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    Ondansetron HCl (GR 38032; SN 307; GR-C507/75)
    Ondansetron HCl (GR 38032; SN 307; GR-C507/75)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0997
    CAS #: 99614-01-4 Purity ≥98%

    Description: Ondansetron HCl (formerly GR 38032F, GR-C507/75; SN307; GR-C507/75; GRC-50775; GR-38032; SN-307; GR38032; Zofran) isan  anti-emetic drug that acts as a potent serotonin 5-HT3 receptor antagonist. It is primarily used to prevent nausea and vomiting caused by cancer chemotherapy, and radiation therapy. The 5-HT3A receptor antagonist ondansetron (0.3 nM) reversibly inhibited the 5-HT (30 microM) signal by 70% and at 3 nM it abolished the response. Acute ondansetron administration at the lowest dose (0.1 mg/kg, IP) tested had no effect, while other doses (0.33 and 1 mg/kg, IP) produced improvements in auditory gating.

    References: Behav Brain Res. 2011 Mar 17;218(1):121-8; Prog Neuropsychopharmacol Biol Psychiatry. 2005 Jul;29(6):908-16.

    Related CAS#: 99614-02-5 (free base); 103639-04-9 (Ondansetron hydrochloride dihydrate) 

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    Molecular Weight (MW)329.82
    CAS No.99614-01-4(HCl); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 66 mg/mL (200.1 mM)
    Water: 24 mg/mL (72.8 mM)
    Ethanol: 10 mg/mL (30.3 mM)
    Other infoChemical Name: 1, 2, 3, 9-tetrahydro-9-methyl-3-[(2-methyl-1H-imidazol-1- yl)methyl]-4H-carbazol-4-one, monohydrochloride, dihydrate
    InChi Code: InChI=1S/C18H19N3O.ClH.2H2O/c1-12-19-9-10-21(12)11-13-7-8-16-17(18(13)22)14-5-3-4-6-15(14)20(16)2;;;/h3-6,9-10,13H,7-8,11H2,1-2H3;1H;2*1H2
    SMILES Code: O=C1C(CN2C=CN=C2C)CCC(N3C)=C1C4=C3C=CC=C4.[H]Cl.[H]O[H].[H]O[H]
    SynonymsGR 38032F; GRC 50775; SN 307; GR-38032F; GRC-50775; SN-307; GR38032F; GRC50775; SN307; GR 38032F; trade name: Zofran. Code names: 

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    In Vitro

    In vitro activity: Ondansetron decreases the intensity of withdrawal signs such as increased defecation, jumping and wet-dog shakes, elevated the nociceptive threshold values which are decreased by precipitated withdrawal, but produces no change in urination, rectal temperature or salivation. Ondansetron and granisetron significantly enhances gastric emptying of glass beads and improves cisplatin-induced slowing of gastric emptying in rats. Ondansetron exhibits a biphasic dose-response profile in mice, with antidepressant-like effects peaking at 0.1 mg/kg, in the forced swim and tail suspension tests. Ondansetron pretreatment augments the antidepressant effects of fluoxetine and venlafaxine but does not influence the effects of desipramine or 8-hydroxy-2-(di-n-propylamino) tetralin. Ondansetron (10 mg/kg) reverses hyperactivity in the open field, and decreases the percentage entry and time spent in open arms in the elevated plus maze. Ondansetron, a selective and potent 5HT3 receptor antagonist, is shown to be effective at blocking the amphetamine-induced disruption of LI at a dose of 0.01 mg/kg, but not at 0.1 mg/kg. Ondansetron is able to attenuate increases in dopamine activity, produces pharmacologically with amphetamine without affecting baseline dopamine activity. Ondansetron facilitates performance in young adult and aged animals, and inhibits an impairment in habituation induced by scopolamine, electrolesions or ibotenic acid lesions of the nucleus basalis magnocellularis. Ondansetron and arecoline antagonizes a scopolamine-induced impairment. 

    Cell Assay: 5-HT evoked transient inward currents (EC50 = 3.4 microM; Hill coefficient = 1.8) that were blocked by the 5-HT3 receptor antagonist ondansetron (IC50 = 103 pM). The 5-HT3A receptor antagonist ondansetron (0.3 nM) reversibly inhibited the 5-HT (30 microM) signal by 70% and at 3 nM it abolished the response.

    In VivoAcute ondansetron administration at the lowest dose (0.1 mg/kg, IP) tested had no effect, while other doses (0.33 and 1 mg/kg, IP) produced improvements in auditory gating. Different doses of ondansetron were injected intraperitoneally (i.p.) at fixed times during the day to determine both the sublethal (TD50) and lethal (LD50) doses, which were, respectively, 3.7 +/- 0.6 mg/kg and 4.6 +/- 0.5 mg/kg. ondansetron (0.25-1.0 mg/kg, subcutaneously) given before the challenge dose of ethanol (2.4 g/kg, intraperitoneally) injection, significantly and dose dependently attenuated the expression of sensitization. In addition, ondansetron (1.0 mg/kg, subcutaneously) given before ethanol injection on days 1, 4, 7, and 10 significantly blocked the development (days 1, 4, 7, and 10), and expression (day 15) of sensitization to the locomotor stimulant effect of ethanol injection.  
    Animal model Mice
    Formulation & Dosage 0.1 mg/kg, 0.33 and 1 mg/kg, i.p.
    ReferencesEur J Pharmacol. 1997 Dec 11;340(2-3):111-9; Jpn J Pharmacol. 1995 Nov;69(3):205-14. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.

    Antagonism of the contractile response to 5-HT in the mouse ileum by granisetron, tropisetron, ondansetron and MDL 72222. Br J Pharmacol. 2000 Dec; 131(8): 1716–1722.
    The ability of the 5-HT3 receptor selective antagonist, ondansetron, to inhibit the 5-HT-induced inward current in GI vagal afferent neurons is dependent upon extracellular glucose concentration. PLoS One. 2011 Jan 28;6(1):e16519.
    5-HT3A CNiFER: Ondansetron antagonism. Neurogastroenterol Motil. 2012 Oct;24(10):e476


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