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- TargetMol
- T3346
- 2026年07月07日
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- CAS号：
612847-09-3
- 规格：
1mLx10mM(inDMSO)/1mg/2mg/5mg/10mg/25mg/50mg/100mg
| 规格： | 1mLx10mM(inDMSO) | 产品价格： | ￥729.0 |
|---|---|---|---|
| 规格： | 1mg | 产品价格： | ￥274.0 |
| 规格： | 2mg | 产品价格： | ￥382.0 |
| 规格： | 5mg | 产品价格： | ￥642.0 |
| 规格： | 10mg | 产品价格： | ￥1040.0 |
| 规格： | 25mg | 产品价格： | ￥1824.0 |
| 规格： | 50mg | 产品价格： | ￥2728.0 |
| 规格： | 100mg | 产品价格： | ￥3880.0 |
Product Introduction
Bioactivity
| 名称 | AKT inhibitor VIII |
| 描述 | AKT inhibitor VIII (AKTi-1/2) is a highly specific Akt1/2 inhibitor (IC50: 58/210 nM). The selectivity for Akt1 is higher about 36-fold than Akt3. |
| 细胞实验 | The cell growth inhibitory effect of AKTi-1/2 is studied using the 96 h sulforhodamine B assay (SRB). Drug concentrations that inhibited 50% of cell growth (IC50) are calculated for each compound in GraphPad Prism 6.0 using non-linear regression analysis and sigmoidal dose–response (variable slope) equation.(Only for Reference) |
| 激酶实验 | Kinase screen: Briefly, all assays (25.5 μl at 21°C for 30 min) are performed using a Biomek 2000 Laboratory Automation Workstation in a 96-well format. Reactions contains 5–20 mU purified kinase along with substrate peptide or protein and are initiated by the addition of 10 mM MgAcetate and 5, 20, or 50 μM ATP ([γ-33P]-ATP, 800 cpm/pmol). |
| 体外活性 | Akti-1/2 (50 mg/kg,i.p.)抑制小鼠肺中基底和IGF-刺激的Akt1/2磷酸化作用. |
| 体内活性 | 在基于细胞的IPKA (C33A)试验中,AKT inhibitor VIII可抑制Akt1/2（IC50：305/2086 nM）。在MCF7,HT29和A2780细胞中,AKT inhibitor VIII可使caspase-3活性急剧增加从而诱导细胞凋亡。在肝细胞中,AKT inhibitor VIII可阻断胰岛素对PEPCK的调节,以及G6Pase表达和FOXO1活性。AKT inhibitor VIII通过阻断PKB还可使PAR-1-介导的血小板聚集显著增强。在HCC827,NCI-H522,NCI-1651和PC-9细胞中,AKT inhibitor VIII抑制细胞生长（IC50：4.7/7.25/9.5 μM）,AKT inhibitor VIII与gefitinib联用会增强对细胞生长和凋亡的抑制。 |
| 存储条件 | Powder: -20°C for 3 years | In solvent: -80°C for 1 year Shipping with blue ice/Shipping at ambient temperature. |
| 溶解度 | 10% DMSO+40% PEG300+5% Tween 80+45% Saline : 2 mg/mL (3.63 mM), Sonication is recommended. DMSO : 255 mg/mL (462.26 mM), Heating is recommended. |
| 关键字 | Protein kinase B | PKB | Inhibitor | inhibit | Apoptosis | Akt3 | Akt2 | Akt1 | AKT inhibitor VIII | Akt |
| 相关产品 | Formamide | Urea | Dimethyl phthalate | Aceglutamide | Alginic acid | Cysteamine hydrochloride | Metronidazole | Sildenafil citrate | Citric Acid Triammonium | Stavudine | Tamoxifen | Ethyl linoleate |
| 相关库 | Inhibitor Library | Bioactive Compound Library | Bioactive Compounds Library Max | Anti-Pancreatic Cancer Compound Library | Autophagy Compound Library | Kinase Inhibitor Library | Neural Regeneration Compound Library | Anti-Aging Compound Library | Highly Selective Inhibitor Library | Stem Cell Differentiation Compound Library | NO PAINS Compound Library | Immunology/Inflammation Compound Library |
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文献和实验化，只能说在在细胞凋亡途径中Akt参与，但不能说明Akt与细胞凋亡途径的上下游关系。 所有建议楼主使用Akt的inhibitor来证明最好。 以上是我个人一点想法，good luck! yuanyuan_626 rarazhuzhu wrote: 谈谈我的看法 楼主想要验证细胞凋亡途径中是否有Akt/PKB参与 首先要确认你的细胞在某种刺激
for the determination of mTOR inhibition by rapamycin and WYE-125132 in assays of recombinant mTOR enzyme, immunprecipitated native mTOR complexes, growth factor- and amino acid-induced cellular phosphorylation cascades as well as the PI3K/AKT/mTOR hyperactive breast
non-ATP competitive allosteric Akt inhibitor with IC50 of 8 nM,12 nM, 65 mM for Akt1, Akt2 and Akt3 respectively； The phase II clinical trials of MK-2206 against the treatment of endometrial cancer are recruiting participant Dana-Farber Cancer
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