Ginsenoside F2

Ginsenoside F2 at a Glance

Ginsenoside F2 is a protopanaxadiol (PPD)-type dammarane saponin of Asian ginseng (Panax ginseng). Structurally it is a partly stripped-down version of the abundant marker saponins — a diglucoside carrying one sugar at each of two positions — and that structure is the key to what it is: not a headline plant constituent but a metabolic intermediate, a transient waystation on the deglycosylation path from ginsenoside Rb1 down to compound K ^{1,6Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →}.

Because it sits mid-chain, F2 is barely present in raw ginseng and is often undetectable in unprocessed root; it accumulates instead when the big saponins are broken down — by steaming and fermentation, by gut bacteria after ingestion, or by deliberate enzymatic conversion in the lab ^{5,6,7Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 7Shin KC · 2014Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by β-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 — biocatalysisView study →}. Its scientific interest is almost entirely as an isolated molecule in cell and animal models, where it has produced two distinctive signals — apoptosis coupled with protective autophagy in breast cancer stem cells, and mitochondrial/AMPK-driven cytotoxicity in glioblastoma ^{1,2Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →Reference 2Kim TJ et al. · 2021In vitroGinsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function — in vitroView study →}. There is no human efficacy data for F2, and — like its PPD relatives — it is poorly absorbed intact by mouth ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}.

A Metabolic Intermediate (Rd → F2 → Compound K)

F2’s real identity is best understood not as a fixed ingredient but as a step in a conveyor belt. The dominant protopanaxadiol saponin of ginseng, ginsenoside Rb1, is progressively deglycosylated — sugars are cleaved off one at a time — along the route Rb1 → Rd → F2 → compound K, ending at the highly absorbable aglycone protopanaxadiol ^{6,8Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 8Hasegawa H · 2004ReviewProof of the mysterious efficacy of ginseng: metabolic activation of ginsenoside — deglycosylation by intestinal bacteria and esterification with fatty acid — reviewView study →}. F2 is the penultimate intermediate: it has lost the sugars that made Rb1 and Rd large and polar, but not yet the last one that yields compound K.

This transformation is carried out by gut microbiota after oral ginseng (species such as Bacteroides and Clostridium, and lactic-acid bacteria, run the hydrolysis) ^{9Reference 9Kang A et al. · 2016AnimalGut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats — animal modelView study →}, and it can be reproduced industrially with β-glucosidase enzymes or bacterial fermentation to manufacture F2 deliberately ^{6,7Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 7Shin KC · 2014Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by β-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 — biocatalysisView study →}. In a human pharmacokinetic study, F2 was undetectable in plasma after ordinary red-ginseng extract but became measurable after a bioconverted ginseng preparation — direct evidence that F2 exposure depends on that deglycosylation step happening, whether in the gut or in the factory ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}.

Two honesties follow from this, and they run through everything below:

• Isolate vs. plant. Every efficacy signal for F2 comes from the purified molecule applied to cells or animals — not from eating ginseng, where F2 is a fleeting trace species ^{1,2,3Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →Reference 2Kim TJ et al. · 2021In vitroGinsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function — in vitroView study →Reference 3Park SH et al. · 2016AnimalProtective effects of ginsenoside F2 on 12-O-tetradecanoylphorbol-13-acetate-induced skin inflammation in mice — animal modelView study →}.
• Intermediate vs. endpoint. F2 is a transient metabolite. Much of its own downstream fate is conversion to compound K, the more absorbable and heavily studied endpoint metabolite that carries much of the PPD-pathway’s pharmacology ^{6,8Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 8Hasegawa H · 2004ReviewProof of the mysterious efficacy of ginseng: metabolic activation of ginsenoside — deglycosylation by intestinal bacteria and esterification with fatty acid — reviewView study →}. Attributing a whole-pathway effect to F2 specifically is difficult when F2 is, by design, on its way to becoming something else.

What It's Used For

F2’s evidence base is small, entirely preclinical, and built on the isolated molecule. Two anticancer signals dominate it; a skin anti-inflammatory and a cytoprotective antioxidant finding round it out.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume, tempered for isolate-vs-plant match and bioavailability. A beta, not a validated metric. Every row rests on isolated F2 in cells or rodents (no human efficacy data), so scores are capped accordingly. Each application links to its write-up.

01Breast cancer stem cells (apoptosis + autophagy)Shaky30%Isolated F2 in a breast-CSC model; well-characterised mechanism; no human data ^{1Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →}

02Glioblastoma cytotoxicity (mitochondrial / AMPK)Shaky26%Isolated F2 in glioblastoma cells; single-lab mechanism study ^{2Reference 2Kim TJ et al. · 2021In vitroGinsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function — in vitroView study →}

03Anti-inflammatory (skin)Shaky20%Isolated F2 in a mouse TPA skin-inflammation model ^{3Reference 3Park SH et al. · 2016AnimalProtective effects of ginsenoside F2 on 12-O-tetradecanoylphorbol-13-acetate-induced skin inflammation in mice — animal modelView study →}

04Antioxidant / cytoprotectiveShaky16%Isolated F2 vs. H₂O₂ injury in vitro ^{4Reference 4Liu D et al. · 2019In vitroLiu D, Zhang C, et al. (2019). [Protective effects of ginsenoside F2 on hydrogen peroxide-induced cell injury] — in vitro. Wei Sheng Yan Jiu (Journal of Hygiene Research), 48(3), 452–457. https://pubmed.ncbi.nlm.nih.gov/31133133/View study →}

Mechanisms

The load-bearing mechanistic nuance is the autophagy contrast: F2’s autophagy in breast cancer stem cells is a survival response the cell mounts against the drug, which is why the interesting therapeutic idea is F2 plus an autophagy blocker ^{1Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →}.

Pharmacokinetics

F2 inherits the poor oral bioavailability of the protopanaxadiol saponins: as a diglucoside it is large and polar, and PPD-type ginsenosides in this family are absorbed intact at only single-digit percentages, most of the dose passing to the colon for microbial processing ^{9,10Reference 9Kang A et al. · 2016AnimalGut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats — animal modelView study →Reference 10Xu QF et al. · 2003AnimalPharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats — animal modelView study →}. The defining PK fact for F2 is its intermediate status — it is generated and consumed along the Rb1 → Rd → F2 → compound K chain, so it exists in a moving equilibrium rather than accumulating ^{6Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →}. Human data make this concrete: in healthy volunteers, F2 was not detectable in plasma after standard red-ginseng extract, but appeared (C_max ≈ 5.8 ng/mL, T_max ≈ 6–7 h, half-life ≈ 10 h) after a bioconverted ginseng preparation in which the parent saponins had already been partially deglycosylated — showing that whether you see any F2 at all depends on that conversion step occurring ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}. Practically, an oral ginseng dose delivers very little intact F2 to tissue, and much of what forms is en route to compound K ^{6,8Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 8Hasegawa H · 2004ReviewProof of the mysterious efficacy of ginseng: metabolic activation of ginsenoside — deglycosylation by intestinal bacteria and esterification with fatty acid — reviewView study →}.

Clinical Trials

There are no registered clinical trials of isolated ginsenoside F2. All human ginseng evidence is at the whole-extract level, where F2 is a trace (often undetectable) species — so no clinical benefit can be attributed to F2 specifically. The one human dataset that touches F2 is a pharmacokinetic study, not an efficacy trial ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}.

Last checked: July 2026.

Isolate vs. Plant Studies

F2 is an unusually clear case of the isolate-vs-plant gap. All of its pharmacology is isolated-molecule work — purified F2 dosed onto breast cancer stem cells, glioblastoma cells, mouse skin, or peroxide-stressed cells ^{1,2,3,4Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →Reference 2Kim TJ et al. · 2021In vitroGinsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function — in vitroView study →Reference 3Park SH et al. · 2016AnimalProtective effects of ginsenoside F2 on 12-O-tetradecanoylphorbol-13-acetate-induced skin inflammation in mice — animal modelView study →Reference 4Liu D et al. · 2019In vitroLiu D, Zhang C, et al. (2019). [Protective effects of ginsenoside F2 on hydrogen peroxide-induced cell injury] — in vitro. Wei Sheng Yan Jiu (Journal of Hygiene Research), 48(3), 452–457. https://pubmed.ncbi.nlm.nih.gov/31133133/View study →}. That is not a strength here the way it can be for an established drug, because the isolate barely exists in the plant: raw ginseng contains F2 only in trace amounts, and human plasma shows none after ordinary ginseng extract ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}. So the whole-plant evidence for ginseng cannot be routed through F2, and the F2 evidence cannot be routed back to ginseng intake. There is also an intermediate-vs-endpoint caveat unique to metabolites like this: because F2 is continuously converted to compound K, a dish of stable F2 does not model the transient exposure a body actually experiences ^{6,8Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 8Hasegawa H · 2004ReviewProof of the mysterious efficacy of ginseng: metabolic activation of ginsenoside — deglycosylation by intestinal bacteria and esterification with fatty acid — reviewView study →}. Where F2 is likely to matter clinically, if anywhere, is in processed, fermented or enzymatically bioconverted ginseng products engineered to raise minor-saponin content — the only setting where measurable F2 reaches the blood ^{5,7Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →Reference 7Shin KC · 2014Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by β-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 — biocatalysisView study →}.

Prevalence in Nature

Ginsenoside F2 occurs across the Panax genus — Asian ginseng (Panax ginseng), American ginseng (P. quinquefolius) and notoginseng (P. notoginseng) — and, in analogous dammarane form, in jiaogulan (Gynostemma pentaphyllum). But unlike the marquee saponins Rb1 and Rg1, which sit at milligrams per gram of root, F2 is a minor, often trace, constituent of raw material and is frequently below detection in unprocessed ginseng ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}.

Its abundance is a processing story rather than a botanical one. F2 is enriched when the large parent saponins are broken down: by steaming and heat (red-ginseng manufacture), by fermentation, by gut microbiota after ingestion, and by deliberate enzymatic conversion ^{5,6,7Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 7Shin KC · 2014Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by β-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 — biocatalysisView study →}. This is why F2 (with Rg3, Rk1, Rg5 and compound K) shows up in “bioconverted” or fermented ginseng products but not in a plain water extract ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}. No clean, reproducible percentage-of-dry-weight figure for native F2 exists to tabulate — its natural level is best described as trace to undetectable.

Discovery & Synthesis

Ginsenoside F2 was catalogued among the minor dammarane saponins during the twentieth-century chemical surveys of Panax ginsenosides, but it drew little attention until the 2000s, when interest in the deglycosylation cascade — how gut bacteria turn indigestible ginseng saponins into absorbable actives — put the Rb1 → Rd → F2 → compound K chain in the spotlight ^{6,8Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →Reference 8Hasegawa H · 2004ReviewProof of the mysterious efficacy of ginseng: metabolic activation of ginsenoside — deglycosylation by intestinal bacteria and esterification with fatty acid — reviewView study →}.

Manufacture today is by conversion, not extraction, precisely because the plant contains so little. F2 is produced by enzymatic hydrolysis of the abundant saponins — for example a β-glucosidase from Thermus thermophilus that selectively cleaves the outer glucose at the C-20 position of larger ginsenosides to yield F2 ^{7Reference 7Shin KC · 2014Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by β-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 — biocatalysisView study →} — and by microbial biotransformation, such as fermenting ginsenoside Rb1 with Leuconostoc mesenteroides to give a mixture of Rd, F2 and compound K ^{6Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →}. These biocatalytic routes are the practical way to obtain gram quantities of an otherwise scarce molecule for research and for enriched-ginseng products.

Patents: not yet researched.

Toxicity & Safety

Ginsenoside F2 carries a low toxicity flag, consistent with the protopanaxadiol ginsenoside family and with the fact that it is a natural human metabolite of everyday ginseng use — it forms transiently in the gut of anyone who takes ginseng and is present at trace levels at most ^{5,6Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →Reference 6Quan LH et al. · 2011Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformationView study →}. Its selective toxicity to cancer cells in the studies above is the intended pharmacology, not a general-toxicity signal ^{1,2Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →Reference 2Kim TJ et al. · 2021In vitroGinsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function — in vitroView study →}. That said, there is no dedicated repeat-dose, genotoxicity or reproductive-toxicity dataset for isolated F2, so its safety profile is inferred from the class and from ginseng as a whole rather than directly characterised; absence of findings is not evidence of safety.

Safety at a Glance

✅ Low / no toxicity

• Low expected toxicity. A natural PPD-type ginseng metabolite, formed transiently in the gut and present only in trace amounts in raw ginseng.
• No isolate safety package. No dedicated repeat-dose, genotoxicity or reproductive-toxicity studies exist for pure F2 — the profile is inferred, not measured.
• Bioconverted/fermented products change exposure. Products engineered to raise minor-saponin content deliver measurable F2 (and compound K) that ordinary ginseng does not — a different exposure than traditional use ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}.

Reproductive and pregnancy/lactation decisions belong to the ginseng herb or the specific product where intake is decided, not to this molecule page; no reproductive-toxicity dataset exists for isolated F2.

Dosage

There is no established human dose of isolated ginsenoside F2. It is a research compound and a transient metabolite, not a standardised supplement. The anticancer, anti-inflammatory and antioxidant effects above come from cell and rodent studies dosing purified F2 at experimental concentrations chosen for the assay, none of which translate to a human oral dose ^{1,2,3,4Reference 1Mai TT et al. · 2012In vitroGinsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitroView study →Reference 2Kim TJ et al. · 2021In vitroGinsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function — in vitroView study →Reference 3Park SH et al. · 2016AnimalProtective effects of ginsenoside F2 on 12-O-tetradecanoylphorbol-13-acetate-induced skin inflammation in mice — animal modelView study →Reference 4Liu D et al. · 2019In vitroLiu D, Zhang C, et al. (2019). [Protective effects of ginsenoside F2 on hydrogen peroxide-induced cell injury] — in vitro. Wei Sheng Yan Jiu (Journal of Hygiene Research), 48(3), 452–457. https://pubmed.ncbi.nlm.nih.gov/31133133/View study →}. The only human exposure figures are pharmacokinetic: after a bioconverted ginseng preparation, plasma F2 peaked around 5.8 ng/mL — vanishingly small, and zero after ordinary ginseng extract ^{5Reference 5Kim HJ et al. · 2022Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic studyView study →}. In practice, any human intake of F2 happens indirectly, as a minor and largely transient product of taking (especially processed or fermented) ginseng, where it is one of many saponins and its individual contribution is unknown.

These are doses studied in research and are not a personal recommendation.

References

1. Mai TT, Moon J, Song Y, et al. (2012). Ginsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells — in vitro. Cancer Letters, 321(2), 144–153. https://pubmed.ncbi.nlm.nih.gov/22326284/
2. Kim TJ, Kim HJ, Kang M, et al. (2021). Ginsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function — in vitro. Phytomedicine, 83, 153483. https://pubmed.ncbi.nlm.nih.gov/33578358/
3. Park SH, Seo W, Eun HS, et al. (2016). Protective effects of ginsenoside F2 on 12-O-tetradecanoylphorbol-13-acetate-induced skin inflammation in mice — animal model. Biochemical and Biophysical Research Communications, 478(4), 1713–1719. https://pubmed.ncbi.nlm.nih.gov/27596969/
4. Liu D, Zhang C, et al. (2019). [Protective effects of ginsenoside F2 on hydrogen peroxide-induced cell injury] — in vitro. Wei Sheng Yan Jiu (Journal of Hygiene Research), 48(3), 452–457. https://pubmed.ncbi.nlm.nih.gov/31133133/
5. Kim HJ, Oh TK, Kim YH, et al. (2022). Pharmacokinetics of ginsenoside Rb1, Rg3, Rk1, Rg5, F2, and compound K from red ginseng extract in healthy Korean volunteers — human pharmacokinetic study. Evidence-Based Complementary and Alternative Medicine, 2022, 8427519. https://pubmed.ncbi.nlm.nih.gov/35111231/
6. Quan LH, Piao JY, Min JW, et al. (2011). Biotransformation of ginsenoside Rb1 to prosapogenins, gypenoside XVII, ginsenoside Rd, ginsenoside F2, and compound K by Leuconostoc mesenteroides — biotransformation. Journal of Ginseng Research, 35(3), 344–351. https://pubmed.ncbi.nlm.nih.gov/23717079/
7. Shin KC, Oh DK. (2014). Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by β-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 — biocatalysis. Biotechnology Letters, 36(6), 1191–1199. https://pubmed.ncbi.nlm.nih.gov/24563303/
8. Hasegawa H. (2004). Proof of the mysterious efficacy of ginseng: metabolic activation of ginsenoside — deglycosylation by intestinal bacteria and esterification with fatty acid — review. Journal of Pharmacological Sciences, 95(2), 153–157. https://pubmed.ncbi.nlm.nih.gov/15215638/
9. Kang A, Zhang S, Zhu D, et al. (2016). Gut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats — animal model. Chemico-Biological Interactions, 258, 187–196. https://pubmed.ncbi.nlm.nih.gov/27613481/
10. Xu QF, Fang XL, Chen DF. (2003). Pharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats — animal model. Journal of Ethnopharmacology, 84(2–3), 187–192. https://pubmed.ncbi.nlm.nih.gov/12648814/

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