Ambeed.cn

首页 / / / PI3K / AZD 6482

AZD 6482 {[allProObj[0].p_purity_real_show]}

货号:A560000 同义名: KIN-193

AZD 6482(KIN-193) 是一种高效且选择性的p110β抑制剂,IC50为0.69 nM。

AZD 6482 化学结构 CAS号:1173900-33-8
AZD 6482 化学结构
CAS号:1173900-33-8
AZD 6482 3D分子结构
CAS号:1173900-33-8
AZD 6482 化学结构 CAS号:1173900-33-8
AZD 6482 3D分子结构 CAS号:1173900-33-8
规格 价格 会员价 库存 数量
{[ item.pr_size ]}

{[ getRatePrice(item.pr_rmb, 1,1) ]}

{[ getRatePrice(item.pr_rmb_sale, 1,1) ]} {[ suihuo_tips(item.pr_am, item.pr_size) ]}

{[ getRatePrice(item.pr_rmb, 1,1) ]}

{[ getRatePrice(item.pr_rmb,item.pr_rate,1) ]} {[ suihuo_tips(item.pr_am, item.pr_size) ]}
{[ getRatePrice(item.pr_rmb, 1,1) ]}{[ suihuo_tips(item.pr_am, item.pr_size) ]} {[ getRatePrice(item.pr_rmb_sale, 1,1) ]} {[ getRatePrice(item.pr_rmb,item.pr_rate,item.mem_rate) ]} {[ getRatePrice(item.pr_rmb,1,item.mem_rate) ]} 现货 咨询 - +
购物车0 收藏 询单

AZD 6482 纯度/质量文件 产品仅供科研

货号:A560000 标准纯度: {[allProObj[0].p_purity_real_show]}
批次查询: 批次纯度:

全球学术期刊中引用的产品

Cell, 2024, 101755. Ambeed. [ A399663 ]
EMBO J., 2024. Ambeed. [ A295334 ]
JMC, 2024, 67(20): 18265-18289. Ambeed. [ A538667 , A341145 , A117430 , A172297 ]
JMC, 2024. Ambeed. [ A210558 , A1518164 ]
Cell Death Discov., 2024, 10, 436. Ambeed. [ A384235 ]
更多 >
产品名称 C2β p110α p110β p110γ p110δ PI3K Vps34 其他靶点 纯度
A66 +

C2β, IC50: 462 nM

++

p110α, IC50: 32 nM

99%+
Taselisib +

C2β, IC50: 292 nM

++++

PI3Kα, Ki: 0.29 nM

+++

PI3Kβ, Ki: 9.1 nM

++++

PI3Kγ, Ki: 0.97 nM

++++

PI3Kδ, Ki: 0.12 nM

+

hVps34, IC50: 374 nM

99%+
Gedatolisib ++++

PI3Kα, IC50: 0.4 nM

+++

PI3Kγ, IC50: 5.4 nM

mTOR 98%
HS-173 ++++

PI3Kα , IC50: 0.8 nM

99%+
Serabelisib +++

PI3Kα, IC50: 21 nM

99%+
GNE-477 ++++

PI3Kα, IC50: 4 nM

mTOR 98%
YM-201636 +

p110α, IC50: 3.3 μM

PIKfyve 98%
AS-252424 +

PI3Kα, IC50: 935 nM

++

PI3Kγ, IC50: 33 nM

99%
Alpelisib +++

PI3Kα, IC50: 5 nM

99%+
AS-604850 +

PI3Kα, IC50: 4.5 μM

+

PI3Kγ, IC50: 0.25 μM

98+%
SF2523 ++

PI3Kα, IC50: 34 nM

++

PI3Kγ, IC50: 158 nM

DNA-PK,mTOR 99%+
Inavolisib ++++

PI3K alpha, IC50: 0.038 nM

99%+
Bimiralisib ++++

PI3Kα, Kd: 1.5 nM

+++

PI3Kβ, Kd: 11 nM

++

PI3Kγ, Kd: 25 nM

++

PI3Kδ, Kd: 25 nM

mTOR 99%+
GSK1059615 ++++

PI3Kα, IC50: 0.4 nM

++++

PI3Kβ, IC50: 0.6 nM

+++

PI3Kγ, IC50: 5 nM

++++

PI3Kδ, IC50: 2 nM

mTOR 98%
GSK2636771 98%
Fimepinostat +++

PI3Kα, IC50: 19 nM

++

PI3Kβ, IC50: 54 nM

++

PI3Kδ, IC50: 39 nM

99%+
VS-5584 ++++

PI3Kα, IC50: 2.6 nM

+++

PI3Kβ, IC50: 21 nM

++++

PI3Kγ, IC50: 3.0 nM

++++

PI3Kδ, IC50: 2.7 nM

mTOR 99%
Dactolisib ++++

p110α1, IC50: 4 nM

++

p110β, IC50: 75 nM

+++

p110γ, IC50: 5 nM

+++

p110δ, IC50: 7 nM

98+%
PI-103 ++++

p110α, IC50: 2 nM

++++

p110β, IC50: 3 nM

+++

p110γ, IC50: 15 nM

++++

p110δ, IC50: 3 nM

DNA-PK,mTOR 99%+
PI-3065 +

p110β, IC50: 1078 nM

+++

p110δ, IC50: 15 nM

99%+
Voxtalisib ++

PI3Kα, IC50: 39 nM

++

PI3Kβ, IC50: 113 nM

+++

PI3Kγ, IC50: 9 nM

++

PI3Kδ, IC50: 43 nM

DNA-PK,mTOR 99%+
AZD-8835 +++

PI3Kα, IC50: 6.2 nM

+

PI3Kβ, IC50: 431 nM

++

PI3Kγ, IC50: 90 nM

+++

PI3Kδ, IC50: 5.7 nM

98%
Pilaralisib analogue ++

PI3Kα, IC50: 39 nM

++

PI3Kβ, IC50: 36 nM

+++

PI3Kγ, IC50: 23 nM

++

PI3Kδ, IC50: 36 nM

99%+
ZSTK474 +++

PI3Kα, IC50: 16 nM

++

PI3Kβ, IC50: 44 nM

++

PI3Kγ, IC50: 49 nM

+++

PI3Kδ, IC50: 4.6 nM

++

PI3K, IC50: 37 nM

98%
AS-605240 ++

PI3Kα, IC50: 60 nM

+

PI3Kβ, IC50: 270 nM

+++

PI3Kγ, IC50: 8 nM

+

PI3Kδ, IC50: 300 nM

98%
TGX-221 +++

p110β, IC50: 5 nM

++

p110δ, IC50: 0.1 μM

99%+
PF-04691502 ++++

PI3Kα, Ki: 1.8 nM

++++

PI3Kβ, Ki: 2.1 nM

++++

PI3Kγ, Ki: 1.9 nM

++++

PI3Kδ, Ki: 1.6 nM

mTOR 98+%
GDC-0084 ++++

PI3Kα, Ki app: 2 nM

++

PI3Kβ, Ki app: 46 nM

+++

PI3Kγ, Ki app: 10 nM

++++

PI3Kδ, Ki app: 3 nM

mTOR 99%+
Buparlisib ++

p110α, IC50: 52 nM

+

p110β, IC50: 166 nM

+

p110γ, IC50: 262 nM

++

p110δ, IC50: 116 nM

+

Vps34, IC50: 2.4 μM

mTOR 98%
LY294002 +

p110α, IC50: 0.5 μM

+

p110β, IC50: 0.97 μM

+

p110δ, IC50: 0.57 μM

DNA-PK 99%+
AZD 6482 +

PI3Kα, IC50: 870 nM

+++

PI3Kβ, IC50: 10 nM

++

PI3Kδ, IC50: 80 nM

DNA-PK 99%+
Pictilisib ++++

p110α, IC50: 3 nM

++

p110β, IC50: 33 nM

++

p110γ, IC50: 75 nM

++++

p110δ, IC50: 3 nM

mTOR 99%+
PKI-402 ++++

PI3Kα, IC50: 2 nM

+++

PI3Kβ, IC50: 7 nM

+++

PI3Kγ, IC50: 16 nM

+++

PI3Kδ, IC50: 14 nM

mTOR 99+%
Copanlisib ++++

PI3Kα, IC50: 0.5 nM

++++

PI3Kβ, IC50: 3.7 nM

+++

PI3Kγ, IC50: 6.4 nM

++++

PI3Kδ, IC50: 0.7 nM

99%+
Omipalisib ++++

p110α, Ki: 0.019 nM

++++

p110β, Ki: 0.13 nM

++++

p110γ, Ki: 0.06 nM

++++

p110δ, Ki: 0.024 nM

99%+
Izorlisib +++

PI3Kα, IC50: 14 nM

++

PI3Kβ, IC50: 0.12 μM

++

PI3Kγ, IC50: 36 nM

+

PI3Kδ, IC50: 0.50 μM

99%+
AZD8186 ++

PI3Kα, IC50: 35 nM

++++

PI3Kβ, IC50: 4 nM

+++

PI3Kδ, IC50: 12 nM

98+%
KU-0060648 ++++

PI3Kα, IC50: 4 nM

++++

PI3Kβ, IC50: 0.5 nM

+

PI3Kγ, IC50: 0.59 μM

++++

PI3Kδ, IC50: 0.1 nM

DNA-PK 99%
Apitolisib +++

p110α, IC50: 5 nM

++

p110β, IC50: 27 nM

+++

p110γ, IC50: 14 nM

+++

p110δ, IC50: 7 nM

mTOR 98%+
CZC24832 +

PI3Kβ, IC50: 1.1 μM

++

PI3Kγ, IC50: 27 nM

98+%
BGT226 maleate ++++

PI3Kα, IC50: 4 nM

++

PI3Kβ, IC50: 63 nM

++

PI3Kγ, IC50: 38 nM

mTOR 99%+
TG 100713 ++

PI3Kα, IC50: 165 nM

+

PI3Kβ, IC50: 215 nM

++

PI3Kγ, IC50: 50 nM

+++

PI3Kδ, IC50: 24 nM

98%+
PI3K-IN-1 ++

PI3Kα, IC50: 39 nM

++

PI3Kβ, IC50: 113 nM

+++

PI3Kγ, IC50: 9 nM

++

PI3Kδ, IC50: 43 nM

DNA-PK,mTOR 98+%
TG100-115 +

PI3Kα, IC50: 1.3 μM

+

PI3Kβ, IC50: 1.2 μM

++

PI3Kγ, IC50: 83 nM

+

PI3Kδ, IC50: 235 nM

98%
PIK-90 +++

PI3Kα, IC50: 11 nM

+

PI3Kβ, IC50: 350 nM

+++

PI3Kγ, IC50: 18 nM

++

PI3Kδ, IC50: 58 nM

99%+
PIK-294 +

p110β, IC50: 490 nM

++

p110γ, IC50: 160 nM

+++

p110δ, IC50: 10 nM

99%+
Duvelisib ++++

PI3Kβ, Ki: 1564 pM

++

PI3Kγ, Ki: 243 pM

++++

PI3Kδ, Ki: 23 pM

99%+
GDC-0326 ++++

PI3Kα, Ki: 0.2 nM

++

PI3Kβ, Ki: 26.6 nM

+++

PI3Kγ, Ki: 10.2 nM

++++

PI3Kδ, Ki: 4 nM

98%
Quercetin Dihydrate +

PI3Kβ, IC50: 5.4 μM

+

PI3Kγ, IC50: 2.4 μM

+

PI3Kδ, IC50: 3.0 μM

95%
Quercetin +

PI3Kβ, IC50: 5.4 μM

+

PI3Kγ, IC50: 2.4 μM

+

PI3Kδ, IC50: 3.0 μM

Sirtuin,Src,PKC 97%
Leniolisib +

PI3Kα, IC50: 0.244 μM

+

PI3Kβ, IC50: 0.424 μM

+

PI3Kγ, IC50: 2.23 μM

+++

PI3Kδ, IC50: 0.011 μM

DNA-PK 99%+
PIK-108 98%
Eganelisib +++

PI3Kγ, IC50: 16 nM

99%+
CAY10505 98%
IPI-3063 ++++

p110δ, IC50: 2.5 nM

99%
Nemiralisib ++++

PI3Kδ, pKi: 9.9

99%+
PF-4989216 ++++

p110α, IC50: 2 nM

++

p110γ, IC50: 65 nM

++++

p110δ, IC50: 1 nM

99%+
PIK-75 HCl +++

p110α, IC50: 5.8 nM

++

p110γ, IC50: 76 nM

+

p110δ, IC50: 0.51 μM

DNA-PK 99%+
Tenalisib ++

PI3Kγ, IC50: 33.2 nM

++

PI3Kδ, IC50: 24.5 nM

95+%
Acalisib +++

p110δ, IC50: 14 nM

99%+
Umbralisib +++

PI3Kδ, IC50: 22.2 nM

99%+
AMG319 +

PI3Kγ, IC50: 850 nM

+++

PI3Kδ, IC50: 18 nM

99%
IC-87114 +

PI3Kγ, IC50: 29 μM

+

PI3Kδ, IC50: 0.5 μM

99%+
Idelalisib ++

p110γ, IC50: 89 nM

++++

p110δ, IC50: 2.5 nM

98%
PIK-293 +

p110γ, IC50: 10 μM

+

p110δ, IC50: 0.24 μM

99%+
Vps34-PIK-III +

PI3Kδ, IC50: 1.2μM

+++

Vps34, IC50: 0.018μM

99%+
GSK2292767 99+%
Seletalisib +

PI3Kγ, IC50: 282 nM

+++

PI3Kδ, IC50: 12 nM

99%+
P110δ-IN-1 ++++

P110δ, IC50: 0.6 nM

98%
PI3Kδ-IN-5 ++++

PI3Kδ, IC50: 0.9 nM

98%
SRX3207 +

PI3K alpha, IC50: 244 nM

+

PI3K gamma, IC50: 9790 nM

+

PI3K delta, IC50: 388 nM

Syk 98%
Parsaclisib HCl ++++

PI3Kδ, IC50: 1 nM

98%
IHMT-PI3Kδ-372 +++

PI3Kδ, IC50: 14 nM

98%
Trigonelline Akt 99%+
Wortmannin ++++

PI3K, IC50: 3 nM

DNA-PK,MLCK 99%+
Samotolisib DNA-PK 99%+
GNE-317 99%+
Oroxin B PTEN,Akt 99%+
NU 7026 +

PI3K, IC50: 13 μM

DNA-PK 98+%
Deguelin Akt 99%+
Ailanthone ATM/ATR,CDK,Akt 98%
Resibufogenin ROS 98%
KU-57788 +

PI3K, IC50: 5 μM

DNA-PK,mTOR 99%+
Cinobufagine Akt 98%
α-Linolenic acid 97% GC
MTX-211 EGFR 98%
PI3K/mTOR Inhibitor-2 ++++

PI3K, IC50: 3.4 nM

mTOR 99%+
SPP-86 99%+
(E)-Akt inhibitor-IV 98%
Vps34-IN-1 ++

Vps34, IC50: 25 nM

98%
SAR405 ++++

Vps34, IC50: 1.2 nM

98+%
3-Methyladenine +

PI3Kγ, IC50: 60 μM

+

Vps34, IC50: 25 μM

Autophagy 98%
Vps34-IN-4 +++

VPS34, IC50: 15 nM

98%+
Autophinib +++

Vps34, IC50: 19 nM

Autophagy 97%
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。

AZD 6482 生物活性

靶点
  • p110β

    PI3Kβ, IC50:10 nM

  • p110α

    PI3Kα, IC50:870 nM

  • p110δ

    PI3Kδ, IC50:80 nM

描述 An in vitro kinase assay demonstrates that AZD 6482 (KIN-193) is highly potent in the inhibition of p110β’s kinase activity (IC50 of 0.69 nM) and has 200, 20, and 70-fold selectivity over p110α, p110δ, and p110γ isoforms, respectively. AZD 6482 also exhibits selectivity of ~80 fold over PI3K-C2β and DNA-PK and more than 1,000-fold over other phosphatidylinositol-3 kinase–related kinases (PIKKs). When tumors reach a volume of ~500 mm3, the tumor-bearing mice receives a single IP injection of AZD 6482 (10 mg/kg). The plasma concentration of AZD 6482 is highest at 1 hour post-injection and declined to undetectable levels by 4h. Concentrations of AZD 6482 in both the CA-p110α- and CA-p110β-driven tumors parallel the plasma concentrations. Analyses of tumor lysates harvested at various time points after AZD 6482 injection reveal that the phosphorylation of AKT is significantly reduced at 1hour after AZD 6482 injection in Rat1-CA-p110β tumors, but remain unchanged in Rat1-CAp110α tumors[3]. KIN-193 is efficacious specifically in blocking AKT signaling and tumor growth that are dependent on p110β activation or PTEN loss. Broad profiling across a panel of 422 human tumor cell lines shows that the PTEN mutation status of cancer cells strongly correlates with their response to KIN-193[3]. Further investigation on AZD6482 profile revealed that mutations in RB1, KRAS, NRAS and APC contributed in drug resistance. Changes in both AZD6482-sensitive and -resistant gene sets showed limited impact on prognosis. Western blotting showed AZD6482 did not induce changes in a panel of major downstream effectors of AKT, but substantially increased PMS2 level. AZD6482 also selectively inhibited migration, invasiveness, and colony formation of ccRCC cells with SETD2 mutations[4].

AZD 6482 细胞研究

细胞系 浓度 检测类型 检测时间 活动说明 数据源
human 639-V cell Growth inhibition assay Inhibition of human 639-V cell growth in a cell viability assay, IC50=1.63144 μM SANGER
human 786-0 cell Growth inhibition assay Inhibition of human 786-0 cell growth in a cell viability assay, IC50=1.31283 μM SANGER
human A427 cell Growth inhibition assay Inhibition of human A427 cell growth in a cell viability assay, IC50=0.99505 μM SANGER
human A498 cell Growth inhibition assay Inhibition of human A498 cell growth in a cell viability assay, IC50=0.11795 μM SANGER

AZD 6482 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT00853450 Antiplatelet Effect Phase 1 Completed - Sweden ... 展开 >> Research Site Lund, Sweden 收起 <<
NCT00688714 Antiplatelet Effect Phase 1 Completed - -

AZD 6482 参考文献

[1]Weigelt B, Warne PH, et al. PI3K pathway dependencies in endometrioid endometrial cancer cell lines. Clin Cancer Res. 2013 Jul 1;19(13):3533-44.

[2]Nylander S, Kull B, et al. Human target validation of phosphoinositide 3-kinase (PI3K)β: effects on platelets and insulin sensitivity, using AZD6482 a novel PI3Kβ inhibitor. J Thromb Haemost. 2012 Oct;10(10):2127-36.

[3]Jing Ni,et al. Functional characterization of an isoform-selective inhibitor of PI3K-p110β as a potential anticancer agent. Cancer Discov. 2012 May;2(5):425-33.

[4]Jun Wang,et al. High selectivity of PI3Kβ inhibitors in SETD2-mutated renal clear cell carcinoma. J BUON. Sep-Oct 2015;20(5):1267-75.

AZD 6482 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

2.45mL

0.49mL

0.24mL

12.24mL

2.45mL

1.22mL

24.48mL

4.90mL

2.45mL

AZD 6482 技术信息

CAS号1173900-33-8
分子式C22H24N4O4
分子量 408.45
别名 KIN-193
运输蓝冰
存储条件

液体 -20°C:3-6个月-80°C:12个月

粉末 Keep in dark place,Inert atmosphere,Store in freezer, under -20°C

溶解度

DMSO: 50 mg/mL(122.41 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

动物实验配方
Ambeed 相关网站 Ambeed.cn Ambeed.com
Ambeed
关于我们
联系我们
资讯中心
网站地图
产品手册
  • 批次文件查询
  • 客户支持
    技术支持
    专业术语
    缩略词释义
    质量手册
    产品咨询
    计算器
    活动政策
    订购方法
    积分商城
    活动声明
    联系我们
    400-920-2911 sales@ambeed.cn tech@ambeed.cn
    Ambeed 只为有资质的科研机构、医药企业基于科学研究或药证申报的用途提供医药研发服务,不为任何个人或者非科研性质用途提供服务。