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VE-822

Cat. No. M3115
VE-822 Structure
Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mg USD 110 In stock
50mg USD 350 In stock
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Quality Control
Biological Activity

VE-822 is an ATR inhibitor with IC50 of 19 nM.

Protocol
Cell Experiment
Cell lines
Preparation method
Concentrations
Incubation time
Animal Experiment
Animal models mice bearing PSN-1 or MiaPaCa-2 tumors
Formulation saline
Dosages 60 mg/kg
Administration Oral gavage
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Chemical Information
Molecular Weight 463.55
Formula C24H25N5O3S
CAS Number 1232416-25-9
Purity 100.00%
Solubility DMSO 20 mg/mL
Storage at -20°C
Customer Product Validations & Biological Datas
Source Cancer Res (2017). Figure 7. VE-822 (Abmole Bioscience)
Method Colony formation assay
Cell Lines AKC cell lines
Concentrations 1 μM
Incubation Time 24 h
Results We next assessed the therapeutic efficacy of an ATR inhibitor (VE-822) with or without gemcitabine in a subcutaneous transplantation model. Intriguingly, while ATR inhibition significantly reduced tumor progression from AKC lines, it had negligible effects on KC tumors.
Rating
Source Sci Rep (2017). Figure 6. VE-822 (Abmole Bioscience)
Method oral
Cell Lines Xenograft mouse model
Concentrations 30 mg/kg
Incubation Time 1–3 day
Results While vehicle-treated xenograft tumors derived from H-82 (Fig. 6D), H-526 (Fig. 6E) and H-69 (Fig. 6F) cells displayed a rapid growth, both VE-822 and PF-477736 treatment led to a massively delayed tumor growth in all three models, which was mimicked by a substantial reduction in Ki67 staining on histological examination in tumors that were excised following completion of treatment (Fig. 6G,H).
Rating
Source Sci Rep (2017). Figure 4. VE-822 (Abmole Bioscience)
Method oral
Cell Lines Xenograft mouse model
Concentrations 30 mg/kg
Incubation Time 1–3 day
Results Contrary to these substantial therapeutic effects inflicted by VE-822 and PF-477736 in SCLC-bearing animals, we only observed a minute survival extension in VE-822- and PF-477736-treated NSCLC-bearing mice.
Rating
Source Sci Rep (2017). Figure 3. VE-822 (Abmole Bioscience)
Method Immunofluorescence
Cell Lines SCLC and NSCLC cells
Concentrations 0.75 μM
Incubation Time 48 h
Results Fully in line with our immunofluorescence data, SCLC cell lines displayed a significantly stronger γH2AX signal following VE-822 and PF-477736 treatment, than their NSCLC counterparts
Rating
Source Sci Rep (2017). Figure 2. VE-822 (Abmole Bioscience)
Method Flow cytometry
Cell Lines SCLC and NSCLC cell
Concentrations 0.1 μM, 0.75 μM, 3.0 μM
Incubation Time 48 h
Results Of note, the slow growing cell line RP2 was less sensitive to VE-822 and PF-477736, compared to cell lines RP1, 3 and 4. The rapidly proliferating SCLC cell line RP5 displayed the most pronounced sensitivity to the cell cycle checkpoint abrogating agents VE-822 and PF-477736.
Rating
Source Cancer Res (2017). VE-822, Figure 7. (AbMole BioScience)
Method
Cell Lines KP-, KPAfl/Δ- and KPAΔ/Δ cells
Concentrations 0.1μM
Incubation Time
Results As shown in Figure 7A-C, VE-822 treatment (30mg/kg, orally, days 1-3, 8-10, 15-17) of KP- and KPAfl/Δ-tumor bearing mice did not result in any significant tumor volume changes, compared to vehicle-treated controls.
Rating
Source Cancer Res (2017). VE-822, Figure 5. (AbMole BioScience)
Method
Cell Lines KP-, KPAfl/Δ- and KPAΔ/Δ cells
Concentrations 0.1μM
Incubation Time 72 h
Results VE-822 exposure led to a substantial and significant reduction in surviving KPAΔ/Δ colonies, compared to vehicle controls (p < 0.0001) (Fig. 5E, F). Of note, the cytotoxic effect of VE-822 was significantly more pronounced in KPAΔ/Δ cells, compared to KP- and KPAfl/Δcells (p < 0.0001 and p < 0.0001, respectively) (Fig. 5D). VE-822 was genotoxic in all three genotypes and induced maximal damage at 24 hours following drug exposure (Fig. 5I, J, S8B).
Rating
Product Citations
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  Catalog
Abmole Inhibitor Catalog 2017




Keywords: VE-822 supplier, ATM/ATR, inhibitors

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