Novel Theophanous Derivatives Field of the invention The present invention relates to S1P1/EDG1 receptor agonists of Formula (I) and their use as active ingredients in the preparation of pharmaceutical compositions. The invention also concerns related aspects including processes for the preparation of the compounds, pharmaceutical compositions containing a compound of the Formula (I), and their use as compounds improving vascular function and as immunomodulating agents, either alone or in combination with other active compounds or therapies. A further aspect of the invention relates to novel compounds of Formulae (II) and (III) that serve as intermediates to prepare compounds of Formula (I). Background of the invention The human immune system is designed to defend the body against foreign micro¬organisms and substances that cause infection or disease. Complex regulatory mechanisms ensure that the immune response is targeted against the intruding substance or organism and not against the host. In some cases, these control mechanisms are unregulated and autoimmune responses can develop. A consequence of the uncontrolled inflammatory response is severe organ, cell, tissue or joint damage. With current treatment, the whole immune system is usually suppressed and the body's ability to react to infections is also severely compromised. Typical drugs in this class include azathioprine, chlorambucil, cyclophosphamide, cyclosporin, or methotrexate. Corticosteroids which reduce inflammation and suppress the immune response, may cause side effects when used in long term treatment. Nonsteroidal anti-infammatory drugs (Unsaid) can reduce pain and inflammation, however, they exhibit considerable side effects. Alternative treatments include agents that activate or block cytokine signaling. Orally active compounds with immunomodulating properties, without compromising immune responses and with reduced side effects would significantly improve current treatments of uncontrolled inflammatory disease. In the field of organ transplantation the host immune response must be suppressed to prevent organ rejection. Organ transplant recipients can experience some rejection even when they are taking immunosuppressive drugs. Rejection occurs most frequently in the first few weeks after transplantation, but rejection episodes can also happen months or even years after transplantation. Combinations of up to three or four medications are commonly used to give maximum protection against rejection while minimizing side effects. Current standard drugs used to treat the rejection of transplanted organs interfere with discrete intracellular pathways in the activation of T-type or B-type white blood cells. Examples of such drugs are cyclosporin, daclizumab, basiliximab, everolimus, or FK506, which interfere with cytokine release or signaling; azathioprine or leflunomide, which inhibit nucleotide synthesis; or 15-deoxyspergualin, an inhibitor of leukocyte differentiation. The beneficial effects of broad immunosuppressive therapies relate to their effects; however, the generalized immunosuppression which these drugs produce diminishes the immune system's defense against infection and malignancies. Furthermore, standard immunosuppressive drugs are often used at high dosages and can cause or accelerate organ damage. Description of the invention The present invention provides novel compounds of Formula (I) that are agonists for the G protein-coupled receptor S1P1/EDG1 and have a powerful and long-lasting immunosuppressive effect which is achieved by reducing the number of circulating and infiltrating T- and B-lymphocytes, without affecting their maturation, memory, or expansion. The reduction of circulating T- / B-lymphocytes as a result of S1P1/EDG1 agonism, possibly in combination with the observed improvement of endothelial cell layer function associated with S1P1/EDG1 activation, makes such compounds useful to treat uncontrolled inflammatory disease and to improve vascular functionality. The compounds of the present invention can be utilized alone or in combination with standard drugs inhibiting T-cell activation, to provide a new immunosuppressive therapy with a reduced propensity for infections when 3 compared to standard immunosuppressive therapy. Furthermore, the compounds of the present invention can be used in combination with reduced dosages of traditional immunosuppressant therapies, to provide on the one hand effective immunosuppressive activity, while on the other hand reducing end organ damage associated with higher doses of standard immunosuppressive drugs. The observation of improved endothelial cell layer function associated with S1P1/EDG1 activation provides additional benefits of compounds to improve vascular function. The nucleotide sequence and the amino acid sequence for the human S1P1/EDG1 receptor are known in the art and are published in e.g.: HIa, T., and Maciag, T. J. Biol Chem. 265 (1990), 9308-9313; WO 91/15583 published 17 October 1991; WO 99/46277 published 16 September 1999. The potency and efficacy of the compounds of Formula (I) are assessed using a GTPyS assay to determine EC50 values and by measuring the circulating lymphocytes in the rat after oral administration, respectively (see in Examples). i) The invention relates to novel thiophenes of the Formula (I), wherein R"* represents methyl, trifluoromethyl, or ethyl; R^ represents hydrogen, Ci.4-alkyl, methoxy, or halogen; R^ represents hydrogen, Ci.4-alkyl, Ci.4-alkoxy, or halogen; 4 R4 represents hydrogen, Ci.4-alkyl, o.r halogen; R5 represents hydrogen; R6 represents hydrogen or hydroxyls; in case R^ represents hydroxyl, R^ can in addition represent hydroxyl; n represents 0; m represents 0 or 1; and in case m represents 1, n can in addition represent 1; and salts as well as solvent complexes of such compounds. The general terms used hereinbefore and hereinafter preferably have, within this disclosure, the following meanings, unless otherwise indicated: Where the plural form is used for compounds, salts, pharmaceutical compositions, diseases and the like, this is intended to mean also a single compound, salt, or the like. Any reference hereinbefore or hereinafter to a compound of Formula (I), (II) or (III) is to be understood as referring also to enantiomers, mixtures of enantiomers such as racemates, diastereomers, mixtures of diastereomers, and mixtures of enantiomers and diastereomers such as diastereomeric racemates, as well as salts (especially pharmaceutically acceptable salts) and solvent complexes (including hydrates) of such compounds, and morphological forms, as appropriate and expedient. The term Ci.4-alkyl, alone or in combination with other groups, means saturated, branched or preferably straight chain groups with one to four carbon atoms. preferably one to three carbon atoms. Examples of Ci-4-alkyl groups are methyl, ethyl, n-propels, /so-propel, n-butyl, /so-butyl, sec-butyl, and tern-butyl. The term Ci.4-alkoxy means an R-0 group, wherein R is a Ci.4-alkyl. Preferred examples of Ci-4-alkoxy groups are methoxy, they, prosody, and iso-propoxy. The term halogen means flour, chloral, broom or iodole, preferably fluoro or chloro. Salts are preferably the pharmaceutically acceptable salts of the compounds of Formula (I). Salt-forming groups are groups or radicals having basic or acidic properties. Compounds having at least one basic group or at least one basic radical, for ex¬ample amino, a secondary amino group not forming a peptide bond or a pyridyl radical, may form acid addition salts, for example with inorganic acids. When several basic groups are present mono- or poly-acid addition salts may be formed. Compounds having acidic groups, such as a carboxy group or a phenolic hydroxy group, may form metal or ammonium salts, such as alkali metal or alkaline earth metal salts, for example sodium, potassium, magnesium or calcium salts, or ammonium salts with ammonia or suitable organic amines, such as tertiary monoamines, for example triethylamine or tri-(2-hydroxyethyl)-amine, or heterocyclic bases, for example A/-ethyl-piperidine or A/,A/-dimethylpipera2ine. Mixtures of salts are possible. Compounds having both acidic and basic groups can form internal salts. For the purposes of isolation or purification, as well as in the case of compounds that are used further as intermediates, it is also possible to use pharmaceutically unacceptable salts, e.g. the picrates. Only pharmaceutically acceptable, non-toxic salts may be used for therapeutic purposes, however, and those salts are therefore preferred. The expression pharmaceutically acceptable salts encompasses either salts with inorganic acids or organic acids like hydrochloric acid, hydrobromic acid, hydroid acid, sulfuric acid, sulfamic acid, phosphoric acid, nitric acid, phosphorous acid, nitrous acid, citric acid, formic acid, acetic acid, oxalic acid, malefic acid, lactic acid, tartaric acid, fanatic acid, benzoic acid, Mandela acid, cinnamon acid, polemic acid, stearic acid, glutamic acid, aspartic acid, methanesulfonic acid, ethanesulfonic acid, ethanedisulfonic acid, p-toluenesulfonic acid, salicylic acid, succinct acid, trifluoroacetic acid, and the like that are non toxic to living organisms or, in case the compound of Formula (I) is acidic in nature, with an inorganic base like an alkali or earth alkali base, e.g. sodium hydroxide, potassium hydroxide, calcium hydroxide and the like. For other examples of pharmaceutically acceptable salts, reference can be made to "Salt selection for basic drugs", Int. J. Pharm. (1986), 33, 201-217. The compounds of the Formula (I), (II) or (III) may contain one or more asymmetric carbon atoms and can be prepared in fonn of pure isomers (preferred) or mixtures of isomers such as mixtures of enantiomers like racemates, mixtures of diastereomers, or mixtures of enantiomers and diasteromers such as diastereomeric racemates. The present invention encompasses all these forms. Mixtures can be separated in a manner known per se, e.g. by column chromatography, thin layer chromatography (TLC), high performance liquid chromatography (HPLC), or crystallization. ii) A particular embodiment of the invention relates to hyphened derivatives according to embodiment i), wherein R'^ represents an ethyl group. iii) A particular embodiment of the invention relates to hyphened derivatives according to embodiment i), wherein R'' represents a methyl group. iv) A particular embodiment of the invention relates to hyphened derivatives according to embodiment i), wherein R'' represents a trifluoromethyl group. v) Another particular embodiment of the invention relates to hyphened derivatives according to any one of the embodiments i) to iv), wherein R2 represents a methoxy group, and R3 and R4 represent hydrogen. vi) Another particular embodiment of the invention relates to hyphen derivatives according to any one of the embodiments i) to iv), wherein R2 represents hydrogen, and R3 and R4 represent Ci.4-alkyl. vii) Another particular embodiment of the invention relates to hyphened derivatives according to embodiment vi), wherein R3 and R4 represent a methyl group. viii) Another particular embodiment of the invention relates to hyphened derivatives according to embodiment vi), wherein R^ and R^ represent an ethyl group. ix) A particularly preferred embodiment of the invention relates to hyphen derivatives according to embodiment vi), wherein R^ represents a methyl group, and R" represents an ethyl group. x) Another particular embodiment of the invention relates to hyphened derivatives according to any one of the embodiments i) to iv), wherein R2 represents hydrogen, R3 represents a methoxy group, and R4 represents a chlorine atom. xi) Another particular embodiment of the invention relates to hyphened derivatives according to any one of the embodiments i) to iv), wherein R^ represents hydrogen, R3 represents a methyl group, and R4 represents a chlorine atom. xii) Another particular embodiment of the invention relates to hyphened derivatives according to any one of the embodiments i) to xi), wherein R^ and R^ represent hydrogen. xiii) Another particularly preferred embodiment of the invention relates to hyphened derivatives according to embodiment xii), wherein n represents 0 and m represents 1. xiv) Another particular embodiment of the invention relates to hyphened derivatives according to embodiment xii), wherein n represents 1 and m represents 1. XV) Another particular embodiment of the invention relates to hyphened derivatives according to any one of the embodiments i) to xi), wherein m represents 1, and R^ and R^ represent hydroxy. xvi) Another particular embodiment of the invention relates to thiophene derivatives according to embodiment xv), wherein n represents 0. xvii) Another particular embodiment of the invention relates to thiophene dehvatives according to any one of the embodiments i) to xi), wherein R^ represents hydrogen, and R6 represents hydroxy. xviii) A further special embodiment of the invention relates to thiophene derivatives according to embodiment i), wherein R1 represents trifluoromethyl, methyl or ethyl, R2, R5 and R® represent hydrogen, R3 and R4 represent Ci-4-alkyl, n represents 0, and m represents 1. xix) Specific thiophene compounds according to Formula (I) are; 3-{4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-2,6-dimethyl-phenyl}-propionic acid; 3-{4-[3-(5,5-dimethyl-3-trifluoromethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-2-ethyl-6-methyl-phenyl}-propionic acid; 3-{2-ethyl-6-methyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-propyl]-phenyl}-propionic acid; and 3-{2-ethyl-4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-6-methyl-phenyl}-propionic acid. XX) A further specific thiophene compound according to Formula (I) is 3-{2,6-dimethyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-. propyl]-phenyl}-propionic acid. wherein R1 R2, R3, R4, R5, R6, n and m are as defined for Formula (I) above, and R7 represents hydrogen, methyl, ethyl, or tert-butyl; and salts as well as solvent complexes of such compounds. xxii) Yet another aspect of the invention relates to novel thiophenes of Formula (III) wherein R\ R^, R^ and R* are as defined for Formula (i) above, and R^ represents hydrogen, methyl, ethyl, or tert-butyl; and salts as well as solvent complexes of such compounds. The compounds of Formula (I) and their pharmaceutically acceptable salts can be used as medicaments, e.g. in the form of pharmaceutical compositions for enteral, parental or topical administration. They can be administered, for example, perorally. e.g. in the form of tablets, coated tablets, drakes, hard and soft legatine capsules, solutions, emulsions or suspensions, rectally, e.g. in the forms of suppositories, parent rally, e.g. in the form of injection solutions or infusion solutions, or topically, e.g. in the form of ointments, creams or oils. The production of the pharmaceutical compositions can be ‘effected in a manner which will be familiar to any person skilled in the art (see for example Mark Gibson, Editor, Pharmaceutical Reformulations and Formulation, IHS Health Group, Englewood, CO, USA, 2001; Remington, The Science and Practice of Pharmacy, 20th Edition, Philadelphia College of Pharmacy and Science) by binging the described compounds of Formula (1) or their pharmaceutically acceptable salts, optionally in combination with other therapeutically valuable substances, into a agential administration form together with suitable, non-toxic, inert, pharmaceutically acceptable solid or liquid carrier materials and, if desired, usual pharmaceutical adjutants. The pharmaceutical compositions comprising a compound of Formula (1) are useful for the prevention and/or treatment of diseases or disorders associated with an activated immune system. Such diseases or disorders are selected from the group consisting of rejection of transplanted organs, tissue or cells; graft-versus-host diseases brought about by transplantation; autoimmune syndromes including rheumatoid arthritis; systemic lupus erythematosus; antiphospholipid syndrome; Hashimoto's thyroiditis; lymphocytic thyroiditis; multiple sclerosis; myasthenia gravis; type I diabetes; verities; eviscerates; sclerotic; Kawasaki's disease, eve-retinitis; posterior uveitis; uveitis associated with Behcet's disease; uveomeningitis syndrome; allergic encephalomyelitis; chronic allograft vasculopathy; post-infectious autoimmune diseases including rheumatic fever and post-infectious glomerulonephritis; inflammatory and hyperproliferative skin diseases; psoriasis; psoriatic arthritis; atopic dermatitis; myopathy; mystifies; osteomyelitis; contact dermatitis; eczematous dermatitis; seborrhoeic dermatitis; lichen planus; pemphigus; bullous pemphigoid; epidermolysis bullosa; urinary; angioedema; viscidities; erythema; cutaneous eosinophilia; acne; scleroderma; alopecia aureate; keratoconjunctivitis; vernal conjunctivitis; dermatitis; herpetic keratinize; dystrophies epithelialis cornea; corneal glaucoma; ocular pemphigus; Moore’s ulcer; ulcerative keratinize; sclerosis; Graves' ophthalmopathy; Vogt-Keying-Harada syndrome; sarcoidosis; pollen allergies; reversible obstructive airway disease; bronchial asthma; allergic asthma; intrinsic asthma; exthnsic asthma; dust asthma; chronic or inveterate asthma; late asthma and airway hyper-responsiveness; bronchiolitis; bronchitis; endometriosis; orchid’s; gastric ulcers; ischemic bowel diseases; inflammatory bowel diseases; necrotizing enterocolitis; intestinal lesions associated with thermal burns; coeliac disease; porcinis; eosinophilic gastroenteritis; mastocytosis; Crohn's disease; ulcerative colitis; vascular damage caused by ischemic diseases and thrombosis; atherosclerosis; fatty heart; myocarditis; cardiac infarction; botrytis syndrome; cachexia due to viral disease; vascular thrombosis; migraine; rhinitis; eczema; interstitial nephritis; Ida-induced nephropathy; Good pasture’s syndrome; hemolytic-uremic syndrome; diabetic nephropathy; glomerulosclerosis; glomerulonephritis; tubulointerstitial neophytes; interstitial cystitis; multiple myositis; Guillain-Barre syndrome; Métier’s disease; polyneuritis; multiple neuritis; militias; mononeuritis; radiculopathy; hyperthyroidism; Basehor’s disease; thyrotoxicosis; pure red cell aphasias; aplastic anemia; hypo plastic anemia; idiopathic thrombocytopenic purpura; autoimmune hemolytic anemia; autoimmune thrombocytopenia; agranulocytosis; pernicious anemia; megaloblastic anemia; anerythroplasia; osteoporosis; fibroid lung; idiopathic interstitial pneumonia; dermatomyositis; leukoderma vulgarism; ichthyoids Volga’s; photo allergic sensitivity; cutaneous T cell lymphoma; polyarteritis nodes; Huntington's chorea; Siena’s chorea; myocardosis; myocarditis; scleroderma; Waggener’s glaucoma; Sjogren's syndrome; adiposis; eosinophilic fascistic; lesions of gingiva, periodontium, alveolar bone, substantiate ossea dentis; male pattern alopecia or alopecia similes; muscular dystrophy; epidermal; Salary’s syndrome; hypophysitis; chronic adrenal insufficiency; Addison's disease; ischemia-reperfusion injury of organs which occurs upon preservation; antitoxin shock; pseudo membranous colitis; colitis caused by drug or radiation; ischemic acute renal insufficiency; chronic renal insufficiency; lung cancer; malignancy of lymphoid ohgin; acute or chronic lymphocytic leukemia; lymphoma; pulmonary emphysema; cataracta; siderosis; retinitis pigmentosa; senile macular degeneration; viral scarring; corneal alkali burn; dermatitis erythema; balloons dermatitis; cement dermatitis; gingivitis; periodontitis; sepsis; pancreatitis; peripheral artery disease; carcinogenesis; solid cancer tumors; metastasis of carcinoma; hypobaropathy; autoimmune hepatitis; primary billiard cirrhosis; sclerosing cholangitis; partial liver resection; acute liver necrosis; cirrhosis; alcoholic cirrhosis; hepatic failure; fulminant hepatic failure; late-onset hepatic failure; and "acute-on-chronic" liver failure. Preferred diseases or disorders to be treated and/or prevented with the compounds of Formula (I) are selected from the group consisting of rejection of transplanted organs such as kidney, liver, heart, lung, pancreas, cornea, and skin; graft-versus-host diseases brought about by stem cell transplantation; autoimmune syndromes including rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, psoriasis, psoriatic arthritis, thyroiditis such as Hashimoto's thyroiditis, uveo-retinitis; atopic diseases such as rhinitis, conjunctivitis, dermatitis; asthma; type I diabetes; post-infectious autoimmune diseases including rheumatic fever and post-infectious glomerulonephritis; solid cancers and tumor metastasis. Particularly preferred diseases or disorders to be treated and/or prevented with the compounds of Formula (I) are selected from the group consisting of rejection of transplanted organs selected from kidney, liver, heart and lung; graft-versus-host diseases brought about by stem cell transplantation; autoimmune syndromes selected from rheumatoid arthritis, multiple sclerosis, apophasis, psoriatic arthritis, Crohn's disease, and Hashimoto's thyroiditis; and atopic dermatitis. The present invention also relates to a method for the prevention or treatment of a disease or disorder mentioned herein comprising administering to a subject a pharmaceutically active amount of a compound of Formula (I). Furthermore, compounds of the Formula (1) are also useful, in combination with one or several immunomodulating agents, for the prevention and/or treatment of the diseases and disorders mentioned herein. According to a preferred embodiment of the invention, said agents are selected from the group consisting of immunosuppressants, corticosteroids, Naiad’s, cytotoxic drugs, adhesion molecule inhibitors, cytokines, cytokine inhibitors, cytokine receptor antagonists and recombinant cytokine receptors. The present invention also relates to the use of a compound of Formula (I) for the preparation of a pharmaceutical composition, optionally for use in combination with one or several immunomodulating agents, for the prevention or treatment of the diseases and disorders mentioned herein. The present invention also relates to pro-drugs of a compound of Formula (I) that convert in vivo to the compound of Formula (I) as such. Any reference to a compound of Formula (I) is therefore to be understood as referring also to the corresponding pro-drugs of the compound of Formula (I), as appropriate and expedient. The compounds of Formula (I) can be manufactured by the methods given below, by the methods given in the Examples or by analogous methods. Optimum reaction conditions may vary with the particular reactants or solvents used, but such conditions can be determined by a person skilled in the art by routine optimization procedures. Compounds of the Formula (I) of the present invention can be prepared according to the general sequence of reactions outlined below. Only a few of the synthetic possibilities leading to compounds of Formula (I) are described. The compounds of Formula (I) may be prepared by reacting a compound of Structure 1 with a base such as aq. Leah, aq. NaOH, aq. KOH, etc. or an acid such as aq. HCI, TFA, etc. in the presence or absence of additional solvents such as THF, dioxane, DMF, DMSO, DCM etc. Compounds of Structure 1 may be prepared by hydrogenation of a compound of Formula (II), or in case n represents 0, m represents 1 and R5 and R6 represent hydrogen, by hydrogenation of a compound of Formula (III) in the presence of a catalyst such as Pd/C, Pt/C etc. in a solvent such as methanol, ethanol, THF etc., or mixtures thereof. Compounds of Formula (II) may be prepared by condensing a compound of Structure 2 with a compound of Structure 3 in the presence of HCI in a solvent such as ethanol, isopropanol, etc., or mixtures thereof, or in the presence of NaOH, LiOH, or KOH in a solvent such as methanol, ethanol, isopropanol, or mixtures thereof, at temperatures preferably between 0°C and 70°C. Similarly, a compound of Formula (III) may be prepared by condensing a compound of Structure 2 with a compound of Structure 4. A compound of Structure 2 may be prepared by reacting a compound of Structure 5, wherein R is metliyl, ethyl or trifluoromethyl, with Viola in a solvent such as diethyl ether, or THF or mixtures thereof at temperatures between -20°C and 35°C. Alternatively, a compound of Structure 2 may also be prepared by reacting a compound of Structure 6, wherein R is methyl, ethyl or trifluoromethyl, with methyl magnesium bromide, methyl magnesiumchloride, or methyl magnesium iodide. The Weiner amide of Structure 6 may be prepared by reacting an acid of Structure 5 with N,0-dimethylhydroxylamine hydrophone in the presence of a coupling reagent such as EDC, DCC, etc. (Lit. e.g. M. Mentzel, H. M. R. Hoffmann, Journal fur Praktische Chemie/Chemiker-Zeltung 339 (1997), 517-524; J. Singh, N. Satyamurthi, I. S. Aidhen, Journal fuer Praktische Chemie (Weinheim, Germany) 342 (2000), 340-347; V. K. Khiestkin, D. G. Mazhukin, Current Organic Chemistry 7 (2003), 967-993). f The compounds of Structure 5 may be prepared by reacting a compound of Structure 7 with an aq. base such as aq. NaOH, aq. LiOH, aq. KOH, etc. or an acid such as aq. HCI, TFA, etc. in a solvent such as water, ethanol, methanol, THF, etc., or mixtures thereof. The compounds of Structure 7 are prepared by treating a compound of Structure 8 with a non-aqueous base such as NaOMe, NaOEt, KO-tert-Bu, DBU, etc. in a solvent such as methanol, ethanol, THF, DMF, etc., or mixtures thereof, preferably at elevated temperatures. The compounds of Structure 8 are prepared by treating a compound of Structure 9 with a 2-mercaptoacetic acid ester in the presence of a base such a NaH, NaOEt, NaOMe, K-tert-butoxide, etc. in THF, dioxane, DIVIF, ethanol, methanol, etc., or mixtures thereof. In addition, the compounds of Structure 5 may also be prepared in a one-pot-three-step procedure starting from a compound of Structure 9 following the above reaction sequence. The compounds of Structure 9 are prepared by reacting a compound of Structure 10 with a chlorinating agent such as oxalylchloride in a solvent such as DCM, CHCI3, THF, etc. (Lit. e.g. R. E. Mewshaw, Richard E. Tetrahedron Lett. 30 (1989), 3753-3756; F, A. Lakhvich, T. S. Khlebnikova, A. A. Akhrem, Zhurnal Organicheskoi Khimii 25 (1989), 2541-2549). The compounds of Structure 10, wherein R represents hydrogen, methyl or ethyl, may be prepared by maculating the compound of Structure 11 with an prophase vacillating agent such as ethyl or methyl format, methyl or ethyl acetate, methyl or ethyl propionate, chloroformate, acetyl chloride, etc. in the presence of a base such as K-tert-butylate, NaOMe, NaH, LDA, etc. in a solvent such as THF, toluene, EtOH etc. at temperatures between 0 and 60°C. (Lit. e.g. Ch. Kashima, S. Shibata, H. Yokoyama, T. Nishio, Journal of Heterocyclic Chemistry 40 (2003), 773-782; I. Yavari, Issa; M. Bayat, Tetrahedron 59 (2003), 2001-2005; J. P. Konopelski, J. Lin, P. J. Wenzel, H. Deng, G. I. Elliott, B. S. Grettenberger, Organic Letters 4 (2002), 4121-4124; C. Wiles, P. Watts, S. J. Haswell, E. Pombo-Villar, Tetrahedron Letters 43 (2002), 2945-2948; R. Faure, A. Frideling, J.-P. Galy, I. Alkorta, J. Elguero, Heterocyclic 57 (2002), 307-316; via imine: M. Hammadi, D. Villemin, Synthetic Communications 26 (1996), 2901-2904). The compound of Structure 11 is prepared according to procedures known to a person skilled in the art (Lit. e.g. M. E. Flaugh, T. A. Crowell, D. S. Farlow, Journal of Organic Chemistry 45 (1980), 5399-5400; A. M. Badger, M. J. Dimartino, C. K. Mirabelli, E. N. Cheeseman, J. W. Dorman, D. H. Picker, D. A. Schwartz, Eur. Pat. Appl. EP 310321 A2 (1989); N. R. Natale, R. O. Hutchins, Organic Preparations and Procedures International 9 (1977), 103-108; L. M. Rice, B. S. Sheth, J. W. Wheeler, Journal of Heterocyclic Chemistry 10 (1973), 731-735). In addition, the compounds of Structure 5, wherein R represents a methyl or ethyl group, are preferably prepared from a compound of Structure 5 wherein R represents hydrogen (Structure 12) by reacting the latter compound with an excess 18 of a strong base such as n-BuLi, tert-BuLi, LDA, etc. in a solvent such as THF, diethyl ether, etc. followed by the appropriate alkyl ting agent (e.g. methyl iodide, ethyl iodide, Lit. e.g. W.-D. Liu, C.-C. Chi, l.-F. Pai, A.-T. Wu, W.-S. Chung, Journal of Organic Chemistry 67 (2002), 9267-9275; D. W. Knight, A. P. Nott, Tetrahedron Letters 21 (1980), 5051-5054; R. Raap, Canadian Journal of Chemistry 49 (1971), 2155-2157). The compounds of Structure 2 wherein R'' represents a trifluoromethyl group are preferably prepared by the sequence outlined below. Hence, the compound of Structure 12 is transformed into its Weinreb amide of Structure 13, which is iodinated upon treatment with a strong base such as LDA followed by the addition of iodine in a solvent such as THF at low temperature (e.g. -78°C). The iodinated compound of Structure 14 is reacted with methyl chlorodifluoroacetate as described in the literature (e.g. D. E. Nichols, S. Frescas, D. Marona-Lewicka, X. Huang, B. L. Roth, G. A. Gudelksy, J. F. Nash, J. Med. Chem. 37 (1994), 4346-4351) to give the trifluoromethyl compound of Structure 15. Treatment of the compound Structure 15 with a methyl Grignard reagent or methyl lithium furnishes the compound of Structure 2 wherein R^ represents a trifluoromethyl group. The following schemes Illustrate synthetic routes to prepare compounds of Structure 3 and 4. (Lit. e.g. H. Kotsuki, P. K. Datta, H. Suenaga, Synthesis 1996, 470-472; for bromide or iodide instead of triflate see e.g. V. P. Baillargeon, J. K. Stille, J. Am. Chem. Soc. 108 (1986), 452-461; M. J. Gomez-Escalonilla, F. Lunge, J.-M. Rueff, L. Oswald, J. F. Nierengarten, Tetrahedron Lett. 43 (2002), 7507-7511; H. Aust, D. lctentry-t>,D-aimetnyi-4,b,b,/-ietranyaro-Denzoic]thiophen-1-yl)-Ethan one (400 mg, 1.69 mol), 3-(4-formyl-2,6-dimethyl-phenyl)-propionic acid (419 mg, 2.03 mol) and NaOH (1.7 g, 42.5 mol) in methanol (17 mol) is stirred at 75'°C for 75 min before it is diluted with 1 N aq. HCI and extracted twice with EA. The organic extracts are dried over MgS04, filtered and evaporated. The crude product is purified by CC on silica gel eluting with DCM containing 6% of methanol to give 3-{4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propenyl]-2,6-dimethyi-phenyl}-propionic acid (620 mg) as a pale yellow solid; LC-MS: tR = 1.17 min; [M+1] = 425.34; ^H NMR(CDCl3): 5 7.68 (d, J = 15.8 Hz, 1H), 35 7,28 (s, 2H), 7.27 (d, J = 15.8 Hz, 1H), .3.18 (t, J = 7.0 Hz, 2H), 3.06-2.98 (m, 2H), 2.78 (q, J = 7.6 Hz, 2H), 2.54-2.48 (m, 2H), 2.39 (s, 6H), 2.34 (s, 2H), 1.58 (t, J = 7.0 Hz, 2H), 1.32 (t, J = 7.6 Hz, 3H). A solution of 1-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-Ethan one (143 mg, 0.606 mol) and 3-(2-ethyl-4-formyl-6-methyl-phenyl)-propionic acid (200 mg, 0.908 mol) in ethanol (15 mL) is treated with 5 N HCI in isopropanol (3 mL). The dark brown reaction mixture is stirred at rt for 3 h, then at 50°C for 48 h before DIPEA (4 mol) is added. The solvent is removed in vacuum and the crude product is purified by prep. HPLC (Grom-Sil 120 0DS-4-HE, 30x75 mm, 10 ^im, acetonitrile/water (0.5% HCOOH), 10% to 95% acetonitrile) to give 3-{2-ethyl-4-[3-(3-ethyl-5,5-dlmethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propenyl]-6-methyl-phenyl}-propionic acid ethyl ester (157 mg) as a yellow oil; LC-MS: tp = 1.27 min,[M+1]= 467.43. A solution of 1-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-Ethan one (200 mg, 0.846 mol) and 3-(2-ethyl-4-formyl-6-methyl-phenyl)-acrylic 36 acid (203 mg, 0.931 mmol) in methanolic NaOH (8 mL, 10 g NaOH in 100 mL methanol) is stirred at rt for 3 In before it is carefully acidified to pH 1 by adding 2 N aq. HCI, The mixture is extracted twice with DCM and the organic extracts are washed with water and brine, dried over MgS04, filtered and evaporated. The crude product is crystallised from acetonitrile (40 mL) to give 3-{2-ethyl-4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-ben2o[c]thiophen-1-yl)-3-oxo-propenyl]-6-methyl-phenylj-acrylic acid (222 mg) as yellow crystals. From the mother liquor a second crop (29 mg) of product can be obtained after purification by prep. HPLC (Grom-Sil 120 0DS-4-HE, 30x75 mm, 10 ^m, acetonitrile/water (0.5% HCOOH), 20% to 95% acetonitrile); LC-MS: [R = 1.20 min, [M+1] = 437.31. 3-{2-Ethyl-6-methyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-propenyl]-phenyl}-acrylic acid is prepared from 1-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1 -yl)-Ethan one and 3-(2-ethyl-4-formyl-6-methyl-phenyl)-acrylic acid in analogy to Intermediate 2B; LC-MS: tp = 1.17 min; [M+1] = 423.34; ^H NMR (CDCI3): 5 7.97 (d, J = 16.4 Hz, 1H), 7.68 (d, J = 15.2 Hz, 1H), 7.33 (s, 2H), 7.28 (d, J = 15.8 Hz, 1H), 6.13 (d, J = 15.8 Hz, 1H), 3.16 (t, J = 7.0 Hz, 2H), 2.77 (q, J = 7.6 Hz, 2H), 2.41 (s, 3H), 2.39 (s, 3H), 2.32 (s, 2H), 1.57 (t, J = 6.4 Hz, 2H), 1.24 (t, J = 7.6 Hz, 3H), 1.00 (s, 6H). Intermediate 4 3-{4-[3-(5,5-Dimethyl-3-trifluoromethyl-4,5,6,7-tetrahyclro-benzo[c]thiophen-1-y!)-3-oxo-propenyl]-2-ethyl-6-methyl-phenyl}-propionic acid ethyl ester is prepared In analogy to Intermediate 2A starting from Scaffold F and Building Block D; LC-MS: IR = 1,29 min. rM+1l = 506.68. 3-{2,6-Dimethyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-propenyl]-phenyl}-acrylic acid (570 mg) is obtained by condensing Scaffold D (415 mg, 1.87 mmol) with Building Block B (381 mg, 1.87 mmol) in analogy to Intermediate 2B; LC-MS: tR= 1.17 min, [M+1] = 409,21. To a solution of 3-{4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propenyl]-2,6-climethyl-phenyl}-propionic acid (610 mg, 1.44 mol) and DIPEA (204 mg, 1.58 mol) in ethanol (30 mol) is added Pd/C (300 mg, 10% Pd, moistened with 50% water). The slurry is stirred at rt for 18 h under 1 atm H2. The mixture is filtered and the filtrate is evaporated. The crude product is purified by prep. HPLC (Grom-Sil 120 0DS-4-HE, 30x75 mm, 10 |am, acetonitrile/water (0.5% HCOOH), 20% to 95% acetonitrile) to give 3-{4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-2,6-dimethyl-phenyl}-propionic acid (460 mg) as a colourless lyophilizes; LC-MS: tp = 1.15 min; [M+1] = 427.40; ^H NMR (CDCI3): 5 6.91 (s, 2H), 3.10-2.90 (m, 8H), 2.73 (q, J = 7.6 Hz, 2H), 2.53-2.46 (m, 2H), 2.32 (s, 6H), 2.30 (s, 2H), 1.54 (t, J = 7.0 Hz, 2H), 1.28 (t, J = 7.6 Hz, 3H), 0.97 (s, 6H). a) To a solution of 3-{2-ethyl-4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propenyl]-6-methyl-phenyl}-propionlc acid ethyl ester (153 mg, 0.328 mmol) in ethanol, Pd/C (80 mg, 10% Pd, moistened with 50% water) is added and the resulting slurry is stirred at rt for 72 h under 1 bar of H2. The reaction mixture is filtered and the filtrate is evaporated. The crude product is purified by prep. HPLC (Grom-Sil 120 0DS-4-HE, 30x75 mm, 1Q ^m, acetonitrile/water (0.5% HCOOH), 20% to 95% acetonitrile) to give 3-{2-ethyl-4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-6-methyl-phenyl}-propionic acid ethyl ester (95 mg) as an amorphous solid; LC-MS: tp = 1.26 min, [M+1] = 469.40. b) A solution of 3-{2-ethyl-4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-ben20[c]thiophen-1-yl)-3-oxo-propyl]-6-methyl-phenyl}-propionic acid ethyl ester (92 mg, 0,196 mmol) in ethanol (2 mL) is treated with 2 N aq. NaOH (2 mol). The solution is stirred at rt for 1 h before the solvent is removed in vacuum. The residue is dissolved in 2 N aq. HCI, and extracted with EA. The organic extract is washed with brine, dried over Na2S04, filtered and evaporated to give 3-{2-ethyl-4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-6-methyl-phenylj-propionic acid as an amorphous solid; LC-MS: XR - 1.16 min; [M+1] = 441.36; ^H NMR (CDCI3): 5 6.95 (s, 1H), 6.93 (s, 1H), 3.12-2.94 (m, 8H), 2.74 (q, J = 7.6 Hz, 2H), 2.66 (q, J = 7.6 Hz, 2H), 2.56-2.48 (m, 2H), 2.36 (s, 3H), 2.32 (s, 2H), 1.56 (t, J = 7.0 Hz, 2H), 1.29 (t, J = 7.6 Hz, 3H), 1.24 (t, J = 7.6 Hz, 3H). To a solution of 3-{2-ethyl-6-methyl-4-[3-oxo-3-(3,5,5-thmethyl-4,5,6,7-tetrahydro- benzo[c]thiophen-1-yl)-progeny]-phenyl}-acrylic acid (Intermediate 3; 340 mg, 0.805 mmol) and DIPEA (182 mg, 1.41 mol) in ethanol, Pd/C (340 mg, 10% Pd, moistened with 50% water) is added and the resulting slurry is stirred at SOX for 72 h under 10 bar of H2. Another portion of Pd/C is added and stirring is continued for 16 h at 50°C under 10 bar of H2. The reaction mixture is filtered and the filtrate is evaporated. The crude product is purified by prep. HPLC (Grom-Sil 120 0DS-4-HE, 30x75 mm, 10 ^m, acetonitrile/water (0.5% HCOOH), 20% to 95% acetonitrile) to give 3-{2-ethyl-6-methyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro- benzo[c]thiophen-1-yl)-propyl]-phenyl}-propionic acid (154 mg) as a colourless foam; LC-MS: tR = 1.15 min, [M+1] = 427.30. Example 4 3-{4-[3-(5,5-Dimethyl-3-trifluoromethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-2-ethyl-6-methyl-phenyl}-propionic acid is prepared in analogy to Example 2 starting from Intermediate 4; LC-MS: tp = 1.17 min, [M+1] = 481.36. 3-{2,6-Dimethyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-propyl]-phenyl}-propionic acid (430 mg) is obtained starting from Intermediate 5 (548 mg, 1.34 mol) in analogy to Example 3; LC-MS: tR = 1.13 min; [M+1] = 413.34; ^H NMR (CDCI3): 5 0,97 (s, 6 H), 1.53 (t, J = 6.7 Hz, 2 H), 2.28 (s, 2H), 2.32 (s, 6H), 2.33 (s, 3H), 2.45-2.54 (m, 2 H), 2,89-2.99 (m, 4 H), 2.99-3.10 (m, 4 H), 6.91 (s, 2 H), Example 6:,GTPyS assay to determine EC50 values GTPyS binding assays are performed in 96 well micro titer plates (Nun, 442587) in a final volume of 200 |jl, using membrane preparations of CHO cells expressing recombinant human SI PI receptor. Assay conditions are 20 mM Hopes (Fluke, 54461), 100 mM NaCI (Fluka, 71378), 5 mM MgCb (Fluka, 63064), 0,1% BSA (Calbiochem, 126609), 1 MM GDP (Sigma, G-7127), 2,5% DMSO (Fluka, 41644), 50 pM 35S-GTPyS (Amersham Biosciences, SJ1320). The pH is 7.4. Test compounds are dissolved and diluted in 100% DMSO and pre-incubated at room temperature for 30 min in 150 pi of the above assay buffer, in the absence of ^^S-GTPyS. After addition of 50 pi of ^^S-GTPyS, the assay is incubated for 1 h at rt. The assay is terminated by transfer of the reaction mixture to a Multiscreen plate (Millipore, MAHFC1H60) using a cell harvester from Packard Biosciences, and the plates are washed with ice-cold 10 mM Na2HP04/NaH2P04 (70%/30%), dried, sealed at the bottom and, after addition of 25 pi MicroScint20 (Packard Biosciences, order no. 6013621), sealed on the top. Membrane-bound ^^S-GTPyS is measured with a TopCount from Packard Biosciences. EC50 is the concentration of agonist inducing 50 % of the maximal specific ^^S-GTPyS binding. Specific binding is determined by subtracting non-specific binding from maximal binding. Maximal binding is the amount of cap bound to the Multiscreen plate in the presence of 10 pM of SIP. Non-specific binding is the amount of binding in the absence of an agonist in the assay. Table 1 shows the EC50 value of a compound of the present invention. The EC50 value was determined according to the method described above. Example 7: Assessment of In vivo Efficacy The efficacy of the compounds of Formula (I) is assessed by measuring the circulating lymphocytes after oral administration of 3 to 30 mg/kg of a compound of Formula (I) to normotensive male Wister rats. The animals are housed in climate-controlled conditions with a 12 h-light/dark cycle, and have free access to normal rat chow and drinking water. Blood is collected before and 3, 6 and 24 h after drug administration. Full blood is subjected to hematology using Advia Hematology system (Bayer Diagnostics, Zurich, Switzerland). All data are presented as mean ± SEM. Statistical analyses are performed by analysis of variance (ANOVA) using Statistics (Stat Soft) and the Student-Newman-Keuls procedure for multiple comparisons. The null hypothesis is rejected when p < 0.05. As an example, Table 2 shows the effect on lymphocyte counts 6 h after oral administration of 10 mg/kg of a compound of the present invention to normotensive male Waster rats as compared to a group of animals treated with vehicle only. Claims wherein R1 represents nnethyl, trifluoromethyl, or ethyl; R2 represents hydrogen, Ci-4-alkyl, methoxy, or halogen; R^ represents hydrogen, Ci.4-alkyl, Ci-4-alkoxy, or halogen; R* represents hydrogen, Ci.4-alkyl, or halogen; R* represents hydrogen; R6 represents hydrogen or hydroxy; in case R6 represents hydroxy, R5 can in addition represent hydroxy; n represents 0; m represents 0 or 1; and in case m represents 1, n can in addition represent 1; 44 and salts as well as solvent complexes of such compounds. 2. A compound according to claim 1, wherein R1 represents an ethyl group. 3. A compound according to claim 1, wherein R'' represents a methyl group. 4. A compound according to claim 1, wherein R"* represents a trifluoromethyl group. 5. A compound according to any one of claims 1 to 4, wherein R^ represents a methoxy group, and R^ and R* represent hydrogen. 6. A compound according to any one of claims 1 to 4, wherein R^ represents hydrogen, and R^ and R* represent Ci.4-alkyl. 7. A compound according to claim 6, wherein R^ and R* represent a methyl group. 8. A compound according to claim 6, wherein R^ and R* represent an ethyl group. 9. A compound according to claim 6, wherein R^ represents a methyl group, and R* represents an ethyl group. 10. A compound according to any one of claims 1 to, 4, wherein R^ represents hydrogen, R^ represents a methoxy group, and R^ represents a chlohne atom. 11. A compound according to any one of claims 1 to 4, wherein R^ represents hydrogen, R^ represents a methyl group, and R* represents a chlorine atom. 12. A compound according to any one of claims 1 to 11, wherein R^ and R^ represent hydrogen. 13. A compound according to claim 12, wherein n represents 0, and m represents 1. 14. A compound according to claim 12, wherein n represents 1, and m represents 1. 15. A compound according to any one of claims 1 to 11, wherein m represents 1, and R^ and R® represent hydroxy. 16. A compound according to claim 15, wherein n represents 0. 17. A compound according to any one of claims 1 to 11, wherein R^ represents hydrogen, and R® represents hydroxy. 18. A comopund according to claim 1 selected from the group consisting of: 3-{4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-2,6-dimethyl-phenyl}-propionic acid; 3-{4-[3-(5,5-dimethyl-3-trifluoromethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-2-ethyl-6-methyl-phenyl}-propionic acid; 3-{2-ethyl-6-methyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-propyl]-phenyl}-propionic acid; and 3-{2-ethyl-4-[3-(3-ethyl-5,5-dimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-3-oxo-propyl]-6-methyl-phenyl}-propionic acid. 19. A compound according to claim 1 which is 3-{2,6-dimethyl-4-[3-oxo-3-(3,5,5-trimethyl-4,5,6,7-tetrahydro-benzo[c]thiophen-1-yl)-propyl]-phenyl}-propionicacid. 20. A pharmaceutical composition comprising a compound according to any one of claims 1 to 19 and a pharmaceutically acceptable carrier. 21. A compound according to any one of claims 1 to 19, or a pharmaceutical composition according to claim 20, for use as a medicament. 22. Use of a compound according to any one of claims 1 to 19 for the preparation of a pharmaceutical composition for the prevention or treatment of diseases or disorders associated with an activated immune system. 23. The use according to claim 22 for the prevention or treatment of diseases or disorders selected from the group consisting of rejection of transplanted organs such as kidney, liver, heart, lung, pancreas, cornea, and sl