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    Doxapram (AHR-619, Dopram, Stimulex or Respiram)
    Doxapram (AHR-619, Dopram, Stimulex or Respiram)

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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 #: V0087
    CAS #: 309-29-5Purity ≥98%

    Description: Doxapram (AHR619, Dopram, Stimulex or Respiram) is a novel potent respiratory stimulant that acts by inhibiting the potassium channels such as TASK-1, TASK-3, TASK-1/TASK-3 with EC50 of 410 nM, 37 μM, 9 μM, respectively. It is a medication used in intensive care settings to stimulate the respiratory rate in patients with respiratory failure.

    References:  2006 Mar;102(3):779-85.

    Related CAS: 7081-53-0 (HCl)  309-29-5 (free base)

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    Molecular Weight (MW) 378.51
    Formula C24H30N2O2
    CAS No. 309-29-5 (free base); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: > 10 mM 
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Chemical Name 1-ethyl-4- (2-morpholin-4-ylethyl)- 3,3-diphenyl-pyrrolidin-2-one
    Synonyms AHR619; AHR-619; AHR 619; Dopram, Stimulex or Respiram.
    SMILES Code O=C1N(CC)CC(CCN2CCOCC2)C1(C3=CC=CC=C3)C4=CC=CC=C4


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    In Vitro

    In vitro activity: Doxapram is a respiratory stimulant that inhibits TASK-1, TASK-3, TASK-1/TASK-3 heterodimeric channel function with EC50 of 410 nM, 37 μM, 9 μM, respectively. Doxapram preferentially stimulated the release of dopamine. It was also seen to directly inhibit Ca(2+)-independent K+ currents. Doxapram was a more potent inhibitor of the Ca(2+)-activated K+ currents recorded under control conditions. Doxapram (at 15-150 μM) also evoked 3H overflow in a concentration dependent manner, and doxapram-evoked release was inhibited by the Ca2+ channel blocker nifedipine (5 μM). The effects of doxapram on type I cells show similarities to those of the physiological stimuli of the carotid body, suggesting that doxapram may share a similar mechanism of action in stimulating the intact organ. 


    Kinase Assay: Doxapram inhibited TASK-1 (half-maximal effective concentration [EC50], 410 nM), TASK-3 (EC50, 37 microM), and TASK-1/TASK-3 heterodimeric channel function (EC50, 9 microM). 


    Cell Assay: Doxapram (1-100 microM) caused rapid, reversible and dose-dependent inhibitions of K+ currents recorded in type I cells (IC50 approximately 13 microM). doxapram was also seen to directly inhibit Ca(2+)-independent K+ currents. Doxapram was a more potent inhibitor of the Ca(2+)-activated K+ currents recorded under control conditions. Doxapram (10 microM) was without effect on L-type Ca2+ channel currents recorded under conditions where K+ channel activity was minimized and was also without significant effect on K+ currents recorded in the neuronal cell line NG-108 15, suggesting a selective effect on carotid body type I cells. The effects of doxapram on type I cells show similarities to those of the physiological stimuli of the carotid body, suggesting that doxapram may share a similar mechanism of action in stimulating the intact organ.

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    References  2006 Mar;102(3):779-85.


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

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