Akt
信号通路图
研究领域
- 抑制剂选择性比较
- 溶解性比较
| 目录号 | 产品目录 | 溶解度(25°C) | ||
|---|---|---|---|---|
| 水 | DMSO | 酒精 | ||
| S1078 | MK-2206 2HCl | <1 mg/mL | 14 mg/mL | <1 mg/mL |
| S1037 | Perifosine (KRX-0401) | 8 mg/mL | <1 mg/mL | 15 mg/mL |
| S1113 | GSK690693 | <1 mg/mL | 39 mg/mL | <1 mg/mL |
| S2808 | Ipatasertib (GDC-0068) | <1 mg/mL | 92 mg/mL | 92 mg/mL |
| S8019 | AZD5363 | <1 mg/mL | 86 mg/mL | <1 mg/mL |
| S5313 | SC66 | -1 mg/mL | 55 mg/mL | -1 mg/mL |
| S2743 | PF-04691502 | <1 mg/mL | 14 mg/mL | <1 mg/mL |
| S1558 | AT7867 | <1 mg/mL | 68 mg/mL | 5 mg/mL |
| S1117 | Triciribine | <1 mg/mL | 64 mg/mL | <1 mg/mL |
| S2635 | CCT128930 | <1 mg/mL | 68 mg/mL | 6 mg/mL |
| S2670 | A-674563 | 72 mg/mL | 72 mg/mL | 18 mg/mL |
| S1556 | PHT-427 | <1 mg/mL | 82 mg/mL | 60 mg/mL |
| S3056 | Miltefosine | 81 mg/mL | <1 mg/mL | 81 mg/mL |
| S2310 | Honokiol | <1 mg/mL | 53 mg/mL | <1 mg/mL |
| S7127 | TIC10 Analogue | <1 mg/mL | 11 mg/mL | <1 mg/mL |
| S7492 | Uprosertib (GSK2141795) | <1 mg/mL | 85 mg/mL | 85 mg/mL |
| S7963 | TIC10 | <1 mg/mL | 77 mg/mL | 77 mg/mL |
| S7776 | Akti-1/2 | <1 mg/mL | 22 mg/mL | <1 mg/mL |
| S8339 | Miransertib (ARQ 092) HCl | <1 mg/mL | 75 mg/mL | 4 mg/mL |
| S7521 | Afuresertib (GSK2110183) | <1 mg/mL | 85 mg/mL | 85 mg/mL |
| S7563 | AT13148 | <1 mg/mL | 62 mg/mL | <1 mg/mL |
| S8132 | Deguelin | <1 mg/mL | 78 mg/mL | 78 mg/mL |
| S7863 | SC79 | <1 mg/mL | 72 mg/mL | 72 mg/mL |
特异性亚型抑制剂
- Akt抑制剂（23）
- 新Akt产品
| 产品目录 | 产品描述 | 文献引用 | 实验数据 |
|---|---|---|---|
| S1078 |
MK-2206 2HClMK-2206 2HCl是一种高度选择性的Akt1/2/3抑制剂，在无细胞试验中IC50分别为8 nM/12 nM/65 nM；对250种其他蛋白激酶没有抑制活性。Phase 2。 |
Inhibition of AKT signaling abolishes MKK4 phosphorylation on Ser78 in injured axons. Cultures of sensory neurons were treated with 5 µM MK-2206 or 5 µM GDC-0068 for 1 hr prior to axotomy. Axonal proteins harvested at indicated time points after axotomy were subjected to immunoblot analysis.
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| S1037 |
Perifosine (KRX-0401)Perifosine (KRX-0401)是一种新型的Akt抑制剂，在MM.1S细胞中IC50为4.7 μM，靶向作用于Akt的pleckstrin同源结构域。Phase 3。 |
Tumor growth of 827 GSC-derived xenografts
treated with an AKT inhibitor perifosine (30 mg/kg
body weight). Twenty-three days after tumor
implantation in mice, perifosine was administered
by intraperitoneal injection (daily for 5 days). Error
bars represent SD. Five mice per group, *p < 0.01.
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| S1113 |
GSK690693GSK690693是 一种泛Akt抑制剂，靶向作用于Akt1/2/3，在无细胞试验中IC50为2 nM/13 nM/9 nM，也对AGC激酶家族:PKA，PrkX和PKC同工酶敏感。Phase 1。 |
UPN cells were treated with GSK690693 or MK2206 (1 uM) for 1h followed by LPA (10 uM), EGF or IGF-1 (10 ng/ml) for another 1h and Western blot was performed. Band intensities of phospho-AKT (p-AKTS473), phospho-S6 (p-S6S240/S244), phospho-YB-1 (p-YB-1S102) and YB-1 were quantified and normalized to the intensity of ERK2. It directly determined the role of AKT using two potent, AKT inhibitors with distinct actions—a catalytic domain inhibitor, GSK690693, and an allosteric inhibitor, MK2206 -in UPN and SKOV3 cells, which showed appreciable AKT and YB-1 phosphorylation upon growth factor stimulation. GSK690693 increased basal and growth factor-induced AKT phosphorylation due to blocking a negative feedback loop downstream of AKT, whereas MK2206 abolished both basal and growth-factor-induced AKT phosphorylation.
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| S2808 |
Ipatasertib (GDC-0068)Ipatasertib (GDC-0068)是一种高选择性的pan-Akt抑制剂，靶向作用于Akt1/2/3，在无细胞试验中IC50为5 nM/18 nM/8 nM，比作用于PKA选择性高620倍。Phase 2。 |
-S280804W1120150906.gif)
-S280804W1120150906.gif)
Inhibition of AKT signaling abolishes MKK4 phosphorylation on Ser78 in injured axons. Cultures of sensory neurons were treated with 5 µM MK-2206 or 5 µM GDC-0068 for 1 hr prior to axotomy. Axonal proteins harvested at indicated time points after axotomy were subjected to immunoblot analysis.
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| S8019 |
AZD5363AZD5363有效抑制Akt(Akt1/Akt2/3)的所有亚型，在无细胞试验中IC50为3 nM/8 nM/8 nM，对P70S6K/PKA也具有相似的抑制效果，而对ROCK1/2抑制活性较低。Phase 2。 |
G-H. Analysis of cells treated with AZD5363 (500 nM) for 24 hrs. G.Western analysis of whole cell lysates. H. Cells labeled with Annexin V-FITC for 6h were imaged. Individual points are average for replicates assessed in duplicate. Midlines are the average ± S.D. Student’s T-test.
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| S5313New |
SC66SC66 is an allosteric inhibitor which displays a dual-inhibitory function toward AKT activity with IC50 values of 0.77, 2.85 and 0.47 μg/ml in HepG2, Huh7 and Hep3B cells after 72 h treatment, respectively. |
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| S2743 |
PF-04691502PF-04691502是一种ATP竞争性的PI3K(α/β/δ/γ)/mTOR双重抑制剂，在无细胞试验中Ki为1.8 nM/2.1 nM/1.6 nM/1.9 nM和16 nM，对Vps34， AKT， PDK1， p70S6K， MEK， ERK， p38 和 JNK 几乎没有作用活性。Phase 2。 |
BMDMs from WT animals were treated with different concentrations of PI3K inhibitors (500 nmol/L PF4691502, PI-103, BKM120 and 25 μmol/L SF1126) followed by hypoxia for 4 hours for Western blots. These macrophages were either used for lysate preparation (nuclear extracts for HIFα or WCE for pAKT and AKT) and Western blot analysis.
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| S1558 |
AT7867AT7867是一种有效的，ATP竞争性的Akt1/2/3和p70S6K/PKA抑制剂，无细胞试验中IC50分别为32 nM/17 n/47 nM和85 nM/20 nM，对AGC激酶家族以外几乎没有抑制活性。 |
(B) Treatment of HEK293T cells with the AKT inhibitors MK2206 or AT7867 abolished EGF (20 ng, 15 min)-induced binding of AKT and pT308AKT to CNK1 and also their residual interaction found in non-stimulated cells.
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| S1117 |
TriciribineTriciribine是一种DNA synthesis抑制剂，也抑制PC3细胞系中的Akt和CEM-SS，H9，H9IIIB，U1细胞中的HIV-1，IC50分别为130 nM和20 nM；对PI3K/PDK1没有抑制作用；作用于缺乏腺苷激酶的细胞，活性降低5000倍。Phase 1/2。 |
Effects of FAK A., PI3K B. or Akt C. inhibition in D-Hep2/AURKA cells on dormancy-related protein expression as analyzed by western blotting. P130 and E2F4 levels were increased, while P107 and Ki67 were decreased. Dormancy-related protein ratio in D-Hep2/AURKA cells treated with TAE226 D., Omipalisib E. or Triciribine F.
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| S2635 |
CCT128930CCT128930是一种有效的，ATP竞争性的，选择性Akt2抑制剂，无细胞试验中IC50为6 nM，作用于Akt2比作用于紧密相关的PKA激酶选择性高28倍。 |
Western blot analysis of pPRAS40 (T246), pS6 (S240/S244), and pS6 (S235/S236) proteins in (A) HeyA8 cells and (B) SKOV3 cells treated with 3.33 μM or 10 μM inhibitors (BX795 or CCT128930) in three-dimensional cell culture for 25 hours. Ten percent fetal b
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| S2670 |
A-674563A-674563是一种Akt抑制剂，在无细胞试验中Ki为11 nM，对PKA适度有效，作用于Akt1比作用于PKC选择性高30多倍。 |
Cell survival was determined using a WST-1 assay in the human lung cancer cells A549 A. and NCI-H358 B. following treatment with either an AKT1 specific inhibitor, A-674563 (black circle and line) or a pan-AKT inhibitor MK-2206 (gray square and line). *p < 0.05.
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| S1556 |
PHT-427PHT-427是作用于Akt和PDPK1的双重抑制剂，对Akt和PDPK1的PH结构域具有高度亲和力，Ki分别为2.7 μM和5.2 μM。 |
Luciferase reporter assays. 32D/BCR-ABL cells transfected with the reporter construct containing 1548 bp of the Atf5 promoter were treated with either DMSO, imatinib (5 μM for 24 hours), LY294002 (20 μM for 48 hours), PHT-427 (20 μM for 24 hours), or JAK inhibitor I (10 μM for 24 hours). Error bars represent SD. |
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| S3056 |
MiltefosineMiltefosine作用于癌细胞系A431和HeLa，抑制PI3K/Akt活性，ED50分别为17.2 μM和8.1 μM，是第一个用于治疗内脏利什曼病的口服药物，有效对抗前鞭毛体和无鞭毛体。 |
Effects of a miltefosine co-treatment with celecoxib on steatohepatitis, hepatocyte apoptosis, Akt activation and p53 expression in the liver of MCD-diet fed mice. Mice were fed the control diet, an MCD diet, an MCD diet with celecoxib (20 mg/kg/day) treatment, or an MCD diet co-treatment with celecoxib and miltefosine (50 mg/kg/day) for 3 weeks. (C) TUNEL-stained sections of liver samples are representative of the indicated groups (magnification×400). Abbreviations: MCD, methionine and choline deficient; CON, control; CEL, celecoxib; MTF, miltefosine. |
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| S2310 |
HonokiolHonokiol是木兰的有效成分，抑制Akt磷酸化，且促进ERK1/2磷酸化。Phase 3。 |
(B) Cleaved PARP, Bax and Bcl2 protein expression was evaluated by immunoblotting of KRAS mutant cells lysates after 48 h of honokiol (10, 20, 40, and 60 μM) treatment. ∗∗P < 0.01 and ∗∗∗P < 0.001 for comparison between control group and honokiol-treated group. |
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| S7127 |
TIC10 AnalogueTIC10 Analogue是一种TIC10的类似物，其抑制Akt和ERK活性，通过FoxO3a诱导TRAIL，具有优越的耐药性，可以穿透血脑屏障，具有超强的稳定性，和改善的药代动力学。Phase 1/2。 |
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| S7492 |
Uprosertib (GSK2141795)Uprosertib (GSK2141795)是一种选择性的，ATP竞争性的，具有口服活性的Akt抑制剂，其对Akt 1/2/3的 IC50分别为180 nM, 328 nM和38 nM。Phase 2。 |
Parental cell line wastreated with Akt inhibitor (GSK2141795) and BGJ398. The 5 uM BGJ398 resistant cell line was treated with GSK2141795, BGJ398, and 2 concentrations of GSK2141795 and varying dosages of BGJ398. The parental cell line treated with GSK2141795, the dark green line, indicates minimal effect of the inhibitor compared to the resistant cell line treated GSK2141795, the light purple line.
However, when the resistant cell line is treated with both GSK2141795 and BGJ398 there is a greater decrease in cell viability compared to the resistant cell line that is treated only with GSK2141795.
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| S7963 |
TIC10TIC10抑制Akt和ERK活性，通过FoxO3a诱导TRAIL，具有优越的耐药性，可以穿透血脑屏障，具有超强的稳定性，和改善的药代动力学性能。Phase 1/2。 |
Established HCC cell lines, HepG2 (A-C) and Huh-7 (D), primary human HCC cells (D, "Pri_1/Pri _2"), as well as HL-7702 human hepatocytes (D) and primary human adult hepatocytes ("Hepatocytes", D), were either left untreated ("C", same for all figures), or treated with applied concentration of TIC10 (0.1-30 μM), cells were then cultured in conditional medium for applied time; Cell proliferation was tested by MTT assay (A and D), clonogenicity assay (B) and [H3] Thymidine incorporation assay (C). Experiments in this figure were repeated for five times, with similar results obtained. n = 5 for each repeat. Bars stand for mean ± SD. *p < 0.05 vs. group "C".
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| S7776 |
Akti-1/2Akti-1/2是高度选择性的Akt1/Akt2抑制剂，IC50分别为58 nM/210 nM，对Akt1的选择性比对Akt3高36倍。 |
AKTi-1/2 inhibits human HCC cells in vitro. Human HCC HepG2 cells (A–F), Huh-7 cells (G), primary human HCC cells (“Pri HCC”, G) or the primary liver cells (“Pri liver cells”, G) were treated with/out applied concentrations of AKTi-1/2 for indicated time; Cell survival (A, B and G), proliferation (C and D) and apoptosis (E and F) were tested by the listed assays. Data were shown as the mean (n = 5) with the standard deviation (SD). Experiments in this figure were repeated three times, with similar results were obtained. *P < 0.05 vs. “C” (untreated control) group.
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| S8339 |
Miransertib (ARQ 092) HClARQ 092是新型的、具有口服生物活性的、选择性的AKT抑制剂，在晚期实体肿瘤中具有较好的、可调控的安全性。 |
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| S7521 |
Afuresertib (GSK2110183)Afuresertib (GSK2110183)是一种有效的，口服生物可利用的 Akt 抑制剂，对Akt1，Akt2，和 Akt3 的 Ki 分别为 0.08 nM，2 nM，和 2.6 nM。Phase 2。 |
Analysis of the mechanism of action of the enhanced anti‑tumor effect of the combination therapy of suboptimal doses of pomalidomide plus dexamethasone and afuresertib in MM cells. (A‑C) The altered expression of protein substrates was analyzed in two MM cell lines that were treated with suboptimal doses of PD, or AFU, or the PD and AFU combination. The XG‑7 and U266 cell lines were subjected to the indicated treatments for 48 and 72 h, respectively. (A) Caspases, (B) substrates related mainly to the working mechanism of IMiDs, (C) substrates mainly related to the working mechanism of afuresertib, and (D) two primary MM cell cultures, were subjected to the analysis in the same manner as the two MM cell lines. In the expression panel of p‑FoxO3a/FoxO1, the upper band represents p‑FoxO3a and the lower band represents p‑FOXO1. PD, pomalidomide plus dexamethasone; AFU, Afuresertib; MM, multiple myeloma; IMiDs, immunomodulatory drugs.
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| S7563 |
AT13148AT13148是一种口服的，ATP竞争性的，多AGC kinase抑制剂，对Akt1/2/3，p70S6K，PKA，和ROCKI/II的IC50分别为38 nM/402 nM/50 nM，8 nM，3 nM，和6 nM/4 nM。Phase 1。 |
AT13148 exerts cytotoxic and anti-proliferative activity against human gastric cancer cells. Human gastric cancer cells (HGC-27, AGS, SNU-601, N87 and MKN-28 lines) or GEC-1 gastric epithelial cells were treated with applied concentration of AT13148 for indicated time, cell survival (A and E), cell proliferation (B and F), cell cycle distribution (C, for HGC-27 cells) and cell death (D, for HGC-27 cells) were tested by the described assays, separately. Data were presented as mean ± SD. “Ctrl” stands for untreated control cells (For all figures). “hr/hrs” stands for hour/hours (For all figures). Experiments in this figure were repeated for five times. *p < 0.05 vs. “Ctrl” group.
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| S8132 |
DeguelinDeguelin，一种从植物中分离出来的天然产物，是PI3K/Akt的抑制剂。 |
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| S7863 |
SC79SC79是一种大脑渗透性Akt磷酸化激活剂，也是一种Akt-PH域易位抑制剂。 |
The molecular structure along with the molecular weight (MW) of SC79 were presented (A). ARPE-19 cells were treated with applied concentration of SC79 (0.1–10 μg/mL, or 2.74–27.41 μM) for 1 h, p-Akt (Ser-473) and Akt1 expression was tested by Western blots and was quantified (B) n = 4). ARPE-19 cells (C and D) primary murine RPE cells ("Primary RPE", (E)) or HLECs (F) pretreated with applied concentration of SC79 for 30 min, were subjected to UV radiation (30 mJ/cm2), cells were further cultured for 24 h, and cell viability was tested by MTT assay (C, E and F); Cell death was detected by trypan blue staining assay (D). "Ctrl" stands for untreated control group (Same for all figures). For each assay, n = 5. Experiments in this figure were repeated three times to insure consistency of results. *p < 0.05 vs. “Ctrl” group (C–F). **p < 0.05 vs. UV only group (C-F).
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