19-epi-Scholaricine
Based on 1 Customer Validation
19-epi-Scholaricine is an orally active indole alkaloid. 19-epi-Scholaricine downregulates the expression of profibrotic/apoptotic proteins (HRAS, HSP90AA1, KDR) and upregulates the expression of cell cycle-related protein (CDK2). 19-epi-Scholaricine suppresses ROS production and reduces the release of inflammatory mediators, thereby attenuating podocyte apoptosis, renal inflammation and oxidative stress by inhibiting AKT/mTOR. 19-epi-Scholaricine can be used in the research of chronic glomerulonephritis and membranous nephropathy.
For research use only. We do not sell to patients.
- Purity: 99.14%
- CAS No.: 132923-06-9
- Formula: C20H24N2O4
- Molecular Weight:356.42
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Storage:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
All VEGFR Isoforms
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Biological Activity
19-epi-Scholaricine (10-50 μM; 24 h) protects ADR-stimulated MPC5 cells from injury, and significantly increases cell viability after 24 h of treatment at the concentration of 50 μM[1].
19-epi-Scholaricine (50 μM; 24 h) regulates the expression of CGN-related targets in ADR-induced MPC5 cells, downregulating HRAS, HSP90AA1 and KDR while upregulating CDK2[1].
19-epi-Scholaricine (50 μM; 24 h) significantly reduces the level of ROS production in ADR-stimulated MPC5 cells[1].
19-epi-Scholaricine (1-20 μM; 25 h) inhibits the release of NO in LPS (HY-D1056)-induced mouse podocyte MPC5 cells[2].
19-epi-Scholaricine (1 μM; 25 h) downregulates the gene expression of Tnf-α and Il-6 in LPS-induced mouse podocyte cell line MPC5[2].
19-epi-Scholaricine (1 μM; 25 h) upregulates the expression of circadian rhythm and AKT/mTOR pathway genes in LPS-stimulated mouse podocyte cell line MPC5[2].
19-epi-Scholaricine (1 μM; 24 h) reduces lipopolysaccharide (LPS)-induced reactive oxygen species (ROS) production in the mouse podocyte cell line MPC5[2].
19-epi-Scholaricine (1 μM; 24 h) restores the mitochondrial membrane potential of LPS-stimulated mouse podocytes MPC5[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:adriamycin (ADR)-stimulated murine glomerular podocyte (MPC5) cells
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Concentration:10, 20, 40 and 50 μM
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Incubation Time:24 h
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Result:Increased the survival rate of ADR-stimulated MPC5 cells; the 50 μM concentration produced a statistically significant increase relative to the ADR-only model group.
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Cell Line:adriamycin (ADR)-stimulated murine glomerular podocyte (MPC5) cells
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Concentration:50 μM
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Incubation Time:24 h
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Result:Downregulated the protein expression of HRAS, HSP90AA1, and KDR, and upregulated the protein expression of CDK2 in ADR-stimulated MPC5 cells, reversing the expression changes induced by ADR.
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Cell Line:adriamycin (ADR)-stimulated murine glomerular podocyte (MPC5) cells
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Concentration:50 μM
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Incubation Time:24 h
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Result:Downregulated the mRNA expression of hras, hsp90aa1, and kdr and upregulated the mRNA expression of cdk2 in ADR-stimulated MPC5 cells, reversing the expression changes induced by ADR.
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Cell Line:MPC5 murine podocytes (LPS-stimulated)
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Concentration:1 μM
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Incubation Time:1 h pre-incubation, then 24 h LPS stimulation
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Result:Significantly reduced the LPS-induced expression of Tnf-α and IL-6 genes in MPC5 cells, restoring levels to near normal.\nUpregulated the expression of Arntl, Cry1, Akt, mTor, and Bcl-2/Bax genes in LPS-stimulated MPC5 cells.
19-epi-scholaricine (1.0 mg/kg; oral gavage; daily; 6 weeks) exhibits superior or comparable therapeutic efficacy to prednisone at 2 mg/kg in a mouse model of membranous nephropathy, as evidenced by reduced urinary protein, restored renal function, suppressed inflammation and oxidative stress, improved histopathology, and modulation of the ARNTL/AKT/mTOR pathway[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR mice (male, 32-36 g, adriamycin-induced)[1]
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Dosage:1 mg/kg
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Administration:p.o.; daily; 28 days
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Result:Reduced urinary protein levels from 11.51 mg/24 h (model group) to 8.84 mg/24 h at day 7.
Attenuated the ADR-induced decrease in serum albumin (ALB) from 30.74 U/L (model group) to 35.92 U/L, and in serum total protein (TP) from 51.01 U/L (model group) to 55.63 U/L.
Reduced serum urea nitrogen (BUN) levels from 9.49 μmol/L (model group) to 8.44 μmol/L.
Ameliorated kidney histopathological damage, including reduced diffuse proliferation of glomerular tracts and decreased lymphocyte/plasma cell infiltration.
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Animal Model:ICR (male, 25 ± 3 g, membranous nephropathy induced by 5 mg/kg C-BSA tail vein injection every 3 days for 6 doses)[2]
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Dosage:1.0 mg/kg
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Administration:oral gavage; daily; 6 weeks
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Result:Reduced 24-hour urinary protein from 9.9 to 6.2 mg.
Increased the urine creatinine (Ucr)/blood creatinine (Scr) ratio from 42.7 to 76.5.
Decreased renal C3 deposition integrated fluorescence signal from 2.1 to 0.52.
Reduced renal IL-1β expression from 4.4 to 1.4.
Normalized oxidative stress markers (malondialdehyde, glutathione, superoxide dismutase, catalase) in kidney homogenates.
Ameliorated histopathological renal lesions including lymphocyte infiltration, loosely stained cytoplasm, and glomerular basement membrane (GBM) thickening to near-normal levels.
Upregulated renal expression of circadian rhythm genes (Arntl, Cry1) and downregulated phosphorylated AKT/mTOR pathway components.
Chemical Information
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CAS No. 132923-06-9
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Appearance Solid
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Molecular Weight 356.42
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Formula C20H24N2O4
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Color Light yellow to light brown
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SMILES
O=C(C1=C2[C@]3(C4=CC=CC(O)=C4N2)[C@@](C[C@@]1([H])[C@@]5([H])[C@H](O)C)([H])N(C5)CC3)OC
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Purity & Documentation
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Data Sheet (284 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Guo R, et al. Pharmacological investigation of indole alkaloids from Alstonia scholaris against chronic glomerulonephritis. Phytomedicine. 2023;118:154958. [Content Brief]
[2]. Tian CB, et al. Managing circadian rhythm involved in alleviating membranous nephropathy by alkaloids of Alstonia scholaris. Phytomedicine. 2025;148:157467. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)