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    Quinine HCl Dihydrate
    Quinine HCl Dihydrate

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    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V0309
    CAS #: 6119-47-7Purity ≥98%

    Description: Quinine HCl dihydrate (Quinine hydrochloride dihydrate) is a novel, potent naturally occuring compound with a variety of biological activities such as anti-malarial, antipyretic, analgesic , anti-inflammatory properties.  

    References: Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10942-7; Eur J Pharmacol. 1995 Dec 27;294(1):353-5.

    Related CAS #: 130-95-0 (Quinine free base) 60-93-5 (2HCl)   6119-70-6 (sulfate dihydrate)   804-63-7 (sulfate)    549-49-5 (HBr)   

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    • 香港大学
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    Molecular Weight (MW)396.91 
    CAS No.6119-47-7  
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 79 mg/mL (199.0 mM)
    Water: 43 mg/mL (108.33 mM
    Ethanol: 79 mg/mL (199.0 mM)
    SMILESCOC1=CC2=C(N=CC=C2[[email protected]]([[email protected]@]3([H])[[email protected]](C[[email protected]@H]4C=C)CC[[email protected]@]4([H])C3)O)C=C1.Cl.O.O
    Synonyms6'-Methoxycinchonidine; Quinine; Chinin; Chininum; (8S,9R)-Quinine; Qualaquin; Odan Brand of Quinine Sulfate; Plough Brand of Quinine Sulfate; Prosana Brand of Quinine Bisulfate; Quinamm; Quinbisan; Quinbisul; Quindan; Quinine HCl; Quinine hydrochloride dihydrate;

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    In Vitro

    In vitro activity: Quinine blocks Cx36 and Cx50 junctional currents in a reversible and concentration-dependent manner with half maximal blocking concentrations of 32 mM and 73 mM, respectively. Quinine induces slow transitions between open and fully closed states that decreased open probability of the channel. Quinine thus offers a potentially useful method to block certain types of gap junction channels, including those between neurons that are formed by Cx36. Quinine, a K+ channel blocker, prevents formation of tumor necrosis factor (TNF) as well as the subsequent hepatic DNA fragmentation and liver enzyme leakage. Quinine elicits Fos-like immunoreactivity (FLI) concentrated in the medial third of the nucleus; acid elicited more broadly distributed FLI concentrated farther laterally. Quinine has a relatively weak effect on doxorubicin accumulation but was able to completely restore doxorubicin sensitivity in the resistant cells. Quinine also modifies the intracellular tolerance to doxorubicin, which suggests that it is able to modify drug distribution within the cells. Quinine primarily blocks the whole cell potassium currents (IK) in a voltage-dependent manner. Quinine also reduces the size of sodium currents (INa) in a use-dependent manner, while leaving calcium currents (ICa) relatively unaffected.

    In VivoIn patients with cerebral malaria receiving the standard dose of 10 mg/kg every eight hours, plasma quinine concentrations consistently exceeded 10 mg/liter, reaching a peak 60 ± 25 hours (mean ± 1 S.D.) after treatment was begun and then declining. Quinine total clearances (CI) and total apparent volumes of distribution (Vd) were significantly lower than in uncomplicated malaria (CI, 0.92 ± 0.42 compared with 1.35 ± 0.6 ml/min/kg, p = 0.03; Vd, 1.18 ± 0.37 compared with 1.67 ± 0.34 liter/kg, p = 0.0013)
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    Am J Med, 1982. 73(4): p. 564-72.; Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10942-7; Eur J Pharmacol. 1995 Dec 27;294(1):353-5. 

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


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