non-malignant diseases. mentioned above. The invention also relates to the use of the compounds according to the present invention for the production of pharmaceutical compositions for inhibiting the activity of the deacetylase histone in the treatment of diseases that respond to such inhibition or to the functional consequences thereof. The invention also relates to a method for treating, preventing or alleviating the diseases, disorders, conditions and / or conditions mentioned herein in a mammal, in particular a human patient, comprising administering a pharmacologically active and therapeutically effective amount. and tolerable of one or more of the compounds according to the present invention to such mammal in need thereof. The invention also relates to the compounds in accordance with this invention for use in the treatment and / or prophylaxis of diseases, especially the diseases mentioned. The invention also relates to pharmaceutical compositions comprising one or more of the compounds according to this invention and a pharmaceutically acceptable diluent or carrier. The invention also relates to pharmaceutical compositions according to this invention having histone deacetylase inhibitory activity. The invention also relates to pharmaceutical compositions according to this invention having apoptosis-inducing activity. The invention also relates to pharmaceutical compositions according to this invention having antiproliferative activity. The invention also relates to the use of a pharmaceutical composition comprising one or more of the compounds according to this invention and a pharmaceutically acceptable diluent or carrier in the manufacture of a pharmaceutical product, such as for example a commercial container, for use in the treatment and / or prophylaxis of diseases as mentioned. Also, the invention also relates to an article of manufacture, which comprises packaging material and a pharmaceutical agent contained in such packaging material, wherein the pharmaceutical agent is therapeutically effective in inhibiting the effects of deacetylase histories, alleviating the symptoms of a disorder related to histone deacetylase, and wherein the packaging material comprises a label or package insert indicating that the pharmaceutical agent is useful for preventing or treating mid-histiocyte deacetylase, and wherein A pharmaceuic agent comprises one or more of the compounds of formula I according to the invention. The packaging material, label and package insert equals or resembles what is generally considered packaging material, labels and standard package inserts for pharmaceutical agents having related utilities. The pharmaceutical compositions according to this invention are prepared by processes that are known per se and familiar to the person skilled in the art. As pharmaceutical compositions, the compounds of the invention (= active compounds) are used either as sols, or preferably in combination with suitable excipients and / or pharmaceutical adjuvants, for example in the form of iables, reveries, capsules, tablets, suppositories, patches. (for example, such as TTS), emulsions, suspensions, gels or solutions, the content of the active compound is preferably between 0.1 and 95% and where it can be achieved, by the appropriate choice of auxiliaries and / or excipients, a form of pharmaceutical administration (for example a delayed release form or an enteric form) suitable exactly for the active compound and / or desired action event. The person skilled in the art is familiar with auxiliaries, vehicles, excipieníes, diluyeníes, carriers or adjuvants that are suitable for the formulations, preparations or pharmaceutical compositions desired on the basis of their knowledge knowledge. In addition to the solvents, gel formers, ointment bases, and other excipients of the active compound can be used, for example antioxidants, dispersants, emulsifiers, preservatives, solubilizers, dyes, complex agents or permeation promoters. Depending on the particular disease to be treated or prevented, other therapeutic active agents, which are normally administered to treat or prevent that disease, may optionally be co-administered with the compounds according to the present invention. As used herein, other therapeutic agents that are normally administered to bring or prevent a paricular disease are known to be appropriate for the disease being treated. In a further aspect of the present invention, the derivatives of N-sulfonylpyrrole according to this invention or salts of such compounds of formula I, which function by inhibiting histone deacetylases, can be combined with standard therapeutic agents used for the aforesaid diseases. In a particular embodiment, the N-sulfonylpyrro derivatives! can be combined with one or more of the anti-cancer agents known in the art, such as, for example anti-cancer agents specific targets and / or chemotherapeutic agents known in the art. Examples of known chemo-therapeutic anti-cancer agents used in cancer therapy include, but are not limited to, (i) alkylation / carbamylation agents such as cyclophosphamide (Endoxan®), ifosfamide (Holoxan®), thioiepa (Thiotehpa Lederle®) , melphalan (Alkeran®), or chloroethylnitriosurea (BCNU); (il) platinum derivatives such as cis-platinum (Plafinex® BMS), oxaliplatin or carboplafin (Cabroplat® BMS); (ili) amphiphilic agents / inhibitors of tubulin such as vinca-alkaloids (vincrysin, vinblasyin, vinorelbine), isolates such as taxol (Paclitaxel®), taxoire (Docetaxel®) and the like, as well as new formulations and conjugates thereof; (iv) topoisomerase inhibitors such as anicycline (exemplified by Doxorubicin / Adriblastin®), epipodophyllotoxins (exemplified by Etoposide / Efopophos®) and field analogues (exemplified by Topoiecan / Hycamfin®); (v) pyrimidine aniagonists such as 5-fluorouracil (5-FU), capecitabine (Xeloda®), arabinosilcytosine / cytarabine (Alexan®) or gemcifabine (Gemzar®); (vi) antagonists of pure purines such as 6-mercaptopurine (Puri-Nethol®), 6-thioguanine or fludarabine (Fludara®) and finally (vile) folic acid antagonists such as metofrexa (Farmifrexaf®). Examples of target-specific anti-cancer drugs used in standard or experimental cancer therapy include, but are not limited to, (i) kinase inhibitors such as, for example, Glivec (Imatinib®), ZD-1 839 / lressa (Gefitinib®) Bay43-9006 (Sorafenib®), SU 1 1248 (Sutente®) or OSI-774 / Tarceva (Erlotinib®); (il) proteasome inhibitors such as PS-341 (Velcade®); (ili) 90 protein inhibitors. heat shock tai such as 17-allylaminogeldanamycin (17-AAG); (iv) vascular targeting agents (VAT) and fai anti-angiogenic drugs such as the VEGF Avastin antibody (Bevacizumab®) or KDR's kinase inhibitor PTK787 / ZK222584 (Vaialanib®); (v) monoclonal antibodies such as Hercepfin (Trastuzumab®) or Mab Thera / Riiuxan (Rituximab®), mutants as well as conjugates of monoclonal antibodies and antibody fragments; (vi) oligonucleotide-based therapeutic agents such as G-3139 / Genasense (Oblimersen®); (vile) protease inhibitors; (vili) hormonal therapeutic agents such as anti-esírógenos (for example Tamoxifen), anti-androgenos (for example Flutamida or Casodex), analogs of LH RH (for example Leuprolide, Goserelin or Triptorelin) and aromatase inhibitors. Other known anti-cancer agents that can be used by combination therapy include bleomycin, retinoids such as transreinoic acid tofal (ATRA), DNA methyltransferase inhibitors such as the 2-deoxycytidine derivative Decylabine (Docagen®), alanosine, cyclohexins as inerleukin-2, inermers such as interferon a2 or interferon- ?, TRAIL agonists and TNF-R and finally histone deacetylase inhibitors other than the sulfonylpyrrole derivatives as described in the present invention such as SAHA, PXD101, MS275, MGCD01 03, Depsipeptide / FK228, NVP-LBH589 volproic acid and buíiraíos. As exemplary amphi- cancer agencies for use in combination with the compounds according to this invention in the co-therapies mentioned in the present in the following drugs may be mentioned, without being restricted thereto, 5 FU, actinomycin D, ABARELIX, ABCIXIMAB, ACLARUBICIN, ADAPALENA, ALEMTUZUMAB, ALTRETAMINE, AMINOGLUTETIMIDA , AMIPRILOSA, AMRUBICIN, ANASTROZOLA, ANCITABIN, ARTEMISININ, AZATIOPRINA, BASILIXIMAB, BENDAMUSTINA, B1CALUTAMIDA, BLEOMICIN, BROXURIDINE, BUSULFAN, CAPECITABIN, CARBOPLATIN, CARBOCUONA, CARMUSTINA, CETRORELIX, CLORAMBUCIL, CLORMETIN, CISPLATINE, CLADRIBINE, CLOMIFENA, CYCLOPHOSFAMIDE, DACARBAZINE, DACLIZUMAB, DACTINOMYCIN, DAUBORUBICIN, DESLORELIN, DEXRAZOXANE, DOCETAXEL, DOXIFLURIDINE, DOXORUBICIN, DROLOXIFENA, DROSTANOLONE, EDELFOSINA, EFLORNITIN, EMITEFUR, EPIRUBICIN, EPITIOSTANOL, EPTAPLATIN, ERBITUX, ESTRAMUSTINA, ETOPOSIDA, EXEMESTANA, FADROZOLA, FINASTERIDA, FLOXURIDINE, FLUCITOSIN, FLUDARABIN, FLUORURACIL, FLUTAMIDA, FORMESTANA, FOSCARNET, FOSFESTROL, FOTEMUSTIN, FULVESTRANT, GEFITINIB, GEMCITABIN, GLIVEC, GOSERELIN, GUSPERIMUS, HERCEPTIN, IDARUBICIN, IDOXURIDINE, IFOSFAMIDE, IMATINIB, IMPROSULFAN, INFLIXIMAB, IRINOTECAN, LANREOTIDE, LETROZOLA, LEUPRORELIN, LOBAPLAT1N, LOMUSTINE, MELFALAN, MERCAPTOPUR1NA, METOTREXATE, METUREDEPA, MIBOPLATIN, MIFEPRISTONE, MILTEFOSINA, MIRIMOSTIM, MITOGUAZONA, MITOLACTOL, MITOMYCIN, MITOXANTRONE, MIZORIBINE, MOTEXAFIN, NARTOGRASTIM, NEBAZUMAB, NEDAPLATIN, NILUTAMIDE, NIMUSTIN, OCTREOTIDE, ORMELOXIFEN, OXALIPLATIN, PACLITAXEL, PALIV1ZUMAB, PEGASPARGASE, PEGFILGRASTIM, PENTETREOTIDE, PENTOSTATIN, PERFOSFAMIDE, PIPOSULFAN, P1RARUBICIN,. 'PLICAMICINA, PREDNIMUSTIN, PROCARBAZINE, PROPAGERMANIUM, PROSPIDIUM CHLORIDE, RALTITREXED, RANIMUSTIN, RANPIRNASE, RASBURICASE, RAZOXANE, RITUXIMAB, RIFAMPICIN, RITROSULFAN, ROMURTIDA, RUBOXISTAURIN, SARGRAMOSTIM, SATRAPLATIN, SIROLIMUS, SOBUZOXANA, SPIROMUSTINA, STREPTOZOCIN, TAMOXIFEN, TASONERMIN, TEGAFUR, TEMOPORFIN, TEMOZOLOMIDE, TENIPOSIDE, TESTOLACTONE, TIOTEPA, TIMALFASIN, TIAMIPR1NA, TOPOTECAN, TOREMIFENA, TRASTUZUMAB, TREOSULFAN, TRIAZIQUONE, TRIMETREXATE, TRIPTORELIN, TROFOSFAMIDE, UREDEPA, VALRUBICIN, VERTEPORFIN, VINBLASTINE, VINCRISTINE, V1NDESINA, VINORELBINA and VOROZOLA. The experience in the technique knows thanks to his experience the daily dose fofa! and the dosage form (s) of the additional co-administered adjunct agency (s). Such total daily dose may vary on a large scale. In practicing the present invention and, depending on the features, characteristics or purposes of their uses mentioned above, the compounds according to the present invention can be administered in combination therapy separately, sequential, simultaneous or chronological steps (for example as combined unit dose forms, such as separate unit dose forms, or as adjacent discrete unit dose forms, as fixed or non-fixed combinations, as a set of parts or as mixtures) with one or more standard therapeutic agents, in particular target-specific anti-cancer or chemotherapeutic agents known in the art, such as those mentioned above. Accordingly, another aspect of the present invention is a combination or pharmaceutical composition comprising a first active ingredient, which is an N-sulfonylpyrrole derivative according to this invention or a salt thereof, a second active ingredient, which is an agent Therapeutic standard, in particular, target specific or chemotherapeutic agent known in the art, as one of the above-mentioned, and optionally a pharmaceutically acceptable portion, diluent and / or excipient for sequential, separate, simultaneous or chronological use in therapy in any order, for example to bring, prevent, or alleviate in a patient diseases that respond to HDAC inhibitor trafficking, such as diseases, disorders or ailments mentioned, in particular cancer. In this context, the present invention also relates to a combination comprising a first active ingredient, which is at least one compound according to this invention, and a second active ingredient, which is at least one standard therapeutic agent. known in the art, for example an analytical agent known in the art, such as, for example, one or more of those mentioned earlier, for separate, sequential, simultaneous or chronological use in therapy; as, for example, in therapy of the diseases mentioned in the present. The term "combination" according to this invention may be present as a fixed combination, non-fixed combination or set of parts. "Fixed combination" is defined as a combination in which the first active ingredient and the second active ingredient are present in a single dose or in a single quantity. An example of a "fixed combination" is a pharmaceutical composition wherein the first active ingredient and the second active ingredient are present in the mixture for simultaneous administration, such as in a formulation. Another example of a "fixed combination" is a pharmaceutical combination wherein the first active ingredient and the second active ingredient are present in a unit without being in the mixture. A "set of parts" is defined as a combination wherein the first active ingredient and the second active ingredient are present in more than one unit. An example of a "parie set" is a combination where the first active ingredient and the second active ingredient are present separately. The components of the set of parts can be administered separately, sequentially, simultaneously or in stages chronologically.

The first and second acive ingredient of a combination or combination of paries according to this invention can be provided as separate formulations (ie, independently of one another), which are subsequently brought together by simultaneous, sequential, separate or chronological use in combination therapy; or packaged and presented together as separate components of a combination pack for simultaneous, sequential, separate or chronological use in combination therapy. The type of pharmaceutical formulation of the first and second active ingredient of a combination or set of parfers according to this invention can be similar, that is, both ingredients are formulated in separate capsules or tablets, or can be different, ie, suitable for different administration forms, such as, for example, an active ingredient formulated as a tablet or capsule and the other formulated for, for example, intravenous administration. The ingredients of the first and second components of the combinations, compositions or conjugates according to this invention may together comprise a therapeutically effective amount for the treatment, prophylaxis or alleviation of a disease responsive to or inhibitory to histone deacetylase inhibition, particularly one of the diseases mentioned in the present. Another aspect of the present invention is a combination comprising, in a non-fixed form, one or more of the derivatives of N-sulfonylpyrrole according to this invention or salts thereof, and one or more of the standard therapeutic agents known in the art, in particular target-specific chemotherapeutic or anti-cancer agents such as those mentioned above, for sequential use, separate, simultaneous or in chronological stages in the therapy in any order, for example, to bring, prevent or alleviate in a patient the diseases that respond to HDAC inhibitor travail, such as the diseases, transoriences or ailments mentioned, in particular cancer. Optionally, the combination includes instructions for use in therapy. Another aspect of the present invention is a combined preparation, such as, for example, a conjugate of parts, comprising a preparation of a first active ingredient, which is a compound according to this invention and a pharmaceutically acceptable carrier or diluent.; a preparation of a second active ingredient, which is a therapeutic agent known in the art, in particular an amph-cancer agent, such as, for example, one of those mentioned above, and a pharmaceutically acceptable diluent or carrier; and optionally, solutions for use in simultaneous, sequential, separate or chronological therapy, for example, for benign and malignant neoplasia or diseases other than cellular neoplasia that respond or are sensitive to the inhibition of histone deacetylases. Another aspect of the present invention is a set of parts which comprises a dosage unit of a first active ingredient, which is a sulfonylpyrrole derivative mentioned above, or a salt thereof, a dosage unit of a second active ingredient, which is a spherical therapeutic agent known in the art, in particular, an anti-cancer agent, such as, for example, an of the aforementioned, and optionally instructions for use in simul-string, sequential or separate therapy, for example to bring up disorders that respond or are sensitive to the inhibition of histones deacetylases, such as, for example, benign or malignant neoplasia, for example, Cancer. Another aspect of the present invention is a pharmaceutical product comprising one or more of the compounds according to this invention, or one or more pharmaceutical compositions comprising such compounds; and one or more therapeutic agents known in the art, in particular ani-cancer agents known in the art, or one or more pharmaceutical compositions comprising such therapeutic agents, such as, for example, those mentioned above, for use in simulin therapy, sequential or separate, for example to treat the diseases mentioned above, in particular cancer. Optionally, this pharmaceutical product comprises instructions for use in such therapy. In this regard, the invention is also related to combinations, compositions, formulations, preparations or assemblies according to the present invention having histone deacetylase inhibitory activity. Another aspect of the present invention is a composition Pharmaceutical such as a unit dosage form comprising, as a mixture, a first active ingredient, which is an N-sulfonylpyrrole derivative according to this invention or a salt thereof, a second active ingredient, which is a standard therapeutic agent known in the art, in particular, chemotherapeutic agent or target specific anticancer known in the art, as one of those mentioned above, and optionally a pharmacologically acceptable carrier, diluent or excipient. Another aspect of the present invention is a commercial package comprising one or more of the compounds according to the present invention together with instructions for simultaneous, sequential or separate use with one or more standard therapeutics known in the art, in parficular anti-cancer agents, such as those mentioned above. The pharmaceutical compositions, combinations, preparations, formulations, assemblies, products, or containers mentioned above may also include more than one of the compounds according to this invention and / or more than one of the standard therapeutic agents known in the art, in particular anti-cancer agents such as those mentioned above. Also, another aspect of the present invention is a method for treating diseases and / or disorders responsive to or responsive to the inhibition of histone deacetylases, such as, for example, cancer, in combination therapy in a patient, comprising administering a pharmacologically active and therapeutically effective and tolerable of a combination, composition, formulation, preparation or pharmaceutical assemblies as described above for such a patient who needs it. Another aspect of the present invention is a method for co-therapeutically treating diseases that respond to or are sensitive to the inhibition of histone deacetylases, such as, for example, the diseases mentioned above, in a patient in need of such treatment comprising administering separately, sequentially concurrent, fixed or non-fixed a pharmacologically active and therapeutically effective and tolerable amount of one or more of the compounds according to the present invention and a pharmacologically active and therapeutically effective and tolerable amount of one or more of the therapeutic agents known in the art, in pariicuiar anti-cancer agents, such as those mentioned above, to patient tala. Also, the compounds according to the present invention can be used in the pre or post-surgical treatment of cancer. Also, the compounds according to the present invention can be used in combination with radiation therapy, particularly in the sensitization of patients suffering from cancer to standard radiation therapy. The administration of the compounds according to this invention, the combinations and the pharmaceutical compositions according to the invention can be carried out in any of the generally accepted modes of administration available in the art.

Examples of suitable modes of administration include delivery, nasal, parenteral, rectal transdermal tropic. The oral and intravenous supply is preferred. For the trafficking of dermayoses, the N-sulfonylpyrrole derivatives of the invention are administered in particular in the form of pharmaceutical compositions which are suitable for topical application. For the production of the pharmaceutical compositions, the compounds of the invention (= active compounds) are preferably mixed with suitable pharmaceutical auxiliaries and further processed to form suitable pharmaceutical formulations. Suitable pharmaceutical formulations are, for example, powders, emulsions, suspensions, sprays, oils, ointments, ointments, creams, pastes, gels or solutions. The pharmaceutical compositions according to the invention are prepared by processes known per se. The dose of the active compounds is carried out in the usual order of magnitude for the histone deacetylase inhibitors. The topical application forms (such as ointments) for the treatment of dermatose contain therefore the active compounds in a concentration of, for example, 0.1-99%. The usual dose in the case of systemic therapy (p.o.) ranges between 0.3 and 30 mg / kg per day, (i.v.) ranges between 0.3 and 30 mg / kg / h. The choice of the optimal dosage regimen and duration of the medication, particularly the optimal dose and the manner of administration of the active compounds necessary in each case they can be determined by a person skilled in the art based on their knowledge. Biological investigations Isolation of HDAC activity of HeLa cell nuclei: The activity of HDAC is isolated from nuclear HeLa extracts according to an original method described by Dignam et al. , (Nucí ACids Res. 1 1, ppl4J5, 1 983). Briefly, isolated nuclei of HeLa cells (CIL SA, Seneife, Belgium) were re-suspended in buffer C (20 mM Hepes pH 7.9, 25% v: v glycerol, NaCl 0.2 M, 1.5 mM MgCl2, 0.2 mM EDTA, 0.5 mM PefaBloc and 0.5 mM DTT) and stirred for 30 minutes on ice. After centrifugation, the supernatant was dialysed in buffer D (40 mM Tris HCl, pH 7.4, 100 mM KCl, 0.2 mM EDTA, 0.5 mM DTT and 25% v: v glycerol) for 5 h at 4 ° C . After dialysis and centrifugation, the supernatant was stored in aliquots at -80 ° C and used for Western blot analysis as well as for enzymatic assay as described below. Isolation of rHDACI: Human HDAC1 fused with flag epitope is stably expressed in Hek293 cells. After mass culture of DMEM with supiemenios and 2% of fetal calf serum, the cells were used and the HDACI-flag was purified by affinity chromatography of M2-agarose as described (Sigma Art. No. A-2220) . The fractions of the purification were analyzed by Western blotting as well as for enzymatic activity as described earlier. HDAC fluorimetric activity assay: The assay of the activity of the HDAC enzyme was performed as described by Wegener et al. (Chem. & Biol. 10. 61 -68, 2003). Briefly, 40 μl of a 1 'dilution: 100 (= 0.4 μl) Nuclear HeLa exfracto (mixture of class I and IL HDACs), 29 μl of enzyme buffer buffer (15 mM Tris HCl pH 8.1, 0.25 mM EDTA, NaCl 250 mM, 10% v: v glycerol) and 1 μl of test compound was added to a well of a 96-well microtiter plate and the reaction started by addition of 30 μl of substrate (Ac-NH-GGK (Ac) -AMC, final concentration of 25 μM and final volume of 100 μl). After incubation for 90 minutes at 30 ° C, the reaction was terminated with the addition of 25 μl of stop solution (50 mM Tris HCl pH 8, 1 00 mM NaCl, 0.5 mg / ml trypsin and 2 μM TSA). After incubation at ambient temperature for another 40 min., Fluorescence was measured using a Wallac Vicíor 1420 multi-eikinic counter (Ex 355 nm, Em 460 nm) for quantification of AMC (7-amino-4-methylcoumarin) generated by cleavage of trypsin from a deacetylated peptide. To calculate the Cl50 values of fluorescence in wells without the test compound 1% DMSO (negative control) was set as 100% enzymatic activity and fluorescence in wells with 2 μM TSA (positive control) was set at 0% enzymatic activity. The corresponding Cl 50 values of the compounds for the HDAC inhibitory activity were determined from the curves of concentration-effect by non-linear regression. The HDAC inhibitory activity expressed by CI5Q values for the compounds selected according to the present invention is shown in the following Table 1, wherein the numbers of the compounds correspond to the numbers of the examples.

Table 1: HDAC inhibitory activity (isolated activity of HDAC from the HeLa nuclear extract) The enzymatic assay of HDAC1 is performed with minor modifications with recombinant flag-HDAC1 protein isolated from HEK293 cell lysates. Approximately 14 ng / well of flag-HDAC1 were incubated with 6 μM of subtraction Ac-NH-GGK (Ac) -AMC for 3 h at 30 ° C. The completion of the reaction and all stages were carried out as described for the HeLa cell nuclear extracts as source for the enzymatic activity of HDAC. Recombinant human HDACI expressed in Hek293 cells is inhibited by Examples 4, 5, 8 to 11, 25 and 28 with an IC 50 = 0.95 nM. Histone H3 cellular hyperacetylation assay: To evaluate the cellular efficacy of a histone deacetylase inhibitor in vitro, an assay was performed on 96-well clear bottom black plates and optimal for use on the Cellomics platform "ArrayScan IL" for calculation quantitative of hisíone aceylation. The pro-cell uses a polyclonal rabbit antibody, specifically bound to the acetylated lysine 23 of a human H3 hisinone in fixed cells with an Alexa Fluor 488 labeled goat anti-rabbit IgG used for contrainination (Braunger et al., AACR annual conference 2003, abstract 4556). 5 x 103 HeLa cervical carcinoma cells / well (ATCC CC 1 -2) in 200 μl of Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal calf serum was grown on the day 1 on Packard display plates (Packard view plates) and incubated for 24 hours under standard cell culture conditions. On day 2, 2 μl of test compound (100 x final concentration) was added and the incubation continued for another 24 h. On day 3, the culture medium was discarded and the adhered cells were fixed for 15 min at room temperature by adding 1 00 μl of fixation buffer agent (3.7% v: v formaldehyde in phosphate buffered saline / PBS) . After discarding the binding buffer and a PBS bath, the cells were permeabilized at ambient temperature by the addition of 1 μl / well permeabilization buffer. (30.8 mM NaCl, 0.54 mM Na2HPO4, 0.31 mM KH2PO4, 5% v: v Triton X-100) for 1 5 minutes at room temperature. After discarding the permeabilization buffer and adding 1 00 μl / well of blocking solution (PBS with 0.05% v: v Tween 20 and 5% p: v of powdered milk) for 30 minutes at room temperature, 1 was added. antibody (ani-K23 histone H3 antibody, Cell Signaling No. 9674) in blocking solution (50 μl / well). After incubation for 1 h at 37 ° C, the wells were washed 5 times for 5 minutes at room temperature with wash buffer (PBS with 0.05% v: v Tween 20) before the addition of the 2nd antibody (anti-goat). rabbit IgG Alexa Fluor 488; MoBiTec No. A-1 1008) in blocking solution (50 μl / well). After the additional incubation of 30 min. At 37 ° C, the wells were washed 5 times for 5 minutes at T.A. with 100 μl of wash buffer at ambient temperature. Finally, 100 μl / well of PBS were added and the image analysis was performed on the Cellomics platform "ArrayScan IL". For the calculation of the EC50 values, the nuclear fluorescence in the cells treated with or without a reference HDAC inhibitor such as SAHA or NVP-LBH-589 respectively was taken as a positive and negative conírol. For the determination of EC50, the percentage of positive cells was determined and the EC50 calculation was performed from concentration-effect curves by non-linear regression. The histone acetylation cell power expressed by EC50 values for the compounds selected according to the present invention is shown in the following Table 2, wherein the numbers of the comps correspond to the numbers of the examples. Table 2: induction of hyperaceilation of H3K23 hisinone in cervical carcinoma cells HeLa Cellular cytotoxicity assay: The amphiparaprivative activity of the histone deacetylase inhibitory compounds as described herein was evaluated with the HeLa cervical carcinoma cell line (ATCC CCL2) using the Alamar Blue cell viability assay (Resazurin). (O'Brien et al., Eur J Biochem 267, 5421-5426, 2000). Resazurin is reduced to fluorescent resorufin by cellular hydrogenase activity, co-related to viable proliferative cells. The test compounds were dissolved as 10mM solutions of dimethyl sulfoxide (DMSO) and subsequently diluted in semi-logarithmic steps. The HeLa cells were grown in 96-well flat bottom plates at a density of 3,000 cells per well in a volume of 200 μl per well. 24 hours after culturing 1 μl each of the dilutions of the compounds were added to each well of the 96-well plate. Each dilution of compound was evaluated in quadruplicate. Wells containing untreated control cells were filled with 200 μl of DMEM medium containing 0.5% v: v DMSO. The cells were then incubated with the substances for 48 hours at 37 ° C in an atmosphere, moistened with 5% carbon dioxide. To determine the viability of the cells, 20 μl of a Resazurin solution (Sigma, 90 mg / l) were added. After 4 hours of incubation at 37 ° C the fluorescence was measured at an extension of 544 nm and an emission of 590 nm. For the calculation of cell viability, the emission value of untreated cells was fixed at 100% viability and the emission rates of the treated cells were fixed in relation to the values of the untreated cells. Viabilities were expressed as% of values. The corresponding Cl50 values of the compounds for cytotoxic activity were determined from the concentration-effect curves by means of non-linear regression. The anti-proliferative / kypotoxic power expressed by Cl50 values for the compounds selected according to the present invention is shown in the following table 3, where the numbers of the compounds correspond to the numbers of the examples.

Table 3: Cytotoxicity in HeLa cervical carcinoma Induction to apoptosis The induction of apoptosis is measured using the ELISA (Art. No. 1774425, Roche Biochemicals, Mannheim, Germany.) A549 NSCLC cells are grown in 96-well flat bottom plates at a density of 3 x. 1 0 E3 cells / well in a total volume of 100 μl / well 24 hours after the culture, 1 μl of each of the dilutions of the compound in DMEM is added in a total volume of 1 μl in each well of final volume 200 μl / well). Each dilution of compound is evaluated at least in triplicate. The wells containing unframed conirol cells are filled with 200 μl of DMEM containing 0.5% vol of DMSO. The cells are incubated with the test compound for 48 hours at 37 ° C in a humidified atmosphere containing 5% carbon dioxide. According to a positive control for the induction of apoptosis, the cells are treated with 50 μM of Cisplatin (Gry Pharmaceuíicals, Kirchzaríen, Germany). The medium is extracted and the cells are used in 200 μl of lysis buffer. After centrifugation as described by the manufacturer, 10 μl of cell lysate is processed as described in the protocol. The degree of apoptosis is calculated as follows: The absorbance at 405 nm obtained with lysates of cells treated with 50 μM of cisplatin is fixed as 100 cpu (cisplatin units), while an absorbance at 405 nm of 0.0 is set as 0.0 cpu . The degree of apoptosis is expressed as cpu in relation to the value of 1 00 cpu achieved with the lysates obtained from cells treated with 50 μM of cisplatin. It is desired that the compounds according to this invention tested in the above assays have an induction effect of apoptosis when tested in this assay.

Claims (9)

1. Compounds of formula 1 (wherein R 1 is hydrogen, C 1-4 alkyl, halogen, or C 1-4 alkoxy, R 2 is hydrogen or C 1-4 alkyl, R 3 is hydrogen or C 1-4 alkyl, R 4 is hydrogen, C 1-4 alkyl, halogen, or C1-4 alkoxy, R5 is hydrogen, C1-4alkyl halogen, or C1-4alkoxy, R6 is -T1-Q1, wherein T1 is a bond, or C1-4alkylene, Q1 is Ar1, A1a, Hh1, or There wherein Ar1 is phenyl, or phenyl substituted by R61 and / or R62, wherein R61 is C1-4 alkyl, or -T2-N (R611) R612, wherein either T2 is a bond, and R611 is hydrogen, C1-4 alkyl, C2-4 hydroxyalkyl, C1-4 alkyl alkoxy C2-4, phenylalkyl C1-4, or Har1-C1-4alkyl, wherein Har1 is optionally substituted by R6111 and / or R6112, and is a ring unsaturated heteroaromatic 5 to 10 membered monocyclic or fused bicyclic comprising one to three heteroatoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, wherein R6111 is halogen, or C1-4alkyl, R6112 is C 1-4 alkyl, and R 612 is hydrogen, C 1-4 alkyl, C 1-4 alkyloxyC 2-4 alkyl or C 2-4 hydroxyalkyl, or R 611 and R 612 together or with the inclusion of the nihologen atom, to which they are linked they form a heyerocyclic ring He1, wherein Het1 is morpholino, thiomorpholino, S-oxo-thiomorpholino, S, S-dioxo-thiomorpholino, piperidino, pyrrolidino, piperazino, or 4N- (C1-4 alkyl) -piperazino, or T2 is C1-4 alkylene, or C2-4 alkylene interrupted by oxygen, and R611 is hydrogen, C1-4 alkyl, C2-4 hydroxyalkyl, C1-4 alkoxyC2-4alkyl, phenylC1-4alkyl, or Har1-C1-4alkyl, wherein Har1 is optionally replaced by R6111 and / or R6112, and is an unsaturated heteroaromatic ring of 5 to 10 monocyclic members or fused bicyclic comprising one to three heteroatoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, wherein R6111 is halogen, or C1-4alkyl, R6112 is C1-4alkyl, and R612 is hydrogen, C1-4alkyl, C1-4alkoxyC2-4alkyl or C2-4 hydroxyalkyl, OR61 1 and R612 together or with the inclusion of the nitrogen atom, to which they are bonded form a heterocyclic ring Het1, wherein Het1 is morpholino, thiomorpholino, S-oxo-thiomorpholino, S, S-dioxo-thiomorpholino, piperidino, pyrrolidino, piperazino, 4N- (C 1-4 alkyl) -piperazino, imidazolo, pyrrolo or pyrazolo, R62 is C 1-4 alkyl, C 1-4 alkoxy, halogen, cyano, C 1-4 alkoxy C 1-4 alkyl, C 1-4 alkylcarbonylamino, or C 1-4 alkylsulfonylamino, Aa 1 is a bisaryl radical formed by two aryl groups, which are independently selected from a group consisting of in phenyl and naphthyl, and which are linked by a single bond, Hh1 is a bis-heteroaryl radical consisting of two heteroaryl groups, which are independently selected from a group consisting of 5 or 6 monocyclic heteroaryl radicals comprising one or two hetero-atoms, each of which is selected ione of the group consisting of nitrogen, oxygen and sulfur, and which are joined by a single bond, Ah i is a heteroaryl radical or aryl-heteroaryl radical formed by a heteroaryl group selected from the group consisting of 5- or 6-membered heteroaryl radicals monocyclics comprising one or two heyerogens, each of which is selected from the group consisting of nihologen, oxygen and sulfur, and an aryl group selected from the group consisting of phenyl and naphthyl, wherein such aryl groups and heteroaryl are linked by a single bond, R7 is hydroxyl, or Cyc1, wherein Cyc1 is a ring system of formula wherein A is C (carbon), B is C (carbon), R71 is hydrogen, halogen, C1-4alkyl, or C1-4alkoxy, R72 is hydrogen, halogen, C1-4alkyl, or C1-4alkoxy, M including A and B is either an Ar2 ring or a Har2 ring, where Ar2 is a benzene ring, Har2 is a monocyclic 5 or 6 membered unsaturated heteroaromatic ring comprising one to three hetero-atoms, each of which which is selected from the group consisting of nitrogen, oxygen and sulfur, and the salts of these compounds. 2. Compounds of formula 1 according to the claim 1, wherein R 1 is hydrogen, C 1-4 alkyl, halogen, or C 1-4 alkoxy, R 2 is hydrogen or C 1-4 alkyl, R 3 is hydrogen or C 1-4 alkyl, R4 is hydrogen, C1-4alkyl, halogen, or C1-4alkoxy, R5 is hydrogen, C1-4alkyl, halogen, or C1-4alkoxy, R6 is -T1-Q1, wherein T1 is a bond, or alkylene C1-4, Q1 is Ar1, Aa1, Hh1, or A, where Ar1 is phenyl, or phenyl substituted by R61 and / or R62, wherein R61 is C1-4alkyl, or -T2-N (R611) R612, wherein T 2 is a bond, C 1-4 alkylene, or C 2-4 alkylene interrupted by oxygen, R 611 is hydrogen, C 1-4 alkyl, C 2-4 hydroxyalkyl, C 1-4 alkyloxy C2-4, phenylC1-4 alkyl, or Har1-C1-4 aiquil, wherein Har1 is optionally substituted with R6111 and / or R6112, and is a 5 to 10 membered fused monocyclic or bicyclic heteroaromatic ring comprising one a Ferrous atoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, wherein R6111 is halogen, or C1-4alkyl, R6112 is C1-4alkyl, R612 is hydrogen, C1-4alkyl, C1alkoxy -C2-4alkyl or C2-4 hydroxyalkyl, R62 is C1-4alkyl, C1-4alkoxy, halogen, cyano, C1-4alkoxy C1-4alkyl, C1-4alkylaminocarbonylamino, or C1-4alkylsulfonylamino, A1a is a radical bisaryl consisting of two aryl groups, which are selected independently from the group consisting of phenyl and naphthyl, and which are linked by a single bond, Hh 1 is a bis-heteroaryl radical formed by two heteroaryl groups, which are independently selected from a group consisting of 5- or 6-membered monocyclic heteroaryl radicals comprising one or two hetero-atoms, each of which is selected from the group consisting of in nitrogen, oxygen and sulfur, and which are attached by a single bond, Ah is a heteroaryl-aryl radical or an aryl-heteroaryl radical formed by a heteroaryl group selected from a group consisting of 5- or 6-membered monocyclic heteroaryl radicals comprising one or two hetero-atoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, and an aryl group selected from the group selected from a group consisting of phenyl and naphthyl, wherein such aryl groups and heteroaryl are linked by a single bond, R7 is hydroxyl, or Cyc1, where C and d is a ring system of formula wherein A is C (carbon), B is C (carbon), R71 is hydrogen, halogen, C 1-4 alkyl, or C 1-4 alkoxy, R 72 is hydrogen, halogen, C 1-4 alkyl, or C 1-4 alkoxy , M including A and B is either an Ar2 ring or a Har2 ring, where Ar2 is a benzene ring, Har2 is a 5 or 6 membered monocyclic monocyclic ring, comprising one to three heteroazines, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, and the salts of these compounds. 3. Compounds of formula I according to claim 1, wherein R1 is hydrogen, or C1-4 alkyl, R2 is hydrogen, or C1-4 alkyl, R3 is hydrogen, or C1-4 alkyl, R4 is hydrogen, or C1-4 alkyl, R5 is hydrogen, or C1-4 alkyl, R6 is -T1-Q1, where T1 is a bond, or C1-4 alkylene, Q1 is Ar1, Aa1, Hh1, or A, where Ar1 is phenyl, or R61-substituted phenyl, wherein R61 is C1-4 alkyl, or -T2-N (R611) R612, wherein either T2 is a bond, 'R611 is hydrogen, C1-4 alkyl, phenylalkyl C1-4 , or Har1-C1-4 alkyl, where Har1 is either an unsaturated 5-membered monocyclic hepatoaromatic ring comprising one, two or three heteroatoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, or a 6-membered unsaturated monocyclic heteroaromatic ring comprising one or two or a 9-membered, bicyclic, fused bicyclic hephenoaromatic ring comprising one, two or three hetero-atoms, each selected from the group consisting of nitrogen, oxygen and sulfur, or a bicyclic, fused bicyclic heteroarylary ring. 10 members comprising one or two hetero-atoms, each of which is selected from the group consisting of nihorogen, oxygen and sulfur, and R612 is hydrogen, C1-4 alkyl, or C2-4 hydroxyalkyl, or R61 1 and R612 together and including the nifrogen atom to which they are bonded, form a heterocyclic ring Het1, wherein Het1 is morpholino, or T2 is alkylene C1 -4, R61 1 is hydrogen, C 1-4 alkyl, phenylalkyl C 1-4, or Har 1-C 1-4 alkyl, wherein Har 1 is either a 5-membered monocyclic unsaturated heteroaromatic ring comprising one, two or three heteroatoms, each one of which is selected from the group consisting of nitrogen, oxygen and sulfur, or a 6-membered monocyclic unsaturated heteroaromatic ring comprising one or two nihologen atoms, or a 9-membered bicyclic unsaturated bicyclic ring comprising one, two or three hetero-axons, each of which is selected from the group consisting of ni- orogen, oxygen and sulfur, or a 10-membered bi- cyclic unsaturated bicyclic heteroaromatic ring comprising one or two heteroatoms, each of which is selected from the group consisting of nitrogen, oxygen and sulfur, and R612 is hydrogen, C1-4alkyl, or C2-4 hydroxyalkyl, or R61 1 and R612 together or with the inclusion of the nitrogen atom, to which they are linked, form a heterocyclic ring Het1, wherein He1 is morpholino, Aa1 is a radical biphenyl, Hh1 is a bipyridyl, pyrazolyl-pyridinyl, imidazolyl-pyridinyl or pyridinyl-thiophenyl radical, there is a pyridinyl-phenyl, pyrazolyl-phenyl, or imidazolyl-phenyl radical, R7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. 4. Compounds of formula I according to claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is-T1 -Q1, Aa1, Hh1, or Ah i, where T1 is a bond, or C1-2 alkylene, Q1 is Ar1, wherein Ar1 is phenyl, or R61-substituted phenyl, wherein R61 is C1-4 alkyl, or -T2-N (R611) R612, wherein either T2 is a bond, R611 is hydrogen, C1 alkyl -4, phenylalkyl C1-2, or Har1-C1-2 alkyl, wherein Har1 is pyridinyl, benzimidazolyl, benzoxazolyl, benzofuraryl, benzoylphenyl or indolyl, and R612 is hydrogen, C1-4alkyl, or C2-3 hydroxyalkyl, or R611 and R612 junes and including nitrogen atom, to which they are bound, form a heterocyclic ring Het1, where Het1 is morpholino, or T2 is C1-2 alkylene, R611 is hydrogen, C1-4alkyl, phenylalkyl C1-2 or Har1-C1-2 alkyl, wherein Har1 is pyridinyl, benzimidazolyl, benzoxazolyl, benzofuranyl benzothiophenyl or indolyl, and R612 is hydrogen, C1-4alkyl, or C2-3 hydroxyalkyl, or R611 and R612 together and including lump of nitrogen to which they are bound form a heterocyclic ring Het1, where He1 is morpholino, Aa1 is a biphenyl radical, Hh1 is a adipic bipyridyl, pyrazolyl-pyridinyl, imidazolyl-pyridinyl or pyridinyl-iiophenyl, there is a pyridinyl-phenyl radical, pyrazolyl-phenyl, or imidazolyl-phenyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. 5. Compounds of formula 1 according to the claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1-Q1, Aa1, Hh1, Ahí, or benzyl, where T1 is a bond, Q1 is Ar1 , wherein Ar1 is phenyl, or R61-substituted phenyl, wherein R61 is C1-4 alkyl, or -T2-N (R611) R612, wherein either T2 is a bond, R611 is C1-4 alkyl, and R612 is C1-4alkyl, or T2 is C1-2alkylene, R611 is hydrogen, C1-4alkyl, phenylalkyl C1-2, or Har1-C1-2alkyl, wherein Har1 is pyridinyl, or indolyl, and R612 is hydrogen, C1-4 alkyl, or C2-3 hydroxyalkyl, or R61 1 and R612 together and including the nitrogen atom to which they are attached, form a heterocyclic ring Het1, where Het1 is morpholino, 'Aa1 is 1, 1'-bifen-4-yl or 1, 1'-bifen-3-yl, Hh1 is a pyridinyl-thiophenyl radical, there is a 3- (pyridinyl) -phenyl, 3- (pyrazolyl) -phenyl, 4- radical (pipdinil) - phenyl or 4- (pyrazolyl) -phenyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. 6. Compounds of formula 1 according to the claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1 -Q1, Aa1, Hh1, Ah1, or benzyl, where T1 is a bond, Q1 is Ar1, wherein Ar1 is phenyl, 3- (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is metyl, or -T2-N (R61 1) R612, wherein either T2 is a bond , R61 1 is meyilo, and R612 is methyl, or T2 is methylene, R61 1 is hydrogen, methyl, isobutyl, benzyl, Har1-methyl, or 2 (Har1) - efyl wherein Har1 is pyridinyl or indolyl, and R612 is hydrogen, me yl, or 2-hydroxy -ylenyl, or R61 1 and R612 together and including the nitrogen atom, to which they are bonded, form a heterocyclic ring Het1, wherein Het1 is morpholino, Aa1 is 1, 1'-bifen-4-yl or 1.1 '-bifen-3-yl, Hh1 is a pyridinyl-iiophenyl radical, Ah i is a 3- (pyridinyl) -phenyl, 3- (pyrazolyl) -phenyl, 4- (pyridinyl) -phenyl or 4- (pyrazolyl) radical -phenyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of compound esus. 7. Compounds of formula 1 according to the claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1 -Q1, Aa1, Hh1, Aya, or benzyl, where T1 is a bond, Q1 is Ar1, where Ar1 is phenyl, 3- (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is methyl, or -T2-N (R61 1) R612, wherein either T2 is a bond, R61 1 is methyl, and R612 is methyl, T2 is methylene, R61 1 is hydrogen, methyl, isobutyl, benzyl, Har1 -methyl, or 2 (Har1) -ethyl wherein Har1 is pyridinyl or indolyl, and R612 is hydrogen, methyl, or 2-hydroxy-ethyl, or R61 1 and R612 together and including the nitrogen atom, to which they are linked, form a heterocyclic ring Het1, wherein Het1 is morpholino, Aa1 is 1, 1'-bifen-4-i1o or 1, 1'-bifen-3 -yl, Hh 1 is a pyridinyl-thiophenyl radical, Ah i is a 3- (pyridinyl) -phenyl, 3- (pyrazolyl) -phenyl, 4- (pyridinyl) -phenyl or 4- (pyrazolyl) r-phenyl radical, R 7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. 8. Compounds of formula 1 according to the claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1-Q1, Aa1, Hh1, Ahi, or benzyl, where T1 is a bond, Q1 is Ar1, where Ar1 is phenyl, - (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is methyl, or -T2-N (R611) R612, wherein either T2 is a bond, R611 is methyl, and R612 is mephyl, or T2 is methylene, R611 is hydrogen, isobuyl, benzyl, Har1-meityl, or 2- (Har1) -ephyl, wherein Har1 is pyridin-3-yl, pyridin-4-yl, indol-2-yl, indole 3-yl or indole-5-yl, and R612 is hydrogen, - or T2 is methylene, R611 is methyl, or 2- (Har1) -elyl, wherein Har1 is indole-2-yl, and R612 is methyl, or T2 is methylene, R611.es 2- (Har1) -ethyl, wherein Har1 is indol-2-yl, and R612 is 2-hydroxy-yl, or T2 is melylene, and R611 and R612 are together and including the Nitrogen, to which they are bound, form a Het1 of the heyrocyclic ring, wherein Het1 is morpholino, Aa1 is 1,1'-biphen-4-yl or 1,1'-biphen-3-yl, Hh1 is 5- (pyridin- 2-yl) -thiophen-2-yl, there is 3- (pyridin-3-yl) -phenyl, 3- (pyridin-4-yl) -phenyl, 3- (pyrazol-1-yl) -phenyl, 3- (1H-pyrazol-4-yl) -phenyl, 4- (pyridin-3-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, 4- (pyrazol-1-yl) -phenyl or 4- (1H-pyrazol-4-yl) -phenyl, R7 is hydroxyl, and the salts of these compounds. 9. Compounds of formula 1 according to the claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1-Q1, Aa1, Hh1, Ahi, or benzyl, where T1 is a bond, Q 1 is Ar1, wherein Ar1 is phenyl, 3- (R61) -phenyl, or 4- (R61) -phenyl, wherein R61 is methyl, or -T2-N (R61 1) R612, wherein either T2 is a bond, R61 1 is methyl, and R612 is methyl, or T2 is methylene, R61 1 is hydrogen, isobutyl, benzyl, Har1 -methyl, or 2- (Har1) -ethyl, wherein Har1 is pyridin-3-yl , pyridin-4-yl, indol-3-yl, or indole-5-yl, and R612 is hydrogen, or T2 is methylene, R61 1 is methyl, or 2- (Har1) -ethyl, wherein Har1 is indole 2-yl, and R612 is methyl, or T2 is methylene, R61 1 is 2- (Har1) -ethyl, wherein Har1 is indole-2-yl, and R612 is 2-hydroxy-yl, or T2 is methylene, and R611 and R612 together and including the nitrogen atom, to which they are bonded, form a Het1 of the heterocyclic ring, wherein Het1 is morpholino, Aa1 is 1,1'-biphen-4-yl or 1,1'-biphen-3 -yl, Hh1 is 5- (pyridin-2-yl) -thiophen-2-yl, there is 3- (pyridin-3-yl) -phenyl, 3- (pyridin-4-yl) -phenyl, 3- ( pyrazol-1-yl) -phenyl, 3- (1H-pyrazol-4-yl) -phenyl, 4- (pyridin-3-yl) -phenyl, 4- (pyridin-4-yl) -phenyl, 4- (pyrazol-1-yl) -phenyl or 4- (1H-pyrazol-4-yl) -phenyl, R7 is 2-aminophenyl, and the salts of these compounds. .10. Compounds of formula 1 according to the claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1-Q1 or biphenyl, where T1 is a bond, or C1-2 alkylene, Q1 is Ar1, wherein Ar1 is phenyl, or phenyl substituted by R61, wherein R61 is C1-4 alkyl, or -T2-N (R6I1) R6.12, wherein T2 is a bond, or C1-2 alkylene, R611 is C1 alkyl -4, or Har1-C1-2 alkyl, wherein Har1 is benzimidazolyl, or indolyl, R6I2 is C1-4 alkyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. 11. Compounds of formula 1 according to claim 1, wherein R1 is hydrogen, R2 is hydrogen, R3 is hydrogen, R4 is hydrogen, R5 is hydrogen, R6 is -T1-Q1, biphenyl, or benzyl, wherein T1 is a bond,, Q1 is Ar1, where Ar1 is phenyl substituted R61, where R61 is methylo, dimethylamino, or -T2-N (R611) R612, wherein T2 is methylene, R611 is methyl, or 2- ( indol-2-yl) ethyl, R612 is metyl, R7 is hydroxyl, or 2-aminophenyl, and the salts of these compounds. 12. A compound of formula 1 according to claim 1, which is selected from 1. (E) -N-hydroxy-3- [1- (loluen-4-sulfonyl) -1-H-pyrrole-3- il] -acrilamide

2. N-hydroxy-3- (1-phenylmethanesulfonyl-1H-pyrrol-3-yl) -acrylamide

3. (E) -3- [1- (biphenyl-4-sulfonyl) -1H-pyrrol-3-yl] -N -hydroxy-acrylamide

4. (E) -3- [1- (4-dimethylamino-benzenesulfonyl) -1 H -pyrrol-3-yl] -N-hydroxy-acrylamide

5. (E) -N- (2-amino-phenyl) -3- [1 - (toluene-4-sulfonyl] -1 H -pyrrol-3-yl] -acrylamide

6. (E) -N- (2-amino-phenyl) -3 (1-phenylmetanesulfonyl-1 H-pyrrole-3 -yl) -acylamide

7. (E) -N- (2-amino-phenyl) -3- [1 - (biphenyl-4-sulfonyl) -1 H -pyrrol-3-yl] -acrylamide

8. (E) -N- (2-amino-phenyl) 3- [1- (4-dimethylamino-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide

9. (E) -N-hydroxy-3- (1 - [4 - (([2- (1 H -indol-2-yl) -ethyl] -methyl-amino) -methyl) -benzenesulfonyl] -1 H -pyrrol-3-yl) -acrylamide 1 0. (E) -3- [1- (4-Dimethylaminomefil-benzenesulfonyl) -1 H -pyrrol-3-yl] -N-hydroxy-acrylamide 1 1. (E) -N-hydroxy-3- [1 - ( 4- { [(Pyridin-3-yl-methyl) -amino] -methyl] -benzenesulfonyl) -1 H -pyrrol-3-yl} -acrylamide 12. (E) -N-hydroxy- 3- [1 - (4- { [(1 H -indol-3-yl-methyl) -amino] -methyl] -benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 13. ( E) -3- { 1 - [4- (benzylamino-methyl) -benzenesulfonyl] -1 H -pyrrol-3-yl.} - N-hydroxy-acrylamide 14. (E) -Nh idroxy-3- { l- [4- (isobuti lam ino-meityl) -bencens ulf onyl] - 1 H-pyrrol-3-yl} acrylamide 15. (E) -N-hydroxy-3-. { 1 - (4- { [(1 H -indol-5-yl-methyl) -amino] -methyl] -benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 16. (E) - N-hydroxy-3- [1 - (4- {[[(pyridin-4-yl-methyl) -amino] -methyl} - benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 17. (E) -3- [1- (4-aminomethyl-benzenesulfonyl) -1 H -pyrro-l-3-yl] -Nh id roxy-acrylamide 1 8. (E) -N-hydroxy-3- [1- (4-pyridin-4-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 19. (E) -N-hydroxy-3- . { 1 - [4- (1 H -pyrazol-4-yl) -benzenesulfonyl] -1 H -pyrrol-3-yl} Acrylamide 20. (E) -N- (2-amino-phenyl) -3- [1- (4-pyridin-4-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 21. . (E) -N- (2-amino-phenyl) -3- [1- (4-pyridin-3-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 22. (E) -N - (2-amino-phenyl) -3-. { 1 - [4- (1 H -pyrazol-4-yl) -benzenesulfonyl] -1 H -pyrrol-3-yl} Acrylamide 23. (E) -3- [1 - (biphenyl-3-sulfonyl) -1 H -pyrrol-3-yl] -N-hydroxy-acrylamide 24. (E) -N-hydroxy-3- [1 - (5-pyridin-2-yl-iiophen-2-sulfonyl) -1 H -pyrrol-3-yl] -acrylamide 25. (E) -N-hydroxy-3-yl- (4-pyrazol-1-yl) -benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 26. (E) -N- (2-amino-phenyl) -3- [1 - (5-pyridin-2-yl-thiophen-2-sulfonyl ) -1 H-pyrrole 3-yl] -acrylamide 27. (E) -Nh idroxy-3- [1 - (4-m orfolin-4-l-methyl-benzenes ulf onyl) - 1 H-pyrrole-3 -l] -acrylamide 28. (E) -N-hydroxy-3-. { 1 - [4- ( { (2-Hydroxy-ethyl) - [2- (1 H -indol-2-yl) -yl] -amino} -methyl) -benzenes ulf onyl] - 1 H -pyrrol-3-il} -acri measure 29. (E) -N-hydroxy-3- [1 - (3-pyridin-4-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] - acrylamide 30. (E) -N- (2-amino-phenyl) -3- [1- (3-pyridin-4-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 31. (E) -N- (2-amino-phenyl) -3- [1- (3-pyridin-3-yl-benzenesulfonyl) -1 H -pyrrol-3-yl] -acrylamide 32. (E ) -N-hydroxy-3-. { l- [3- (1 H -pyrazol-4-yl) -benzenesulfonyl-1 H-pyrrol-3-yl} - acrylamide and 33. (E) -N- (2-amino-phenyl) -3-. { 1 - [3- (1 H -pyrazol-4-yl) -benzenesulfonyl] -1H-pyrrol-3-yl) -acrylamide, and the salts thereof. 3. Compounds of formula 1 according to claim 1 for use in the treatment of diseases. 14. A pharmaceutical composition comprising one or more compounds of formula I according to claim 1 together with customary vehicles and / or pharmaceutical excipients. 15. Use of the compounds of formula 1 according to claim 1 for the manufacture of pharmaceutical compositions for treating diseases that respond or are sensitive to the inhibition of histone deacetylase activity. 16. Use of the compounds of formula I according to claim 1 for the manufacture of pharmaceutical compositions for bringing benign and / or malignant neoplasia, eg as cancer. 17. Use of the compounds of formula I according to claim 1 for the manufacture of pharmaceutical compositions to treat diseases other than malignancy, such as, for example, arthropathies and osteopathological conditions, systemic lupus erythematosus, rheumatoid arthritis, including light muscle cell proliferation. proliferative vascular disorders, atherosclerosis and restenosis, or inflammatory conditions. 8. A method for treating diseases in a patient, comprising administering to said patient an effective and tolerable therapeutic amount of a compound of formula I according to claim 1. 19. A method for bringing benign and / or malignant neoplasia, eg, cancer, in a patient, comprising administering to the patient a therapeutically effective and tolerable amount of a compound of formula I according to claim 1, optionally, simultaneously, sequentially or separately with one or more additional therapeutic agents. 20. A method for bringing non-malignant diseases, such as, for example arthropathies and osteopathological conditions, systemic lupus erythematosus, rheumatoid arthritis, light muscle cell proliferation including proliferative vascular disorders, atherosclerosis and restenosis, or inflammatory conditions, in a patient, comprising administering to such a patient a therapeutically effective and tolerable amount of a compound of formula I according to claim 1, optionally, simultaneously, sequentially or separately with one or more additional therapeutic agents.