COMPOUNDS HAVING CRTH2 ANTAGONIST ACTIVITY The present invention relates to compounds which are useful as Pharmaceuticals, to methods for preparing these compounds, compositions containing them and their use in the treatment and prevention of allergic diseases such as asthma, allergic rhinitis and atopic dermatitis and other inflammatory diseases mediated by prostaglandin Da (PGDa) acting at the CRTH2 receptor on cells including eosinophils, basophils and Th2 lymphocytes. PGD2 is an eicosanoid, a class of chemical mediator synthesised by cells in response to local tissue damage, normal stimuli or hormonal stimuli or via cellular activation pathways. Eicosanoids bind to specific cell surface receptors on a wide variety of tissues throughout the body and mediate various effects in these tissues. PGDa is known to be produced by mast cells, macrophages and Th2 lymphocytes and has been detected in high concentrations in the airways of asthmatic patients challenged with antigen (Murray et al, (1986), N. Engl. J. Med. 315: 800-804). Instillation of PGDa into airways can provoke many features of the asthmatic response including bronchoconstriction (Hardy et al, (1984) N. Engl. J. Med. 311: 209-213; Sampson et al (1997) Thorax 52: 513-518) and eosinophil accumulation (Emery et al, (1989) J. Appl. Physiol. 67: 959-962). The potential of exogenously applied PGD2 to induce inflammatory responses has been confirmed by the use of transgenic mice overexpressing human PGD2 synthase which exhibit exaggerated eosinophilic lung inflammation and Th2 cytokine production in response to antigen (Fujitani et al, (2002) /. Immunol. 168: 443-449). The first receptor specific for PGDj to be discovered was the DP receptor which is linked to elevation of the intracellular levels of cAMP. However, PGD2 is thought to mediate much of its proinflammatory activity through interaction with a G protein-coupled receptor termed CRTH2 (chemoattractant receptor-homologous molecule expressed on Th2 cells) which is expressed by Th2 lymphocytes, eosinophils and basophils (Hirai et al, (2001) J. Exp. Med. 193: 255-261, and EP0851030 and EP-A-1211513 and Bauer et al, EP-A-1170594). It seems clear that the effect of PGD2 on the activation of Th2 lymphocytes and eosinophils is mediated through CRTH2 since the selective CRTH2 agonists 13,14 dihydro-15-keto-PGD2 (DK-PGD2) and 15R-methyl-PGD2 can elicit this response and the effects of PGD2 are blocked by an anti-CRTH2 antibody (Hirai et al, 2001; Monneret et al, (2003) J. Pharmacol. Exp. Ther. 304: 349-355). In contrast, the selective DP agonist BW245C does not promote migration of Th2 lymphocytes or eosinophils (Hirai et al, 2001; Gervais et al, (2001) /. Allergy Clin. Immunol. 108: 982-988). Based on this evidence, antagonising PGD2 at the CRTH2 receptor is an attractive approach to treat the inflammatory component of Th2-dependent allergic diseases such as asthma, allergic rhinitis and atopic dermatitis. EP-A-1170594 suggests that the method to which it relates can be used to identify compounds which are of use in the treatment of allergic asthma, atopic dermatitis, allergic rhinitis, autoimmune disease, reperfusion injury and a number of inflammatory conditions, all of which are mediated by the action of PGD2 at the CRTH2 receptor. Compounds which bind to CRTH2 are taught in WO-A-03066046 and WO-A-03066047. These compounds arc not new but were first disclosed, along with similar compounds, in GB 1356834, GB 1407658 and GB 1460348, where they were said to have anti-inflammatory, analgesic and antipyretic activity. WO-A-03066046 and WO-A-03066047 teach that the compounds to which they relate are modulators of CRTH2 receptor activity and are therefore of use in the treatment or prevention of obstructive airway diseases such as asthma, chronic obstructive pulmonary disease (COPD) and a number of other diseases including various conditions of bones and joints, skin and eyes, GI tract, central and peripheral nervous system and other tissues as well as allograft rejection. The compounds described in these documents are indoles with a carboxylic acid group is at the 3-position of the indole ring system a quinoline, quinazoline or benzothiazole group at the 1-position. The present invention relates to novel compounds which bind to CRTH2 and which will therefore also be useful in the treatment of diseases and conditions mediated by the activity of PGD2 at the CRTH2 receptor. In the present invention there is provided a compound of general formula (I) (Figure Removed) wherein R1, R2, R3 and R4 are independently hydrogen, halo, Ci-Q alkyl, -O(Ci-Cfi alkyl), -CON(R9)2 , -SOR9, -SO2R9, -SO2N(R9)2, -N(R9)2, -NR9COR9, -CO2R9, -COR9, -SR9,-OH,-NO2or-CN; each R9 is independently hydrogen or Ci-Cg alkyl; R5 and R6 are each independently hydrogen, or Cj-Q alkyl or together with the carbon atom lo which they are attached form a Ca-C? cyclonlkyl group; R7 is hydrogen or Ci-Cg alkyl n is 1 or 2; X is a bond or, when n is 2, X may also be a NR9 group; wherein R9 is as defined above; when X is a bond R8 is C1-C6 alkyl, C2-C6 alkenyl, C2-C6 alkynyl, biphenyl or a 9-14 membered bicyclic or tricyclic heteroaryl group; when X is a NR9 group R8 may additionally be phenyl, naphthyl or a 5-7 membered heteroaromatic ring; and the R group is optionally substituted with one or more substituents selected from halo, C1-C6 alkyl, -O(C1-C6)alkyl, aryl, -O-aryl, heteroaryl, -O-heteroaryl, -CON(R9)2, -SOR9, -SO2R9, SO2N(R9)2, -N(R9)2, -NR9COR9, -CO2R9, -COR9, -SR9, -OH,-N02or-CN; wherein R9 is as defined above; or a pharmaceutically acceptable salt, hydrate, solvate, complex or prodrug thereof. The compounds of general formula (I) are antagonists of PGD2 at the CRTH2 receptor and will therefore be useful in the treatment of conditions which are mediated by PGD2 binding to CRTH2. These include allergic diseases, asthmatic conditions and inflammatory diseases, examples of which are allergic asthma, perennial allergic rhinitis, seasonal allergic rhinitis, atopic dermatitis, contact hypersensitivity (including contact dermatitis), conjunctivitis, especially allergic conjunctivitis, eosinophilic bronchitis, food allergies, eosinophilic gastroenteritis, inflammatory bowel disease, ulcerative colitis and Crohn's disease, mastocytosis and also other PGD2-mediated diseases, for example autoimmune diseases such as hyper IgE syndrome and systemic lupus erythematus, psoriasis, acne, multiple sclerosis, allograft rejection, reperfusion injury, chronic obstructive pulmonary disease, as well as rheumatoid arthritis, psoriatic arthritis and osteoarthritis. Similar, but not identical, compounds are disclosed in WO-A-9950268. These compounds differ from those of the present invention in that they do not contain a sulfone/sulfonamide moiety attached to the 3-position of the indole ring. In addition, they are not taught to be useful in the treatment of conditions such as asthma and allergic conditions, which are mediated by PGD2. Rather, they are said to be of use in the treatment of complications arising from diabetes mellitus. PL 65781 and JP 43-24418 also relate to indole derivatives. However, the compounds disclosed in both of these documents differ from the compounds of the present application in that they are indole N-sulfonamides rather than 3-sulfones or 3-sulfonamides like the compounds of the present invention. The compounds disclosed in PL 65781 and JP 43-24418 are similar in structure to indomethacin and, like indomethacin, are said to have anti-inflammatory and antipyretic activity. Thus, although this may not have been appreciated at the time when these documents were published, the compounds they describe are COX inhibitors, an activity which is quite different from that of the compounds of the present invention. Indeed, COX inhibitors are contraindicated in the treatment of many of the diseases and conditions, for example asthma and inflammatory bowel disease, for which the compounds of the present invention are useful, although they may sometimes be used to treat arthritic conditions. Compounds which bind to the CRTH2 receptor are disclosed in WO-A-03/097042 and WO-A-03/097598. These compounds are indole acetic acids but in WO-A-03/097042 the indole system is fused at the 2-3 positions to a 5-7 membered carbocyclic ring. In WO-A-03/097598 there is a pyrrolidine group at the indole 3-position. WO-A-03/101981 and WO-A-03/101961 both relate to CRTH2 antagonists. The compounds described in WO-A-03/101961 are similar in structure to the compounds of the present invention in which X is a bond. They differ from the compounds of general formula (I) because there is an -S- group linked to the indole 3-position in place of the SO or SOj group of the compounds of general formula (I). In addition, the group equivalent to the R8 group in the compounds of general formula (I) is an aryl or heteroaryl group. There are no aliphatic substitutents at this position as with the compounds of general formula (I). It has surprisingly been found that although these compounds have high intrinsic activity, they are less suitable for use as medicaments than the compounds of the present invention. This is because certain of the compounds of WO-A-03/101961 are inhibitors of cytochrome P4sos and this has implications for the metabolism of any pharmacological agent which may be co-administered with these compounds. In contrast, the present inventors have shown that, surprisingly, the compounds of the present invention do not inhibit cytochrome P450S. In addition, our preliminary binding experiments have indicated that the sulfide compounds described in WO-A-03/101961 appear to bind human eosinophils with a low off rate, which could lead to an unpredictable duration of action. WO-A-03/10981 relates to compounds which are of similar structure to the compounds of the present invention except that the substituent at the 3-position of the indole ring system is a phenyl, naphthyl or heteroaryl group with no SO, SOj or SOjNR9 linker as with the compounds of general formula (I). Clearly, the inclusion of a linking group is likely to have a substantial effect on the activity of the compound. Furthermore, the substituent at the indole 3-position cannot be an aliphatic group as in the present invention. WO-A-2004/007451 relates to CRTH2 inhibitors which are similar in structure to the compounds of the present invention in which X is a bond, except that the group A equivalent to the R group of the compounds of general formula (I) is phenyl, naphthyl or a 5-7 membered heteroaromatic group. In fact, all the exemplified compounds have a substituted phenyl group at this position. This is clearly different from the compounds of the present invention where the R8 groups are either a bicyclic or tricyclic heteroaromatic ring or an alkyl, alkenyl or alkynyl group. It is particularly surprising that compounds containing alkyl, alkenyl and alkynyl groups have proved to be so active since they differ markedly in structure from the prior art compounds. In the present specification "C1-C6 alkyl" refers to a straight or branched saturated hydrocarbon chain having one to six carbon atoms and optionally substituted with one or more halo substituents or with one or more C3-C7 cycloalkyl groups. Examples include methyl, ethyl, n-propyl, isopropyl, t-butyl, n-hexyl, trifluoromethyl, 2-chloroethyl, methylenecyclopropyl, methylenecyclobutyl, methylenecyclobutyl and methylenecyclopentyl. "C1-C4 alkyl" and "C1-C18 alkyl" have similar meanings except that they contain from one to four and from one to eighteen carbon atoms respectively. C3-C7 cycloalkyl refers to a saturated 3 to 7 membered carbocyclic ring. Examples of such groups include cyclopropyl, cyclobutyl, cyclopentyl and cyclohexyl. The terms "C2-C6 alkenyl" and "C2-C6 alkynyl" refer straight or branched hydrocarbon chains having from two to six carbon atoms and containing respectively at least one carbon-carbon double bond or at least one carbon-carbon triple bond. As with alkyl groups they may optionally be substituted with one or more halo substituents or with one or more C3-C7 cycloalkyl groups. In the present specification, "halo" refers to fluoro, chloro, bromo or iodo. The terms "aromatic moiety" and "aryl" in the context of the present specification refer to an aromatic ring system having from 5 to 14 ring carbon atoms and containing up to three rings. Examples of aromatic moieties are benzene and naphthalene. Aryl groups may be substituted with one or more substituents chosen from halo, C1-C6 alkyl, C1-C6 alkoxy, a 5-7-membered heterocyclic ring or SOzR9 where R9 is as defined above. The terms "heteroaromatic moiety" and "heteroaryl" refer to an aromatic ring system in which at least one of the ring carbon atoms is replaced by a nitrogen, oxygen or sulfur atom. Examples include single ring systems such as pyridine, pyrimidine, pyrazole, thiophene, oxazole and isoxarolc. Other examples include fused ring systems such as quinoline, isoquinoline, quinazoline, benzthiazole, benzoxazole, bcnzimidazole and indole groups. Unless stated otherwise a heteroaromatic moiety has from 5 to 14 ring carbon atoms but, for example, "5-7 membered heteroatomatic ring" contains 5 to 7 ring atoms. Bicyclic and tricyclic heteroaryl groups contain respectively two or three fused rings. Bicyclic heteroaryl groups may be, for example, 6,6- or 6-5-ring systems such as those exemplified above. As with aryl groups, heteroaryl groups may also be substituted with one or more substituents chosen from halo, C1-C6 alkyl, C1-C6 alkoxy, a 5-7-membered heterocyclic ring or SO2R9 where R9 is as defined above. The term "5 to 7 membered heterocyclic ring" refers to a non-aromatic ring system having from 5 to 7 ring atoms and wherein at least one of the ring carbon atoms is replaced by a nitrogen, oxygen or sulfur atom. Examples include piped dine, morpholine, imidazoline, piperazine and terahydrofuran. Appropriate pharmaceutically and veterinarily acceptable salts of the compounds of general formulae (I) and (II) include basic addition salts such as sodium, potassium, calcium, aluminium, zinc, magnesium and other metal salts as well as choline, diethanolamine, ethanolamine, ethyl diamine and other well known basic addition salts. Where appropriate, pharmaceutically or veterinarily acceptable salts may also include salts of organic acids, especially carboxylic acids, including but not limited to acetate, trifluoroacetate, lactate, gluconate, citrate, tartrate, maleate, malate, pantothenate, adipate, alginate, aspartate, benzoate, butyrate, digluconate, cyclopentanate, glucoheptanatc, glycerophosphate, oxalate, heptanoate, hexanoate, furnarate, nicotinate, pamoate, pectinate, 3-phenylpropionate, picrate, pivalate, proprionate, tartrate, lactobionate, pivolalc, camphorate, undecanuale and succinate, organic sulfonic acids such as methanesulfonate, ethanesulfonate, 2-hydroxyethane sulfonate, camphorsulfonate, 2-naphthalenesulfonate, benzenesulfonate, p-chlorobenzenesulfonate and p-toluencsulfonate; and inorganic acids such as hydrochloride, hydrobromide, hydroiodide, sulfate, bisulfate, hemisulfate, thiocyanate, persulfate, phosphoric and sulfonic acids. Salts which are not pharmaceutically or veterinarily acceptable may still be valuable as intermediates. Prodrugs are any covalently bonded compounds which release the active parent drug according to general formula (I) in vivo. Examples of prodrugs include alkyl esters of the compounds of general fonnula (I), for example the esters of general fonnula (II) below. If a chiral centre or another form of isomeric centre is present in a compound of the present invention, all forms of such isomer or isomers, including enantiomers and diastereoisomers, are intended to be covered herein. Compounds of the invention containing a chiral centre may be used as a racemic mixture, an enantiomerically enriched mixture, or the racemic mixture may be separated using well-known techniques and an individual enantiomer may be used alone. In the compounds of general formula (I), it is preferred that, independently or in any combination: R1 is halo or hydrogen; R2 is halo or hydrogen; R3 is halo or hydrogen; R4 is halo or hydrogen. In more preferred compounds, R1, R3 and R4 are hydrogen, while R2 is halo, particularly fluoro. In preferred compounds of general formula (I), R5 and R6 are each independently hydrogen or C1-C6 alkyl. However, in more active compounds, at least one, and preferably both of R5 and R6 are hydrogen. Compounds of general formula (I) preferably have an R7 group chosen from H or Cr Q alkyl; most suitably R7 is methyl. In particularly preferred compounds of general formula (I), n is 2. When X is a bond, it is preferred that R8 is C1-C6 alkyl, biphenyl or a bicyclic heteroaryl group, any of which may be substituted with halogen, phenyl, -CO2R9 CON(R9)2 or -SO2R9, where R9 is as defined above. More preferred compounds in which X is a bond include those in which R8 is Ci-C4 alkyl, biphenyl or a bicyclic heteroaryl group, any of which may be substituted with phenyl, -CO2R9 CONCR'fe or -SO2R9, where R9 is H or Q-C4 alkyl. When X is NR9, it is preferred that R9 is H or methyl and R8 is: phenyl optionally substituted with one or more halo, C1-C6alkyl or -O(C1-C6 alkyl) groups; C1-C6 alkyl, optionally substituted with aryl; or heteroaryl. More preferably, when X is NR9, R8 is phenyl, benzyl or pyridyl, any of which may optionally be substituted with one or more halo, methyl or methoxy groups. Among the most preferred compounds are the following: 1. [3-(Butane-l-sulfonyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 2. 3-(Biphenyl-4-sulfonyl)-5-fluoro-2-methyl-indol-l-yl]-acetic acid 3. (3 Carboxymethanesulfonyl-5-fluoro-2-methyl-indol-l-yl)-acetic acid 4. (3-Carbamoylmethanesulfonyl-5-fluoro-2-methyl-indol-l-yl)-aceticacid 5. [5-Fluoro-3-(2-methanesulfonyl-ethanesulfonyI)-2-methyl-indol-l -yl]-acetic acid 6. [3-(Benzothiazole-2-sulfonyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 7. [3-(Benzothiazole-2-sulfinyl>5-fluoro-2-methyl-indol-l-yl]-aceticacid 8. [5-Fluoro-2-methyl-3-(quinoline-2-sulfonyl)-indol-l-yl]-aceticacid 9. [5-Fluoro-2-methyl-3-(quinolin-8-ylsulfonyl)-indol-l-yl]-aceticacid 10. (5-Fluoro-2-methyl-3-phenylmethanesulfonyl-lH-indol-l-yl)-aceticacid 11. [3-(4-Chloro-phenylsulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-acetic acid 12. [3-(3-Chloro-phenylsulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 13. [3-(4-Fluoro-phenylsulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 14. [3-(2-Chloro-phenylsulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 15. (3-Benzylsulfamoyl-5-fluoro-2-methyl-indol-l-yl)-acetic acid 16. [5-Fluoro-3-(2-methoxy-phenylsulfamoyl)-2-methyl-indol- l-yl]-acetic acid 17. [5-Huoro-3-(4-methoxy-phenylsulfamoyl)-2-methyl-indol-l-yl]-acetic acid 18. (5-Fluoro-2-methyl-3-phenylsulfamoyl-indol-l-yl)-acetic acid 19. [3-(3,4-Dichloro-benzylsulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 20. [5-Huoro-3-(3-methoxy-phenylsulfamoyl)-2-methyl-indol- l-yl]-acetic acid 21. (5-Fluoro-2-methyI-3-m-tolylsulfamoyl-indol- l-yl)-acetic acid 22. (5-Fluoro-2-methyl-3-p-tolylsulfamoyl-indol-l-yl)-acetic acid 23. [3-(4-Chloro-benzylsulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 24. [3-(Benzyl-methyl-sulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 25. [5-Fluoro-2-methyl-3-(pyridin-3-ylsulfamoyl)-indol-l-yI]-aceticacid; or the Gi-C6 alkyl, aryl, (CH2)mOC(=O)Cl-C6alkyl, (CH2)mN(Rn)2, CH((CH2)mO(C=O)R12)2 esters of any of the above; wherein mis lor 2; R" is hydrogen or methyl; R12 is C,-C,8 alkyl. In a further aspect of the present invention, there is provided a compound of general formula (II) (Figure Removed) wherein R1, R2, R3, R4, R5, R6, n, X, R7 and R8 are as defined for general formula (I); R10 is Q-Qs alkyl, aryl, (CH2)mOC(=O)Ci-C6alkyl, (CH2)mN(Rn)2, CH((CH2)mO(C=0)R12)2; m is 1 or 2; R1' is hydrogen or methyl; RI2isCi-C,8alkyl. Compounds of general formula (II) are novel and may be used as prodrugs for compounds of general formula (I). When the compound of general formula (II) acts as a prodrug, it is later transformed to the drug by the action of an esterase in the blood or in a tissue of the patient. Examples of particularly suitable R10 groups when the compound of general formula (II) is used as a prodrug include: methyl, ethyl, propyl, phenyl, CH2OC(=O)tBu, CH2CH2N(Me)2 CH2CH2NH2 or CH(CH2O(C=O)R12)2 wherein Rn is as defined above. Compounds of general formula (I) wherein R1, R2, R3, R4, R5, R6, R7 and R8 are as defined for general formula (I) and X is a bond, may be prepared from compounds of general formula (la), which is a compound of general formula 00 wherein n is 0 and X is a bond, by oxidation with a suitable oxidising agent such as potassium peroxymonosulfate, m-CPBA, hydrogen peroxide or other well known oxidising reagents. In addition to their use as prodrugs, compounds of formula (It) wherein R10 is Q-Q alkyl may be used in a process for the preparation of a compound of general formula (I), the process comprising reacting the compound of general formula (n) with a base such as sodium hydroxide or lithium hydroxide. The reaction may take place in an aqueous solvent or an organic solvent or a mixture of the two. A typical solvent used for the reaction is a mixture of tetrahydrofuran and water. The same method may be used to prepare compounds of general formula (la) as defined above from compounds of general formula (Ua), which are identical to compounds of general formula (II) except that n is 0. Compounds of general formula (II) and (Ha) in which X is a bond may be prepared from compounds of general formula (II)(Figure Removed) wherein R1, R2, R3, R4, R7 and R8 are as defined for general formula (I) and n is 0, 1 or 2; by reaction with a compound of general formula (IV): X-CR5R6-CO2R10 (IV) wherein R5 and R6 are as defined for general formula (I), R10 is as defined for general formula (II) and X is a leaving group in particular a halo group, for example bromo. The reaction is conducted under strongly basic conditions, for example in the presence of excess sodium hydride, and in a polar organic solvent such as dimethylform amide. Compounds of general formula (TV) are well known and are readily available or can be prepared by methods known to those skilled in the art. Compounds of general formula (HI) wherein R1, R2, R3, R4, R7 and R8 are as defined for general formula (I) and n is 2 can be prepared by reacting a compound of general formula (V) (Figure Removed) wherein R1, R2, R3, R4 and R7 are as defined in general formula (I); with a compound of general formula (VI):herein R8 is as defined in general formula (I). The reaction is carried out in the presence of a Lewis acid such as indium(IQ) bromide. The reaction may be conducted in a polar organic solvent, particularly a chlorinated solvent such as 1,2-dichloroethane Compounds of general formulae (V) and (VI) are well known in the art and are readily available or can be prepared by known methods. Compounds of general formula (II) in which X is NR9 umy be prepared from compounds of general formula (VII): as defined in general formula (II) by reaction with a compound of general formula (VIE): (Figure Removed) wherein R8 and R9 is as defined above for general formula (I). The reaction solvent may be a polar organic solvent such as dichloromethane. Compounds of general formulae (Vm) are well known and are either readily available or can be prepared by methods well known to those skilled in the art. Compounds of general formula (VII) may be prepared from compounds of general formula (DC) (Figure Removed) wherein R1, R2 R3, R4, Rs, R6, and K7 are as defined in general formula (I) and R10 is as defined for general formula (II); by reaction with chlorosulfonic acid. The reaction preferably takes place in a non polar organic solvent. Compounds of general formula (DC) are well known and are readily available or can be prepared by methods well known to those skilled in the art. Compounds of general formula (ID) wherein R1, R2, R3, R4, R7 and R8 are as defined for general formula (I) and n is 0 can be prepared by reacting a compound of general formula (IX) wherein R1, R2, R3, R4 and R7 are as defined in general formula (I) and R10 is as defined for general formula (H) with a compound of general formula (X): R8-SH (X) wherein R8 is as defined in general formula (I). The reaction is carried out in the presence of iodine and potassium iodide. The reaction may take place in an aqueous or an organic solvent or a mixture of the two. A typical solvent used for the reaction is a mixture such as ethanol and water. Compounds of general formula (I) are antagonists of PGD2 at the CRTH2 receptor and compounds of general formula (II) are prodrugs for compounds of general formula (I)- Compounds of general formulae (I) and (II) are therefore useful in a method for the treatment of diseases and conditions mediated by PGD2 at the CRTH2 receptor, the method comprising administering to a patient in need of such treatment a suitable amount of a compound of general formula (I) or (IT). In a third aspect of the invention, there is provided a compound of general formula (I) or (II) for use in medicine, particularly for use in the treatment or prevention of diseases and conditions mediated by PGD2 at the CRTH2 receptor. Furthermore, there is also provided the use of a compound of general formula (I) or (II) in the preparation of an agent for the treatment or prevention of diseases and conditions mediated by PGD2 at the CRTH2 receptor. As mentioned above, such diseases and conditions include allergic asthma, perennial allergic rhinitis, seasonal allergic rhinitis, atopic dermatitis, contact hypersensitivity (including contact dermatitis), conjunctivitis, especially allergic conjunctivitis, eosinophilic bronchitis, food allergies, eosinophilic gastroenteritis, inflammatory bowel disease, ulcerative colitis and Crohn's disease, mastocytosis and also other PGD2-mediated diseases, for example autoimmune diseases such as hyper IgE syndrome and systemic lupus erythematus, psoriasis, acne, multiple sclerosis, allograft rejection, reperfusion injury, chronic obstructive pulmonary disease, as well as rheumatoid arthritis, psoriatic arthritis and osteoarthritis. The compounds of general formula (I) or (II) must be formulated in an appropriate manner depending upon the diseases or conditions they are required to treat. Therefore, in a further aspect of the invention there is provided a pharmaceutical composition comprising a compound of general formula (I) or (II) together with a pharmaceutical excipient or carrier. Other active materials may also be present, as may be considered appropriate or advisable for the disease or condition being treated or prevented. The carrier, or, if more than one be present, each of the carriers, must be acceptable in the sense of being compatible with the other ingredients of the formulation and not deleterious to the recipient. The formulations include those suitable for oral, rectal, nasal, bronchial (inhaled), topical (including eye drops, buccal and sublingual), vaginal or parenteral (including subcutaneous, intramuscular, intravenous and intradermal) administration and may be prepared by any methods well known in the art of pharmacy. The route of administration will depend upon the condition to be treated but preferred compositions are formulated for oral, nasal, bronchial or topical administration. The composition may be prepared by bringing into association the above defined active agent with the carrier. In general, the formulations are prepared by uniformly and intimately bringing into association the active agent with liquid carriers or finely divided solid carriers or both, and then if necessary shaping the product. The invention extends to methods for preparing a pharmaceutical composition comprising bringing a compound of general formula (I) or (H) in conjunction or association with a pharmaceutically or veterinarily acceptable carrier or vehicle. Formulations for oral administration in the present invention may be presented as: discrete units such as capsules, sachets or tablets each containing a predetermined amount of the active agent; as a powder or granules; as a solution or a suspension of the active agent in an aqueous liquid or a non-aqueous liquid; or as an oil-in-water liquid emulsion or a water in oil liquid emulsion; or as a bolus etc. For compositions for oral administration (e.g. tablets and capsules), the term "acceptable carrier" includes vehicles such as common excipients e.g. binding agents, for example syrup, acacia, gelatin, sorbitol, tragacanth, polyvinylpyrrolidone (Povidone), methylcellulose, ethylcellulose, sodium carboxymethylcellulose, hydroxypropylmethylcellulose, sucrose and starch; fillers and carriers, for example corn starch, gelatin, lactose, sucrose, microcrystalline cellulose, kaolin, mannitol, dicalcium phosphate, sodium chloride and alginic acid; and lubricants such as magnesium stearate, sodium stearate and other metallic stearatcs, glycerol stearate stcaric acid, silicone fluid, talc waxes, oils and colloidal silica. Flavouring agents such as peppermint, oil of wintergreen, cherry flavouring and the like can also be used. It may be desirable to add a colouring agent to make the dosage form readily identifiable. Tablets may also be coated by methods well known in the art. A tablet may be made by compression or moulding, optionally with one or more accessory ingredients. Compressed tablets may be prepared by compressing in a suitable machine the active agent in a free flowing form such as a powder or granules, optionally mixed with a binder, lubricant, inert diluent, preservative, surface-active or dispersing agent. Moulded tablets may be made by moulding in a suitable machine a mixture of the powdered compound moistened with an inert liquid diluent. The tablets may optionally be coated or scored and may be formulated so as to provide slow or controlled release of the active agent. Other formulations suitable for oral administration include lozenges comprising the active agent in a flavoured base, usually sucrose and acacia or tragacanth; pastilles comprising the active agent in an inert base such as gelatin and glycerin, or sucrose and acacia; and mouthwashes comprising the active agent in a suitable liquid carrier. For topical application to the skin, compounds of general formula (I) or (II) may be made up into a cream, ointment, jelly, solution or suspension etc. Cream or ointment formulations that may be used for the drug are conventional formulations well known in the art, for example, as described in standard text books of pharmaceutics such as the British Pharmacopoeia. Compounds of general formula (I) or (II) may be used for the treatment of the respiratory tract by nasal, bronchial or buccal administration of, for example, aerosols or sprays which can disperse the pharmacological active ingredient in the form of a powder or in the form of drops of a solution or suspension. Pharmaceutical compositions with powder-dispersing properties usually contain, in addition to the active ingredient, a liquid propellant with a boiling point below room temperature and, if desired, adjuncts, such as liquid or solid non-ionic or anionic surfactants and/or diluents. Pharmaceutical compositions in which the pharmacological active ingredient is in solution contain, in addition to this, a suitable propellant, and furthermore, if necessary, an additional solvent and/or a stabiliser. Instead of the propellant, compressed air can also be used, it being possible for this to be produced as required by means of a suitable compression and expansion device. Parenteral formulations will generally be sterile. Typically, the dose of the compound will be about 0.01 to 100 mg/kg; so as to maintain the concentration of drug in the plasma at a concentration effective to inhibit PGD2 at the CRTH2 receptor. The precise amount of a compound of general formula (I) or (II) which is therapeutically effective, and the route by which such compound is best administered, is readily determined by one of ordinary skill in the art by comparing the blood level of the agent to the concentration required to have a therapeutic effect. Compounds of general formula (I) or (n) may be used in combination with one or more active agents which are useful in the treatment of the diseases and conditions listed above, although these active agents are not necessarily inhibitors of PGDz at the CRTH2 receptor. Therefore, the pharmaceutical composition described above may additionally contain one or more of these active agents. There is also provided the use of a compound of general formula (I) or (II) in the preparation of an agent for the treatment of diseases and conditions mediated by PGDa at the CRTH2 receptor, wherein the agent also comprises an additional active agent useful for the treatment of the same diseases and conditions. %» These additional active agents which may have a completely different mode of action include existing therapies for allergic and other inflammatory diseases including: p2 agonists such as salmeterol; corticostcroids such as flulicasone; antihistamines such as loratidine; leukotriene antagonists such as montelukast; anti-IgE antibody therapies such as omalizumab; anti-infectives such as fusidic acid (particularly for the treatment of atopic dermatitis); anti-fungals such as clotrimazole (particularly for the treatment of atopic dermatitis); immunosuppressants such as tacrolimus and particularly pimecrolimus in the case of inflammatory skin disease. CRTH2 antagonists may also be combined with therapies that are in development for inflammatory indications including: other antagonists of PGDa acting at other receptors such as DP antagonists; inhibitors of phoshodiesterase type 4 such as cilonilast; drugs that modulate cytokine production such as inhibitors of TNFoc converting enzyme (TACE); drugs that modulate the activity of Th2 cytokines IL-4 and EL-5 such as blocking monoclonal antibodies and soluble receptors; PPAR-y agonists such as rosiglitazone; 5-lipoxygenase inhibitors such as zileuton. In yet a further aspect of the invention, there is provided a product comprising a compound of general formula (I) or (TO and one or more of the agents listed above as a combined preparation for simultaneous, separate or sequential use in the treatment of a disease or condition mediated by the action of PGDa at the CRTH2 receptor. The invention will now be described in greater detail with reference to the following non limiting examples and the drawings in which: Figure 1 shows the effects of CRTH2 agonists on calcium mobilisation in CHO/CRTH2 cells. Example 1 - Synthesis of 3-Sulfonvl indole Derivatives (Method A) 1. Synthesis of 3-(Butane-l -sulfonyl)-5-fluoro-2-methyl-lH-indole Indium (III) bromide (94.7 mg, 0.267 mmol) was added in one portion to a stirred solution of 5-fluoro-2-methylindole (50 mg, 0.34 mmol) and butanesulfonyl chloride (418 mg, 2.67 mmol) in 1,2-dichloroethane (2 ml) at room temperature. The mixture was subjected to microwave conditions (85 °C, 150 W) for 45 minutes, cooled to room temperature and then concentrated in vacua to leave a brown residue. Purification by flash column chromatography on silica gel eluting with 10 % ethyl acetate : hexane to 100 % ethyl acetate gave the sulfone (55 mg, 15 %) as an off- white solid. 2. Synthesis of [3-(Butane-l-sulfonyI)-5-fluoro-2-methyl-indol-l-yl]-acetic acid (Compound 1) 3-(Butane-l-sulfonyl)-5-fluoro-2-methyl-lH-indole (55 mg, 0.204 mmol) in DMF (1 ml) was added dropwise over 1 minute to a stirred suspension of sodium hydride (11 mg, 0.29 mmol; 60 % in mineral oil) in DMF (1 ml) at 0 °C. The solution was stirred at 0 °C for 45 minutes and then ethyl bromoacetate (0.032 ml, 0.29 mmol) was added dropwise and the resulting mixture stirred at room temperature for 18 hours. The mixture was adjusted to pH 4 with 10 % citric acid and then extracted into ethyl acetate (2 x 10 ml). The combined organic extracts were dried and concentrated in vacua to leave a residue. The residue was taken up into THF (1 ml) and lithium hydroxide monohydrate (19 mg, 0.464 mmol) in water (1 ml) was then added in one portion at room temperature. The mixture was stirred at room temperature for 3 hours and then the solution adjusted to pH 4 with 10 % citric acid. The product was extracted with ethyl acetate and the combined organic extracts were dried and concentrated in vacua to leave a residue which was triturated with diethyl ether to give the carboxylic acid as an off-white solid (5.4 mg, 8 %), SH (400 MHz, MeOD) 7.57 (IH, dd J 9.8, 2.3 Hz, Ar), 7.43 (IH, dd J 9.1,4.0 Hz, Ar), 7.04 (IH, td / 9.1, 2.5 Hz, Ar), 4.79 (2H, s, C//2CO2H), 3.23-3.19 (2H, m, SO4C#2), 2.70 (3H, s, CCHj), 1.77-1.70 (2H, m, CH2Cff2CH2CH3), 1.47-1.41 (2H, m, CH2CH2C//2CH3), 0.93 (3H, t J 7.6 Hz, CH2CH2CH2CH3); Tr = 1.38 min, m/z (ES+) (M+H)+ 308.24. Tr = 1.82 min (98 %), m/z (ES*) (M+H)+ 328.20. Compound 2 was prepared using the same general method as for Compound 1 but with appropriately chosen starting materials. Compound 2 - 3-(Biphenyl-4-sulfonyl)-5-fluoro-2-methyl-indol-l-yI]-acetic acid 6H (400 MHz, MeOD) 8.03 (2H, d, J 8.6 Hz Ar), 7.80 (2H, d, / 8.6 Hz, Ar), 7.77-7.74 (IH, dd, / 9.6, 2.5Hz, Ar), 7.66-7.64 (2H, dd, J 8.0, 1.3Hz, Ar), 7.49-7.39 (4H, m, Ar), 7.07 (1H, td, / 9.1, 2.5Hz, Ar), 5.07 (2H, s, C//2), 2.76 (3H, s, C//3); Tr = 1.52 min, m/z (ES+) (M+H)+ 424.1. Example 2 - Synthesis of 3-Sulfonvl indole Derivatives (Method B) 1. 2-MethyIsulfanyl-ethanethiol A solution of methyl iodide (10 ml, 22.82 g, 0.161 mol) in acetone (50ml) was added dropwise to a stirred suspension of ethane dithiol (11.24 ml, 12.62 g, 0.134 mol) and potassium carbonate (37.04 g, 0.268 mol) in acetone (150 ml). The resulting mixture was stirred at room temperature for 4 hours. Water (150 ml) was added, and the mixture stirred for a further 15 minutes. The reaction mixture was extracted with dichloromethane (3 x 200 ml), the organic washings combined, dried over sodium sulfate and evaporated (maintaining pressure above 200 mbar to ensure no co-evaporation of product) to give 2-methylsulfanyl-ethanethiol. LC/MS showed <5% starting material and a 2:1 mixture of mono and bis-methylated material. The material was used in the next step with no further purification. 2. [5-FIuoro-2-methyI-3-(2-methylsuIfanyl-ethyIsuIfanyI)-indol-l-yI]-acetic acid ethyl ester To a stirred solution of (5-fluoro-2-methyl-indol-l-yl)-acetic acid ethyl ester (1.20g, S.lOmmol) and 2-methylsulfanyl-ethanethiol (1.04g, 6.12mmol) in 1:1 EtOH:H2O (40ml) at room temperature was added iodine (1.29g, S.lOmmol) and potassium iodide (0.847g, 5.10mmol). The mixture was heated to 100°C and stirred for 2 hours, then stirred at room temperature for 16 hours. The reaction mixture was quenched by the careful addition of saturated NaHCOs 10uM). Compounds of general formula CD bound to CRTH2 receptor expressed in CHO cells with a range of affinity varying from very high to moderate. In fact the Ki values determined in competition versus [3H]PGD2 varied from 500 pM to 1 uM. Compounds of general formula (I) had no activity (or very weak activity) at the DP and TP receptors. The binding selectivity of the compounds of general formula (I) for CRTH2 receptor was greater than 200 fold for CRTH2 receptor, compared to DP and TP receptors. Calcium mobilisation Assay Cells were seeded onto poly-D-lysine coated 96-well plates at a density of 80,000 cells per well and incubated at 37°C overnight to allow the cells to adhere. Cells were washed twice with HBSS and incubated for Ih at 37°C in 100//1 HBSS and 100^1 calcium-3-dye (Molecular Devices) solution, supplemented with 4mM probenecid. Changes in fluorescence were monitored over a 50s time course with agonist addition at 17s using a Flexstation (Molecular Devices). Effect 0/CRTH2 agonists on calcium mobilisation in CHO-CRTH2 cells PGDj caused a dose-dependent increase in inuucellular Ca2* mobilisation in CHO/CRTII2 cells, wilh an EC50 = 2.4 ± O.SnM (n=3) (Figure 1). Effect of compounds of general formula (I) on the calcium mobilisation induced by PGD2 PGDj-stimuIated Ca2* flux was fully inhibited by the compounds of general formula (I) and the ICso value for each compound in the calcium assay was comparable to its Ki value in Radioligand binding. ICso values of compounds of general formula (I) varied from 5 nM to 1 u,M. The results for several compounds of general formula (I) are shown in Table 2. Increasing doses of the compounds of general formula (I) caused a dose-dependent and parallel shift of the PGDa dose response curve in CHO/CRTH2 cells, thereby indicating that the compounds are competitive CRTH2 antagonists. The antagonistic effect of the compounds of general formula (I) appears to be CRTH2 selective, since no inhibitory effect was seen with ATP-stimulated Ca2+ flux in CHO/CRTH2 cells.(Table Removed) CLAIMS 1. A compound of general formula (I) (Figure Removed)wherein R1, R2, R3 and R4 axe independently hydrogen, halo, alkyl, -O(C1-C6 alkyl), -CON(R9)2 , -SOR9, -SOaRB, -SOzN(R9)2, -NR9COR9, -COzR9, -COR9, each R9 is independently hydrogen or C1-C6 alkyl; Rs and R6 are each independently hydrogen, or C1-C6 alkyl or together with the carbon atom to which they are attached form a C3-C7 cycloalkyl group; R7 is hydrogen or C1-C6 alkyl n is I or 2; X is a bond or, when n is 2, X may also be a NR9 group; wherein R9 is as defined above; when X is a bond R8 is C1-C6 alkyl, C1-C6 alkenyl, C1-C6 alkynyl. biphenyl or a 9-14 membered bicyclic or tricyclic heteroaryl group; when X is a NR9 group R* may additionally be phenyl, naphthyl or a 5-7 membered heteroaromatic ring; and the R8 group is optionally substituted with one or more subsiituents selected from halo, C1-C6 alkyl. -0(C1-C6 )alkyl, aryl, -O-aryl, heteroaryt, -O-heteroaryl, -CON(R9)2, -SOR9, -SOzR9, SOzNCR9)2, -NCR9)2 -NR9COR9, -COzR9, -COR9, -SR9, •OH,-NO2or-CN; wherein Rp is as defined above; or a pharmaceutically acceptable salt, hydrate, solvate, complex or prodrug thereof. 2. A compound of general formula (II): (Figure Removed)-wherein R1. R2, R3. R4. R5 . R6. n,-R10 is C1-C6 alkyl, aryl, (CH2)mOC(=O)C,-C«alkyl, mis lor 2; Rn is hydrogen or methyl; R12 is C1-C18 alkyl. 3. A compound as claimed in claim 1 or claim 2 wherein, independently or in any combination: R' is halo or hydrogen; R2 is halo or hydrogen; R3 is halo or hydrogen; R4 is halo or hydrogen. 4. A compound as claimed in any one of claims 1 to 3 wherein R1, R3 and R4 are hydrogen and R2 is halo. 5. A compound as claimed in claim 4 wherein Rz is fluoro. 6. A compound as claimed in any one of claims 1 to 5 wherein R5 and R* are each independently hydrogen or C1-C4 alky]. 7. 'A compound as claimed in claim 6 wherein at least one of R5 and R6 are hydrogen. 8. A compound as claimed in claim 7 wherein both R5 and R6 are hydrogen. 9. A compound as claimed in any one of claims I to 8 wherein R7 is H or alkyl. . 10. A compound as claimed in claim 9 wherein R7 is methyl. 11. A compound as claimed in any one of claims 1 to 1 0 wherein n is 2. 12. A compound as claimed in any one of claims 1 to 1 1 wherein X is a bond and R8 is C]-Q alkyl. biphenyl or a bicyclic heteroaryl group, any of which may be substituted with halogen, phenyl, -COjR9 CON(R*)2 or -SOjR9, where R9 is as defined above. 13. A compound as claimed in claim 12 wherein R' is Q-Cj alkyl, biphenyl, a bicyclic heteroaryl group or a 5-7 membered heterocyclic ring, any of which may be substituted with phenyl, -COjR9 CON(R9)2 or -S02R9. where R9 is H orC1-C8 alkyl. 14. A compound as claimed in any one of claims 1 to 11 wherein X is NR9, R9 is H or methyl and R* is: phenyl optionally substituted with one or more halo, C1-C86 alkyl or -O(C1-C6 alkyl) groups; C1-C6 alkyl, optionally substituted with aryl; or heteroaryl. 15. A compound as claimed in claim 14, wherein R8 is phenyl, benzyl or pyridyl, any of which may optionally be substituted with one or more halo, methyl or methoxy groups. 16. [3-(ButaTje-l-sulfemyl)-5-fluoro-2-methyl-indol-l-ylJ-acetic acid 3-(Biphenyl-4-sulfonyl)-5-fluoro-2-inethyl-indo!-l-yl)'aceticacid (3-CarBoxymethane8ulfony1-5-fluoro-Z-methyl-indol-l-yl)-aceticacid (3-Caibamoylmethanesulfonyl-5-fluon>-2-niethyl-iiidoI-l-yJ)-aceticacid [5-Fluoro-3-(2-memanesulfonyl-ethanesulfonyl)-2-mediyl-indol-l-yl]"aceticacid [3-(Benzoihi8zole-2-sulfonyl)-5-fluoro-2-methyl-indoH-yl)-aceticacid [3-(Benzothiazole-2-sulfinyl)-5-fluoro-2-methyl-indol-l -yl]-acetic acid [5-FluoTO-2-naethyl-3-(quinoIine-2-8ulfonyl)-Jndol-l-yl]-aceticacid fS"Fluoro-2-methyl-3-(quinolin-8-ylsulfonylHndol-l-yI]-aceticacid (5-Fluoro-2-m«hyl-3-phenylmethanesulfanyl-iH-indoM'yl>-acetic add [3-(4-Chloro-phenylsulfamoyl)-5-fluoro-2-meihyI-indol-l-yl]-aceticacid [3-(3-Chloro-phenylsulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid (3-(4-Fluon)-phwnyl6ulfamoyl)-5-fluoro-2-nieihyl-indol-l-yl]-acedcacid [3-(2^hlcm>-phenylsiilfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid (3-Ben2ylfiulfamoyl-5-fluoro-2-methyHndol-l-yl)-aceticacid {5-Fluoro-3-(2-meihoxy-phenylsulfamoyl)-2-methyl-indol-l-yl]-aceticacid [5-Ruoro-3-(4"methoxy-phenylsulfwioyl)-2-methyl-indol-l-yl]-aceticaci4 (5-Fluoro-2-meihyl-3-phenylsulfamoyHndol-l-yl)-acetic8cid [3-(3,4-Dichloro-benzylsulftnioyl).5-fluoro-2-raethyJ-indol-l-yl]-aceticacid [5-Fluoro-3-(3-methoxy-phenylsu|famoyl)-2-methyl-radoH-yl]-aceticacid (5-Fluoro-2-methyl-3-m-tolyl5ulfamoyl-indol-l-yl)-aceticacid (5-FLUORA"2-methyI-3-p-tolylsulfamoyl-indol-l-yl)-aceUc acid [3.(4-ChJoro-benzylsulfamoyl)-5-fluoro-2-roethyI-indo]-l-yl]-aceticadd [3-(Benzyl-methyl-sulfamoyl)-5-fluoro-2-methyl-indol-l-yl]-aceticacid 42 [5-Huoro-2-meihyl-3-(pyridin-3-yl5ulfamoyl)-indol-l-yl]-acetic acid; or the C.-Ce alky], aryl, (C^)fflOC(=O)C,-Cfialkyl, CH((CH2)fnO(CsO)Rl2)2 esters of any of the above; wherein m is 1 or 2; R" is hydrogen or methyl; RuisC,-C,8alkyl. 17. A process for the preparation of a compound of general formula (I) as claimed in any one of claims 1 to 13 or 16 wherein n is 1 or 2 and X is a bond, die process comprising treating a compound of general formula (la), which is a compound of general formula (I) wherein n is 0 and X is a bond, by oxidation with a suitable oxidising agent. 18. A process for the preparation of a compound of general formula (I) as claimed in any one of claims 1 to 16, the process comprising reacting a compound of general formula (II) as defined in claim 2 and wherein R10 is C|-C« alkyi with a base. 19. A compound as claimed in any one of claims 1 to 16 for use in medicine. 20. A compound as claimed in any one of claims 1 to 16 for use in the treatment of allergic asthma, perennial allergic rhinitis, seasonal allergic rhinitis, alopic dermatitis, contact hypersensitivity (including contact dermatitis), conjunctivitis, especially allergic conjunctivitis, eosinophilic bronchitis, food allergies, eosinophilic gastroenteritis, inflammatory bowel disease, ulcerative colitis and Crohn's disease, mastocytosis, another PGD2-mediated disease, for example autoimmune diseases such as hyper IgE syndrome and systemic lupus erythematus, psoriasis, acne, multiple sclerosis, allograft rejection, reperfusion injury and chronic obstructive pulmonary disease; or rheumatoid arthritis, psoriatic arthritis or osteoarthritis. 21. The use of a compound as claimed in any one of claims 1 to 16 in the preparation of an agent for the treatment or prevention allergic asthma, perennial llergic rhinitis, seasonal allergic rhinitis, atopic dermatitis, contact hypersensitivity (including contact dermatitis), conjunctivitis, especially allergic conjunctivitis, eosinophilic bronchitis, food allergies, eosinophilic gastroenteritis, inflammatory bowel disease, ulcerative colitis and Crohn's disease, mastocytosis, another POP2-mediated disease, for example autoimmune diseases such as hyper IgE syndrome and systemic lupus erythematus, psoriasis, acne, multiple sclerosis, allograft rejection, reperfusion injury and chronic obstructive pulmonary disease; or rheumatoid arthritis, psoriatic arthritis or osteoarthritis. 22. A pharmaceutical composition comprising a compound as claimed in any one of claims 1 to 16 together with a pharmaceutical excipient or carrier, 23. A composition as claimed in claim 22 formulated oral, rectal, nasal, bronchial (inhaled), topical (including eye drops, buccal and sublingual), vaginal or parenteral (including subcutaneous, intramuscular, intravenous andintradermal) administration. 24. A composition as claimed in claim 23 formulated for oral, nasal, bronchial or topical administration. 25. A composition as claimed in any one of claims 22 to 24 containing one or more additional active agents useful in the treatment of diseases and conditions mediated by POD* at the CRTH2 receptor. 26. A composition as claimed in claim 25, wherein the additional active agents are selected from: p2 agonists such as salmeterol; corticosteroids such as fluticaeone; antirustaminefi such as loratidine; leukotriene antagonists such as montclukast; anti-IgE antibody therapies such as oraalizumab; anti-infectivea such as fusidic acid (particularly for the treatment of atopic dermatitis); anti-fung&ls such as clotrimazole (particularly for the treatment of atopic dermatitis); immunosuppressancs such as tacrolimus and particularly piraecrolimus in the case of inflammatory skin disease; other antagonists of PGD2 acting at other receptors such as DP antagonists; inhibitors of phoshodiesterase type 4 such as cilonilast; drugs that modulate cytokine production such as inhibitors of TNFa converting enzyme (PACE); drugs thai modulate the activity of Th2 cytokines IL-4 and IL-5 such as blocking monoclonal antibodies and soluble receptors; PPAR-γ agonists such as rosiglitazone; 5-Iipoxygenase inhibitors such as zileuton. 27. A process for the preparation of a pharmaceutical composition as claimed in any one of claims 22 to 26 comprising bringing a compound as claimed in any one of claims 1 to 16 in conjunction or association with a pharmaceutically or veterinarily acceptable carrier or vehicle. 28. A product comprising a compound as claimed in any one of claims 1 to 16 and one or more of the agents listed in claim 26 as a combined preparation for simultaneous; separate or sequential use in the treatment of a disease or condition mediated by the action of PGDz at the CRTH2 receptor. 29. The use as claimed in claim 21, wherein the agent also comprises an additional active agent useful for the treatment of diseases and conditions mediated by FGD2 at the CRTH2 and/or DP receptor. 30. The use as claimed in claim 29, wherein the additional active agent is the agents listed in claim 26.