Tenacissoside H


CAS No. : 191729-45-0

(Synonyms: Tenacissimoside C)

191729-45-0
Price and Availability of CAS No. : 191729-45-0
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Cat. No. : HY-N0670
M.Wt: 794.97
Formula: C42H66O14
Purity: >98 %
Solubility: DMSO : 100 mg/mL (ultrasonic)
Introduction of 191729-45-0 :

Tenacissoside H (Tenacissimoside C) is a compound found in Caulis Marsdeniae Tenacissimae. Tenacissoside H shows anti-inflammation, anti-tumor and neuroprotective effects. Tenacissoside H inhibits PI3K/Akt and NF-κB signaling pathway. Tenacissoside H inhibits cancer cells proliferation, S phase arrest, and inhibits tumor growyh in mice. Tenacissoside H promotes neurological recovery of ischemia-reperfusion injury in mice by inhibiting inflammation and apoptosis. Tenacissoside H can be used for the research of cancer, inflammation and neurological diseases, such as esophageal cancer and cerebral ischemia[1][2]. In Vitro:Tenacissoside H (2-10 mg/mL; 24-48 h) potently inhibits human esophageal carcinoma EC9706 cell proliferation in a time- and dose-dependent manner, with IC50 values of 9.81 mg/mL at 24 h and 6.45 mg/mL at 48 h[1].
Tenacissoside H (10 mg/mL; 24 h) blocks human esophageal carcinoma EC9706 cells from entering the S phase from the G1 phase, significantly reducing the percentage of cells in the S phase to 12.82% relative to the blank control group[1].
Tenacissoside H (10 mg/mL; 1-7 days) downregulates PI3K and NF-κB p65 mRNA expression in human esophageal carcinoma EC9706 cells[1]. In Vivo:Tenacissoside H (100 mg/kg; i.p.; twice weekly; 14 days) produces inhibition of esophageal tumor growth in nude mice, reduces PCNA expression, and downregulates proteins in the PI3K/Akt-NF-κB signaling pathway[1].
Tenacissoside H (20-80 mg/kg; i.p.; daily; 5 consecutive days 30 minutes before operation) dose-dependently protects male C57BL/6 mice against cerebral ischemia-reperfusion injury, with the 80 mg/kg dose producing the most significant improvements in neurological function, reduction in brain damage, and modulation of inflammatory and oxidative stress pathways via the TrkB signaling axis[2].

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