2,6-Dihydroxypurine
Catalog No: CFN91728
2,6-Dihydroxypurine, a plant alkaloid found in tea, coffee, and cocoa, is a mild stimulant of the central nervous system. 2,6-Dihydroxypurine also acts as an intermediate product on the pathway of purine degradation.Furthermore, Xanthines act as antagonists for adenosine receptors, with selectivity depending on whether there are substitution of alkyl groups.
IC50 & Target: Microbial Metabolite; Human Endogenous Metabolite
2,6-Dimethoxy-1,4-benzoquinone
Catalog No: CFN98883
2,6-Dimethoxy-1,4-benzoquinone exhibits strong antibacterial activities against S. pyogenes, S. mitis, and S. mutans with MIC values of 7.8, 7.8, and 15.6 ug/mL, and MBC values of 7.8, 7.8, and 31.2 ug/mL, respectively. 2,6-Dimethoxy-1,4-benzoquinone can produce genotoxic effects in patients taking dimethophrine.
20(R)-Ginsenoside Rg3
Catalog No: CFN98170
20(R)-Ginsenoside Rg3 has anticarcinogenic, neuroprotective, anti-aging and antifatigue activities, it has a wide spectrum of targets including caspase-3, MMP-2, MMP-9,HIF-1a,VEGF,IL-1,IL-6 and TNF-a.
20(R)-Ginsenoside Rh2
Catalog No: CFN90340
20(R)-Ginsenoside Rh2, a minor stereoisomer of ginsenoside Rh2, possesses matrix metalloproteinase inhibitory. 20(R)-Ginsenoside Rh2 has anticancer, anti- proliferation, anti-inflammatory and antioxidative activities, it also shows selective osteoclastgenesis inhibitory activity. 20(R)-Ginsenoside Rh2 reduce apoptotic rate significantly, enhance the activity of caspase-3 and induces apoptosis in human lung adenocarcinoma A549 cells.
20(S)-Ginsenoside Rh2
Catalog No: CFN99971
Ginsenoside Rh2 has memory-enhancing ,anti-osteoporosis, antitumor, antidiabetic, antiallergic, and anti-inflammatory effects, it potently protects ischemia-reperfusion brain injury, also inhibits prostaglandin-E_2 synthesis in lipopolysaccharide-stimulated RAW264.7 cells. It can inhibit the tendency of apoptosis, and reverse the impaired β-cell growth potential by modulating Akt/Foxo1/PDX-1 signaling pathway and regulating cell cycle proteins; it suppresses RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions, not excluding the involvement of NF-κB and ERK.
