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Palomid 529

SKU: orb1305138

Description

Palomid 529

Research Area

Cell Biology, Signal Transduction

Images & Validation

Key Properties

CAS Number914913-88-5
MW406.43
Purity99.03%
FormulaC24H22O6
SMILESCOc1ccc(COc2cc3oc(=O)c4cc(ccc4c3cc2OC)C(C)O)cc1
TargetmTOR,Apoptosis
Solubility10% DMSO+90% Corn Oil:2.5 mg/mL (6.15 mM);DMSO:50 mg/mL (123.02 mM);Ethanol:< 1 mg/mL (insoluble or slightly soluble)

Bioactivity

In Vivo
Palomid 529 not only reduces the proliferation of ischemic retina but also improves the tissue and structure of vasculogenesis. It inhibits endothelial cell proliferation mediated by VEGF and bFGF, with IC50 values of 20 nM and 30 nM, respectively. Additionally, Palomid 529 induces apoptosis in endothelial cells and reduces the phosphorylation of pAktS473, pGSK3βS9, and pS6 induced by the vascular endothelial growth factor VEGF-A. In the lung cancer NCI-60 cell line, Palomid 529 exhibits potent antiproliferative activity, with a GI50< 35 μM. Furthermore, it significantly enhances the antiproliferative effect of radiation on prostate cancer cells (PC-3), demonstrating concentration-dependent growth inhibition in PC-3 cells. Palomid 529 inhibits radiation-induced p-Akt activation and reduces the Bcl-2/Bax ratio in PC-3 cells.
In Vitro
Palomid 529 effectively inhibits tumor growth, angiogenesis, and vascular permeability. In the rabbit retinal detachment model, it significantly suppresses the proliferation of Müller cells, the formation of neuroglial scars, and photoreceptor cell death. Additionally, Palomid 529 dose-dependently inhibits Ad-VEGF-A-driven angiogenesis and, when administered orally to nude mice, restrains the growth of C6V10 gliomas. Compared to the control group, treatment with Palomid 529 in PC-3 tumor-bearing mice results in a 57.1% reduction in tumor growth. It also markedly suppresses tumor growth in mouse models of Brca1 deficiency by inhibiting the Akt and mTOR signaling pathways.
Cell Research
Human umbilical vascular endothelial cells (HUVEC) are used. The proliferation assay is carried out by seeding the HUVECs in 96-well plates at a density of 1,000 per well in complete medium. Following a 24-hour plating period, the cells are starved for 24 hours in 0.5% serum before being treated with Palomid 529 in the presence of 10 ng/mL basic fibroblast growth factor (bFGF) or VEGF in complete medium. After 48 hours, cell number is determined using a colorimetric method. The results are expressed as the percentage of the maximal bFGF or VEGF response in the absence of Palomid 529. Nonproliferating endothelial cells are assayed by growing HUVECs to quiescence in 96-well plates and treating with Palomid 529 for 48 hours. Initially, 5,000 cells per well are seeded and confluence is achieved the next day. The plates are incubated for another 24 hours to ensure growth arrest before treatment with Palomid 529. (Only for Reference)

Storage & Handling

StoragePowder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
Expiration Date12 months from date of receipt.
DisclaimerFor research use only

Alternative Names

Palomid 529, Palomid529, Palomid-529, P-529, P529, mTORC2, mTORC1, mTOR, inhibit, P 529, Mammalian target of Rapamycin, Inhibitor, Apoptosis, SG 00529, SG00529, SG-00529

Similar Products

  • Palomid 529 [orb1222997]

    >98% (HPLC)

    914913-88-5

    406.4

    C24H22O6

    5 mg, 10 mg, 25 mg, 50 mg, 1 g, 500 mg, 200 mg, 100 mg
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Key Properties

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Palomid 529 (orb1305138)

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Available Sizes

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5 mg
$ 80.00
1 ml x 10 mM (in DMSO)
$ 90.00
10 mg
$ 110.00
25 mg
$ 170.00
50 mg
$ 240.00
100 mg
$ 340.00
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