Cannabis Sativa

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Devazepide
Clinical data
ATC code
  • none
Identifiers
  • N-(1-methyl-2-oxo-5-phenyl-3H-1,4-benzodiazepin-3-yl)-1H-indole-2-carboxamide
CAS Number
PubChem CID
IUPHAR/BPS
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.208.547 Edit this at Wikidata
Chemical and physical data
FormulaC25H20N4O2
Molar mass408.461 g·mol−1
3D model (JSmol)
  • O=C(c2cc1ccccc1[nH]2)N[C@H]3/N=C(\c4ccccc4N(C3=O)C)c5ccccc5
  • InChI=1S/C25H20N4O2/c1-29-21-14-8-6-12-18(21)22(16-9-3-2-4-10-16)27-23(25(29)31)28-24(30)20-15-17-11-5-7-13-19(17)26-20/h2-15,23,26H,1H3,(H,28,30)/t23-/m1/s1 ☒N
  • Key:NFHRQQKPEBFUJK-HSZRJFAPSA-N ☒N
 ☒NcheckY (what is this?)  (verify)

Devazepide[1] (L-364,718, MK-329) is benzodiazepine drug, but with quite different actions from most benzodiazepines, lacking affinity for GABAA receptors and instead acting as an CCKA receptor antagonist.[2] It increases appetite and accelerates gastric emptying,[3][4] and has been suggested as a potential treatment for a variety of gastrointestinal problems including dyspepsia, gastroparesis and gastric reflux.[5] It is also widely used in scientific research into the CCKA receptor.[6][7]

Synthesis[edit]

Devazepide is synthesised in a similar manner to other benzodiazepines.[8][9]

See also[edit]

References[edit]

  1. ^ US 4820834, Evans, Ben E.; Freidinger, Roger M. & Bock, Mark G., "Benzodiazepine analogs", published 1989-04-11, assigned to Merck & Co. Inc. 
  2. ^ Hill DR, Woodruff GN (September 1990). "Differentiation of central cholecystokinin receptor binding sites using the non-peptide antagonists MK-329 and L-365,260". Brain Research. 526 (2): 276–83. doi:10.1016/0006-8993(90)91232-6. PMID 2257485. S2CID 23851131.
  3. ^ Cooper SJ, Dourish CT (December 1990). "Multiple cholecystokinin (CCK) receptors and CCK-monoamine interactions are instrumental in the control of feeding". Physiology & Behavior. 48 (6): 849–57. doi:10.1016/0031-9384(90)90239-z. PMID 1982361. S2CID 24850080.
  4. ^ Cooper SJ, Dourish CT, Clifton PG (January 1992). "CCK antagonists and CCK-monoamine interactions in the control of satiety". The American Journal of Clinical Nutrition. 55 (1 Suppl): 291S–295S. doi:10.1093/ajcn/55.1.291s. PMID 1728842.
  5. ^ Scarpignato C, Varga G, Corradi C (1993). "Effect of CCK and its antagonists on gastric emptying". Journal of Physiology, Paris. 87 (5): 291–300. doi:10.1016/0928-4257(93)90035-r. PMID 8298606. S2CID 23725376.
  6. ^ Weller A (July 2006). "The ontogeny of postingestive inhibitory stimuli: examining the role of CCK". Developmental Psychobiology. 48 (5): 368–79. doi:10.1002/dev.20148. PMID 16770766.
  7. ^ Savastano DM, Covasa M (October 2007). "Intestinal nutrients elicit satiation through concomitant activation of CCK(1) and 5-HT(3) receptors". Physiology & Behavior. 92 (3): 434–42. doi:10.1016/j.physbeh.2007.04.017. PMID 17531277. S2CID 5566756.
  8. ^ Evans BE, Rittle KE, Bock MG, DiPardo RM, Freidinger RM, Whitter WL, et al. (December 1988). "Methods for drug discovery: development of potent, selective, orally effective cholecystokinin antagonists". Journal of Medicinal Chemistry. 31 (12): 2235–46. doi:10.1021/jm00120a002. PMID 2848124.
  9. ^ EP 1492540, Jackson, Karen, "The use of devazepide as analgesic agent", published 2005-01-05, assigned to ML Laboratories plc 
source: https://en.wikipedia.org/wiki/Devazepide

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