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Liquiritigenin Estrogen/progestogen Receptor agonist

Cat.No.S3929

Liquiritigenin (4',7-Dihydroxyflavanone), the most active estrogenic compound from the root of Glycyrrhizae uralensis Fisch, selectively binds to ERβ with an IC50 value of 7.5 μM and activates multiple ER regulatory elements and native target genes with Erβ but not ERα.
Liquiritigenin Estrogen/progestogen Receptor agonist Chemical Structure

Chemical Structure

Molecular Weight: 256.25

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Quality Control

Batch: Purity: 98.7557%
98.7557

Solubility

In vitro
Batch:

DMSO : 51 mg/mL (199.02 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 51 mg/mL

Water : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 256.25 Formula

C15H12O4

Storage (From the date of receipt)
CAS No. 578-86-9 Download SDF Storage of Stock Solutions

Synonyms 4',7-Dihydroxyflavanone Smiles C1C(OC2=C(C1=O)C=CC(=C2)O)C3=CC=C(C=C3)O

Mechanism of Action

Targets/IC50/Ki
ERβ
VEGF
In vitro
Liquiritigenin-treated murine osteoblastic MC3T3-E1 cells shows an increased alkaline phosphatase activity and enhances phosphorylation of Smad1/5 compared with untreated cells. Moreover, this compound inhibits osteoclast differentiation, its bone-resorption activity through slightly decreases the phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and inhibitor of nuclear factor kappa B-α ; however, the phosphorylation of Akt and p38 slightly increase in bone marrow-derived osteoclasts. The expression levels of the osteoclast marker proteins nuclear factor of activated T-cell cytoplasmic-1, Src, and cathepsin K diminish. This chemical is shown to exert the following pharmacological effects: increased cell growth, increased alkaline phosphatase activity, promotion of collagen synthesis, and the mineralization of osteoblastic MC3T3-E1 cells. It inhibits serum-induced HIF-1α and VEGF expression via the AKT/mTOR-p70S6K signaling pathway in HeLa cells.
In vivo
Liquiritigenin inhibits the growth of tumors in nude mice originating from human cervical cancer cell line HeLa cells, and reduces angiogenesis in a dose dependent manner. This compound effectively reduces the levels of pro-inflammatory cytokines and the expressions of p-p65NF-κB and p-IκBα. Furthermore, its preconditioning could down-regulate the immobility time in tail suspension test (TST), forced swimming test (FST) and up-regulate BDNF and TrkB contents in hippocampus. Thus, this chemical has antidepressant activity that might be attributed to its anti-inflammatory property and BDNF/TrkB signaling pathway.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/27107388/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01199250 Not yet recruiting
Lynch Syndrome|Recurrent Uterine Corpus Carcinoma|Stage I Uterine Corpus Cancer|Stage II Uterine Corpus Cancer|Stage III Uterine Corpus Cancer|Stage IV Uterine Corpus Cancer
Gynecologic Oncology Group|National Cancer Institute (NCI)|GOG Foundation
January 2100 --
NCT04662164 Withdrawn
Type 2 Diabetes Patients
Shanghai HEP Pharmaceutical Co. Ltd.
December 2025 Phase 1|Phase 2
NCT06177132 Not yet recruiting
Vestibular Disorder
University Hospital Ghent|University Ghent
November 2025 Not Applicable
NCT03277170 Not yet recruiting
Asthma; Status|Asthma in Children|Asthma Acute|Asthma Attack|Acute Asthma Exacerbation
Vanderbilt University Medical Center
September 1 2025 Phase 2

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