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Ginkgolic acid C15:0
Catalog No: CFN90339

Reference standards.

Ginkgolic acid C15:1
Catalog No: CFN90161

Ginkgolic acid C15:1 has antibacterial, antiparasitic, and anti-cancer activities, it can suppress lung cancer invasion and migration through the inhibition of PI3K/Akt/mTOR signaling pathway.

Ginkgolic acid C17:1
Catalog No: CFN98508

Ginkgolic acid C17:1 can significantly inhibit enterohemorrhagic Escherichia coli O157:H7(EHEC) biofilm formation on the surfaces of polystyrene and glass, and on nylon membranes.

Ginkgolide A
Catalog No: CFN99638

Ginkgolide A is a platelet-activating factor antagonist, it can inhibit the neurotoxicity of prions or amyloid-beta1-42, may be relevant treatments for prion or Alzheimer's diseases.Ginkgolide A has neuroprotective, and anxiolytic-like effects, it is widely used for the treatment of cardiovascular diseases and diabetic vascular complications, which might be achieved through regulating the STAT3-mediated pathway.

Ginkgolide B
Catalog No: CFN99640

Ginkgolide B has potent neuroprotective, anti-arrhythmias, anti-inflammatory and anti-apoptotic effects, it might be a promising drug on inhibiting platelet function and reducing inflammation in atherosclerosis.Ginkgolide B retards the proliferation and development of mouse embryonic stem cells (ESCs) and blastocysts in vitro and causes developmental injury in vivo.

Ginkgolide C
Catalog No: CFN99639

Ginkgolide C is a potent inhibitor of collagen-stimulated platelet aggregation, it may increase intracellular cAMP and cGMP production and MMP-9 activity, inhibit intracellular Ca(2+) mobilization and TXA(2) production. Ginkgolide C has anti-adipogenic and ameliorating Alzheimer disease effects; it also can increase△LVP significantly,enhances the myocardial systolic and diastolic function of rats,but has no significant effect on HR while it shows inotropic activity.

Ginkgolide J
Catalog No: CFN99149

Ginkgolide J has neuroprotective activity, it can prevent A beta(1-42) induced inhibition of long-term potentiation in the CA1 region of mouse hippocampal slices, it is also capable of inhibiting cell death of rodent hippocampal neurons caused by A beta(1-42). Ginkgolide J can inhibit platelet aggregation induced by ADP or PAF.

Ginkgolide K
Catalog No: CFN91009

Ginkgolide K exerts anti-oxidative stress and neuroprotective effect on ischemic stroke, it has potentially anti- Parkinson's disease activity, it can promote the clearance of A53T mutation alpha-synuclein in SH-SY5Y cells. Ginkgolide K promotes angiogenesis after ischemia stroke through increasing the expression of HIF-1α/VEGF via JAK2/STAT3 pathway, it promotes astrocyte proliferation and migration after oxygen-glucose deprivation via inducing protective autophagy through the AMPK/mTOR/ULK1 signaling pathway. Ginkgolide K can inhibit PAF-induced platelet aggregation and improve nerve injury after cerebral ischemia-reperfusion.

Ginsenoside Compound K
Catalog No: CFN99756

Ginsenoside compound K (C-K) is a metabolite of the protopanaxadiol-type saponins of Panax ginseng C.A. Meyer, has long been used to treat against the development of cancer, inflammation, allergies, and diabetes; C-K acts as a unique HUVEC migration inhibitor by regulating MMP expression, as well as the activity of SPHK1 and its related sphingolipid metabolites. C-K exhibits anti-inflammatory effects by reducing iNOS and COX-2, C-K exhibits an inhibition against the activity of CYP2C9 and CYP2A6 in human liver microsomes with IC50s of 32.0±3.6 μM and 63.6±4.2 μM, respectively. C-K promotes Aβ clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.

Ginsenoside F1
Catalog No: CFN99754

Ginsenoside has been reported to suppress platelet aggregation and to reduce gap junction-mediated intercellular communication, also as a novel anti-skin cancer drug with anti-proliferative and anti-migration features. Ginsenoside F1 has a potential for industrial cosmetic materials, it also has inhibitory effect of elastase and tyrosinase, it significantly reduces ultraviolet-B-induced cell death by maintaining constant levels of Bcl-2 and protects HaCaT cells from apoptosis caused by ultraviolet B irradiation.