Bartogenic acid
Bartogenic acid is an orally active NF-κB inhibitor, found in Barringtonia racemosa fruits. Bartogenic acid increases catalase, superoxide dismutase (SOD), and glutathione levels. Bartogenic acid inhibits lipid peroxidation and suppresses inflammation markers. Bartogenic acid can be used for the research of ovarian cancer, skin cancer, and inflammatory conditions.
For research use only. We do not sell to patients.
- CAS No.: 79355-89-8
- Formula: C30H46O7
- Molecular Weight:518.68
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
NF-κB |
In Vitro
Bartogenic acid (0.1-100 μM; 48 h) inhibits the growth of human ovarian cancer SKOV-3 cells in vitro with an IC50 of 15.72 μM[1].
Bartogenic acid (48 h) potently and selectively induces cytotoxicity in human skin carcinoma SCC-13 cells (IC50=7.5 µM) with a selectivity index of 4.05[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human ovarian cancer SKOV-3 cells
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Concentration:0.1 μM; 1 μM; 10 μM; 50 μM; 100 μM
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Incubation Time:48 h
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Result:Dose-dependently reduced the viability of SKOV-3 cells, with an IC50 value of 15.72 μM after 48 h of treatment.
Decreased as the concentration of bartogenic acid increased.
In Vivo
Bartogenic acid (1-4 mg/kg; p.o./topical; daily; 13.5 weeks) exhibits dose-dependent chemopreventive efficacy against DMBA (HY-W011845)/Croton oil-induced skin cancer in Swiss albino mice, with the 4 mg/kg oral dose achieving the lowest tumor incidence (36.1%) and near-normal antioxidant marker levels and skin architecture[2].
Bartogenic acid (2-10 mg/kg; p.o.; daily for 21 days) protects rats against the primary and secondary arthritic lesions, body weight changes and haematological perturbations induced by CFA (HY-153808)[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:SCID (female, 5 weeks old, subcutaneous inoculation of SKOV-3 cells to establish a xenograft model)[1]
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Dosage:3 mg/kg
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Administration:i.v.; daily; 21 days
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Result:Achieved 41.47% tumor growth inhibition (p < 0.001) compared to vehicle controls, with mean tumor volume of 364.70 mm3 on day 21.
Showed no significant reduction in NF-κB H score, viable tumor cell score, fibrosis score, TGF-β1 levels, or MMP9 levels, but significantly increased necrosis score (p < 0.05).
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Animal Model:Swiss albino (6-8 weeks old, 23-25 gm, DMBA/Croton oil-induced two-stage skin carcinogenesis)[2]
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Dosage:1 mg/kg; 2 mg/kg; 4 mg/kg
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Administration:p.o.; daily; 13.5 weeks; topical; daily; 13.5 weeks
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Result:Reduced tumor incidence to 89.3%, with an average of 9.72 tumors per tumor-bearing mouse, mean tumor volume of 124.8 mm3, and mean tumor weight of 1.01 gm at 1 mg/kg oral dose.
Partially restored glutathione (GSH) content and activities of catalase, superoxide dismutase (SOD), and glutathione peroxidase (GSHPx), with mild histopathological improvement at 1 mg/kg oral dose.
Reduced tumor incidence to 52.4%, with an average of 6.34 tumors per tumor-bearing mouse, mean tumor volume of 89.7 mm3, and mean tumor weight of 0.61 gm at 2 mg/kg oral dose.
Significantly reduced skin malondialdehyde (MDA) levels to 125.7 μg/mg protein, restored GSH content to near-normal levels, significantly increased catalase, SOD, and GSHPx activities, and preserved normal skin architecture with only mild epidermal cell invasion at 2 mg/kg oral dose.
Reduced tumor incidence to 36.1%, with an average of 4.19 tumors per tumor-bearing mouse, mean tumor volume of 45.6 mm3, and mean tumor weight of 0.11 gm at 4 mg/kg oral dose.
Significantly reduced skin MDA levels to 104.5 μg/mg protein, restored GSH content and catalase, SOD, and GSHPx activities to near-normal levels, and preserved fully normal skin architecture with no epidermal thickening or cell invasion at 4 mg/kg oral dose.
Reduced tumor incidence to 48.2%, with an average of 8.21 tumors per tumor-bearing mouse, mean tumor volume of 63.5 mm3, and mean tumor weight of 0.51 gm at 4 mg/kg topical dose.
Reduced skin MDA levels to 141.6 μg/mg protein, restored GSH content and catalase, SOD, and GSHPx activities to near-normal levels, and showed mild to moderate histopathological improvement at 4 mg/kg topical dose.
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Animal Model:Wistar rats (either sex, 100-150 g, Complete Freund’s Adjuvant-induced arthritis)[3]
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Dosage:2 mg/kg; 5 mg/kg; 10 mg/kg
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Administration:p.o.; daily; 21 days
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Result:Reduced primary arthritic lesions to 113% rise in injected paw volume and secondary lesions to 15% rise in non-injected paw volume at 2 mg/kg, 109% rise and 12% rise at 5 mg/kg, and 91% rise and 11% rise at 10 mg/kg (all P < .01).
Resulted in 37 g body weight gain at 2 mg/kg, 36 g gain at 5 mg/kg, and 39 g gain at 10 mg/kg (all P < .01).
Reduced thymus weight to 0.12 g and spleen weight to 0.96 g at 2 mg/kg, 0.12 g and 0.84 g at 5 mg/kg, and 0.085 g and 0.74 g at 10 mg/kg (all thymus weights and 5 mg/kg, 10 mg/kg spleen weights P < .05 or P < .01).
Reduced WBC count to 7.5 ×103/mm3, ESR to 12 mm/h, CRP to 4.4 mg/dL, and RF to 37 IU/mL at 2 mg/kg; increased RBC count to 9 ×106/mm3, reduced WBC count to 7.2 ×103/mm3, increased Hb to 15 mg%, reduced CRP to 2.2 mg/dL, and RF to 33 IU/mL at 5 mg/kg; increased RBC count to 9.8 ×106/mm3, reduced WBC count to 5.6 ×103/mm3, reduced ESR to 11 mm/h, increased Hb to 16 mg%, reduced CRP to 1.4 mg/dL, and RF to 23 IU/mL at 10 mg/kg (all significant vs control, P < .01).
Reduced arthritis score to median 6 (4, 8), flexion pain test score to median 1.5 (1, 2), mobility score to median 1.5 (1, 2), and improved stance score to median 3 (2, 3) at 10 mg/kg (P < .05 or P < .01); 2 mg/kg and 5 mg/kg showed non-significant pain score improvements.
Protected against soft tissue swelling, periarticular bone resorption, bone erosion, and joint space narrowing in the adjuvant-injected paw at 10 mg/kg.
Chemical Information
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CAS No. 79355-89-8
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Molecular Weight 518.68
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Formula C30H46O7
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SMILES
OC([C@]12[C@]([C@@H](C(C)(CC2)C)O)([H])C3=CC[C@@]([C@@]4([C@@]([C@](C)([C@H]([C@@H](C4)O)O)C(O)=O)([H])CC5)C)([H])[C@]5(C)[C@@]3(CC1)C)=O
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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.
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Purity & Documentation
References
[1]. Dubey VK, et al. Tumor-suppressing effect of bartogenic acid in ovarian (SKOV-3) xenograft mouse model. Naunyn Schmiedebergs Arch Pharmacol. 2021;394(8):1815-1826. [Content Brief]
[2]. Patil CR, et al. Chemomodulatory Potential of Bartogenic Acid Against DMBA/Croton Oil Induced Two-Step Skin Carcinogenesis in Mice. J Cancer. 2016;7(14):2139-2147. Published 2016 Oct 23. [Content Brief]
[3]. Patil KR, et al. Anti-Arthritic Activity of Bartogenic Acid Isolated from Fruits of Barringtonia racemosa Roxb. (Lecythidaceae). Evid Based Complement Alternat Med. 2011;2011:785245. [Content Brief]
[4]. Patil KR, et al. Anti-inflammatory activity of bartogenic acid containing fraction of fruits of Barringtonia racemosa Roxb. in acute and chronic animal models of inflammation. J Tradit Complement Med. 2016 Apr 4;7(1):86-93. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Bartogenic acid Related Classifications
HY-N19717 Related Classifications
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