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Chemical Compound Review

Rimonabant HCl     5-(4-chlorophenyl)-1-(2,4- dichlorophenyl)...

Synonyms: CHEMBL558598, Bio-0091, SureCN1186698, CS-0707, CHEBI:651643, ...
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Disease relevance of Acomplia

  • SR 141716A evoked thermal hyperalgesia with an ED50 of 0.0012 fmol [1].
  • Unexpectedly, we found that CB1-mediated effects of SR 141716A included inhibition of MAPK activation by pertussis toxin-sensitive receptor-tyrosine kinase such as insulin or insulin-like growth factor 1 receptors but not by pertussis toxin-insensitive receptor-tyrosine kinase such as the fibroblast growth factor receptor [2].
  • Native cannabinoid receptors were studied in male rat major pelvic ganglion neurons, where it was found that WIN 55,212-2 inhibited and SR 141716A increased Ca2+ currents [3].
  • Experiments with cultured pituitary adenoma cells showed that the CB1 agonist WIN 55,212--2 inhibited GH secretion in most of acromegaly-associated pituitary adenomas tested and that the CB1 antagonist SR 141716A was generally able to reverse this effect [4].
  • Both intraperitoneal (0, 1, 2.5, 5, 10 and 20 mg/kg, n = 7-15 per group) and subcutaneous (0, 10, 20 and 40 mg/kg, n = 6-9 per group) administration of SR 141716A caused emesis (ED(50) = 5.52 +/- 1.23 and 20.2 +/- 1.02 mg/kg, respectively) in the least shrew in a dose-dependent manner [5].

Psychiatry related information on Acomplia

  • SR 141716A administration precipitated several somatic signs that included wet dog shakes, frontpaw tremor, ataxia, hunched posture, tremor, ptosis, piloerection, decreased locomotor activity and mastication, which can be interpreted as being part of a withdrawal syndrome [6].
  • Both cannabinoid agonists WIN 55,212-2 and delta9-tetrahydrocannabinol shortened the modal response time, and cannabinoid antagonist SR 141716A lengthened the modal response time [7].
  • At the efficient dose of 3 mg/kg I.P., SR 141716A reduced the spectral power of the EEG signals typical of SWS but did not affect those of wakefulness [8].
  • The availability of the cannabinoid antagonist, SR 141716A, to precipitate withdrawal following repeated cannabinoid administration provides a model to investigate the mechanisms underlying cannabinoid dependence as well as potential treatments to alleviate withdrawal symptoms [9].
  • Over a 4-hour recording period, SR 141716A (0.1, 0.3, 1, 3, and 10 mg/kg I.P.) dose-dependently increased the time spent in wakefulness at the expense of slow-wave sleep (SWS) and rapid eye movement sleep (REMS), delayed the occurrence of REMS but did not change the mean duration of REMS episodes [8].

High impact information on Acomplia


Chemical compound and disease context of Acomplia


Biological context of Acomplia


Anatomical context of Acomplia

  • By contrast, SR 141716A had no effect on MAPK activation by insulin or IGF1 in CHO cells lacking CB1 receptors, ruling out the possibility of a direct interaction of SR 141716A with the Gi protein [2].
  • Morphine-induced increases in nucleus accumbens dopamine levels were unaltered by SR 141716A [22].
  • Both penile erection and NO2- increase induced by SR 141716A were reduced by the prior injection into the PVN of the cannabinoid CB1 agonists WIN 55,212-2 (5 microg) or HU 210 (5 microg), given into the paraventricular nucleus at doses unable to induce penile erection or to modify NO2- concentration [19].
  • Furthermore, the potentiation of ACh release in the hippocampus by SR 141716A alone suggests either that this compound is an inverse agonist at cannabinoid receptors or it is antagonizing the actions of an endogenous ligand acting on these receptors [23].
  • 5. We conclude that abn-cbd relaxes the rat small mesenteric artery by endothelium-dependent activation of K(+) channels via SR 141716A-sensitive pathways, which do not involve CB(1) and CB(2) receptors [24].

Associations of Acomplia with other chemical compounds


Gene context of Acomplia

  • However, simultaneous application of CRF and WIN 55,212--2 resulted in a synergistic effect on ACTH secretion, and this effect could be abolished by SR 141716A, demonstrating a CB1-mediated effect [4].
  • Moreover, WIN 55,212--2 was able to suppress GHRH-stimulated GH release, and this effect was not blocked by coincubation with SR 141716A, possibly indicating a non-CB1-mediated effect [4].
  • This activation, corresponding to both neuronal cell bodies and the surrounding neuropil, is totally inhibited by the selective antagonist of CB1 cannabinoid receptors, SR 141716A [29].
  • SR 141716A failed to antagonize this activity in either cell line, confirming its specificity for CB1 [30].
  • The inhibitory effects of both ligands on peak L-type Ca2+ currents were abolished by pertussis toxin pretreatment and application of the CB1-receptor antagonist SR-141716A (100 nM, n = 5) [31].

Analytical, diagnostic and therapeutic context of Acomplia


  1. Hypoactivity of the spinal cannabinoid system results in NMDA-dependent hyperalgesia. Richardson, J.D., Aanonsen, L., Hargreaves, K.M. J. Neurosci. (1998) [Pubmed]
  2. A selective inverse agonist for central cannabinoid receptor inhibits mitogen-activated protein kinase activation stimulated by insulin or insulin-like growth factor 1. Evidence for a new model of receptor/ligand interactions. Bouaboula, M., Perrachon, S., Milligan, L., Canat, X., Rinaldi-Carmona, M., Portier, M., Barth, F., Calandra, B., Pecceu, F., Lupker, J., Maffrand, J.P., Le Fur, G., Casellas, P. J. Biol. Chem. (1997) [Pubmed]
  3. SR 141716A acts as an inverse agonist to increase neuronal voltage-dependent Ca2+ currents by reversal of tonic CB1 cannabinoid receptor activity. Pan, X., Ikeda, S.R., Lewis, D.L. Mol. Pharmacol. (1998) [Pubmed]
  4. Normal human pituitary gland and pituitary adenomas express cannabinoid receptor type 1 and synthesize endogenous cannabinoids: first evidence for a direct role of cannabinoids on hormone modulation at the human pituitary level. Pagotto, U., Marsicano, G., Fezza, F., Theodoropoulou, M., Grübler, Y., Stalla, J., Arzberger, T., Milone, A., Losa, M., Di Marzo, V., Lutz, B., Stalla, G.K. J. Clin. Endocrinol. Metab. (2001) [Pubmed]
  5. Delta(9)-tetrahydrocannabinol and synthetic cannabinoids prevent emesis produced by the cannabinoid CB(1) receptor antagonist/inverse agonist SR 141716A. Darmani, N.A. Neuropsychopharmacology (2001) [Pubmed]
  6. Behavioural and biochemical evidence for signs of abstinence in mice chronically treated with delta-9-tetrahydrocannabinol. Hutcheson, D.M., Tzavara, E.T., Smadja, C., Valjent, E., Roques, B.P., Hanoune, J., Maldonado, R. Br. J. Pharmacol. (1998) [Pubmed]
  7. Cannabinoid modulation of time estimation in the rat. Han, C.J., Robinson, J.K. Behav. Neurosci. (2001) [Pubmed]
  8. Arousal-enhancing properties of the CB1 cannabinoid receptor antagonist SR 141716A in rats as assessed by electroencephalographic spectral and sleep-waking cycle analysis. Santucci, V., Storme, J.J., Soubrié, P., Le Fur, G. Life Sci. (1996) [Pubmed]
  9. Precipitated cannabinoid withdrawal is reversed by Delta(9)-tetrahydrocannabinol or clonidine. Lichtman, A.H., Fisher, J., Martin, B.R. Pharmacol. Biochem. Behav. (2001) [Pubmed]
  10. Activation of corticotropin-releasing factor in the limbic system during cannabinoid withdrawal. Rodríguez de Fonseca, F., Carrera, M.R., Navarro, M., Koob, G.F., Weiss, F. Science (1997) [Pubmed]
  11. The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation. De Petrocellis, L., Melck, D., Palmisano, A., Bisogno, T., Laezza, C., Bifulco, M., Di Marzo, V. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  12. Structural features of the central cannabinoid CB1 receptor involved in the binding of the specific CB1 antagonist SR 141716A. Shire, D., Calandra, B., Delpech, M., Dumont, X., Kaghad, M., Le Fur, G., Caput, D., Ferrara, P. J. Biol. Chem. (1996) [Pubmed]
  13. Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral CB1 receptors. Richardson, J.D., Kilo, S., Hargreaves, K.M. Pain (1998) [Pubmed]
  14. R-(+)-[2,3-Dihydro-5-methyl-3-(4-morpholinylmethyl)-pyrrolo-[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphtalenylmethanone (WIN-2) ameliorates experimental autoimmune encephalomyelitis and induces encephalitogenic T cell apoptosis: Partial involvement of the CB(2) receptor. S??nchez, A.J., Gonz??lez-P??rez, P., Galve-Roperh, I., Garc??a-Merino, A. Biochem. Pharmacol. (2006) [Pubmed]
  15. Behavioral evidence for the interaction of oleamide with multiple neurotransmitter systems. Fedorova, I., Hashimoto, A., Fecik, R.A., Hedrick, M.P., Hanus, L.O., Boger, D.L., Rice, K.C., Basile, A.S. J. Pharmacol. Exp. Ther. (2001) [Pubmed]
  16. Capsaicin evokes hypothermia independent of cannabinoid CB1 and CB2 receptors. Ding, Z., Cowan, A., Rawls, S.M. Brain Res. (2005) [Pubmed]
  17. WIN-55,212-2 and SR-141716A alter nicotine-induced changes in locomotor activity, but do not alter nicotine-evoked [(3)H]dopamine release. Rodvelt, K.R., Bumgarner, D.M., Putnam, W.C., Miller, D.K. Life Sci. (2007) [Pubmed]
  18. Activation of mitogen-activated protein kinases by stimulation of the central cannabinoid receptor CB1. Bouaboula, M., Poinot-Chazel, C., Bourrié, B., Canat, X., Calandra, B., Rinaldi-Carmona, M., Le Fur, G., Casellas, P. Biochem. J. (1995) [Pubmed]
  19. The cannabinoid receptor antagonist SR-141716A induces penile erection in male rats: involvement of paraventricular glutamic acid and nitric oxide. Melis, M.R., Succu, S., Mascia, M.S., Sanna, F., Melis, T., Castelli, M.P., Argiolas, A. Neuropharmacology (2006) [Pubmed]
  20. Analgesic, respiratory and heart rate effects of cannabinoid and opioid agonists in rhesus monkeys: antagonist effects of SR 141716A. Vivian, J.A., Kishioka, S., Butelman, E.R., Broadbear, J., Lee, K.O., Woods, J.H. J. Pharmacol. Exp. Ther. (1998) [Pubmed]
  21. Role of different brain structures in the behavioural expression of WIN 55,212-2 withdrawal in mice. Castañé, A., Maldonado, R., Valverde, O. Br. J. Pharmacol. (2004) [Pubmed]
  22. Cannabinoid modulation of opiate reinforcement through the ventral striatopallidal pathway. Caillé, S., Parsons, L.H. Neuropsychopharmacology (2006) [Pubmed]
  23. Electrically evoked acetylcholine release from hippocampal slices is inhibited by the cannabinoid receptor agonist, WIN 55212-2, and is potentiated by the cannabinoid antagonist, SR 141716A. Gifford, A.N., Ashby, C.R. J. Pharmacol. Exp. Ther. (1996) [Pubmed]
  24. Vasodilator actions of abnormal-cannabidiol in rat isolated small mesenteric artery. Ho, W.S., Hiley, C.R. Br. J. Pharmacol. (2003) [Pubmed]
  25. Cannabinoid CB1 receptors fail to cause relaxation, but couple via Gi/Go to the inhibition of adenylyl cyclase in carotid artery smooth muscle. Holland, M., John Challiss, R.A., Standen, N.B., Boyle, J.P. Br. J. Pharmacol. (1999) [Pubmed]
  26. Excitatory transmission to the circular muscle of the guinea-pig ileum: evidence for the involvement of cannabinoid CB1 receptors. Izzo, A.A., Mascolo, N., Borrelli, F., Capasso, F. Br. J. Pharmacol. (1998) [Pubmed]
  27. Conditioned place preference induced by the cannabinoid agonist CP 55,940: interaction with the opioid system. Braida, D., Pozzi, M., Cavallini, R., Sala, M. Neuroscience (2001) [Pubmed]
  28. Effect of the cannabinoid CB1 receptor antagonist SR-141716A on ethanol self-administration and ethanol-seeking behaviour in rats. Economidou, D., Mattioli, L., Cifani, C., Perfumi, M., Massi, M., Cuomo, V., Trabace, L., Ciccocioppo, R. Psychopharmacology (Berl.) (2006) [Pubmed]
  29. Delta 9-tetrahydrocannabinol-induced MAPK/ERK and Elk-1 activation in vivo depends on dopaminergic transmission. Valjent, E., Pagès, C., Rogard, M., Besson, M.J., Maldonado, R., Caboche, J. Eur. J. Neurosci. (2001) [Pubmed]
  30. Molecular cloning, expression and function of the murine CB2 peripheral cannabinoid receptor. Shire, D., Calandra, B., Rinaldi-Carmona, M., Oustric, D., Pessègue, B., Bonnin-Cabanne, O., Le Fur, G., Caput, D., Ferrara, P. Biochim. Biophys. Acta (1996) [Pubmed]
  31. Cannabinoid CB1 receptor of cat cerebral arterial muscle functions to inhibit L-type Ca2+ channel current. Gebremedhin, D., Lange, A.R., Campbell, W.B., Hillard, C.J., Harder, D.R. Am. J. Physiol. (1999) [Pubmed]
  32. Characterization of CB1 receptors on rat neuronal cell cultures: binding and functional studies using the selective receptor antagonist SR 141716A. Jung, M., Calassi, R., Rinaldi-Carmona, M., Chardenot, P., Le Fur, G., Soubrié, P., Oury-Donat, F. J. Neurochem. (1997) [Pubmed]
  33. Cannabinoid receptors on goldfish retinal bipolar cells: electron-microscope immunocytochemistry and whole-cell recordings. Yazulla, S., Studholme, K.M., McIntosh, H.H., Fan, S.F. Vis. Neurosci. (2000) [Pubmed]
  34. SR 141716A, a cannabinoid receptor antagonist, produces hyperalgesia in untreated mice. Richardson, J.D., Aanonsen, L., Hargreaves, K.M. Eur. J. Pharmacol. (1997) [Pubmed]
  35. Effect of the cannabinoid receptor SPECT agent, AM 281, on hippocampal acetylcholine release from rat brain slices. Gifford, A.N., Tang, Y., Gatley, S.J., Volkow, N.D., Lan, R., Makriyannis, A. Neurosci. Lett. (1997) [Pubmed]
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