Palomid 529 (P529)
For research use only.
Catalog No.S2238 Synonyms: SG 00529
CAS No. 914913-88-5
Palomid 529 (P529, SG 00529) inhibits both the mTORC1 and mTORC2 complexes, reduces phosphorylation of pAktS473, pGSK3βS9, and pS6. Phase 1.
Selleck's Palomid 529 (P529) has been cited by 7 publications
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After starved in serum-free medium for 24 h,A549 cells incubated with the indicated concentrations of Palomid529 for 3 h,followed by 20-minute stimolation of 100ng/ml EGF.
Dr. Zhang of Tianjin Medical University. Palomid 529 (P529) purchased from Selleck.
(A) Cell growth rate fromP529 (2 μM) and vehicle treated MFN2 knockout MCF-7 (left) and A549 cells (right). (B) Representative pictures (left) and statistical analysis (right) shown colony formation from P529 and vehicle treated MFN2 knockout MCF-7 and A549 cells. (C,D) In vitro wound closure of P529 and vehicle treated MFN-2 knockout MCF-7 cells (C) and A549 cells (D) from 24 h after scratch assay.
Sci Rep, 2017, 7:41718. Palomid 529 (P529) purchased from Selleck.
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|Description||Palomid 529 (P529, SG 00529) inhibits both the mTORC1 and mTORC2 complexes, reduces phosphorylation of pAktS473, pGSK3βS9, and pS6. Phase 1.|
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) <35 μM. In addition, Palomid 529 significantly enhances the antiproliferative effect of radiation in prostate cancer cells (PC-3). Palomid 529 gives rise to a concentration dependent growth inhibition on PC-3 cells. Doses of 2 and 7μM resulted in 30 and 60% growth inhibition, respectively. Palomid 529 inhibits the radiation-induced p-Akt activation and decreases Bcl-2/Bax ratio in PC-3. Palomid 529 not only inhibits radiation-induced overexpression of Id-1 and VEGF but also down-regulates radiation-induced MMP-2 and MMP-9. 
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. 
Estrogen receptor binding assays:The proteins are produced with rabbit reticulocyte lysates. The amount of template used in each reaction is determined empirically and expression is monitored in parallel reactions where [35S]methionine is incorporated into the receptor followed by gel electrophoresis and exposure to film. Binding reactions of the estrogen receptors (ER) and Palomid 529 are carried out in 100 mL final volumes in TEG buffer [10 mM Tris (pH 7.5), 1.5 mM EDTA, 10% glycerol]. In vitro transcribed-translated receptor (5 μL) is used in each binding reaction in the presence of 0.5 nM [3H]estradiol (E2). Palomid 529 is routinely tested from 10−11 to 10−6 M and diluted in ethanol. The reactions are incubated at 4 °C overnight and bound E2 is quantified by adding 200 mL dextran-coated charcoal. After a 15-minutes rotation at 4 °C, the tubes are centrifuged for 10 minutes and 150 mL of the supernatant are added to 5 mL scintillation mixture for determination of cpm by liquid scintillation counting. The maximum binding is determined by competing bound E2 with only the ethanol vehicle. Controls for background are included in each experiment using 5 mL unprogrammed rabbit reticulocyte lysate. This value, typically 10% to 15% of the maximal counts, is subtracted from all values. The data are plotted and Ki values are calculated. Experiments are conducted at least thrice in duplicate.
-  Xue Q, et al. Cancer Res, 2008, 68(22), 9551-9557.
-  Diaz R, et al. Br J Cancer 2009, 100(6), 932-940.
-  Lewis GP, et al. Invest Ophthalmol Vis Sci, 2009, 50(9), 4429-4435.
|In vitro||DMSO||81 mg/mL (199.29 mM)|
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