Phytochemical Name : Lunasin

Properties Information
PhytoCAT-ID PhytoCAT-643
Phytochemical name or plant extracts Lunasin
PMID 20457246
Literature evidence These compounds arrest the cell cycle in the S- and G1-phases, respectively, acting synergistically to induce apoptosis.
IUPAC name (2R)-4,8-dimethoxy-9-methyl-2-propan-2-yl-2,3-dihydrofuro[2,3-b]quinolin-9-ium
Phytochemicals’ class or type of plant extracts Novel seed peptide
Source of phytochemicals or plant Extracts Glycine max
Geographical availability Amur, China North-Central, China South-Central, China Southeast, Hainan, Inner Mongolia, Japan, Khabarovsk, Korea, Laos, Manchuria, Nansei-shoto, Primorye, Qinghai, Taiwan, Thailand, Tibet, Vietnam, Xinjiang
Plant parts NA
Other cancers Breast cancer
Target gene or protein MMP2, MMP9, NOS, IL-1, IL-6, TNF-α, Src, Akt, ERK, NF-κB, MCP-1
Gene or Protein evidence Meanwhile, we also found that lunasin inhibited the phosphorylation of focal adhesion kinase (FAK), Src, Akt, ERK and nucleus translocation of NF-κB, which indicates that, possibly via competing with αVβ3 or αVβ5/α5β1 integrin, lunasin suppresses the metastasis of breast cancer cells through integrin-mediated FAK/Akt/ERK and NF-κB signaling pathways followed by downregulation of the activity and expression of MMP-2/-9. The 6 h-LSGS presented anti-inflammatory activity on LPS-induced macrophage cells (p < 0.05) by suppressing the release of nitric oxide (NO) and proinflammatory cytokines, including IL-1 and IL-6. The gene expression of NOS, IL-1, IL-6, and TNF-α was significantly inhibited by 6 h-LSGS. Lunasin significantly inhibited interleukin (IL)-6 and macrophage chemoattractant protein (MCP)-1 secretion by TNF-α stimulation, and MCP-1 secretion in the RAW-CM model. This study highlights that lunasin suppressed 3T3-L1 adipocyte inflammation and inhibited 4T1 breast cancer cell migration.
Target pathways FAK/Akt/ERK pathway NF-κB signaling pathway
IC50 NA
Potency Lunasin/aspirin therapy exerts its potent pro-apoptotic effect is at least partially achieved through modulating the extrinsic-apoptosis dependent pathway. Synergistic down-regulatory effects were observed for ERBB2, AKT1, PIK3R1, FOS and JUN signaling genes, whose amplification has been reported as being responsible for breast cancer cell growth and resistance to apoptosis.
Cell line/ mice model MDA-MB-231, 4T1
Additional information  Lunasin/aspirin therapy exerts its potent pro-apoptotic effect is at least partially achieved through modulating the extrinsic-apoptosis dependent pathway. ALS Reversals - Lunasin Regimen
PubChem ID 20054959
Additional PMIDs 31979146 31784283 27175819 20457246 27983683
Additional sources of information https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:60450240-2 . NCT02709330
Safety NA