Therapeutic Targets Database
BIDD Pharmainformatics Databases


Target Validation Information
Target NameCholecystokinin type A receptor    
Type of TargetClinical trial target    
Drug Potency against TargetDexloxiglumideIC50 = 120 nM[1]
PD-170292EC50 = 2 nM[2]
PD-170292EC50 = 2 nM[3]
A-71378IC50 = 0.5 nM[4]
A-71378IC50 = 0.5 nM[1]
Asp-Tyr(SO3Na)-Met-Gly-Trp-Met-Asp-Phe-NH2IC50 = 0.28 nM[5]
PranazepideIC50 = 0.67 nM[6]
VL-0699IC50 = 12700 nM[7]
L-740093IC50 = 1604 nM[8]
L-708474IC50 = 1797 nM[9]
PD-137342IC50 = 18000 nM[10]
PD-140723IC50 = 186 nM[10]
VL-0395IC50 = 197 nM[11]
VL-0494IC50 = 197 nM[12]
PD-140548IC50 = 2.8 nM[10]
PD-135666IC50 = 25.5 nM[10]
PD-137337IC50 = 2500 nM[10]
L-365260IC50 = 280 nM[6]
CR-1795IC50 = 30 nM[13]
PD-136621IC50 = 3100 nM[10]
VL-2799IC50 = 3240 nM[14]
VL-1499IC50 = 4010 nM[11]
CI-988IC50 = 4300 nM[10]
Boc-Asp-Tyr(So3-)-Nle-Gly-Trp-Asp-Phe-NH2IC50 = 5 nM[15]
PD-140547IC50 = 539 nM[10]
PD-138915IC50 = 580 nM[10]
FR-175985IC50 = 62 nM[6]
CR-2345IC50 = 6600 nM[13]
PD-138916IC50 = 850 nM[10]
PD-135118IC50 = 950 nM[10]
Asp-Tyr(SO3H)-Met-Gly-Trp-Met-Asp-Phe-NH2Ki = 0.64 nM[16]
SINCALIDEKi = 0.64 nM[17]
Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-Phe-NH2Ki = 0.93 nM[16]
H-Tyr-D-Ala-Gly-Phe-NH-NH-Phe-Asp-Nle-D-Trp-HKi = 10000 nM[18]
Tyr-D-Phe-Gly-D-Trp-NMeNle-Asp-Phe-NH2Ki = 1100 nM[19]
Boc-D-Glu-Tyr(SO3H)-Nle-D-Lys-Trp-Nle-Asp-Phe-NH2Ki = 1550 nM[16]
Boc-D-Glu-Tyr(SO3H)-Nle-D-Nle-Trp-Nle-Asp-Phe-NH2Ki = 1600 nM[16]
H-Tyr-D-Ala-Gly-Phe-NH-NH-Trp-D-Nle-D-Asp-D-Phe-HKi = 1900 nM[20]
Tyr-D-Ala-Gly-Phe-NH-NH-Phe-Asp-NMeNle-D-Trp-BocKi = 1900 nM[18]
Boc-Glu-Tyr(SO3H)-Nle-D-Lys-Trp-Nle-Asp-Phe-NH2Ki = 1996 nM[16]
Boc-cyclo-(Glu-Tyr-Nle-D-Lys)-Trp-Nle-Asp-Phe-NH2Ki = 1997 nM[16]
1-(4-Chloro-phenyl)-3-(3-pentyl-oct-2-enyl)-ureaKi = 200 nM[21]
Tyr-D-Phe-Gly-D-Trp-Nle-Asp-Phe-NH2Ki = 2000 nM[19]
IQM-95333Ki = 2890 nM[22]
TetragastrinKi = 3 nM[23]
Tyr-D-Ala-Gly-D-Trp-NMeNle-Asp-Phe-NH2Ki = 320 nM[19]
SNF-9007Ki = 3200 nM[19]
Tyr-D-Phe-Gly-Trp-NMeNle-Asp-Phe-NH2Ki = 3600 nM[19]
3,4-Dichloro-N-(3,3-diphenyl-allyl)-benzamideKi = 400 nM[21]
H-Tyr-D-Ala-Gly-Phe-NH-NH-Phe-Asp-Nle-Trp-BocKi = 4100 nM[18]
Tyr-D-Ala-Gly-Trp-NMeNle-Asp-Phe-NH2Ki = 5100 nM[19]
Tyr-D-Ala-Gly-Trp-Nle-Asp-Phe-NH2Ki = 5700 nM[19]
Tyr-D-Ala-Gly-D-Trp-Nle-Asp-Phe-NH2Ki = 6500 nM[19]
H-Tyr-D-Ala-Gly-Phe-NH-NH-D-Trp-Nle-Asp-Phe-HKi = 7000 nM[20]
1-(3,3-Diphenyl-allyl)-3-m-tolyl-ureaKi = 800 nM[21]
Tyr-D-Nle-Gly-Trp-Nle-Asp-Phe-NH2Ki = 9.6 nM[19]
1-(4-Chloro-phenyl)-3-(3,3-diphenyl-allyl)-ureaKi = 90 nM[21]
Tyr-D-Nle-Gly-D-Trp-NMeNle-Asp-Phe-NH2Ki = 910 nM[19]
Tyr-D-Phe-Gly-Trp-Nle-Asp-Phe-NH2Ki = 98 nM[19]
Action against Disease ModelDexloxiglumideDexloxigl uMide, the active enantiomer of loxigl uMide, interacts competitively with CCK(1) receptors as determined in preclinical studies, such as specific radioligand binding assays or functional studies on isolated guinea pig gallbladder, where it inhibited smooth muscle cell contractions induced by cholecystokinin-octapeptide (CCK-8), the most prominent active forms of cholecystokinin. Dexloxigl uMide has a potent antagonistic effect, of a competitive nature, on h uMan gallbladder cholecystokinin type 1 receptors. In isolated h uMan gallbladder, dexloxigl uMide produced a concentration-dependent rightward shift of the cholecystokinin-octapeptide curve, without affecting its maximal response[24]
The Effect of Target Knockout, Knockdown or Genetic VariationsNormal food intake, normal weight[25]
Ref 1Curr Opin Pharmacol. 2007 Dec;7(6):583-92. Epub 2007 Nov 9.Progress in developing cholecystokinin (CCK)/gastrin receptor ligands that have therapeutic potential. To Reference
Ref 2Curr Top Med Chem. 2003;3(8):837-54.CCK1R agonists: a promising target for the pharmacological treatment of obesity. To Reference
Ref 3Curr Top Med Chem. 2007;7(17):1721-33.NPY Y1 and Y5 receptor selective antagonists as anti-obesity drugs. To Reference
Ref 4Curr Pharm Des. 2005;11(3):295-322.Recent developments in the design of specific Matrix Metalloproteinase inhibitors aided by structural and computational studies. To Reference
Ref 5Bioorg. Med. Chem. Lett. 3(5):855-860 (1993) To Reference
Ref 6Bioorg. Med. Chem. Lett. 7(2):169-174 (1997) To Reference
Ref 7J Med Chem. 2006 Apr 20;49(8):2456-62.Anthranilic acid based CCK1 receptor antagonists and CCK-8 have a common step in their "receptor desmodynamic processes". To Reference
Ref 8Bioorg. Med. Chem. Lett. 5(24):3023-3026 (1995) To Reference
Ref 9J Med Chem. 1994 Mar 18;37(6):719-21.High-affinity and potent, water-soluble 5-amino-1,4-benzodiazepine CCKB/gastrin receptor antagonists containing a cationic solubilizing group. To Reference
Ref 10Bioorg. Med. Chem. Lett. 3(5):881-884 (1993) To Reference
Ref 11Bioorg Med Chem. 2009 Jul 15;17(14):5198-206. Epub 2009 Jun 2.2D-QSAR and 3D-QSAR/CoMFA analyses of the N-terminal substituted anthranilic acid based CCK(1) receptor antagonists: 'Hic Rhodus, hic saltus'. To Reference
Ref 12Bioorg Med Chem Lett. 2007 May 15;17(10):2749-55. Epub 2007 Mar 3.Synthesis and evaluation of novel benzimidazole derivative [Bz-Im] and its radio/biological studies. To Reference
Ref 13Bioorg. Med. Chem. Lett. 3(5):861-866 (1993) To Reference
Ref 14Bioorg Med Chem. 2009 Mar 15;17(6):2336-50. Epub 2009 Feb 14.Anthranilic acid based CCK1 receptor antagonists: blocking the receptor with the same 'words' of the endogenous ligand. To Reference
Ref 15J Med Chem. 1987 Aug;30(8):1366-73.Synthesis and biological activities of pseudopeptide analogues of the C-terminal heptapeptide of cholecystokinin. On the importance of the peptide bonds. To Reference
Ref 16J Med Chem. 1989 Jun;32(6):1184-90.Synthesis and binding affinities of cyclic and related linear analogues of CCK8 selective for central receptors. To Reference
Ref 17J Med Chem. 1989 Feb;32(2):445-9.Full agonists of CCK8 containing a nonhydrolyzable sulfated tyrosine residue. To Reference
Ref 18J Med Chem. 2006 Mar 9;49(5):1773-80.Design and synthesis of novel hydrazide-linked bifunctional peptides as delta/mu opioid receptor agonists and CCK-1/CCK-2 receptor antagonists. To Reference
Ref 19J Med Chem. 2006 May 18;49(10):2868-75.Structure-activity relationships of bifunctional peptides based on overlapping pharmacophores at opioid and cholecystokinin receptors. To Reference
Ref 20J Med Chem. 2007 Jan 11;50(1):165-8.Partial retro-inverso, retro, and inverso modifications of hydrazide linked bifunctional peptides for opioid and cholecystokinin (CCK) receptors. To Reference
Ref 21J Med Chem. 1992 Mar 20;35(6):1042-9.Hybrid cholecystokinin-A antagonists based on molecular modeling of lorglumide and L-364,718. To Reference
Ref 22J Med Chem. 1997 Oct 10;40(21):3402-7.Synthesis and stereochemical structure-activity relationships of 1,3-dioxoperhydropyrido[1,2-c]pyrimidine derivatives: potent and selective cholecystokinin-A receptor antagonists. To Reference
Ref 23J Med Chem. 1987 Apr;30(4):729-32.Synthesis and binding affinities of analogues of cholecystokinin-(30-33) as probes for central nervous system cholecystokinin receptors. To Reference
Ref 24Drug Discov Today. 2007 Jul;12(13-14):504-20. Epub 2007 Jun 27.Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 as a promising therapeutic target. To Reference
Ref 25Obes Rev. 2006 Feb;7(1):89-108.Obesity drugs and their targets: correlation of mouse knockout phenotypes with drug effects in vivo. To Reference


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