Molecular Weight(MW): 393.53
A66 is a potent and specific p110α inhibitor with IC50 of 32 nM in a cell-free assay, >100 fold selectivity for p110α over other class-I PI3K isoforms.
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(C) Western blot analyses of pAkt in MMTV-MT tumor derived cells treated with various PI3K inhibitors (in micromolar) as indicated following growth factor starvation. (D) Western blot analyses of pAkt in MMTV-NeuT tumor-derived cells treated with various PI3K inhibitors (in micromolar) as indicated. (*) P < 0.01; (**) P < 0.001 (Student’s t-test).
Genes Dev, 2012, 26: 1573–1586. A66 purchased from Selleck.
(A) Tumor volumes of MMTV-MT tumor transplants treated with various PI3K inhibitors as indicated (n = 12 per group). (B) Tumor volumes of MMTV-NeuT tumor transplants treated with PI3K inhibitors as indicated (control, n = 20; GDC-0941, n = 20; A66, n = 16; and TGX221, n = 16). (*) P < 0.01; (***) P < 0.0001 (Student’s t-test).
Genes Dev, 2012, 26: 1573–1586. A66 purchased from Selleck.
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2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.
|Description||A66 is a potent and specific p110α inhibitor with IC50 of 32 nM in a cell-free assay, >100 fold selectivity for p110α over other class-I PI3K isoforms.|
|Features||Highly selective for the p110α isoform.|
In addition to the wild-type p110α, A66 also potently inhibits the oncogenic forms of p110α such as p110α E545K and p110α H1047R with IC50 of 30 nM and 43 nM, respectively. Unlike PIK-75, A66 displays >100 fold selectivity for p110α over other class-I PI3K isoforms. Among the class-II PI3Ks, class-III PI3K and PI4Ks, A66 only exhibits limited cross-reactivity with the class-II PI3K PI3KC2β and the PI4Kβ isoform of PI4K with IC50 of 462 nM and 236 nM, respectively. A66 exhibits no inhibitory activity against other lipid kinases or the related kinases DNA-PK and mTOR. A66 has a higher degree of specificity compared with PIK-75 when tested at 10 μM against two large panels of 110 protein kinases and 318 kinases. Inhibition of p110α alone by A66 treatment is sufficient to block insulin signalling to Akt/PKB in certain cell lines that harbor H1047R mutations in PIK3CA and have high levels of p110α and class-Ia PI3K activity.  A66 treatment at 0.7 μM induces a 75-80% reduction in focus formation by the highly transforming p85α iSH2 mutants KS459delN, DKRMN-S560del, and K379E, and reduces the phosphorylation of Akt on T308 by all p85 mutants. 
|In vivo||A single dose of A66 at 100 mg/kg induces a profound reduction in the phosphorylation of Akt/PKB and p70 S6 kinase, but not of ERK, in SK-OV-3 tumour tissue in vivo at both 1 hour and 6 hours after dosing. A66 dosed at 100 mg/kg once daily (QD) for 21 days or 75 mg/kg twice daily (BID) for 16 days induces a significant delay in growth of SK-OV-3 xenografted tumors with average TGI of 45.9% and 29.9%, respectively, which is even greater than that induced by the well-established pan-PI3K inhibitor BEZ-235. QD dosing of A66 in the HCT-116 xenograft model also induces a significant reduction in tumour volume with TGI of 77.2%, but causes a non-significant reduction in tumor volume in the U87MG xenograft model.  Administration of A66 at 10 mg/kg in male CD1 mice induces significant impairments in the ITT (insulin tolerance test) and GTT (glucose tolerance test), and an increase in glucose production during a PTT (pyruvate tolerance test), almost to the same level as the pan-PI3K inhibitors. |
|In vitro||DMSO||79 mg/mL (200.74 mM)|
|Ethanol||1 mg/mL (2.54 mM)|
|In vivo||15% Captisol||8 mg/mL|
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