Bavachin NLT 98%

Bavachin, a flavonoid first isolated from seeds of P. corylifolia, acts as a phytoestrogen that activates the estrogen receptors ERα and ERβ with EC₅₀s of 320 and 680 nM, respectively. IC50 & Target: IC50: 320 nM (ERα), 680 nM (ERβ) In Vitro: Bavachin significantly inhibits melanin synthesis and TYR activity. Bavachin (10 µM) inhibits the expression of TYR and JNK proteins, and the expression of TYR, TRP-1, TRP-2, ERK1, ERK2 and JNK2 mRNA in A375 cells. ICI182780 and U0126 cAN significantly reverse the bavachin treatment on the protein expression levels and the mRNA expression of TYR, TRP-1, TRP-2, ERK1, ERK2 and JNK2^[1]. Bavachin accumulates lipid in a dose dependent manner in ORO staining experiments. Bavachin significantly increases the growth of preadipoctye at 10 µM compared with the control cells in MTT assay. Bavachin also increases BrdU incorporation into newly synthesized DNA during pre-adipocyte proliferation. BrdU incorporation is enhanced by insulin and further enhanced by co-treatment with insulin and bavachin at 2 and 10 µM. Bavachin activates adipogenic factors and increases PPARγ transcriptional activity in differentiated adipocytes. Bavachin enhances insulin-stimulated glucose uptake through GLUT4 translocation via Akt and AMPK pathway^[2]. BVN significantly increases both hMAO-A and hMAO-B activities^[3]. Bavachin shows ER ligand binding activity in competitive displacement of [³H] E2 from recombinant ER. The estrogenic activity of bavachin is characterized in a transient transfection system using ERα or ERβ and estrogen-responsive luciferase plasmids in CV-1 cells with an EC₅₀ of 320 nM and 680 nM, respectively. Bavachin increases the mRNA levels of estrogen-responsive genes such as pS2 and PR, and decreases the protein level of ERα by proteasomal pathway^[4].