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Bioactive Products
Cat. No. Information
CFN98592 Psoralidin

Psoralidin possesses potent antidepressant-like, anti-inflammatory, anticancer and chemopreventive properties. Psoralidin is a dual inhibitor of COX-2 and 5-LOX, it is also an agonist for both estrogen receptor (ER)α and ERβ agonist.Psoralidin inhibits LPS-induced iNOS expression via repressing Syk-mediated activation of PI3K-IKK-IκB signaling pathways, it induces reactive oxygen species (ROS)-dependent DNA damage and protective autophagy mediated by NOX4 in breast cancer cells.
CFN97539 Guajadial

Guajadial shows α-glucosidase inhibitory activities significantly and its activity was better than that of Acarbose.Guajadial may act as Selective Estrogen Receptors Modulators (SERMs), therefore holding significant potential for anticancer therapy, it exhibits potent inhibitory effects on the growth of human hepatoma cells.
CFN90859 Notoginsenoside Ft1

Notoginsenoside Ft1 is a novel stimulator of angiogenesis, it stimulates angiogenesis via HIF-1α-mediated VEGF expression, with PI3K/AKT and Raf/MEK/ERK signaling cascades concurrently participating in the process; it has the potential therapeutic effect on human neuroblastoma, it can arrest the proliferation and elicited the apoptosis of SH-SY5Y cells possibly via p38 MAPK and ERK1/2 pathways.Notoginsenoside Ft1 activates both glucocorticoid and estrogen receptors to induce endothelium-dependent, nitric oxide-mediated relaxations in rat mesenteric arteries. Notoginsenoside Ft1 also provides a great potential application of it in clinics for patients with diabetic foot ulcers, it may accelerate diabetic wound healing by orchestrating multiple processes, including promoting fibroblast proliferation, enhancing angiogenesis, and attenuating inflammatory response.
CFN96379 Methyl p-hydroxyphenyllactate

Methyl para-hydroxyphenyllactate(MeHPLA) can suppress the cellular proliferation of estrogen-sensitive MCF-7 breast cancer cells in vitro and to suppress the growth of rat uteri in vivo, high affinity of MeHPLA for the type II estrogen binding site (EBS) suggests that this interaction is responsible for the observed suppression of cell growth.