Devazepide

Last updated
Devazepide
Devazepide.svg
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 InfoCard 100.208.547 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C25H20N4O2
Molar mass 408.461 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 X mark.svgN
  • Key:NFHRQQKPEBFUJK-HSZRJFAPSA-N X mark.svgN
 X mark.svgNYes check.svgY  (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]

Contents

Synthesis

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

See also

References

  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
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.