| Field | Specification |
|---|---|
| Alternative names | Lonchocarpine |
| CAS no. | |
| Applications | |
| Source | Plant — Fabaceae Lonchocarpus sericeus (Poir.) Kunth ex DC. |
| Molecular weight | |
| Molecular formula | C20H18O3 |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Lonchocarpin, also known as Lonchocarpine, is an inhibitor of the Wnt/β-catenin signaling pathway with an IC50 of 4 μM in SW480 pBAR/Renilla cells. Acting downstream of β-catenin stabilization, it blocks β-catenin nuclear localization and TCF-mediated transcription as well as the proliferation and migration of colorectal cancer cells. It also enhances Nrf2/ARE-mediated antioxidant responses in primary astrocytes via AMPK- and JNK-related signaling, reduces H2O2-induced ROS production, and increases expression of HO-1, NQO1 and MnSOD, and can be used in research on colorectal cancer and oxidative stress[1][2]. It is supplied as a solid with the molecular formula C20H18O3 and a molecular weight of 306.36 g/mol.
Physical & Chemical Properties
| CAS Number | 31501-55-0 |
|---|---|
| Molecular Formula | C20H18O3 |
| Molecular Weight | 306.36 g/mol |
| Appearance | Solid |
| Structure Classification | Flavonoids Chalcones |
| SMILES | O=C(/C=C/C1=CC=CC=C1)C2=CC=C3C(C=CC(C)(O3)C)=C2O |
| Signaling Pathway | Stem Cell/Wnt; PI3K/Akt/mTOR; Epigenetics; MAPK/ERK Pathway |
| Initial Source | Plant — Fabaceae Lonchocarpus sericeus (Poir.) Kunth ex DC. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with your institution's chemical hygiene plan.
In Vitro
HO-1, NQO1 and MnSOD expression rises at the protein (16 h) and mRNA (6 h) levels in primary rat astrocytes treated with Lonchocarpin (5-20 μM)[1]. Lonchocarpin (5-20 μM; 3 h) boosts ARE nuclear protein binding and promotes Nrf2 nuclear translocation, and it enhances ARE-mediated transcriptional activity (16 h)[1]. Phosphorylation of AMPK, ERK1/2, JNK and p38 MAPK is increased by Lonchocarpin (5-20 μM; 1 h)[1]. In primary rat astrocytes, Lonchocarpine (20 μM; 16 h) induces HO-1 expression; AMPK and JNK promote this process, p38 MAPK suppresses it, and ERK has no effect[1]. When primary rat astrocytes are pretreated with lonchocarpin (5-20 μM) for 1 h and then exposed to H2O2 (50 μM), H2O2-induced intracellular ROS levels fall and the H2O2-caused decrease in cell viability is attenuated[1]. In primary rat astrocytes, the ARE-mediated transcriptional activity induced by lonchocarpine (20 μM) is regulated positively by AMPK and JNK and negatively by p38 MAPK, and is unaffected by ERK[1]. The binding of nuclear proteins to ARE induced by Lonchocarpine (20 μM) in primary rat astrocytes is regulated positively by AMPK and JNK and negatively by p38 MAPK[1]. In RKO and SW480 cells, Lonchocarpin (1-30 μM; 24 h) suppresses Wnt/β-catenin reporter activity in a concentration-dependent manner, with an IC50 of 4 μM in SW480 pBAR/Renilla cells. Nuclear β-catenin levels are also lowered by Lonchocarpin without a significant drop in total β-catenin, and Wnt/β-catenin signaling is inhibited whether driven by dnTCF4-VP16, wild-type β-catenin, or constitutively active β-catenin S33A, supporting action downstream of β-catenin stabilization and suppression of TCF-mediated transcription[2]. Proliferation of HCT116, SW480 and DLD-1 colorectal cancer cells is inhibited by Lonchocarpin (5-20 μM; 24 h). Specifically, lonchocarpin at 10 μM and 20 μM lowers EdU-positive SW480 cell counts by 50% and 85%, respectively, and EdU-positive DLD-1 cell counts by 40% and 75%, with no significant effect on proliferation of non-tumorigenic IEC-6 cells[2]. Migration of HCT116, SW480 and DLD-1 cells is inhibited by Lonchocarpin (5-20 μM; 24 h): at 20 μM, scratch closure falls by 55%, 55% and 45% in HCT116, SW480 and DLD-1 cells, respectively, and at 10 μM it falls by 40% in SW480 cells, while migration of IEC-6 cells is not significantly affected[2]. Lonchocarpin (20-50 μM) also preferentially lowers the MTT viability signal of colorectal cancer cells[2].
Immunofluorescence[2]
| Cell Line | RKO human colorectal cancer cells |
|---|---|
| Concentration | 10, 20 μM |
| Incubation Time | 24 h |
| Result | Reduced Wnt3a-induced nuclear β-catenin-positive cells from 86% to 54% at 10 μM and to 30% at 20 μM. |
Western Blot Analysis[2]
| Cell Line | RKO human colorectal cancer cells |
|---|---|
| Concentration | 20 μM |
| Incubation Time | overnight |
| Result | Did not significantly reduce total β-catenin protein levels, but reduced β-catenin levels in the nuclear fraction, with corresponding changes in cytosolic β-catenin levels. |
Cell Proliferation Assay[2]
| Cell Line | HCT116, SW480, DLD-1 human colorectal cancer cells, IEC-6 non-tumoral rat intestinal cells |
|---|---|
| Concentration | 5, 10, 20, 30 μM |
| Incubation Time | 24 h |
| Result | Inhibited 33% of EdU-positive HCT116 cells at 5 and 10 μM, and 75% at 30 μM. Inhibited 50% of EdU-positive SW480 cells at 10 μM and 85% at 20 μM. Inhibited 40% of EdU-positive DLD-1 cells at 10 μM and 75% at 20 μM. Showed no effect on EdU-positive IEC-6 cell count at 5, 10, or 20 μM. |
Cell Viability Assay[2]
| Cell Line | HCT116, SW480, DLD-1 human colorectal cancer cells, IEC-6 non-tumoral rat intestinal cells |
|---|---|
| Concentration | 10, 20, 30, 40, 50 μM |
| Incubation Time | 24 h; 48 h; 72 h |
| Result | Reduced absorbance in HCT116, SW480, and DLD-1 cells at 20-50 μM across all time points, while 10 μM had no effect. Reduced absorbance in IEC-6 cells only at 50 μM across all time points, and at 40 μM only at 72 h. |
In Vivo
In AOM/DSS-induced colorectal adenocarcinoma mice, adenocarcinoma tissues show 31% and 38% fewer Ki-67-positive proliferative cells and BrdU-positive cells, respectively, with Lonchocarpin (100 mg/kg/day; i.p.; 4 days); 50 mg/kg/day gives no statistically significant antiproliferative effect[2].
| Animal Model | Male and female 129SvJxC57BL6 mixed mice, 8-12 weeks old, AOM/DSS-induced colorectal adenocarcinoma model[2] |
|---|---|
| Dosage | 50 mg/kg; 100 mg/kg/day |
| Administration | i.p.; daily; 4 days; split into two 50 mg/kg doses every 12 hours (100 mg/kg/day group) |
| Result | Reduced Ki-67-positive cells in adenocarcinomas by 31% compared to vehicle control. Reduced BrdU-positive cells in adenocarcinomas by 38% compared to vehicle control. Showed no statistically significant antiproliferative effects at 50 mg/kg/day dose. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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