Palomid 529

mTORC1,mTORC2

406.43

DMSO ：75 mg/mL (184.5 mM)

Palomid 529 inhibits proliferation and increases apoptosis of endothelial cells. Palomid 529 inhibits both VEGF-driven and bFGF-driven endothelial cell proliferation with IC50 of 20 nM and 30 nM, respectively. Palomid 529 retains the ability to induce endothelial cell apoptosis. Palomid 529 decreases VEGF-A–driven phosphorylation of pAktS473, pGSK3βS9, and pS6. However, Palomid 529 prevents neither phosphorylated mitogen-activated protein kinase (pMAPK) nor pAktT308 as potently as pAktS473. Palomid 529 not only reduces the proliferative response in the ischemic retina but also improves the organization and structure of the vessels that form. Palomid 529 shows a potent antiproliferative activity in the NCI-60 cell lines panel, with growth inhibitory 50 (GI50)

Palomid 529 shows a dose-dependent inhibition of the Ad-VEGF-A–driven angiogenesis following Palomid 529 treatment. Palomid 529 inhibits C6V10 glioma tumor growth in nude mice following i.p. dosing. Palomid 529 decreases AktS473 but not AktT308 signaling. Palomid 529 inhibits C6V10 glioma tumor growth in nude mice following i.p. dosing. Palomid 529 decreases AktS473 but not AktT308 signaling. Palomid 529 inhibits tumor growth, angiogenesis, and vascular permeability. Treatment of PC-3 tumour-bearing mice with Palomid 529 reduced tumour growth to 57.1% compared with controls. Palomid 529 is an effective suppressor of Müller cell proliferation, glial scar formation, and photoreceptor cell death in a rabbit model of retinal detachment (RD). Palomid 529 significantly suppresses Brca1-deficient tumor growth in mice through inhibition of both Akt and mTOR signaling.

P529

C₂₄H₂₂O₆

914913-88-5