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| Molecular weight | |
| Molecular formula | C20H26N2O6S |
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Compound Overview
Quinidine sulfate is an orally active antiarrhythmic agent. It reduces expression of P-gp, inhibits P-gp-mediated efflux, increases intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and increases the proportion of apoptotic cells in the sub-G1 phase. It exerts sustained block and open-channel block effects on IK(f), alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. It has been studied in relation to uterine sarcoma and seizures[1][2][3][4]. It has the molecular formula C20H26N2O6S and a molecular weight of 373.46 g/mol.
Physical & Chemical Properties
| CAS Number | 50-54-4 |
|---|---|
| Molecular Formula | C20H26N2O6S |
| Molecular Weight | 373.46 g/mol |
| SMILES | O=S(O)(O)=O.C=C[C@H]1C[N@](CC[C@H]1C2)[C@@]2([H])[C@@H](O)C3=CC=NC4=CC=C(OC)C=C34.[0.5] |
| Target | Caspase 3 |
| Signaling Pathway | Membrane Transporter/Ion Channel; Epigenetics; Cell Cycle/DNA Damage; Apoptosis |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with your institution's chemical hygiene plan.
In Vitro
Quinidine sulfate (10 μM; 24 h) enhances Paclitaxel-induced cytotoxicity in P-gp-positive MES-SA/DX5 uterine sarcoma cells, lowering the paclitaxel IC50 to 80.56 nM, but leaves paclitaxel cytotoxicity unchanged in P-gp-negative MES-SA uterine sarcoma cells[1]. In paclitaxel-treated P-gp-positive MES-SA/DX5 uterine sarcoma cells, Quinidine sulfate (10 μM; 24 h) significantly raises the sub-G1 apoptotic fraction and thereby strengthens paclitaxel-induced apoptosis[1]. Quinidine blocks in vitro Debrisoquine metabolism in rat liver microsomes, with lower potency than in human liver microsomes[3].
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
In male Lewis rats, Quinidine sulfate (80 mg/kg; p.o.; single dose) potently blocks amphetamine ring hydroxylation: p-hydroxyamphetamine excretion falls to 7.2% and 24.1% of control levels at 24 h and 48 h, respectively, while late-phase amphetamine excretion rises to 542% of the control level[3]. In male NMRI mice, Quinidine sulfate (10-30 mg/kg; intraperitoneal injection; single dose) significantly raises the threshold for pentylenetetrazol-induced tonic convulsions[4].
| 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). |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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