Cajanol
Cajanol is an isoflavanone that can be isolated from the roots of Cajanus cajan (L.) Millsp.. Cajanol inhibits cancer cell proliferation and induces cancer cell apoptosis. Cajanol promotes the expression of Bax, inhibits the expression of Bcl-2, activates caspase-9 and caspase-3, induces PARP cleavage, arrests the cell cycle at the G2/M phase, generates ROS, disrupts mitochondrial membrane potential and triggers cytochrome c release. Cajanol induces bacterial DNA damage, disrupts bacterial cell membranes, and exerts antibacterial activity in vitro. Cajanol reduces the expression of PI3K, inhibits the phosphorylation of Akt and NF-κB, downregulates the expression and transport function of P-gp, restores the sensitivity of drug-resistant cancer cells to Paclitaxel, and inhibits the growth of Paclitaxel-resistant metastatic ovarian tumors. Cajanol is applicable to research related to breast cancer, ovarian cancer and bacterial infections.
Para uso exclusivo en investigación. No vendemos a pacientes.
- No. CAS: 61020-70-0
- Fòrmula: C17H16O6
- Peso molecular:316.31
-
Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Actividad biológica
-
Chemical Information
- Pureza y Documentación
- Referencias
-
Help & FAQs
Ver todos los productos específicos de isoformas Caspase
More
Actividad biológica
Cajanol (0-316 μM; 24-72 h) potently inhibits the growth of human breast cancer MCF-7 cells in a time- and dose-dependent manner, with an IC50 of 54.05 μM at 72 h, 58.32 μM at 48 h, and 83.42 μM at 24 h[1].
Cajanol (16-64 μM; 48 h) induces concentration-dependent G2/M cell cycle arrest, concentration-dependent apoptosis, DNA fragmentation, and typical apoptotic nuclear morphological changes including chromatin condensation and fragmentation, as well as ROS production and mitochondrial membrane potential disruption in human breast cancer MCF-7 cells[1].
Cajanol (16-64 μM; 48 h) induces the activation of caspase-3 and caspase-9, downregulates Bcl-2 expression and upregulates Bax expression, triggers concentration-dependent release of cytochrome c from mitochondria to the cytoplasm, and induces concentration-dependent cleavage of PARP in human breast cancer MCF-7 cells[1].
Cajanol (24 h) inhibits the growth of Gram-positive bacterial strains (Staphylococcus epidermidis, Staphylococcus aureus, Bacillus subtilis) and Gram-negative bacterial strains (Escherichia coli, Proteus vulgaris, Pseudomonas aeruginosa) in vitro. The most susceptible strains (Staphylococcus epidermidis, Staphylococcus aureus, Escherichia coli) have an MIC value of 98.90 μM, while the less susceptible strains (Bacillus subtilis, Proteus vulgaris, Pseudomonas aeruginosa) have an MIC value of 197.8 μM[2].
Cajanol (4-10 h) induces time-dependent cell death and membrane damage, as well as DNA cleavage, in Escherichia coli and Staphylococcus aureus in vitro[2].
Cajanol (2-16 μM; 72 h) concentration-dependently reverses Paclitaxel (HY-B0015) resistance in A2780/Taxol and A549/Taxol cells[3].
Cajanol (2-8 μM; 48 h) concentration-dependently inhibits ABCB1 mRNA expression and P-gp protein in A2780/Taxol cells[3].
Cajanol (2-8 μM; 48 h) inhibits the PI3K/Akt/NF-κB signaling pathway in A2780/Taxol cells in a concentration-dependent manner by reducing PI3K expression, inhibiting Akt phosphorylation, and blocking the phosphorylation and nuclear translocation of NF-κB/p65[3].
Cajanol (2-8 μM; 2 h pre-incubation, 1 h co-incubation with rhodamine-123) concentration-dependently inhibits P-gp-mediated efflux activity in A2780/Taxol cells and increases intracellular rhodamine-123 accumulation[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:MCF-7 human breast cancer cells
-
Concentration:0, 9.88, 19.75, 39.5, 79, 158 and 316 μM
-
Incubation Time:24 h; 48 h; 72 h
-
Result:Inhibited MCF-7 cell growth in a time- and dose-dependent manner.
Reached an IC50 value of 83.42 μM after 24 h treatment, 58.32 μM after 48 h treatment, and 54.05 μM after 72 h treatment.
-
Cell Line:MCF-7 human breast cancer cells
-
Concentration:0, 16, 32 and 64 μM
-
Incubation Time:48 h
-
Result:Increased the G2/M phase cell population from 19.24% (16 μM) to 47.87% (64 μM), compared to 7.55% in untreated controls.
-
Cell Line:MCF-7 human breast cancer cells
-
Concentration:0, 16, 32 and 64 μM
-
Incubation Time:48 h
-
Result:Increased the percentage of annexinV-FITC binding MCF-7 cells in a concentration-dependent manner, reaching 12.84% (16 μM), 47.94% (32 μM), and 78.03% (64 μM).
-
Cell Line:MCF-7 human breast cancer cells
-
Concentration:16-64 μM
-
Incubation Time:48 h
-
Result:Decreased relative Bcl-2 expression from 66.89% (16 μM) to 47.20% (64 μM) in a concentration-dependent manner.
Increased relative Bax expression from 186.36% (16 μM) to 341.36% (64 μM) in a concentration-dependent manner.\nDecreased relative mitochondrial cytochrome c expression from 87.93% (16 μM) to 19.40% (64 μM) in a concentration-dependent manner.
Increased relative cytosolic cytochrome c expression from 190.04% (16 μM) to 503.91 % (64 μM) in a concentration-dependent manner.\nDecreased relative full-length PARP expression from 95.64% (16 μM) to 38.89% (64 μM) in a concentration-dependent manner.
Increased cleaved PARP expression in a concentration-dependent manner, visible as an 85 kDa protein band with disappearance of the 116 kDa band.
-
Cell Line:A2780/Taxol paclitaxel-resistant ovarian cancer cells, A549/Taxol paclitaxel-resistant non-small cell lung cancer cells
-
Concentration:2, 4, 8, 16 μM
-
Incubation Time:72 h (co-incubated with paclitaxel)
-
Result:Reduced the Paclitaxel IC50 in A2780/Taxol cells from 35.85 μM to 25.67 μM (2 μM), 16.25 μM (4 μM), 6.54 μM (8 μM), and 6.05 μM (16 μM), with corresponding fold resistance values of 22.52, 14.51, 5.64, and 5.50, respectively.
Reduced the paclitaxel IC50 in A549/Taxol cells from 289.34 μM to 189.43 μM (2 μM), 68.95 μM (4 μM), 27.9 μM (8 μM), and 23.76 μM (16 μM), with corresponding fold resistance values of 24.35, 9.01, 3.74, and 3.15, respectively.
Exhibited an IC50 of 28.34 μM in A2780/Taxol cells and 87.78 μM in A549/Taxol cells when used alone.
-
Cell Line:A2780/Taxol paclitaxel-resistant ovarian cancer cells
-
Concentration:2, 4, 8 μM
-
Incubation Time:48 h
-
Result:Concentration-dependently downregulated ABCB1 mRNA expression, with 8 μM reducing expression to ~10% of the control level.
Did not significantly change expression of VEGF, MMP-9, Tubα1a, and Tubβ3 mRNA.
-
Cell Line:A2780/Taxol paclitaxel-resistant ovarian cancer cells
-
Concentration:2, 4, 8 μM
-
Incubation Time:48 h
-
Result:Concentration-dependently downregulated P-gp protein expression.
Did not significantly change expression of VEGF, MMP-9, α-tubulin, βIII-tubulin, MRP1, MRP2, and LRP protein.\nConcentration-dependently reduced PI3K protein expression, inhibited Akt phosphorylation, and reduced NF-κB/p65 phosphorylation and nuclear translocation.
Did not significantly change total Akt and total NF-κB/p65 protein expression.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:BALB/c nude (6-week-old female, 18-20 g, subcutaneous inoculation of A2780/Taxol paclitaxel-resistant ovarian cancer cells)[3]
-
Dosage:2 mM/kg (single-agent); 2 mM/kg + 0.5 mM/kg paclitaxel (combination)
-
Administration:i.v.; on days 1, 8, and 15 post-tumor implantation; 24 days monitoring
-
Result:Achieved a final tumor volume of 680 mm3 after 24 days when administered alone.
Reduced final tumor volume to 182.4 mm3 when combined with 0.5 mM/kg paclitaxel.
Maintained an average mouse body weight of ~25 g when combined with paclitaxel.
Significantly inhibited P-gp protein expression in tumor tissues.
Chemical Information
-
No. CAS 61020-70-0
-
Peso molecular 316.31
-
Fòrmula C17H16O6
-
SMILES
O=C1C2=C(O)C=C(OC)C=C2OCC1C3=CC=C(O)C=C3OC
-
Structure Classification
-
Initial Source
-
Envío
Room temperature in continental US; may vary elsewhere.
-
Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
[1]. Luo M, et al. Cajanol, a novel anticancer agent from Pigeonpea [Cajanus cajan (L.) Millsp.] roots, induces apoptosis in human breast cancer cells through a ROS-mediated mitochondrial pathway. Chem Biol Interact. 2010;188(1):151-160. [Content Brief]
[2]. Liu XL, et al. Cajanol inhibits the growth of Escherichia coli and Staphylococcus aureus by acting on membrane and DNA damage. Planta Med. 2011;77(2):158-163. [Content Brief]
[3]. Sui M, et al. Cajanol Sensitizes A2780/Taxol Cells to Paclitaxel by Inhibiting the PI3K/Akt/NF-κB Signaling Pathway. Front Pharmacol. 2021 Dec 8;12:783317. [Content Brief]
[4]. Bouley R, et al. Structural Determinants Influencing the Potency and Selectivity of Indazole-Paroxetine Hybrid G Protein-Coupled Receptor Kinase 2 Inhibitors. Mol Pharmacol. 2017;92(6):707-717. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Cajanol Related Classifications
HY-N10342 Related Classifications
Powered by Bioz
- Cajanol
- 61020-70-0
- Apoptosis
- Bcl-2 Family
- Caspase
- PARP
- Reactive Oxygen Species (ROS)
- Bacterial
- PI3K
- Akt
- NF-κB
- P-glycoprotein
- isoflavanone
- apoptosis
- MCF-7 cells
- Staphylococcus epidermidis
- Staphylococcus aureus
- Bacillus subtilis
- Escherichia coli
- Proteus vulgaris
- Pseudomonas aeruginosa
- A2780/Taxol cells
- A549/Taxol cells
- BALB/c nudemice
- breast cancer
- ovarian cancer
- bacterial infections
- Inhibitor
- inhibitor
- inhibit