FIELD OF THE INVENTION 1. The present invention relates to novel 5-hydroxy-5-aryl-pyrrol-2-ones, their preparation and their use as non-peptide CCK ligands, particularly in pharmaceutical formulations thereof. BACKGROUND OF THE INVENTION 2. Cholecystokinins (CCKs) act as anti-opioid peptides. CCK was initially described as a regulatory hormone found in endocrine cells of the gastro-intestinal (GI) tract Some CCKs share a common amino acid sequence with gastrin, which is involved in control of gastric acid and pepsin secretion. CCKs have also been found throughout the central nervous system (CNS), where they act as neurotransmitter and/or modulator of many important functions. There are various known structures of CCK, identified with reference to the number of amino acids they comprise. For example, CCK-8 a naturally-occurring predominant CCK peptide having only eight amino acids, is the minimum fully-active sequence. Albeit, small amounts of CCK-4 have also been reported. 3. CCKs have multiple function in the physiology and pathology of vertebrate. Pharmaceuticals and biotechs have taken advantage of the pathological properties of the CCKs to develop molecules that block these properties to deliver health and wellness. For instance, CCK plays an important role in the invasiveness and the production of matrix metalloproteinase-9 (MMP-9) in human pancreatic cancer cell lines. The pathway of the invasiveness may be associated with MMP-9 of those lines regulated by CCK. 04. The gut hormone CCK exerts various actions on the gastrointestinal tract, including the regulation of growth. The hormone has been reported to induce hypertrophy and hyperplasia of the pancreas and to enhance chemically-induced pancreatic carcinogenesis in animals. Stimulation of endogenous CCK secretion through the induction of deficiency of intraintestinal proteases and bile salts by trypsin- inhibiting nutrients, bile salt-binding drugs or surgical intervention is also capable of stimulating growth and tumour development in the rat In humans, factors suggested to increase the risk of pancreatic cancer, such as a high-fat- and high- protein- thet or gastrectomy, are known to stimulate plasma CCK secretion. Receptors for CCK have been demonstrated in human pancreatic adenocarcinomas, and CCK has been demonstrated to enhance the pancreatic xenograft growth and growth of gastric and bile duct cancer. 5. The actions of CCK are mediated by two G protein coupled receptor (GPCRs). They are termed as type-A and type-B, reflecting their preferential localisation in the alimentary tract and in the brain, respectively. Recently, these receptors have been re-named as CCK1 and CCK2, respectively, although the original designation is also used hereinbelow with respect to the present invention. The molecular cloning of two CCK receptor subtypes, one from rat and human pancreas and one from human brain, has confirmed the pharmacological classification of the CCK receptors. The differential distribution of CCK1 and CCK2 receptors in the peripheral vs. central nervous system is not absolute, as CCK1 receptors have also been shown to be expressed in discrete regions of the CNS, including the spinal cord, particularly in primates. 6. The functions of the CCK1 receptor in the brain are poorly understood, whereas the CCK2 receptor is known to mediate anxiety, panic attacks, satiety and pain. Therefore, antagonists to CCK receptors and to gastrin have been useful to prevent and treat CCK-related and/or gastrin-related disorders. Just as there are some overlap in the biological activities of CCK and gastrin, antagonists also tend to have affinity for both receptors. 7. Selective CCK receptor antagonists are themselves useful in treating CCK-related disorders of the appetite regulatory systems as well as in potentiating and prolonging opiate-mediated analgesia, thus having utility in the treatment of pain, while selective gastrin antagonists are useful in the modulation of CNS behaviour, as a palliative for gastrointestinal neoplasms, and in the treatment and prevention of gastrin-related disorders of the GI system in humans and animals, such as peptic ulcers, Zollinger-Ellison syndrome, antral G cell hyperplasia and other conditions in which reduced gastrin activity is of therapeutic value. Also, since CCK and gastrin also have trophic effects on certain tumours, antagonists of CCK and gastrin are useful in treating these tumours. 8. Various chemical classes of CCK-receptor antagonists have been reported. These include pyrazolidinones showing good selectivity for CCKb receptors (Howbert, JJ.et al.; Bioorg. Med Chem. Lett. 1993,3,875-880.), ureidoacetamides which are potent and selective ligands for CCKE/gastrin receptors (WO 91/113874), ureidophenoxyacetanilides (Takeda, Y.et al.; Chem. Pharm Bull. 1998,46 , 951- 961), ureidomethylcarbamoylphenylketones (Hagishita, S.; et al., Bioorg. MedChem. 1997,5,1695-1714), and ureidobenzodiazepine derivatives (Evans, B.E.; et al., Proc. Natl. Acad. ScL USA 1986,83,4918-4922). Description of drawings The CCK B antagonist (Example 8) did not show a significant tramadol potentiation. The phenylethyl-derivative (Example 5) had a 4-fold potentiation of the analgesic effect of tramadol. A similar, but smaller activity was observed for the cyclopentyl-derivative (Example 7). The isobutylderivative, at a0.1mg/kg dose, showed a significant anxiolytic effect, which is at a 0.5 mg/kg dose similar to the standard anxiolytic diazepam at a lmg/kg dose. The isobutylderivative Exp 8, showed good antidepressant properties compared to the standard antidepressant at a 1 Omg/kg dose. The 0.5mg dose of the tetramic acid has a greater magnitide than the standard Desimipramine in the forced swimming test SUMMARY OF THE PRESENT INVENTION The objective of the present invention is to provide novel 5-hydroxy-5-aryl-pyrrol- 2-ones derivatives, which preferably act as CCK ligands, and pharmaceutical formulations thereof. According to the present invention there is provided a compound of formula (I): wherein X is selected from hydrogen, a hydroxyl group, a halogen, a substituted or unsubstituted cyclic and heterocyclic moiety, substituted or unsubstituted, linear or branched alkyl, alkyloxy, alkylcaibonyl, alkyloxycarbonyl, alkenyl, alkenyloxy, alkenylcarbonyl, alkenyloxycarbonyl, alkynyl, alkynyloxy, alkynylcarbonyl, alkynyloxycarbonyl, aryl, benzyl, arlyoxy, arylcarbonyl, aryloxycarbonyl and sulphur equivalents of said oxy, carbonyl and oxycarbonyl moieties or as defined for Y, Rand R1. Y is selected from H, hydroxyl, thio, substituted N as defined in R, R1 and X. R is selected from hydrogen, a halogen, an amide, a substituted or unsubstituted cyclic and heterocyclic moiety, a phenyl group, aryl, substituted or unsubstituted, linear or branched alkyl, alkyloxy, alkylcarbonyl, alkyloxycarbonyl, alkenyl, alkenyloxy, alkenylcarbonyl, alkenyloxycarbonyl, alkynyl, alkynyloxy, alkynylcarbonyl, alkynyloxycarbonyl, aryl, benzyl, arlyoxy, arylcarbonyl,aryloxycarbonyl and sulphur equivalents of said oxy, carbonyl and oxycarbonyl moieties, and as in R1,Y and X defined. R1 is selected from H, methyl, alkyl, aryl, substituted aryl, benzyl, C1-18 straight, branched or cyclic, saturated, unsaturated and aromatic hydrocarbyl groups, which aromatic groups may be heterocyclic, cyclic or acyclic and which may optionally be substituted by alkyl, alkoxy, or halo; or R1 and R2 , when taken together with the N- atom to which they are bonded, may form an N-containing saturated, unsaturated or partially unsaturated ring system comprising 3 to 10 ring atoms selected from C, N and O, optionally substituted at any position of the ring by a substituent selected from a halogen, a substituted or unsubstituted cyclic and heterocyclic moiety, substituted or unsubstituted, linear or branched alkyl, alkyloxy, alkylcarbonyl, alkyloxycarbonyl, alkenyl, alkenyloxy, alkenylcarbonyl, alkenyloxycarbonyl, alkynyl, alkynyloxy, alkynylcarbonyl, alkynyloxycarbonyl, aryl, benzyl, arlyoxy, arylcarbonyl, aryloxycarbonyl, sulphur equivalents of said oxy, carbonyl and oxycarbonyl moieties, and as defined for the other substituents and any possible combination thereof. Preferably said alkyl- and aryl containing moieties, more preferably C1-C12 connected to an aromatic system and most preferably is phenyl ethyl or substituted phenyl ethyl groups. Preferred substituents for R are phenyl, substituted phenyl formed by R1 alkyl or alkoxy, phenyl, benzyl, phenyl (C2-4) alkenyl, phenoxy, benzyloxy, halo, oxo or alkyloxycarbonyl. Suitable substituents on the aromatic system are methyl, halogen, benzyl, phenyl, alkoxy carbonyl and oxo. Preferably, said heterocyclic ring is mono-or di- substituted. Preferably, X is H, halo (F, Br, CI, I) or methyl. Preferably, R is H, phenyl, halo, substituted phenyl, aryl and bis aryl, substituted aryl and heteroaryl. It will be understood that formula (I) is intended to embrace all possible isomers, including optical isomers and mixtures thereof, including racemates. It will also be understood that formula (I) is intended to embrace all possible polymorphs, crystal, impurity, //-oxide, ester, hydrate or any combination thereof. In addition, the present invention includes within its scope prodrugs of the compounds of formula (I). In general, such prodrugs will be functional derivatives of the compounds of formula (I) which are readily convertible in vivo into the required compound of formula (I). Conventional procedures for the selection and preparation of suitable prodrug derivatives are described, for example, in "Design of Prodrugs", ed H. Bungaard, Elsevier, 1985. The scope of the invention also extends to salts, particularly physiologically acceptable salts and hydrates of the compounds of formula (I). The pharmaceutically acceptable salts of the compounds of formula (I) include the conventional non-toxic salts or the quarternary ammonium salts of the compounds of formula (I) formed, eg, from non-toxic inorganic or organic acids. The pharmaceutically acceptable salts of formula (I) also include those formed from a base, such as an alkali or alkaline earth metal hydroxide, or an organic base, such as an amine or a quarternary ammonium hydroxide. Some of the synthesized chemical structures that demonstrated significant CCK antagonistic properties are given below. 26. The present invention also resides in the use of a compound of the first aspect as a CCK receptor ligand and/or as a CCK antagonist Preferably, said use is as a selective or mixed CCK1 or CCK2 ligand. Most preferred are mixed antagonists as reported in Lattmann et al. [Lattmann, E., Arayarat, P. and Singh, H. (2000) Review article: Small organic molecules as cholecystokinin antagonists. Science (KKU), 28,288-299 lattmann, E., Billington, D.C., Poyner, D.R., Howitt, S.B. and Offel M. (2001) Synthesis and evaluation of Asperlicin analogues as non-peptidal Cholecystokinin-antagonists. Drug Design and Discovery, 17,219-230 Lattmann, E., Billington, D.C., Poyner, D.R., Howitt, S.B. and Ofifel, M. (2001) Solid phase synthesis of 3-alkylated 1,4-benzodiazepines as non-peptidal Cholecystokinin antagonists. Pharm. Pharm. Lett. 11,5-8 Lattmann, E., Billington, D.C., Poyner, D.R., Arayarat, P., Howitt, S.B., Lawrence, S. and Offel,M. (2002) Combinatorial solid phase synthesis of multiply-substituted 1,4-benzodiazepines and affinity stuthes on the CCK2 receptor (Part 1). Drug Design and Discovery, 18,9-21. Lattmann, E., Sattayasai, J., Billington, D.C., Poyner, D.R., Puapairoj, P., Tiamkao, S., Airarat, W., Singh, H. and Ofifel, M. (2002) Synthesis and evaluation of N i -substituted-3 -propyl-1,4-benzodiazepine-2 -ones as Cholecystokinin (CCK2)-receptor ligands. J. Pharm. Pharm. 54, 827-834 Lattmann, E., Arayarat, P. (2003) Review article: From CNS-drugs to anti-neoplastic agents: Cholecystokinin (CCK)- antagonists as modern anti-cancer agents. Science (KKU) 2003,31, 178-193 Lattmann, E., Sattayasai, J., Boonprakob, J., lattmann, P., Singh, H. (2005) Synthesis and evaluation of N-{5-methyl-3-oxo 1 ,2- 2o(F2)] = 0.0541 Colourless wR(F2) = 0.1165 Mo Kα radiation: λ - 0.71073 A 5136 reflections Triclinic 331 parameters P-l a = 8.3190(13) A b = 12.614(4) A c= 13.8106(18) A a = 93.049(17)° p = 94.791(12)° y= 107.651(19)° Selected geometric parameters (A, °) Cl(l)-C(l) 1.696(4) C1(1)-C(1') 1.695(4) C(l)-C(4) 1.310(5) C(1)C(4’) 1.322(5) C(2)-C(5) 1.511(5) C(2)C(5) 1.524(5) C(2)O(2) 1.410(4) C(2,)-O(2,) 1.400(4) C(3)-O(l) 1.224(5) C(3,)-O(l,) 1.237(4) N(l)-C(l1) 1.448(5) N(l)-C(11) 1.448(5) Example 9 l-Benzyl-4-chloro-5-hydroxy-5-phenyl-1H-dihydro-pyrrol-2-one. Yield = 71 % Melting Point: 165-167 °C Rf (80% ether / 20% petrol ether) = 0.21 Molecular Weight: 299.8 Molecular Formula: C17H14CINO2 MS (APCI(+)): 193/195 (M+l), 300/302 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.31-7.42 (m, ArH, 5H), 7.14-7.27 (m, ArH, 5H), 6.08 (s, CH), 4.59-4.70 (d, CH2,1H), 3.93-4.09 (d, CH2,1H), 3.52-3.79 (bs, OH) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 167.9 (C=O), 155.9 (C-Cl), 137.6 (ArC), 134.4 (ArC), 129.3 (ArC), 128.7 (4xArC), 128.4 (2xArC), 128.4 (ArC), 127.3 (ArC), 126.4 (ArC), 93.2 (C-OH), 43.4 (CH2) p.p.m. IR (KBr-disc) u max: 3446, 3279, 3098, 2931, 2850, 2374, 2334, 1684, 1611, 1456, 1413,1349,1276,1205,1128,1051,696 cm-1. Example 10a (major): 4-Chloro-5-hydroxy-5-phenyl-((5)-(-)-l-phenyl-ethyl)-lH-dihydro- pyrrol-2-one. Yield = 66% Melting Point: 162-164 °C Rf (80% ether / 20% petrol ether) = 0.23 Molecular Weight: 313.8 Molecular Formula: C18H16CINO2 MS (APCI(+)): 193/195 (M+l), 314/316 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.34-7.53 (ArH, 7H), 7.08-7.25 (ArH, 3H), 5.96 (s, CH), 4.16-4.28 (q, N-CH, J= 7.9 Hz), 2.91-3.37 (bs, OH), 1.49-1.58 (d, CH3) p.p.m. ,3C NMR (CDCI3) 250 MHz: δ = 167.3 (C=O), 154.3 (C-Cl), 142.5 (ArC), 134.7 (ArC), 129.4 (ArC), 128.7 (2xArC), 128.4 (2xArC), 127.7 (2xArC), 127.3 (2xArC), 126.4 (ArC), 123.0 (CH-CCI), 93.8 (C-OH), 53.5 (NH-CH), 18.8 (CH3) p.p.m. IR (KBr-disc) u max: 3241, 2983, 2932, 2863, 2366, 2347, 1686, 1661, 1614, 1494, 1456,1425,1356,1258,1202,1025,931,855,755,692 cm"1. Example 10b (minor): 4-Chloro-5-hy droxy-5-pheny 1-1 -((S-)-1 -pheny 1-ethy 1)-1 ,5-dihy dro- pyrrol-2-one. Yield = 8 % Rf (80% ether / 20% petrol ether) = 0.23 Molecular Weight: 313.8 Molecular Formula: C18H16ClNO2 MS (APCI(+)): 193/195 (M+l), 314/316 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.29-7.53 (ArH, 7H), 6.95-7.21 (ArH, 3H), 6.08 (s, CH), 4.59-4.78 (q, N-CH, 7= 7.9 Hz), 6.62-2.71 (bs, OH), 1.49-1.63 (d, CH3) p.p.m. Example 11 4-Chloro-l-cyclohexyl-5-hydroxy-5-plienyl-1H-dihydro-pyrrol-2-one. Yield = 57% Melting Point: 170-172 °C Rf (80% ether / 20% petrol ether) = 0.27 Molecular Weight: 291.8 Molecular Formula: C16H18ClNO2 MS (APCI(+)): 193/195 (M+l), 292/294 (M+) m/z JH NMR (CDCI3) 250 MHz: δ = 7.26-7.61 (m, ArH, 5H), 6.08 (s, CH), 3.72-3.85 (bs, OH), 2.83-3.19 (m, N-CH), 1.21-2.07 (m, overlapping CH2,10H) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 163.9 (C=O), 153.9 (C-Cl), 135.0 (ArC), 129.25 (2xArC), 128.9 (2xArC), 126.4 (ArC), 122.9 (CH-CC1), 96.0 (C-OH), 53.6 (N-CH), 32.8 (CH2), 31.1 (CH2), 29.8 (CH2), 26.2 (2xCH2), 24.2 (CH2) p.p.m. IR (KBr-disc) o max: 3440, 2924, 2858, 2355, 2344, 1641, 1449, 1367, 1250, 1138, 1016,996,742,695 cm-1. Example 12 4-Chloro-5-(4-chloro-phenyl)-l-cyclopropyl-5-hydroxy-1H-dihydro-pyrrol -2-one. Yield = 72% Melting Point: 169-171 °C Rf (80% ether / 20% petrol ether) = 0.19 Molecular Weight: 284.1 Molecular Formula: C13H11Cl2NO2 MS (APCI(+)):227/229/231 (M+l), 284/286/288 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.12-7.32 (m, ArH, 4H), 5.97 (s, CH), 3.98-4.16 (bs, OH, 1.67-1.82 (m, N-CH), 0.24-0.99 (m, overlapping CH2,4H) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 165.8 (C=O), 155.4 (C-Cl), 144.2 (ArC), 133.7 (ArC), 129.0 (2xArC), 127.7 (2xArC), 122.2 (CH-CC1), 91.7 (C-OH), 22.6 (N-CH), 3.7 & 5.2 (CH2, 2XC) p.p.m. IR (KBr-disc) o max: 3433, 3220, 3019, 2935, 2858, 1700, 1675, 1497, 1412, 1251, 1209,1144,1089,1015,940, 844,802,679 cm"1. Example 13 4-Chloro5-(4-chloro-phenyl)-5-hydn)xy-l-isopropyl-1H-dihydro-pyrrol-2-one. Yield =69% Melting Point: 127-130 °C Re (80% ether / 20% petrol ether) = 0.21 Molecular Weight: 286.2 Molecular Formula: C13H13CI2NO2 MS (APCI(+)):227/229231 (M+1), 286/288/290 (M+) m/z NMR (CDCI3) 250 MHz: δ = 7.31-7.48 (m, ArH, 4H), 6.06 (s, CH), 3.33-3.52 (m, N- CH), 1.25-1.37 & 1.10-1.22 (d, CH3,6H), (OH not detected) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 167.1 (C=O), 154.0 (C-Cl), 136.7 (ArC), 133.4 (ArC), 128.9 (2xArC), 128.0 (2xArC), 123.2 (QH-CC1), 92.9 (C-OH), 45.6 (N-CH), 20.1 & 21.3 (CH3, 2XC) p.p.m. IR (KBr-disc) o max: 3272, 2978, 2927, 1691, 1614, 1496, 1429, 1384, 1352, 1249, 1096,1012,936, 846, 801,683 cm"1. Example 14 4-Chloro--5-(4-chloro-phenyl)-5-hydroxy-l-methyl-1H-dihydro-pyrrol-2-one. Yield = 66% Melting Point: 179-181 °C Rf (80% ether / 20% petrol ether) = 0.24 Molecular Weight: 258.1 Molecular Formula: C11H9CI2NO2 MS (APCI(+)): 227/229/231 (M+l), 258/260/262 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.31-7.42 (ArH, 4H), 6.06 (s, CH), 4.56-4.71 (bs, OH), 2.60 (s, CH3) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 167.8 (C=O), 156.0 (C-Cl), 135.5 (ArC), 132.8 (ArC), 129.1 (2xArC), 127.8 (2xArC), 121.6 (CH-CC1), 92.2 (C-OH), 24.4 (CH3) p.p.m. IR (KBr-disc) u max: 3429, 3102, 2970, 2932, 2857, 1677, 1611, 1494, 1475, 1431, 1202,1151,1091,988,928,811,692 cm-1. Example 15 4-Chloro-5-(4-chloro-phenyl-5-hydroxy-l-phenethyl-1H-dihydro-pyrrol-2-one. Yield = 45% Melting Point: 145-148 °C Rf (80% ether / 20% petrol ether) = 0.18 Molecular Weight: 348.2 Molecular Formula: C18H11Cl2NO2 MS (APCI(+)): 227/229/231 (M+1), 348/350/352 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.22-7.49 (m, ArH, 7H), 7.12-7.18 (m, ArH, 2H), 6.13 (s, CH), 3.68-3.79 & 2.64-2.77 (m, N-CH2), 2.88-3.29 (m, Ar-CH2), (OH not detected) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 167.7 (C=O), 155.5 (C-Cl), 138.8 (ArC), 135.5 (ArC), 133.3 (ArC), 129.1 (2xAiC), 128.8 (2xArC), 128,7 (2xArC), 127.7 (2xArC), 126.7 (ArC), 121.9 (CH-CC1), 92.3 (C-OH), 42.0 (N-CH2), 34.5 (Ar-CH2) p.p.m. IR (KBr-disc) o max: 3421, 3228, 2925, 2848, 2370, 2338, 1684, 1658, 1606, 1461, 1406,1248,1190,1097,935,806,697 cm1. Example 16 4-Chloro-5-(4=-chloro-phenyl)-l-hexyl-5-hydroxy-1H-dihydro-pyrrol-2-one. Yield = 49% Melting Point: 169-172 °C Rf (80% ether / 20% petrol ether) = 0.25 Molecular Weight: 328.2 Molecular Formula: C16H19CI2NO2 MS (APCI(+)): 227/229/231 (M+l), 328/330/332 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.31-7.43 (m, ArH, 4H), 6.15 (s, CH), 3.24-3.44 (m, CH2, 1H), 2.67-2.91 m, CH2, 1H), 1.04-1.69 (m, overlapping CH2, 8H), 0.74-0.89 (t, CH3, J=6.3 Hz) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 165.8 (C=O), 155.7 (C-Cl), 140.8 (ArC), 136.9 (ArC), 129.1 (2xArC), 127.8 (2xArC), 91.6 (C-OH), 40.3 (N-CH2), 30.8 (N-CH2-CH2), 29.1 (N- CH2-CH2-CH2), 26.8 (NH-CH2-CH2-CH2-CH2), 22.6 (CH3-CH2), 15.2 (CH3) p.p.m. IR (KBr-disc) u max: 3446,2935,2863,1698, 1413, 1252, 1200,1138,1092,1013,938, 846,814,702 cm-1. Example 17 4-Chloro-5-(4-chloro-phenyl)-l-cyclopentyl-5-hydro-pyrrol-2-one Yield = 73% Melting Point: 157-159 °C Rf (80% ether / 20% petrol ether) = 0.23 Molecular Weight: 312.2 Molecular Formula: C15H15CI2NO2 MS (APCI(+)): 227/229/231 (M+l), 312/314/316 (M+) m/z NMR (CDCI3) 250 MHz: δ = 7.32-7.51 (ArH, 4H), 6.03 (s, CH), 4.95-5.03 (bs, OH), 3.41-3.62 (m, N-CH, J= 9.26 Hz), 1.97-2.19 (m, CH2), 1.68-1.93 (m, overlapping CH2, 8H) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 167.1 (C=O), 154.8 (CH-CC1), 135.2 (ArC), 133.9 (ArC), 128.9 (2xArC), 128.0 (2xArC), 122.3 (CH-CO), 93.0 (C-OH), 54.3 (N-CH), 30.0 & 28.9 (N-CH-CH2, 4XC), 24.5 (N-CH-CH2-CH2,2xC) p.p.m. IR (KBr-disc) o max: 3407, 3276, 2968, 2922, 2883, 2379, 2339, 1691, 1491, 1429, 1367,1249,1203,1092,1013,932, 843,787,709 cm1. Example 18 4-Chloro--5-(4-chloro-phenyl)-5-hydroxy-1-isobutyl-1H-dihydro-pyrrol-2-one. Yield = 76% Melting Point: 155-158 °C Rf (80% ether / 20% petrol ether) = 0.22 Molecular Weight: 300.2 Molecular Formula: C14H15CI2NO2 MS (APCI(+)): 227/229/231 (M+l), 300/302/304 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.30-7.41 (m, ArH, 4H), 6.19 (s, CH), 3.13-3.31 (dd, CH2, J = 8.0 Hz, 1H), 2.49-2.62 (dd, CH2, J = 8.0 Hz, 1H), 1.69-1.83 (m, CH, J= 5.8 Hz), 0.69-0.80 (t, CH3, J= 4.5 Hz, 6H) p.p.m. ,3C NMR (CDCI3) 250 MHz: δ = 163.3 (C=O), 156.3 (CH-CC1), 139.4 (ArC), 134.8 (ArC), 129.1 (2xArC), 127.7 (2xArC), 122.3 (CH-CC1), 95.0 (C-OH), 47.6 (CH2), 27.6 (£H-CH2), 20.4 (CH3, 2XC) p.p.m IR (KBr-disc) u max: 3426, 3252, 2964, 2924, 2850, 1684, 1406, 1209, 1095, 817, 743, 703 cm-1. 1 -Benzyl l-4-chloro-5-(4-chlolophenyl)-5-hydroxy-1H-hydro-pyrrol-2-one. Yield = 59 % Melting Point: 149-152 °C Rf (80% ether / 20% petrol ether) = 0.18 Molecular Weight: 334.2 Molecular Formula: C17H13CI2NO2 MS (APCI(+)): 227/229/231 (M+l),334/336/338 (M+) m/z 1H NMR (CDCI3) 250 MHz: δ = 7.29-7.36 (m, ArH, 4H), 7.06-7.25 (m, ArH, 5H), 6.09 (s, CH), 4.52-4.60 (d, CH2,1H), 3.89-3.98 (d, CH2,1H) p.p.m. 13C NMR (CDCI3) 250 MHz: δ = 167.6 (CO), 155.4 (C-Cl), 137.5 (ArC), 135.3 (ArC), 133.2 (ArC), 129.1 (ArC), 129.0 (ArC), 128.9 (2xArC), 128.6 (ArC), 128.4 (ArC), 127.9 (2xArC), 127.4 (ArC), 121.9 (CH), 92.6 (C-OH), 43.2 (CH2) p.p.m. IR (KBr-disc) u max: 3442,2931,2849,2365,2339,1674, W16,1492,1406,1349 1272, 1199,1094,1018,817,699 cm-1. Biological Evaluation - [125],I-CCK-8 receptor binding essay: 82. CCKA and CCKB receptor binding assays were performed using guinea pig cerebral cortex (CCKB) and rat pancreas (CCKA). Male guinea pig brain tissues were prepared according to the modified method described by Saita et al, [(1994), Eur. J. Pharmacol,269,249-254]. Pancreatic membranes were prepared in a similar way described by Carpenter et al, [(1988), Proc Natl Acad Sci USA, 85,1968-1972]. Briefly, tissues were homogenized in ice cold sucrose (0.32 M, 25 ml) for 15 strokes at 500 rpm and centrifuged at 13000 rpm for 10 mins. The supernatant was re-centrifuges at 13000 rpm for 20 mins. The resulting pellet was re-dispersed to the required volume of buffer at 500 rpm and stored in aliquots at -70°C. 83. Binding was achieved using a radioligand 125I-Bolton-Hunter labeled CCK, NEN at 25 pM. The samples were incubated {with membranes (0.1 mg/ml)} in 20 mM Hepes, ImM EGTA, 5 mM MgCl2,150 mm NaCl, 0.25 mg/ml bacitracin at pH 6.5 for 2 hrs at RT and then suspended by centrifugation at 1100 rpm for 5 minutes. The membrane pellets were washed twice with water and the bound radioactivity was measured in a Packard Cobra Auto-gamma counter (B5005). All binding assays were carried out with L-363,260 as an internal non-specific standard. Controls (no compound) were also added. All samples were made in duplicate and repeated twice. All compounds were initially screened for percentage inhibition at 10 }im. Samples showing an average inhibition of >35% were diluted to 1pm and re- screened and if active diluted again. This enabled the calculation of ICso's of the series of pyrolones and the examples containing a 5-phenyl group are outlined below. Figure 1. Active examples. 84. A selection of 11 highly diverse amines were chosen to undergo nucleophilic attack at the carbonyl group of 5-arylated-furan-2-one ring of the furanone building block, leading to ring opening and recyclisation into pyrrol-2-ones. These included aryl amines, one of which has a chiral centre and amines with simple alkyl- and cyclic alkyl side chains. The 5- arylated-5-hydroxy-pyrrol-2-ones being formed here, all contain a chiral centre and therefore will exist as enantiomers. In order to control the stereochemistry a chiral amine, (5)-(-)-phenylethylamine was to be used. Diasteromers were formed, which could be isolated and biologically tested. Isobutylamine and its homologue isopropylamine were also used as the aforementioned amine again has shown good activity in relation to pain, depression and anxiolytic assays. 85. In summary 3,4-Dichloro-5-phenyl-5H-furan-2-ones were dissolved in ether and cooled on ice. The appropriate amine was added to the cold solution and stirred for 30 minutes, allowing the reaction mixture to slowly warm up to room temperature. After work up, the desired compound was extracted using column chromatography (80% ether, 20% petrol ether) and analysed using NMR, IR and MS. 86. All outlined compounds are chemically stable, white, crystalline molecules and they are formed in good yields. 87. The crystalline isopropyl derivative, which contains a chiral centre (5-position), was analysed by X-ray crystallography. X-ray data can be found in the experimental section. 88. This compound along side the other compounds synthesised here were fully characterised using 'H and 13C NMR, MS and IR spectroscopy. Pharmacology 89. Following the synthesis and characterisation of these novel molecules, the evaluation in a receptor binding assay followed and the results are outlined in the table below (Table 2). Table 2 : Binding affinity 90. The phenyl-ethyl derivative, example 5, is a potent and mixed CCK antagonist The binding is enhanced by replacing the phenyl group with p-chorophenyl and this observation was determined to be a general trend with respect to the analysis of struture -activity-relationships. 91. Long lipophilic N- substituents resulted in a loss of binding affinity. The Isopropyl derivative 8 showed a good affinity towards the CCK B receptor. 92. A cycloalkyl substituent on the N showed micromolar affinity, but the affinity was not enhanced further by the introduction of a chlorine atom into the 5 aryl group. 93. Interestingly, the addition of a methyl group to the benzyl derivative furnished chiral compounds (Example 10a and 10b), which could easily be separated by column chromatography. CLAIMS 1.A compound of formula (I): wherein X is selected from hydrogen, a halogen, a substituted or unsubstituted cyclic and heterocyclic moiety, substituted or unsubstituted, linear or blanched alkyl, alkyloxy, alkylcarbonyl, alkyloxycarbonyl, alkenyl, alkenyloxy, alkenylcarbonyl, and sulphur equivalents of said oxy, carbonyl and oxycarbonyl moieties, Y is selected from a H, hydroxyl group, alkoxy, thioxy, or as defined in X, R, R1. R is selected from hydrogen, a halogen, phenyl, substituted phenyl, a substituted or unsubstituted cyclic and heterocyclic moiety, substituted or unsubstituted, linear or branched alkyl, alkyloxy, alkylcarbonyl, alkyloxycarbonyl, alkenyl, alkenyloxy, alkenylcarbonyl, alkenyloxycarbonyl, alkynyl, alkynyloxy, alkynylcarbonyl, alkynyloxycarbonyl, aryl, benzyl, arlyoxy, arylcarbonyl, aryloxycaibonyl and sulphur equivalents of said oxy, carbonyl and oxycarbonyl moieties, or as defined in X, Y, R1. R1 is selected from H, methyl, benzyl, alkyl, cycloalkyl, aryl, substituted aryl, heteroaryl, C1-18 straight, branched or cyclic, saturated, unsaturated and aromatic hydrocarbyl groups, which aromatic groups may be heterocyclic, cyclic or acyclic and which may optionally be substituted by alkyl, alkoxy, or halo; or R1 when taken together with the N-atom to which they are bonded, may form an N-containing saturated, unsaturated or partially unsaturated ring system comprising 3 to 10 ring atoms selected from C, N and O, optionally substituted at any position of the ring by a substituent selected from a halogen, a substituted or unsubstituted cyclic and heterocyclic moiety, substituted or unsubstituted, linear or branched alkyl, alkyloxy, alkylcarbonyl, alkyloxycarbonyl, alkenyl, alkenyloxy, alkenylcarbonyl, alkenyloxycarbonyl, alkynyl, alkynyloxy, alkynylcarbonyl, alkynyloxycarbonyl, aryl, benzyl, arlyoxy, arylcarbonyl, aryloxycarbonyl, sulphur equivalents of said oxy, carbonyl and oxycarbonyl moieties, and as defined in X, Y, R. 2. A compound as claimed in claim 1, wherein said alkyl-containing moieties are C1-C18, preferably C1-C12. 3. A compound as claimed in claim 1 or 2, wherein said alkenyl- and said alkynyl- containing moieties are C2-C18, preferably C2-C12. 4. A compound as claimed in any preceding claim, wherein R1 taken together with the N-atom to which they are bonded, form an optionally-substituted: pyrrolidinyl, piperidinyl, benzimidazolyl, pynolyl, pyrazolyl, tetrahydropyrazinyl, dihydropyrazolyl, pyrazolyl, 2,3-dihydro-IH-indol-l-yl, pipetrazin-l-yl, morpholin-4-yl or pyrid-l-yl moiety. 5. A compound as claimed in claim 4, wherein substituents on the ring system formed by R1 are selected from C1-6 alkyl or alkoxy, phenyl, benzyl, phenyl (C2-4) alkenyl, phenoxy, benzyloxy, halo, oxo and alkyloxycarbonyl. 6. A compound as claimed in claim 4 or S, wherein system formed by Ri is mono-or di-substituted. 7. A compound as claimed in any one of claims 1 to 3, wherein R1 are, independently, H, C1-6 alkyl, alkenyl, alkynyl, benzyl, and cyclohexyl. 8. A compound as claimed in claim 7, wherein one of R1 is H, C14 alkyl or benzyl and the other is C1-6 alkyl, phenyl, benzyl or phenyl (C2-4) alkyl, cyclohexyl, 1,3-dihydro- 3H-pyrazolyl or morpholin-4-yl. 9. A compound as claimed in any preceding claim, wherein X is selected from H, F, Br, CI, I and methyl. 10. A compound as claimed in claim 1 having the one of following formulae 11. The use of a compound as claimed in any one of claims 1 to 10 as a CCK receptor ligand and/or as a CCK antagonist. 12. The use as claimed in claim 11, wherein said compound is a selective CCK1 , CCK2 or mixed CCK ligand. 13. A method of treatment of a mammal afflicted with a CCK-related condition, or prophylaxis in a mammal at risk of a CCK-related condition by administration of a therapeutically effective amount of a compound as claimed in any one of claims 1 to 12. 14. The use of a compound in accordance with any one of claims 1 to 11 in the preparation of a medicament, for the treatment or prophylaxis of a CCK-related condition. 15. The method of previous claims, wherein said CCK-related conditions is a GI disorder, a CNS disorder caused by CCK interactions with dopamine, other CNS disorder, oncologic disorder, disorder of appetite regulatory systems; Zollinger-Ellison syndrome; antral G cell hyperplasia; or pain. 16. The method or use of claim 15, wherein said GI disorder is selected from irritable bowel syndrome, gastro-oesophageal reflux disease or ulcers, excess pancreatic or gastric secretion, acute pancreatic, or motility disorders; said CNS disorder is selected from neuroleptic disorders, tardive dyskinesia, Parkinson's disease, psychosis or Gilles de la Tourette syndrome, said other CNS disorder is selected from anxiety disorders and panic disorders and said oncologic disorder is selected from small cell adenocarcinomas and primary tumours of the central nervous system glial and neuronal cells. 17. These novel compounds, as CCK antagonists and supported by other pharmacological mechanisms, protect against stress related aging. 18. The use of a compound to potentiate the analgesic effects of SE/ NE reuptake inhibitor. 19. The use of these agents to potentiate the analgesic effect of opiates.