WS3

WS3 (25 nM; 3 days) induces proliferation in senescent passage six primary human fetal RPE cells, with 25 nM WS3 causing a four-fold increase in EdU-positive cells relative to DMSO control, and elicits similar responses in primary adult rat and adult human RPE cells^[1].
WS3 (25 nM; serial passages through passage fifteen, split every three days) supports continuous proliferation of primary human fetal RPE cells through passage fifteen (maximal 1.95 doublings per passage at passage eleven), with proliferation ceasing immediately upon compound removal, and does not induce cell death during senescence^[1].
WS3 (25 nM; from passage six to passage ten) does not induce chromosomal abnormalities or tumorigenic events during long-term culture of primary human fetal RPE cells from passage six to passage ten^[1].
WS3 (25 nM) expanded primary human fetal RPE cells to passage ten differentiate into functional mature RPE monolayers (with cobblestone morphology, pigmentation, tight junctions, RPE marker expression, and POS phagocytosis) upon WS3 removal, and WS3-expanded primary adult human RPE cells similarly differentiate into mature RPE cells with appropriate gene expression^[1].
WS3 induces dose-dependent proliferation of mouse R7T1 β cells with an EC₅₀ of 0.074 μM^[2].
WS3 (50-200 nM; 48 h) potently inhibits NRF2-ARE signaling in A549 cells with an IC₅₀ of 135 nM, selectively reducing NRF2 and downstream target levels via proteasomal/ubiquitin-mediated degradation dependent on the SKP1-CUL1-β-TrCP complex, while sparing normal HUVEC and BEAS-2B cells^[3].
WS3 (50-200 nM; 4-48 h) disrupts the 14-3-3ζ-pGSK3β interaction in A549 cells, activating GSK3β to promote CUL1-β-TrCP-mediated NRF2 ubiquitination and degradation, with this effect reversible via GSK3β or PP2A inhibition^[3].
WS3 (20-400 nM; 24 h-2 week) induces oxidative stress, ferroptosis, and NRF2-dependent growth inhibition in A549 cells, with effects abrogated in NRF2-KO cells^[3].
WS3 (20-200 nM; 48 h-2 week) synergizes with carboplatin and ferroptosis inducers to enhance growth inhibition of A549 cells^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.