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Andrographolide
| Product Name | Andrographolide |
| Price: | $12 / 20mg |
| Catalog No.: | CN08808 |
| CAS No.: | 5508-58-7 |
| Molecular Formula: | C20H30O5 |
| Molecular Weight: | 350.5 g/mol |
| Purity: | >=98% |
| Type of Compound: | Diterpenoids |
| Physical Desc.: | Powder |
| Source: | The herbs of Andrographis paniculata (Burm. f.) Nees |
| Solvent: | Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc. |
| SMILES: | OC[C@]1(C)[C@H](O)CC[C@@]2([C@@H]1CCC(=C)[C@H]2C/C=C/1[C@H](O)COC1=O)C |
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| Description | Andrographolide is a NF-κB inhibitor, which inhibits NF-κB activation through covalent modification of a cysteine residue on p50 in endothelial cells without affecting IκBα degradation or p50/p65 nuclear translocation. |
| Target | p50 |
| In Vitro | Andrographolide (AP) concentration-dependently suppresses receptor activator of nuclear factor kappa B ligand (RANKL)-mediated osteoclast differentiation and bone resorption in vitro and reduces the expression of osteoclast-specific markers. Andrographolide attenuates inflammation by inhibition of TNFα-induced NF-κB activation through covalent modification of reduced Cys62 of p50, without affecting IκBα degradation or p50/p65 nuclear translocation. Andrographolide also inhibits the ERK/MAPK signalling pathway without affecting p38 or JNK signalling. Andrographolide inhibits osteoclast differentiation of RAW 264.7 cells in a concentration-dependent manner. Andrographolide suppresses osteoclast formation in a concentration-dependent manner without any obvious cytotoxic effects, in both BMMs and RAW 264.7 cells. Andrographolide treatment substantially reduces the area of bone resorption. Only approximately 30% of the bone resorption observed in the control group is achieved after treatment with 2.5 μM Andrographolide. Osteoclastic bone resorption is almost completely inhibited after treatment with 10 μM Andrographolide[1]. |
| In Vivo | Treatment with Andrographolide (5 or 30 mg/kg) reduces the extent of bone loss induced by LPS. Moreover, Andrographolide slightly increases the BMD and cortex thickness compared to LPS treatment. Histological examination confirms the protective effects of Andrographolide on LPS-induced bone loss. LPS injection leads to inflammatory bone erosion and increased numbers of TRAP-positive osteoclasts[1]. |
| Cell Assay | Effects of Andrographolide on cell proliferation are determined with a CCK-8. BMMs are plated in 96-well plates at a density of 3×103 cells per well in triplicate. Twenty-four hours later, the cells are treated with increasing concentrations of Andrographolide (0, 2.5, 5, 10 or 20 μM) for 2 days. Next, 10 μL CCK-8 is added to each well, and the plates are then incubated at 37°C for an additional 2 h. The optical density (OD) is then measured with an ELX800 absorbance microplate reader at a wavelength of 450 nm (650 nm reference). The cell viability is calculated[1]. |
| Animal Admin | Mice[1] C57BL/6 mice (8 weeks old) are divided into four groups of seven mice each. Mice are injected i.p. with Andrographolide (5 or 30 mg/kg body weight) or PBS as a control 1 day before injection of LPS (5 μg/g body weight). Andrographolide or PBS is injected intraperitoneally every other day for 8 days. LPS is injected intraperitoneally on days one and four. All mice are killed 8 days after the initial LPS injection, and the left femurs of all animals are scanned with a high-resolution micro-CT at a resolution of 9 μm. |
| Density | 1.2±0.1 g/cm3 |
| Boiling Point | 557.3±50.0 °C at 760 mmHg |
| Flash Point | 195.5±23.6 °C |
| Exact Mass | 350.209320 |
| PSA | 86.99000 |
| LogP | 1.62 |
| Vapour Pressure | 0.0±3.4 mmHg at 25°C |