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Detail of "52-86-8"

  • MSDS Download
  • CAS Number:
  • 52-86-8
  • Name:
  • 1-Butanone,4-[4-(4-chlorophenyl)-4-hydroxy-1-piperidinyl]-1-(4-fluorophenyl)-

  • Superlist Name:
  • Haloperidol
  • Molecular Structure:
  • Formula:
  • C21H23ClFNO2
  • Molecular Weight:
  • 375.90
  • Synonyms:
  • Butyrophenone,4-[4-(p-chlorophenyl)-4-hydroxypiperidino]-4'-fluoro- (6CI,8CI);4-(4-(4-Chlorophenyl)-4-hydroxy-1-piperidinyl)-1-(4-fluorophenyl)-1-butanone;4-(4-Hydroxy-4'-chloro-4-phenylpiperidino)-4'-fluorobutyrophenone;Aloperidin;Bioperidolo;Brotopon;Dozic;Einalon S;Eukystol;Haldol;Haloperin;Keselan;McN-JR 1625;NSC 615296;Peluces;Serenace;Serenelfi;g-[4-(p-Chlorphenyl)-4-hydroxypiperidino]-p-fluorbutyrophenone;
  • EINECS:
  • 200-155-6
  • Density:
  • 1.239 g/cm3
  • Melting Point:
  • 152 °C
  • Boiling Point:
  • 529.034 °C at 760 mmHg
  • Flash Point:
  • 273.75 °C
  • Appearance:
  • white crystalline powder
  • Hazard Symbols:
  • ToxicT
  • Risk Codes:
  • 60-61-25-36/37/38-43
  • Safety:
  • 53-26-36/37/39-45 Details
  • Transport Information:
  • UN 2811 6.1/PG 3

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CAS No.52-86-8 Haloperidol

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CAS No.52-86-8 Haloperidol

EINECS:200-155-6 Molecular Formula: C21H24ClFNO2 Molecular Weight: 376.8716 Boiling point: 529°C at 760 mmHg Flash point:273.8°C

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CAS No.52-86-8 Haloperidol

Haloperidol EINECS: 200-155-6 C21H24ClFNO2 376.8716 InChI: InChI=1/C21H23ClFNO2/c22-18-7-5-17(6-8-18)21(26)11-14-24(15-12-21)13-1-2-20(25)16-3-9-19(23)10-4-16/h3-10,26H,1-2,11-15H2/p+1

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CAS No.52-86-8 Haloperidol

product Name Haloperidol Synonyms haloperidol methanol solution; Haloperidol,98%; 4-(4-chlorophenyl)-1-[4-(4-fluorophenyl)-4-oxobutyl]-4-hydroxypiperidinium Molecular Formula C21H24ClFNO2 Molecular Weight 376.8716 InChI InChI=1/C21H23ClFNO2/c22-18-7-5-17(6-8-18)21(26)11-1

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CAS No.52-86-8 Haloperidol

Molecular structure: Boiling point: 529 ° C at 760 mmHg Flash point: 273.8 ° C The steam pressure: 5.07 mmHg at 25 ° C E-12

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Haloperidol(Haldol)) is an antipsychotic and butyrophenone.

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Reference

Postsynaptic receptors are not essential for dopaminergic feedback regulation
Postsynaptic receptors are not essential for dopaminergic feedback regulation. Di Chiara, G.; Porceddu, M. L.; Fratta, W.; Gessa, G. L. (Inst. Pharmacol., Univ. Cagliari, Cagliari, Italy). Nature (London), 267(5608), 270-2 (English) 1977. CODEN: NATUAS. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Destruction of striatal dopamine [51-61-6]-sensitive adenylate cyclase [9012-42-4] by kainic acid (3 .mu.g, intrastriatally) did not modify dopamine concns. but increased 3,4-dihydroxyphenyl acetate (I) [102-32-9] levels by 100% in lesioned striatum. Homolateral turning obsd. 24 h after lesioning was stimulated by apomorphine-HCl [314-19-2] (0.1-0.5 mg/kg, s.c.) and reversed into contralateral turning by haloperidol [52-86-8] (0.3 mg/kg, i.p.). The increases in striatal I in response to haloperidol or fluphenazine-HCl [146-56-5] were higher in lesioned animals than in controls. I concns. were decreased by apomorphine in both control and lesioned striatum. Haloperidol and apomorphine were mutually antagonistic. An interaction with postsynaptic dopamine receptors is not essential for the changes in dopamine metab. produced by neuroleptics and apomorphine, suggesting that dopamine receptors are not essential for dopaminergic feedback regulation.
Dopamine receptor binding enhancement accompanies lesion-induced behavioral supersensitivity
Dopamine receptor binding enhancement accompanies lesion-induced behavioral supersensitivity. Creese, Ian; Burt, David R.; Snyder, Solomon H. (Dep. Pharmacol. Exp. Ther., Johns Hopkins Univ. Sch. Med., Baltimore, Md., USA). Science, 197(4303), 596-8 (English) 1977. CODEN: SCIEAS. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) The binding of tritiated haloperidol [52-86-8] to rat striatal dopamine receptors increased after lesion (made by injection of 6-hydroxydopamine) of the nigrostriatal dopamine pathway in those rats which were behaviorally supersensitive, as reflected by apomorphine-induced contralateral rotations. The enhanced binding was associated with an increased no. of receptor sites with no change in their affinity.
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