Astragaloside VI Inhibitor

Solid. Powder

98.00%

Store at -20 degree C for 3 years powder
-80 degree C for 2 years in solvent

947.11

<1mg/ml refers to the product slightly soluble or insoluble

C47H78O19

C[C@]12[C@@]3([H])[C@@]4(CC[C@@]1([C@]([C@@]5(O[C@H](C(C)(O)C)CC5)C)([H])[C@@H](O)C2)C)[C@@]6([C@@](C(C)([C@@H](O[C@@]7([H])[C@@H]([C@H]([C@H](O)CO7)O)O[C@]8([H])O[C@@H]([C@@H](O)[C@H](O)[C@H]8O)CO)CC6)C)([H])[C@@H](O[C@]9([H])O[C@@H]([C@@H](O)[C@H](O)[C@H]9O)CO)C3)C4

84687-45-6

EGFR

In the simple non-infected wound model, wound healing in mice is accelerated by Astragaloside VI, wherein the time required for wound closure is shortened by approximately 2-4 days, compared to that in the control group. Topical treatment with Astragaloside VI reduces the volume of pus produced, compared to the control group. Astragaloside VI treated wounds show an accelerated rate of healing, compared to the control and vaseline groups. By day 22, the Astragaloside VI -treated wounds fully close, whereas the blank and vaseline-treated wounds do not fully close until day 26. Astragaloside VI increases blood vessel formation in both the non-infected and infected wound models [1]. Astragaloside VI could effectively activate EGFR/MAPK signaling cascades, promote NSCs proliferation and neurogenesis in transient cerebral ischemic brains, and improve the repair of neurological functions in post-ischemic stroke rats [2].

Angiogenesis; EGFR; JAK/STAT signaling; Tyrosine Kinase/Adaptors