Estrogenic effect

Estriol 3-sulfate
Catalog No: CFN90080

Estriol 3-sulfate acts through the hydrolyzed E3, E3-17-S is inactive because it is not hydrolyzed, so Estriol 3-sulfate can play an important role in the biological responses of this mammary cancer cell line.
Acteoside
Catalog No: CFN97048

Acteoside is a lipase inhibitor, has neuroprotective, anti-obesity,anti-inflammatory, antioxidant, anticancer, cytotoxic,antihypertensive, analgesic, and antimetastatic activities. Acteoside can promote nerve growth factor and tropomycin receptor kinase A expression, inhibit arachidonic acid release and prostaglandin E2 production induced by 0.5 microM melittin. Acteoside can protect the cells from X‑ray induced damage through enhancing the scavenging activity of ROS, decreasing the Bax/Bcl-2 ratio and downregulating the activity of procaspase-3, as well as modulating the mitogen‑activated protein kinase signaling pathways.
Sagittatoside A
Catalog No: CFN90139

Sagittatoside A selectively activates estrogen response element (ERE)-luciferase activity via ERα, and sagittatoside A and icariin induces ERα phosphorylation at serine 118 residue.
Isoliquiritigenin
Catalog No: CFN97542

Isoliquiritigenin has hepatoprotective, chemopreventive, antitumor, vasorelaxant, anti-platelet, anti-allergic, antiviral, antioxidant and anti-inflammatory effects, it can induce growth inhibition and apoptosis through downregulating AA metabolic network and the deactivation of PI3K/Akt in human breast cancer. Isoliquiritigenin also has the ability to protect cells from AA+iron-induced H2O2 production and mitochondrial dysfunction, which is mediated with GSK3β phosphorylation downstream of AMPK.
Gypenoside XVII
Catalog No: CFN90193

Gypenoside XVII confers protection against Aβ25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, inactivation of GSK-3β and activation of Nrf2/ARE/HO-1 pathways. Gypenoside XVII has protective effects to the cellular and rodent models of Alzheimer's disease by activating TFEB.