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Ginsenoside F1


  • Brand : BIOFRON

  • Catalogue Number : BF-G1005

  • Specification : 98%

  • CAS number : 53963-43-2

  • Formula : C36H62O9

  • Molecular Weight : 638.87

  • PUBCHEM ID : 9809542

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

roots of Panax ginseng C.A.Mey.

Structure Type



Standards;Natural Pytochemical;API




β-D-Glucopyranoside, (3β,6α,12β)-3,6,12-trihydroxydammar-24-en-20-yl/Ginsenoside F1/GINSENOSIDEF1/Ginsenoside-F1/(3β,6α,12β)-3,6,12-Trihydroxydammar-24-en-20-yl β-D-glucopyranoside




1.2±0.1 g/cm3


Methanol; DMSO

Flash Point

408.4±32.9 °C

Boiling Point

751.7±60.0 °C at 760 mmHg

Melting Point



InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:53963-43-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Ginsenosides are the principal active components of ginseng and are considered attractive candidates for combination cancer therapy because they can kill tumors and have favorable safety profiles. However, the overall benefit of ginsenosides remains unclear, particularly in cancer immunosurveillance, considering the controversial results showing repression or promotion of immune responses. Here we identify a potentiating role of ginsenoside F1 (G-F1) in cancer surveillance by natural killer (NK) cells. Among 15 different ginsenosides, G-F1 most potently enhanced NK cell cytotoxicity in response to diverse activating receptors and cancer cells. G-F1 also improved cancer surveillance in mouse models of lymphoma clearance and metastatic melanoma that rely on NK cell activity. G-F1-treated NK cells exhibited elevated cytotoxic potential such as upregulation of cytotoxic mediators and of activation signals upon stimulation. NK cell potentiation by G-F1 was antagonized by insulin-like growth factor (IGF)-1 blockade and recapitulated by IGF-1 treatment, suggesting the involvement of IGF-1. Thus, our results suggest that G-F1 enhances NK cell function and may have chemotherapeutic potential in NK cell-based immunotherapy. We anticipate our results to be a starting point for further comprehensive studies of ginsenosides in the immune cells mediating cancer surveillance and the development of putative therapeutics.


IGF-1; cancer surveillance; cytotoxicity; ginsenoside; natural killer cell


Ginsenoside F1 Promotes Cytotoxic Activity of NK Cells via Insulin-Like Growth Factor-1-Dependent Mechanism.


Kwon HJ1, Lee H1, Choi GE1,2, Kwon SJ1, Song AY1, Kim SJ1, Choi WS1, Hwang SH3, Kim SC4, Kim HS1,5.

Publish date

2018 Nov 28




Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by d-galactose via suppressing p38MAPK-dependent NF-κB activity. A specific inhibitor of p38MAPK, SB203580 significantly decreased the secretion of IL-6 and IL-8, the major components of SASPs. Additionally, treatment of senescent astrocytes with NF-κB inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-κB was required for SASP. Importantly, conditioned media from senescent astrocytes promoted the migration of glioblastoma cells, such as U373-MG, U251-MG and U87-MG assessed by scratch wound healing. This migration was significantly decreased by F1 treatment in senescent astrocytes. Interestingly, IL-8, the main mediator regulating glioblastoma cell invasion, was suppressed in both transcriptional and protein level. Herein, we propose ginsenoside F1 as a potential therapeutic strategy for reducing the deleterious contribution of senescent astrocytes in aged brain and related diseases.

Copyright © 2018 Elsevier B.V. All rights reserved.


Astrocytic senescent; Ginsenoside F1; Glioblastoma; NF-κB; SASP; p38MAPK


Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype.


Hou J1, Cui C1, Kim S2, Sung C3, Choi C4.

Publish date

2018 Mar 1




Ischemic stroke is one of the most lethal and highly disabling diseases that seriously affects the human health and quality of life. A therapeutic angiogenic strategy has been proposed to alleviate ischemia-induced injury by promoting angiogenesis and improving cerebrovascular function in the ischemic regions. The insulin-like growth factor 1 (IGF-1)/insulin-like growth factor 1 receptor (IGF1R) axis is crucial for cerebral angiogenesis and neurogenesis. However, effective drugs that prevent cerebral ischemic injury by inducing cerebral angiogenesis via activation of the IGF1R pathway are lacking. Here, we screened a pro-angiogenic agent ginsenoside F1 (GF1), a ginseng saponin isolated from a traditional Chinese medicine that was widely used in ischemic stroke treatment. It promoted the proliferation, mobility and tube formation of human umbilical vein endothelial cells and human brain microvascular endothelial cells, as well as pericytes recruitment to the endothelial tubes. GF1 stimulated vessel sprouting in the rat arterial ring and facilitated neovascularization in chicken embryo chorioallantoic membrane (CAM). In the in vivo experiments, GF1 rescued the axitinib-induced vascular defect in zebrafish. It also increased the microvessel density (MVD) and improved focal cerebral blood perfusion in the rat middle cerebral artery occlusion (MCAO) model. Mechanism studies revealed that GF1-induced angiogenesis depended on IGF1R activation mediated by the autocrine IGF-1 loop in endothelial cells. Based on our findings, GF1-induced activation of the IGF-1/IGF1R pathway to promote angiogenesis is an effective approach to alleviate cerebral ischemia, and GF1 is a potential agent that improves cerebrovascular function and promotes recovery from ischemic stroke.

Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.


Angiogenesis; Axitinib (PubChem CID: 131871370); Cerebral ischemia; Ginsenoside F1; Ginsenoside F1 (PubChem CID: 53447401); Insulin-like growth factor 1; Insulin-like growth factor 1 receptor; OSI-906 (PubChem CID:11640390)


Ginsenoside F1 promotes angiogenesis by activating the IGF-1/IGF1R pathway.


Zhang J1, Liu M1, Huang M1, Chen M1, Zhang D2, Luo L2, Ye G1, Deng L3, Peng Y1, Wu X4, Liu G4, Ye W5, Zhang D6.

Publish date

2019 Jun

Description :

Ginsenoside F1, an enzymatically modified derivative of Ginsenoside Rg1, demonstrates competitive inhibition of CYP3A4 activity and weaker inhibition of CYP2D6 activity.