| 词条 | CPHPC |
| 释义 |
| Verifiedfields = changed | verifiedrevid = 414040402 | ImageFile=CPHPC.png | ImageSize=200px | IUPACName=(2R)-1-[6-[(2R)-2-Carboxypyrrolidin-1-yl]-6-oxohexanoyl]pyrrolidine-2-carboxylic acid | OtherNames=Ro 63-8695 |Section1={{Chembox Identifiers | IUPHAR_ligand = 8256 | ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} | ChemSpiderID = 111662 | UNII_Ref = {{fdacite|changed|FDA}} | UNII = WO97N24A47 | InChI = 1/C16H24N2O6/c19-13(17-9-3-5-11(17)15(21)22)7-1-2-8-14(20)18-10-4-6-12(18)16(23)24/h11-12H,1-10H2,(H,21,22)(H,23,24)/t11-,12-/m1/s1 | InChIKey = HZLAWYIBLZNRFZ-VXGBXAGGBC | ChEMBL_Ref = {{ebicite|correct|EBI}} | ChEMBL = 25263 | StdInChI_Ref = {{stdinchicite|correct|chemspider}} | StdInChI = 1S/C16H24N2O6/c19-13(17-9-3-5-11(17)15(21)22)7-1-2-8-14(20)18-10-4-6-12(18)16(23)24/h11-12H,1-10H2,(H,21,22)(H,23,24)/t11-,12-/m1/s1 | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} | StdInChIKey = HZLAWYIBLZNRFZ-VXGBXAGGSA-N | CASNo_Ref = {{cascite|correct|??}} | CASNo=224624-80-0 | PubChem=125516 | SMILES = O=C(O)[C@@H]2N(C(=O)CCCCC(=O)N1[C@@H](C(=O)O)CCC1)CCC2 }} |Section2={{Chembox Properties | Formula=C16H24N2O6 | MolarMass=340.37 g/mol | Appearance= | Density= | MeltingPt= | BoilingPt= | Solubility= |Section3={{Chembox Hazards | MainHazards= | FlashPt= | AutoignitionPt = }}CPHPC (R-1-[6-[R-2-carboxy-pyrrolidin-1-yl]-6-oxo-hexanoyl] pyrrolidine-2-carboxylic acid) is a proline-derived small molecule able to strip amyloid P (AP) from deposits by reducing levels of circulating serum amyloid P (SAP). The SAP-amyloid association has also been identified as a possible drug target for anti-amyloid therapy, with the recent development and first stage clinical trials of CPHPC for amyloidosis.[1] CPHPC has also been patented for possible treatment of Alzheimer's disease.[2] MechanismThe symmetrical nature of CPHPC allows it to bind to two molecules of AP (the SAP subunits). This allows five molecules of CPHPC to bind two SAP pentamers together by the B/binding face blocking the binding on to existing amyloid deposits.[3] References1. ^{{cite journal| vauthors = Pepys MB, Herbert J, Hutchinson WL, Tennent GA, Lachmann HJ, Gallimore JR, Lovat LB, Bartfai T, Alanine A, Hertel C, Hoffmann T, Jakob-Roetne R, Norcross RD, Kemp JA, Yamamura K, Suzuki M, Taylor GW, Murray S, Thompson D, Purvis A, Kolstoe S, Wood SP, Hawkins PN | title = Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis | journal = Nature | volume = 417 | issue = 6886 | pages = 254–9 | year = 2002 | pmid = 12015594 | doi = 10.1038/417254a }} {{DEFAULTSORT:Cphpc}}2. ^Pharmaceutical Formulations for the Treatment of Alzheimer's Disease {{Cite patent|WO|2008014232 }} 3. ^Reducing the Supply of Amyloid Fibril Precursor Proteins, MedScape Today 2 : Pyrrolidines|Amino acid derivatives |
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