Ginsenoside F1

• CAS: 53963-43-2
• Catalog Number: ACM53963432-1
• Category: Main Products
• Molecular Weight: 638.87
• Molecular Formula: C36H62O9
• Synonyms: 3β,6α,12β-Trihydroxy-5α-dammar-24-en-20-yl β-D-glucopyranoside
• IUPAC Name: (2R,3S,4S,5R,6S)-2-(hydroxymethyl)-6-[(2S)-6-methyl-2-[(3S,5R,6S,8R,9R,10R,12R,13R,14R,17S)-3,6,12-trihydroxy-4,4,8,10,14-pentamethyl-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-17-yl]hept-5-en-2-yl]oxyoxane-3,4,5-triol
• SMILES: CC(=CCC[C@@](C)([C@H]1CC[C@@]2([C@@H]1[C@@H](C[C@H]3[C@]2(C[C@@H]([C@@H]4[C@@]3(CC[C@@H](C4(C)C)O)C)O)C)O)C)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO)O)O)O)C
• InChI: InChI=1S/C36H62O9/c1-19(2)10-9-13-36(8,45-31-29(43)28(42)27(41)23(18-37)44-31)20-11-15-34(6)26(20)21(38)16-24-33(5)14-12-25(40)32(3,4)30(33)22(39)17-35(24,34)7/h10,20-31,37-43H,9,11-18H2,1-8H3/t20-,21+,22-,23+,24+,25-,26-,27+,28-,29+,30-,31-,33+,34+,35+,36-/m0/s1
• InChI Key: XNGXWSFSJIQMNC-FIYORUNESA-N
• Boiling Point: 751.7±60.0 °C
• Melting Point: >165 °C (dec.)
• Flash Point: 409.1ºC
• Density: 1.23±0.1 g/ml
• Appearance: White powder
• Exact Mass: 638.43900
• pKa: 12.94±0.70

Case Study

Ginsenoside F1 for the Activation of UCP1-Dependent Thermogenesis in Obesity-Induced Insulin Resistance

Meng Y, et al. Food Science and Human Wellness, 2023, 12(6), 2061-2072.

Ginsenoside F1 was investigated for its thermogenic potential via UCP1 activation. Using a UCP1-luciferase reporter assay, F1 was screened from a ginsenoside library and identified as a potent activator. Pull-down assays and pharmacological inhibition confirmed its specific binding to β3-adrenergic receptors, initiating the cAMP/PKA/CREB signaling cascade. In vivo experiments in high-fat diet-induced diabetic mice demonstrated that intraperitoneal administration of F1 significantly reduced body weight and improved glucose tolerance. Proteomic analysis of adipose tissue revealed upregulation of thermogenesis- and lipolysis-related proteins, alongside suppression of fatty acid synthesis enzymes. Moreover, F1 enhanced mitochondrial respiration in both adipocytes and hepatocytes, outperforming norepinephrine.

Cardioprotective Mechanism Study for Ginsenoside F1 against Pirarubicin-Induced Cardiotoxicity via Nrf2 and AKT/Bcl-2 Pathways

Zhang Y, et al. Journal of Ginseng Research, 2023, 47(1), 06-116.

Ginsenoside F1 (GF1), a metabolite of ginsenosides Re and Rg1, was experimentally applied to counteract pirarubicin (THP)-induced cardiotoxicity in vitro and in vivo. In H9c2 cardiomyocytes and rat models, GF1 was evaluated for its antioxidative and anti-apoptotic activities. Biochemical markers including MDA, CK-MB, c-TnT, LDH, SOD, and GSH were quantified using ELISA. Western blotting assessed the expression of Nrf2-regulated genes (HO-1, Gst, GCLM) and AKT/Bcl-2 pathway proteins. Trigonelline and imidazoquinoxaline (IMQ) were used to inhibit Nrf2 and AKT, respectively. GF1 treatment promoted Nrf2 nuclear translocation and AKT/Bcl-2 activation, attenuating myocardial oxidative damage and apoptosis. The absence of protection with inhibitors confirmed pathway involvement. This study demonstrates the precise application of GF1 in modulating cardioprotective signaling, suggesting its therapeutic potential against anthracycline cardiotoxicity.

Ginsenoside F1 for the Attenuation of Eosinophilic Inflammation in Chronic Rhinosinusitis via NK Cell Modulation

Kim S-J, et al. Journal of Ginseng Research, 2021, 45(6), 695-705.

Ginsenoside F1 (G-F1) was experimentally applied to a murine model of chronic rhinosinusitis (CRS) to evaluate its immunomodulatory potential. Histological analysis revealed that G-F1 treatment markedly reduced sinonasal epithelial hyperplasia, mucosal thickening, and eosinophil/mast cell infiltration. qPCR and ELISA assays demonstrated that G-F1 suppressed Th2 cytokines IL-4 and IL-13, along with hematopoietic prostaglandin D synthase expression. Unlike dexamethasone, G-F1 preserved macrophage activity while enhancing natural killer (NK) cell function. NK cell depletion nullified G-F1's therapeutic effects, indicating a direct role in mediating its anti-inflammatory action. These findings support the use of Ginsenoside F1 as a selective immunotherapeutic agent targeting NK cells to resolve eosinophilic inflammation in CRS, distinguishing it from conventional corticosteroids.

Ginsenoside F1-Enriched Extract (SGB121) for Reversing Scopolamine-Induced Neurotoxicity: In Vitro and In Vivo Applications

Bastola T, et al. Journal of Functional Foods, 2020, 74, 104165.

The neuroprotective efficacy of Ginsenoside F1-enriched extract SGB121 was assessed using scopolamine-induced neuronal impairment models. In vitro, SH-SY5Y neuroblastoma cells were pretreated with SGB121 and subsequently exposed to scopolamine. SGB121 significantly reversed scopolamine-induced apoptosis, restored mitochondrial membrane potential, and reactivated phosphorylation of Akt, GSK3β, and ERK. In vivo, ICR mice received oral SGB121 once daily for 7 days before behavioral assessment via Y-maze and passive avoidance tests. Results indicated marked recovery of scopolamine-induced memory impairment. Western blotting of hippocampal tissue confirmed that SGB121 restored phosphorylated ERK and CREB levels and upregulated BDNF expression. Additionally, SGB121 suppressed acetylcholinesterase expression in both cell cultures and hippocampal tissue. These findings highlight the potent neuroprotective and cognitive benefits of Ginsenoside F1, supporting its potential as a therapeutic candidate in neurodegenerative disease intervention.