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Chemical Compound Review

Selfotel     (2S,4R)-4- (phosphonomethyl)piperidine- 2...

Synonyms: GNF-Pf-157, Selfotel, (+)-, CHEMBL39664, SureCN120234, CGS-19755, ...
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Disease relevance of Selfotel

  • Termination of Acute Stroke Studies Involving Selfotel Treatment. ASSIST Steering Committed [1].
  • Both the visceral hyperalgesia and the decrease in somatic pain thresholds were prevented by prior intrathecal CGS-19755 or NBQX injections [2].
  • Furthermore, CGS-19755, 10 mg/kg intraperitoneally, begun either before or after ischemia substantially reduced calcium influx into ischemic neurons as evidenced by reduced calcium-calmodulin binding [3].
  • We conclude that CGS-19755 prevents calcium entry into ischemic neurons and may be effective therapy for very acute cerebral ischemia [3].
  • When CGS-19755 was combined with mild hypothermia the effects of repetitive ischemia were completely abolished in all but one gerbil [4].

Psychiatry related information on Selfotel

  • In contrast, mice that had received the repeated treatment regimen of CGS 19755 increased motor activity in response to challenge doses of 30 and 54 mg/kg [5].
  • CGS 19755 inhibited convulsions elicited by maximal electroshock in rat (ED50 = 3.8 mg/kg i.p. 1 hr after administration) and in mouse (ED50 = 2.0 mg/kg i.p. 0.5 hr after administration) [6].
  • MK-801 (0.01-0.03 mg/kg, i.v.) and CGS-19755 (1-10 mg/kg, i.v.) significantly augmented scopolamine-induced deficit in the non-delayed maze task and impaired the short-term memory in the 5-min delay-interposed task [7].
  • CGS 19755 (3.0 mg/kg) attenuated performance, decreased nose-pokes (an activity necessary to trigger the presentation of the discriminative stimulus and the presentation of the response levers), and increased response latencies (time from 'opportunity to leverpress' to 'actual leverpress') [8].

High impact information on Selfotel

  • NMDA receptor antagonist (CGS-19755, 20 nmol) or AMPA/kainate receptor antagonist (NBQX, 20 nmol) was injected intrathecally before low-pH injections [2].
  • The in vivo neuroprotective effect and brain levels of cis-4-phosphonomethyl-2-piperidine carboxylic acid (CGS 19755), a competitive N-methyl-D-aspartate (NMDA) antagonist, were compared with its in vitro neuroprotective effects [9].
  • BACKGROUND AND PURPOSE: CGS 19755 is a competitive N-methyl-D-aspartate (NMDA) receptor antagonist that limits neuronal damage in animal stroke models [10].
  • CSF and brain levels of CGS 19755 were 12 microM and 5 microM, respectively, at 1 h, 6 microM and 5 microM at 2 h, and 13 microM and 7 microM at 4 h [9].
  • METHODS: CGS-19755 (30 mg/kg) or LY233053 (100 mg/kg) was administered 5, 30, or 60 minutes after reversible spinal cord ischemia in rabbits, induced by temporary occlusion of the infrarenal aorta [11].

Chemical compound and disease context of Selfotel


Biological context of Selfotel

  • Under these conditions, NAAG exhibits apparent inhibition constants (IC50) of 500, 790, and 8.8 microM in the kainate, AMPA, and CGS-19755 receptor binding assays, respectively [17].
  • In crude P2 fractions, no evidence was obtained to suggest that CGS 19755 is taken up by an active transport system [6].
  • CGS 19755 decreased tidal volume and had little effect on frequency of respiration [18].
  • Glutamate and NMDA were found concentration-dependently, and in a manner that could be antagonized by CGS 19755 and MK-801, to produce cell death [19].
  • The competitive excitatory amino acid antagonist cis-4-phosphonomethyl-2-piperidine-carboxylic acid (CGS 19755) increased the latency for monkeys to remove their tails from warm water (analgesia); larger doses produced ataxia, loss of righting, salivation, and eliminated reactivity to stimulation (anesthesia) [18].

Anatomical context of Selfotel

  • Cortical but not basal ganglia infarct volume was significantly smaller in rats receiving CGS-19755 than in the carrier-treated group [20].
  • Delayed injection (5 and 10 h postischaemia) of CGS 19755 (10 and 30 mg/kg) and MK801 (1 and 3 mg/kg) did not provide any protection against pyramidal cell loss [21].
  • We conclude that CGS-19755 crosses the blood-brain barrier very slowly, even in acutely ischemic tissue [22].
  • In the working memory task, CGS 19755 and 3-[(+-)-2-carboxypiperazin-4-yl]propyl-1-phosphonic acid at 10 and 32 ng/side, injected bilaterally into the dorsal hippocampus before testing, produced a significant increase in the number of errors (attempts to pass through two incorrect panels of the three panel-gates at four choice points) [23].
  • Triphenyltetrazolium-determined injury volume of the ipsilateral caudate nucleus in cats treated with NPC 17742 (105 +/- 25 [SEM] mm3), MK-801 (97 +/- 22 mm3), and CGS 19755 (97 +/- 13 mm3) was less than in control cats (198 +/- 21 mm3) [24].

Associations of Selfotel with other chemical compounds


Gene context of Selfotel

  • Also one single episode of spreading depression gave rise to a significant increase of cortical BDNF mRNA levels (to 207% of control), which was attenuated (by 61%) after administration of the competitive NMDA receptor antagonist CGS 19755 [29].
  • It inhibited the binding of the selective NMDA receptor antagonist, [3H]-((+/-)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonate (CPP), with a Ki of 35 nM, and was 4, 5 and 7 fold more potent than the antagonists [+/-)-cis-4-phosphonomethylpiperidine-2-carboxylic acid) (CGS 19755), CPP and D-AP5, respectively [30].
  • In the group where only CGS-19755 was used, significant neuronal protection was evident in the hippocampus (CA1 and CA3), striatum, and medial geniculate nucleus [4].
  • NMDA-induced decreases in ChAT and glutamic acid decarboxylase (GAD) activities were prevented by CGS-19755 (10-40 mg/kg) and MK-801 (1-10 mg/kg) [31].
  • When CGS 19755 was applied with picrotoxin, somatostatin release was the same as levels obtained in the control group with TTX [32].

Analytical, diagnostic and therapeutic context of Selfotel


  1. Termination of Acute Stroke Studies Involving Selfotel Treatment. ASSIST Steering Committed. Davis, S.M., Albers, G.W., Diener, H.C., Lees, K.R., Norris, J. Lancet (1997) [Pubmed]
  2. Altered visceral sensation in response to somatic pain in the rat. Miranda, A., Peles, S., Rudolph, C., Shaker, R., Sengupta, J.N. Gastroenterology (2004) [Pubmed]
  3. CGS-19755, a competitive NMDA receptor antagonist, reduces calcium-calmodulin binding and improves outcome after global cerebral ischemia. Grotta, J.C., Picone, C.M., Ostrow, P.T., Strong, R.A., Earls, R.M., Yao, L.P., Rhoades, H.M., Dedman, J.R. Ann. Neurol. (1990) [Pubmed]
  4. CGS-19755 is neuroprotective during repetitive ischemia: this effect is significantly enhanced when combined with hypothermia. Shuaib, A., Ijaz, S., Mazagri, R., Senthilsevlvan, A. Neuroscience (1993) [Pubmed]
  5. Behavioral tolerance and sensitization to CGS 19755, a competitive N-methyl-D-aspartate receptor antagonist. Boast, C.A., Pastor, G., Gerhardt, S.C., Hall, N.R., Liebman, J.M. J. Pharmacol. Exp. Ther. (1988) [Pubmed]
  6. CGS 19755, a selective and competitive N-methyl-D-aspartate-type excitatory amino acid receptor antagonist. Lehmann, J., Hutchison, A.J., McPherson, S.E., Mondadori, C., Schmutz, M., Sinton, C.M., Tsai, C., Murphy, D.E., Steel, D.J., Williams, M. J. Pharmacol. Exp. Ther. (1988) [Pubmed]
  7. NMDA antagonists potentiate scopolamine-induced amnesic effect. Li, H.B., Matsumoto, K., Tohda, M., Yamamoto, M., Watanabe, H. Behav. Brain Res. (1997) [Pubmed]
  8. Effects of CGS 19755 and dizocilpine (MK 801) on delayed time discrimination performance. Berz, S., Bättig, K., Welzl, H. Behav. Brain Res. (1992) [Pubmed]
  9. Correlation of CGS 19755 neuroprotection against in vitro excitotoxicity and focal cerebral ischemia. Pérez-Pinzón, M.A., Maier, C.M., Yoon, E.J., Sun, G.H., Giffard, R.G., Steinberg, G.K. J. Cereb. Blood Flow Metab. (1995) [Pubmed]
  10. Safety and tolerability of the glutamate antagonist CGS 19755 (Selfotel) in patients with acute ischemic stroke. Results of a phase IIa randomized trial. Grotta, J., Clark, W., Coull, B., Pettigrew, L.C., Mackay, B., Goldstein, L.B., Meissner, I., Murphy, D., LaRue, L. Stroke (1995) [Pubmed]
  11. Delayed therapy of experimental ischemia with competitive N-methyl-D-aspartate antagonists in rabbits. Madden, K.P., Clark, W.M., Zivin, J.A. Stroke (1993) [Pubmed]
  12. Neuronal protection correlates with prevention of calcium-calmodulin binding in rats. Grotta, J.C., Picone, C.M., Dedman, J.R., Rhoades, H.M., Strong, R.A., Earls, R.M., Yao, L.P. Stroke (1990) [Pubmed]
  13. Excitatory amino acid antagonists and memory: effect of drugs acting at N-methyl-D-aspartate receptors in learning and memory tasks. Parada-Turska, J., Turski, W.A. Neuropharmacology (1990) [Pubmed]
  14. Effects of N-methyl-D-aspartate receptor antagonists on cisplatin-induced emesis in the ferret. Lehmann, A., Kärrberg, L. Neuropharmacology (1996) [Pubmed]
  15. Role of hypothermia in the mechanism of protection against serotonergic toxicity. I. Experiments using 3,4-methylenedioxymethamphetamine, dizocilpine, CGS 19755 and NBQX. Farfel, G.M., Seiden, L.S. J. Pharmacol. Exp. Ther. (1995) [Pubmed]
  16. Genetic differences in the effects of competitive and non-competitive NMDA receptor antagonists on locomotor activity in mice. Liljequist, S. Psychopharmacology (Berl.) (1991) [Pubmed]
  17. Interactions between N-acetylaspartylglutamate and AMPA, kainate, and NMDA binding sites. Valivullah, H.M., Lancaster, J., Sweetnam, P.M., Neale, J.H. J. Neurochem. (1994) [Pubmed]
  18. Analgesic, anesthetic, and respiratory effects of the competitive N-methyl-D-aspartate (NMDA) antagonist CGS 19755 in rhesus monkeys. France, C.P., Winger, G.D., Woods, J.H. Brain Res. (1990) [Pubmed]
  19. Characterization of the N-methyl-D-aspartate (NMDA) receptor in the embryonic chick brain. Jacobsson, S.O., Hedin, H., Sellström, A., Fowler, C.J. Naunyn Schmiedebergs Arch. Pharmacol. (1998) [Pubmed]
  20. The effects of a competitive NMDA receptor antagonist (CGS-19755) on cerebral blood flow and pH in focal ischemia. Takizawa, S., Hogan, M., Hakim, A.M. J. Cereb. Blood Flow Metab. (1991) [Pubmed]
  21. Protection by NMDA antagonists against selective cell loss following transient ischaemia. Swan, J.H., Meldrum, B.S. J. Cereb. Blood Flow Metab. (1990) [Pubmed]
  22. In vivo distribution of CGS-19755 within brain in a model of focal cerebral ischemia. Hogan, M.J., Gjedde, A., Hakim, A.M. J. Neurochem. (1992) [Pubmed]
  23. Effects of intrahippocampal injections of N-methyl-D-aspartate receptor antagonists and scopolamine on working and reference memory assessed in rats by a three-panel runway task. Ohno, M., Yamamoto, T., Watanabe, S. J. Pharmacol. Exp. Ther. (1992) [Pubmed]
  24. Comparative analysis of brain protection by N-methyl-D-aspartate receptor antagonists after transient focal ischemia in cats. Miyabe, M., Kirsch, J.R., Nishikawa, T., Koehler, R.C., Traystman, R.J. Crit. Care Med. (1997) [Pubmed]
  25. Identification of subunit- and antagonist-specific amino acid residues in the N-Methyl-D-aspartate receptor glutamate-binding pocket. Kinarsky, L., Feng, B., Skifter, D.A., Morley, R.M., Sherman, S., Jane, D.E., Monaghan, D.T. J. Pharmacol. Exp. Ther. (2005) [Pubmed]
  26. Cloning and functional characterization of human heteromeric N-methyl-D-aspartate receptors. Hess, S.D., Daggett, L.P., Crona, J., Deal, C., Lu, C.C., Urrutia, A., Chavez-Noriega, L., Ellis, S.B., Johnson, E.C., Veliçelebi, G. J. Pharmacol. Exp. Ther. (1996) [Pubmed]
  27. Diphenylhydantoin potentiates the EEG and behavioural effects induced by N-methyl-D-aspartate antagonists in rats. Popoli, P., Pèzzola, A., Sagratella, S. Psychopharmacology (Berl.) (1994) [Pubmed]
  28. Differential effects of N-methyl-D-aspartate receptor blockade on eticlopride-induced immediate early gene expression in the medial and lateral striatum. Keefe, K.A., Adams, A.C. J. Pharmacol. Exp. Ther. (1998) [Pubmed]
  29. Rapid increase of BDNF mRNA levels in cortical neurons following spreading depression: regulation by glutamatergic mechanisms independent of seizure activity. Kokaia, Z., Gidö, G., Ringstedt, T., Bengzon, J., Kokaia, M., Siesjö, B.K., Persson, H., Lindvall, O. Brain Res. Mol. Brain Res. (1993) [Pubmed]
  30. CGP 37849 and CGP 39551: novel and potent competitive N-methyl-D-aspartate receptor antagonists with oral activity. Fagg, G.E., Olpe, H.R., Pozza, M.F., Baud, J., Steinmann, M., Schmutz, M., Portet, C., Baumann, P., Thedinga, K., Bittiger, H. Br. J. Pharmacol. (1990) [Pubmed]
  31. CGS-19755 and MK-801 selectively prevent rat striatal cholinergic and gabaergic neuronal degeneration induced by N-methyl-D-aspartate and ibotenate in vivo. Schoepp, D.D., Salhoff, C.R., Hillman, C.C., Ornstein, P.L. J. Neural Transm. Gen. Sect. (1989) [Pubmed]
  32. Gamma-aminobutyric acid-glutamate interaction in the control of somatostatin release from hypothalamic neurons in primary culture: in vivo corroboration. Rage, F., Benyassi, A., Arancibia, S., Tapia-Arancibia, L. Endocrinology (1992) [Pubmed]
  33. Behavioral pharmacological profile of CGS 19755, a competitive antagonist at N-methyl-D-aspartate receptors. Bennett, D.A., Bernard, P.S., Amrick, C.L., Wilson, D.E., Liebman, J.M., Hutchison, A.J. J. Pharmacol. Exp. Ther. (1989) [Pubmed]
  34. Effects of competitive N-methyl-D-aspartate antagonists on midbrain dopamine neurons: an electrophysiological and behavioral comparison to phencyclidine. French, E.D., Ferkany, J., Abreu, M., Levenson, S. Neuropharmacology (1991) [Pubmed]
  35. Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury. The Executive Committee of the International Selfotel Trial. Juul, N., Morris, G.F., Marshall, S.B., Marshall, L.F. J. Neurosurg. (2000) [Pubmed]
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