Xanthatin NLT 98%

Xanthatin is isolated from Xanthium strumarium leaves. Xanthatin exhibits strong antitumor activities against a variety of cancer cells through apoptosis persuasion and shows anti-inflammatory activities by inhibiting PGE2 synthesis and 5-lipoxygenase activity^[1]. Xanthatin is a potent and orally active inhibitor of VEGFR2 kinase activity with an IC₅₀ of 3.8 μM and prominently blocks the phosphorylation of VEGFR2 at Tyr951 site. Xanthatin inhibits angiogenesis and has the potential for the investigation of breast cancer^[2]. IC50 & Target: IC50: apoptosis; 3.8 μM (VEGFR2 kinase); 2.63 µg/mL (T. b. brucei)^[1] In Vitro: Xanthatin is against T. b. brucei with an IC₅₀ value of 2.63 µg/mL and exhibits weak irreversible inhibition of parasite specific trypanothione reductase^[1].
Xanthatin (0-40 μM; 24 hours) has obscure inhibition effect on the proliferation of HUVEC in the absence of VEGF^[2].
Xanthatin (5-40 μM; 24 hours) inhibits breast cancer cell proliferation in a dose responsive manner. Xanthatin inhibits HCC1937, MDA-MB-415, SK-BR-3, MCF-7 and MDA-MB-231 with IC₅₀ values of 81 μM, 31 μM, 38 μM, 30 μM, and 17 μM, respectively^[2].
Xanthatin (0-10 μM; 24 hours) dose dependently suppresses the phosphorylation of STAT3 (Ser727), at the same time, it also results in a rapid dephosphorylation of down-stream kinases of STAT3, including PI3K and Akt, including PI3K (p-PI3K p85 _tyr458) and Akt^[2].
In Vivo: Xanthatin (intragastric administration; 20 mg/kg; once daily; 25 days) leads to significant inhibition of tumor volume. And this compound is well-tolerated and exhibits no significant difference in weight compares to the vehicle group^[2].