AZD8055

	产品编号	CFN60002
	CAS编号	1009298-09-2
	分子式 = 分子量	C₂₅H₃₁N₅O₄ = 465.5
	产品纯度	>=98%
	物理属性	Powder
	化合物类型	Alkaloids
	植物来源
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产品名称	产品编号	CAS编号	包装	QQ客服
AZD8055	CFN60002	1009298-09-2	1mg	QQ客服：1457312923
AZD8055	CFN60002	1009298-09-2	5mg	QQ客服：1457312923
AZD8055	CFN60002	1009298-09-2	10mg	QQ客服：1457312923
AZD8055	CFN60002	1009298-09-2	20mg	QQ客服：1457312923

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Description:

AZD8055 is a novel ATP-competitive mTOR inhibitor with IC50 of 0.8 nM in MDA-MB-468 cells with excellent selectivity (∼1,000-fold) against PI3K isoforms and ATM/DNA-PK. AZD8055 induces caspase-dependent apoptosis and also induces autophagy. Phase 1.

Targets:

mTOR | PI3K | Autophagy

In vitro:

Pediatr Blood Cancer,2012 Feb;58(2):191-9.

Initial testing (stage 1) of the mTOR kinase inhibitor AZD8055 by the pediatric preclinical testing program.[Pubmed: 21337679]

AZD8055 is a small molecule ATP-competitive inhibitor of the serine/threonine kinase mTOR that regulates cap-dependent translation through the mTORC1 complex and Akt activation through the mTORC2 complex.
METHODS AND RESULTS:
Procedures AZD8055 was tested against the PPTP in vitro panel at concentrations ranging from 1.0 nM to 10 µM and against the PPTP in vivo panels at a dose of 20 mg/kg administered orally daily x 7 for 4 weeks. In vitro the median relative IC(50) for AZD8055 against the PPTP cell lines was 24.7 nM. Relative I/O values >0% (consistent with a cytostatic effect) were observed in 8 cell lines and 15 cell lines showed Relative I/O values ranging from -4.7 to -92.2% (consistent with varying degrees of cytotoxic activity). In vivo AZD8055 induced significant differences in EFS distribution compared to controls in 23 of 36 (64%) evaluable solid tumor xenografts, and 1 of 6 evaluable ALL xenografts. Intermediate activity for the time to event activity measure (EFS T/C >2) was observed in 5 of 32 (16%) solid tumor xenografts evaluable. The best response was stable disease. PD2 (progressive disease with growth delay) was observed in 20 of 36 (55.6%) evaluable solid tumor xenografts. AZD8055 significantly inhibited 4E-BP1, S6, and Akt phosphorylation following day 1 and day 4 dosing, but suppression of mTORC1 or mTORC2 signaling did not predict tumor sensitivity.
CONCLUSIONS:
AZD8055 demonstrated broad activity in vitro, but at the dose and schedule studied demonstrated limited activity in vivo against the PPTP solid tumor and ALL panels.

Br J Cancer,2011 Mar 29;104(7):1116-25.

Effect of PI3K- and mTOR-specific inhibitors on spontaneous B-cell follicular lymphomas in PTEN/LKB1-deficient mice[Pubmed: 21407213]

The PI3K-mTOR (phosphoinositide 3-kinase-mammalian target of rapamycin kinase) pathway is activated in the majority of tumours, and there is interest in assessing whether inhibitors of PI3K or mTOR kinase have efficacy in treating cancer. Here, we define the effectiveness of specific mTOR (AZD8055) and PI3K (GDC-0941) inhibitors, currently in clinical trials, in treating spontaneous B-cell follicular lymphoma that develops in PTEN(+/-)LKB1(+/hypo) mice.
METHODS AND RESULTS:
The PTEN(+/-)LKB1(+/hypo) mice were administered AZD8055 or GDC-0941, and the volumes of B-cell follicular lymphoma were measured by MRI. Tumour samples were analysed by immunohistochemistry, immunoblot and flow cytometry. The AZD8055 or GDC-0941 induced ∼40% reduction in tumour volume within 2 weeks, accompanied by ablation of phosphorylation of AKT, S6K and SGK (serum and glucocorticoid protein kinase) protein kinases. The drugs reduced tumour cell proliferation, promoted apoptosis and suppressed centroblast population. The AZD8055 or GDC-0941 treatment beyond 3 weeks caused a moderate additional decrease in tumour volume, reaching ∼50% of the initial volume after 6 weeks of treatment. Tumours grew back at an increased rate and displayed similar high grade and diffuse morphology as the control untreated tumours upon cessation of drug treatment.
CONCLUSIONS:
These results define the effects that newly designed and specific mTOR and PI3K inhibitors have on a spontaneous tumour model, which may be more representative than xenograft models frequently employed to assess effectiveness of kinase inhibitors. Our data suggest that mTOR and PI3K inhibitors would benefit treatment of cancers in which the PI3K pathway is inappropriately activated; however, when administered alone, may not cause complete regression of such tumours.

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	2.1482 mL	10.7411 mL	21.4823 mL	42.9646 mL	53.7057 mL
5 mM	0.4296 mL	2.1482 mL	4.2965 mL	8.5929 mL	10.7411 mL
10 mM	0.2148 mL	1.0741 mL	2.1482 mL	4.2965 mL	5.3706 mL
50 mM	0.043 mL	0.2148 mL	0.4296 mL	0.8593 mL	1.0741 mL
100 mM	0.0215 mL	0.1074 mL	0.2148 mL	0.4296 mL	0.5371 mL

产品名称	产品编号	CAS编号	分子式 = 分子量	位单	联系QQ
YM155 (Sepantronium Bromide); YM155 (Sepantronium Bromide)	CFN60046	781661-94-7	C₂₀H₁₉BrN₄O₃ = 443.29	5mg	QQ客服：2056216494
3′-甲氧基,3,7,4′-三羟基黄酮; Geraldol	CFN70311	21511-25-1	C₁₆H₁₂O₆ = 300.3	5mg	QQ客服：2159513211
Butyraxanthone B; Butyraxanthone B	CFN92696	1141754-81-5	C₂₈H₃₀O₆ = 462.5	5mg	QQ客服：1413575084
金圣草(黄)素; Chrysoeriol	CFN98785	491-71-4	C₁₆H₁₂O₆ = 300.3	5mg	QQ客服：215959384

AZD8055

AZD8055

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