1. Membrane Transporter/Ion Channel Epigenetics Cell Cycle/DNA Damage Apoptosis
  2. P-glycoprotein PARP Caspase Apoptosis Potassium Channel
  3. Quinidine hydrochloride

Quinidine hydrochloride is an orally active antiarrhythmic agent. Quinidine hydrochloride reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine hydrochloride exerts sustained block and open-channel block effects on IK(f). Quinidine hydrochloride alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine hydrochloride can be used in studies related to uterine sarcoma and seizures.

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Quinidine hydrochloride

Quinidine hydrochloride Chemical Structure

CAS No. : 1668-99-1

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Description

Quinidine hydrochloride is an orally active antiarrhythmic agent. Quinidine hydrochloride reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine hydrochloride exerts sustained block and open-channel block effects on IK(f). Quinidine hydrochloride alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine hydrochloride can be used in studies related to uterine sarcoma and seizures[1][2][3][4].

In Vitro

Quinidine (10 μM; 24 h) hydrochloride potentiates Paclitaxel (HY-B0015)-induced cytotoxicity in P-gp-positive MES-SA/DX5 uterine sarcoma cells (reducing paclitaxel IC50 to 80.56 nM) but does not alter paclitaxel cytotoxicity in P-gp-negative MES-SA uterine sarcoma cells[1].
Quinidine (10 μM; 24 h) hydrochloride significantly increases the sub-G1 apoptotic portion in paclitaxel-treated P-gp-positive MES-SA/DX5 uterine sarcoma cells, enhancing paclitaxel-induced apoptosis[1].
Quinidine inhibits the in vitro metabolism of Debrisoquine in rat liver microsomes, with lower potency than observed in human liver microsomes[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay[1]

Cell Line: P-gp-negative MES-SA uterine sarcoma cells, P-gp-positive MES-SA/DX5 uterine sarcoma cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Did not significantly alter the cytotoxicity of paclitaxel in MES-SA cells, with paclitaxel IC50 remaining comparable to paclitaxel alone (19 nM vs. 18 nM).
Strongly potentiated paclitaxel-induced cytotoxicity in MES-SA/DX5 cells, reducing the IC50 of paclitaxel from 13851 nM to 81 nM.
Showed no significant cytotoxicity up to 100 μM in either cell line.\nShowed concentration-dependent cytotoxicity with docetaxel against MES-SA cells.
Enhanced docetaxel-induced cytotoxicity in MES-SA/DX5 cells more potently than hydrocinchonine, alongside cinchonine.
Showed no significant cytotoxicity up to 100 μM in either cell line.

Cell Cycle Analysis[1]

Cell Line: P-gp-positive MES-SA/DX5 uterine sarcoma cells (paclitaxel-treated)
Concentration: 10 μM
Incubation Time: 24 h
Result: Significantly increased the sub-G1 apoptotic portion (G0 = 27.19) in paclitaxel-treated MES-SA/DX5 cells, whereas paclitaxel alone induced minimal sub-G1 accumulation (G0 = 0.05).
In Vivo

Quinidine (80 mg/kg; p.o.; single administration) hydrochloride potently inhibits amphetamine ring hydroxylation in male Lewis rats, reducing the excretion of p-hydroxyamphetamine to 7.2% and 24.1% of the control group levels at 24 h and 48 h, respectively, while increasing the late-phase excretion of amphetamine to 542% of the control group level[3].
Quinidine (10-30 mg/kg; intraperitoneal injection; single administration) hydrochloride significantly elevates the threshold of pentylenetetrazol-induced tonic convulsions in male NMRI mice[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Lewis (male, 175-225 g)[3]
Dosage: 80 mg/kg
Administration: p.o.; single dose
Result: Reduced urinary excretion of p-hydroxyamphetamine to 7.2% of vehicle-control levels in the 0-24 h collection period.
Reduced urinary excretion of p-hydroxyamphetamine to 24.1% of vehicle-control levels in the 24-48 h collection period.
Increased amphetamine excretion to 542% of control levels in the 24-48 h period.
Excreted an average of 0.40 μmol p-hydroxyamphetamine and 7.80 μmol amphetamine in the 0-24 h period.
Excreted an average of 3.60 μmol amphetamine and a significantly reduced amount of p-hydroxyamphetamine relative to controls in the 24-48 h period.
Achieved total combined excretion of amphetamine and p-hydroxyamphetamine over 48 h equal to 79.7% of the administered dose, which was not significantly different from control groups.
Animal Model: NMRI (male, 5-6 weeks old, 25-30 g)[4]
Dosage: 10 mg/kg; 20 mg/kg; 30 mg/kg
Administration: i.p.; single dose
Result: Did not alter the pentylenetetrazole threshold dose for onset of myoclonic twitch.
Significantly increased the pentylenetetrazole threshold dose for onset of tonic hind limb extension compared to saline-treated controls (p < 0.05).
Molecular Weight

360.88

Formula

C20H25ClN2O2

CAS No.
SMILES

O[C@H]([C@]1([H])[N@@]2C[C@@H]([C@](CC2)([H])C1)C=C)C3=CC=NC4=C3C=C(OC)C=C4.Cl

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Please store the product under the recommended conditions in the Certificate of Analysis.

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Product Name:
Quinidine hydrochloride
Cat. No.:
HY-W115674
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