Swerchirin
Swerchirin is an orally active, plant-derived xanthone that acts as an inhibitor of the Raf/MEK/ERK signaling pathway. Swerchirin downregulates the expression of phosphorylated MEK and phosphorylated ERK, induces mitochondrial apoptosis and cell cycle arrest, regulates Bcl-2 family proteins, triggers cytochrome c release, activates caspases, and drives PARP cleavage. Swerchirin reduces blood glucose levels in rat models under fasting, fed, glucose-loaded conditions, and following treatment with Tolbutamide (HY-B0401). Swerchirin can be used in research related to ovarian cancer, liver injury, and diabetes.
For research use only. We do not sell to patients.
- CAS No.: 521-65-3
- Formula: C15H12O6
- Molecular Weight:288.25
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
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Caspase 3 |
Caspase-9 |
Bax |
Bcl-2 |
PARP |
MEK |
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| SK-OV-3 | IC50 |
20 μM
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Antiproliferative activity against human ovarian cancer SKOV3 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
Antiproliferative activity against human ovarian cancer SKOV3 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
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33721473 |
Swerchirin (10-40 μM; 48 h) potently inhibits the viability of human ovarian cancer SKOV3 cells in a concentration-dependent manner, with an IC50 of 20 μM[1].
Swerchirin (10-40 μM; 24 h) induces G2/M cell cycle arrest in human ovarian cancer SKOV3 cells in a concentration-dependent manner in vitro[1].
Swerchirin (10-40 μM; 6-72 h) reduces the mitochondrial membrane potential of human ovarian cancer SKOV3 cells in a concentration-dependent manner in vitro[1].
Swerchirin (10-40 μM; 48 h) induces apoptosis in human ovarian cancer SKOV3 cells in a concentration-dependent manner[1].
Swerchirin (10-40 μM) regulates the expression of apoptosis-related proteins in human ovarian cancer SKOV3 cells in a concentration-dependent manner, upregulating pro-apoptotic proteins and downregulating the anti-apoptotic protein Bcl-2[1].
Swerchirin (10-40 μM) inhibits the Raf/MEK/ERK signaling pathway in human ovarian cancer SKOV3 cells in vitro in a concentration-dependent manner by downregulating the expression of phosphorylated MEK and phosphorylated ERK[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human ovarian cancer SKOV3 cells
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Concentration:10, 20, 40 μM
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Incubation Time:48 h
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Result:Exhibited a concentration-dependent anti-proliferative effect on SKOV3 cells, reducing cell viability significantly.
Achieved an IC50 of 20 μM after 48 hours of incubation.
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Cell Line:human ovarian cancer SKOV3 cells
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Concentration:10, 20, 40 μM
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Incubation Time:24 h
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Result:Caused a concentration-dependent increase in the percentage of SKOV3 cells in the G2/M phase.
Increased the G2/M population from 10.34% (control) to 21.69% at 10 μM, to 26.14% at 20 μM, and to 30.21% at 40 μM.
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Cell Line:human ovarian cancer SKOV3 cells
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Concentration:10, 20, 40 μM
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Incubation Time:48 h
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Result:Induced apoptosis in SKOV3 cells in a concentration-dependent manner.
Increased the apoptotic cell population from 5.2% (control) to 11.3% at 10 μM, 35.7% at 20 μM, and 67.8% at 40 μM.
Swerchirin (5-250 mg/kg; p.o.; single administration) produces a dose-dependent, sustained hypoglycemic effect in fed male CF albino rats, with an ED50 of 23.1 mg/kg for achieving a 40% hypoglycemic effect that lasts up to 7 h[3].
Swerchirin (50 mg/kg; p.o.; single administration) reduces blood glucose by 39% in fasted male CF albino rats at 3 h and maintains blood glucose levels below baseline for 24 h[3].
Swerchirin (50 mg/kg; p.o.; single administration) inhibits the post-glucose-load blood glucose peak and delays blood glucose recovery in glucose-loaded male CF albino rats[3].
Swerchirin (20 mg/kg; p.o.; single dose) enhances the hypoglycemic effect of Tolbutamide in pretreated male CF albino rats, with the maximum hypoglycemic effect observed at 4 h[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Swiss mice (male, 20-25 g, paracetamol-induced hepatotoxicity model)[2]
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Dosage:3 mg/kg; 6 mg/kg; 12.5 mg/kg; 25 mg/kg; 50 mg/kg
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Administration:p.o.; single dose 1 hour before 600 mg/kg paracetamol
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Result:Reduced paracetamol‑provoked serum ALT, AST and ALP rises dose‑dependently; it achieved 80.0 % (ALT), 51.5 % (AST), 43.5 % (ALP) reduction at 6 mg/kg, 78.0 % (ALT), 45.8 % (AST), 37.2 % (ALP) reduction at 12.5 mg/kg, 69.2 % (ALT), 43.9 % (AST), 33.3 % (ALP) reduction at 25 mg/kg, and 67.0 % (ALT), 41.3 % (AST), 29.4 % (ALP) reduction at 50 mg/kg.
Exerted no changes to serum ALT, AST and ALP relative to control mice when dosed alone across 3‑50 mg/kg.
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Animal Model:CF albino rats (male, 140-165 g, fed model)[3]
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Dosage:5 mg/kg; 10 mg/kg; 20 mg/kg; 50 mg/kg; 100 mg/kg; 250 mg/kg
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Administration:p.o.; single dose
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Result:Exhibited a dose-dependent blood sugar lowering effect.
Induced significant blood sugar lowering at 1, 3, 4, and 7 hours, which persisted up to 24 hours at 5 mg/kg.
Induced ~40% blood sugar lowering within 3 hours, which continued up to 24 hours at 10 mg/kg, 20 mg/kg, 50 mg/kg, 100 mg/kg, and 250 mg/kg.
Decreased blood sugar levels from an initial 107.9 mg/dl to 71.9 mg/dl at 1 hour, 60.1 mg/dl at 3 hours, 57.9 mg/dl at 4 hours, 43.4 mg/dl at 7 hours, and 27.1 mg/dl at 24 hours at 50 mg/kg.
Achieved an ED50 of 23.1 mg/kg for 40% blood sugar lowering up to 7 hours.
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Animal Model:CF albino rats (male, 140-165 g, fasted model)[3]
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Dosage:50 mg/kg
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Administration:p.o.; single dose
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Result:Lowered blood sugar by 39% at 3 hours compared to controls.
Decreased blood sugar levels from an initial 63.3 mg/dl to 48.5 mg/dl at 1 hour, 37.9 mg/dl at 3 hours, 44.7 mg/dl at 4 hours, 46.9 mg/dl at 7 hours, and 41.3 mg/dl at 24 hours.
Maintained blood sugar levels below initial fasting levels at 24 hours.
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Animal Model:CF albino rats (male, 140-165 g, glucose-loaded model)[3]
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Dosage:50 mg/kg
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Administration:p.o.; single dose
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Result:Suppressed the post-glucose blood sugar peak, reducing it from a control peak of 131.8 mg/dl to 94.3 mg/dl at 30 minutes post-glucose.
Decreased blood sugar levels to 60.9 mg/dl at 1 hour and 48.5 mg/dl at 3 hours post-glucose.
Slowed recovery to fasting levels compared to controls.
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Animal Model:CF albino rats (male, 140-165 g, tolbutamide-pretreated model)[3]
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Dosage:20 mg/kg
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Administration:p.o.; single dose
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Result:Enhanced the blood sugar lowering effect of tolbutamide, with maximum lowering observed at 4 hours.
Decreased blood sugar levels from an initial 82.6 mg/dl to 42.8 mg/dl at 1 hour, 40.5 mg/dl at 3 hours, 39.4 mg/dl at 4 hours, and 43.6 mg/dl at 7 hours.
Chemical Information
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CAS No. 521-65-3
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Molecular Weight 288.25
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Formula C15H12O6
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SMILES
O=C1C2=C(C=C(C=C2O)OC)OC3=C1C(O)=CC=C3OC
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)