标签归档：akt

PI3K/AKT-IN-1

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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

PI3K/AKT-IN-1 

PI3K/AKT-IN-1 是一种有效的 PI3K/AKT 双重抑制剂 (PI3Kγ、PI3Kδ 和 AKT 的 IC50分别为 6.99 μM、4.01 μM 和 3.36 μM)。PI3K/AKT-IN-1 具有抗癌活性，其作用机制是抑制 PI3K/AKT 通路，诱导 caspase 3 依赖性凋亡 (apoptosis)。

PI3K/AKT-IN-1

PI3K/AKT-IN-1 Chemical Structure

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

PI3K/AKT-IN-1 is an effective PI3K/AKT dual inhibitor (IC50 of 6.99, 4.01 and 3.36 μM for PI3Kγ, PI3Kδ and AKT, respectively). PI3K/AKT-IN-1 has anticancer activity and acts by inhibiting PI3K/AKT axis and inducing caspase 3 dependent apoptosis[1].

IC50 & Target[1]

PI3Kγ

6.99 μM (IC50)

PI3Kδ

4.01 μM (IC50)

Akt

3.36 μM (IC50)

体外研究
(In Vitro)

PI3K/AKT-IN-1 (compound 7f) (0.04-100 µM; 48 hours) has high cytotoxic activity on both cell lines with better activity on leukaemia cell line (K562 IC50=2.62 µM) than on the breast cancer cell line (MCF-7 IC50=3.22 µM)[1].
PI3K/AKT-IN-1 (2.62 µM) can promote S-phase cell cycle arrest and apoptosis induction in K562 cells[1].
PI3K/AKT-IN-1 (2.62 µM; 48 hours) causes an increase in the percentage of Annexin-V positive apoptotic cells both in the early and late stage[1].
PI3K/AKT-IN-1 (2.62 µM; 48 hours) markedly reduces the expression of PI3K, AKT, Cyclin D1 and NF-κB[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay

Cell Line: MCF-7 and K562 cells[1]
Concentration: 0.04-100 µM
Incubation Time: 48 hours
Result: Demonstrated high cytotoxic activity on both cell lines with better activity on leukaemia cell line (K562 IC50=2.62 µM) than on the breast cancer cell line (MCF-7 IC50=3.22 µM).

Cell Cycle Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time:
Result: Promoted S-phase cell cycle arrest and apoptosis induction.

Apoptosis Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time: 48 hours
Result: Caused an increase in the percentage of Annexin-V positive apoptotic cells both in the early and late stage.

Western Blot Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time: 48 hours
Result: Markedly reduced the expression of PI3K, p-PI3K, AKT, p-AKT, Cyclin D1 and NF-κB.

体内研究
(In Vivo)

PI3K/AKT-IN-1 (2000 mg/kg; p.o.; single) is non-toxic and is well tolerated by experimental animals[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female rats (180-200g)[1]
Dosage: 2000 mg/kg
Administration: p.o.; single
Result: The median lethal dose (LD50) was greater than the test dose (2000 mg/kg).

分子量

467.54

Formula

C23H25N5O4S
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. El-Dydamony NM, et al. Pyrimidine-5-carbonitrile based potential anticancer agents as apoptosis inducers through PI3K/AKT axis inhibition in leukaemia K562. J Enzyme Inhib Med Chem. 2022;37(1):895-911.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

PI3K/AKT-IN-1

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

PI3K/AKT-IN-1 

PI3K/AKT-IN-1 是一种有效的 PI3K/AKT 双重抑制剂 (PI3Kγ、PI3Kδ 和 AKT 的 IC50分别为 6.99 μM、4.01 μM 和 3.36 μM)。PI3K/AKT-IN-1 具有抗癌活性，其作用机制是抑制 PI3K/AKT 通路，诱导 caspase 3 依赖性凋亡 (apoptosis)。

PI3K/AKT-IN-1

PI3K/AKT-IN-1 Chemical Structure

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

PI3K/AKT-IN-1 is an effective PI3K/AKT dual inhibitor (IC50 of 6.99, 4.01 and 3.36 μM for PI3Kγ, PI3Kδ and AKT, respectively). PI3K/AKT-IN-1 has anticancer activity and acts by inhibiting PI3K/AKT axis and inducing caspase 3 dependent apoptosis[1].

IC50 & Target[1]

PI3Kγ

6.99 μM (IC50)

PI3Kδ

4.01 μM (IC50)

Akt

3.36 μM (IC50)

体外研究
(In Vitro)

PI3K/AKT-IN-1 (compound 7f) (0.04-100 µM; 48 hours) has high cytotoxic activity on both cell lines with better activity on leukaemia cell line (K562 IC50=2.62 µM) than on the breast cancer cell line (MCF-7 IC50=3.22 µM)[1].
PI3K/AKT-IN-1 (2.62 µM) can promote S-phase cell cycle arrest and apoptosis induction in K562 cells[1].
PI3K/AKT-IN-1 (2.62 µM; 48 hours) causes an increase in the percentage of Annexin-V positive apoptotic cells both in the early and late stage[1].
PI3K/AKT-IN-1 (2.62 µM; 48 hours) markedly reduces the expression of PI3K, AKT, Cyclin D1 and NF-κB[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay

Cell Line: MCF-7 and K562 cells[1]
Concentration: 0.04-100 µM
Incubation Time: 48 hours
Result: Demonstrated high cytotoxic activity on both cell lines with better activity on leukaemia cell line (K562 IC50=2.62 µM) than on the breast cancer cell line (MCF-7 IC50=3.22 µM).

Cell Cycle Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time:
Result: Promoted S-phase cell cycle arrest and apoptosis induction.

Apoptosis Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time: 48 hours
Result: Caused an increase in the percentage of Annexin-V positive apoptotic cells both in the early and late stage.

Western Blot Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time: 48 hours
Result: Markedly reduced the expression of PI3K, p-PI3K, AKT, p-AKT, Cyclin D1 and NF-κB.

体内研究
(In Vivo)

PI3K/AKT-IN-1 (2000 mg/kg; p.o.; single) is non-toxic and is well tolerated by experimental animals[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female rats (180-200g)[1]
Dosage: 2000 mg/kg
Administration: p.o.; single
Result: The median lethal dose (LD50) was greater than the test dose (2000 mg/kg).

分子量

467.54

Formula

C23H25N5O4S
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. El-Dydamony NM, et al. Pyrimidine-5-carbonitrile based potential anticancer agents as apoptosis inducers through PI3K/AKT axis inhibition in leukaemia K562. J Enzyme Inhib Med Chem. 2022;37(1):895-911.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

PI3K/AKT-IN-1

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

PI3K/AKT-IN-1 

PI3K/AKT-IN-1 是一种有效的 PI3K/AKT 双重抑制剂 (PI3Kγ、PI3Kδ 和 AKT 的 IC50分别为 6.99 μM、4.01 μM 和 3.36 μM)。PI3K/AKT-IN-1 具有抗癌活性，其作用机制是抑制 PI3K/AKT 通路，诱导 caspase 3 依赖性凋亡 (apoptosis)。

PI3K/AKT-IN-1

PI3K/AKT-IN-1 Chemical Structure

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

PI3K/AKT-IN-1 is an effective PI3K/AKT dual inhibitor (IC50 of 6.99, 4.01 and 3.36 μM for PI3Kγ, PI3Kδ and AKT, respectively). PI3K/AKT-IN-1 has anticancer activity and acts by inhibiting PI3K/AKT axis and inducing caspase 3 dependent apoptosis[1].

IC50 & Target[1]

PI3Kγ

6.99 μM (IC50)

PI3Kδ

4.01 μM (IC50)

Akt

3.36 μM (IC50)

体外研究
(In Vitro)

PI3K/AKT-IN-1 (compound 7f) (0.04-100 µM; 48 hours) has high cytotoxic activity on both cell lines with better activity on leukaemia cell line (K562 IC50=2.62 µM) than on the breast cancer cell line (MCF-7 IC50=3.22 µM)[1].
PI3K/AKT-IN-1 (2.62 µM) can promote S-phase cell cycle arrest and apoptosis induction in K562 cells[1].
PI3K/AKT-IN-1 (2.62 µM; 48 hours) causes an increase in the percentage of Annexin-V positive apoptotic cells both in the early and late stage[1].
PI3K/AKT-IN-1 (2.62 µM; 48 hours) markedly reduces the expression of PI3K, AKT, Cyclin D1 and NF-κB[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay

Cell Line: MCF-7 and K562 cells[1]
Concentration: 0.04-100 µM
Incubation Time: 48 hours
Result: Demonstrated high cytotoxic activity on both cell lines with better activity on leukaemia cell line (K562 IC50=2.62 µM) than on the breast cancer cell line (MCF-7 IC50=3.22 µM).

Cell Cycle Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time:
Result: Promoted S-phase cell cycle arrest and apoptosis induction.

Apoptosis Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time: 48 hours
Result: Caused an increase in the percentage of Annexin-V positive apoptotic cells both in the early and late stage.

Western Blot Analysis

Cell Line: K562 cells[1]
Concentration: 2.62 µM
Incubation Time: 48 hours
Result: Markedly reduced the expression of PI3K, p-PI3K, AKT, p-AKT, Cyclin D1 and NF-κB.

体内研究
(In Vivo)

PI3K/AKT-IN-1 (2000 mg/kg; p.o.; single) is non-toxic and is well tolerated by experimental animals[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female rats (180-200g)[1]
Dosage: 2000 mg/kg
Administration: p.o.; single
Result: The median lethal dose (LD50) was greater than the test dose (2000 mg/kg).

分子量

467.54

Formula

C23H25N5O4S
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. El-Dydamony NM, et al. Pyrimidine-5-carbonitrile based potential anticancer agents as apoptosis inducers through PI3K/AKT axis inhibition in leukaemia K562. J Enzyme Inhib Med Chem. 2022;37(1):895-911.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

MS143

发表于由
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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

MS143 

MS143 是一种有效的 AKT 降解剂，在 PC3 细胞中 DC50=46 nM，GI50=0.8 µM。MS143 通过劫持泛素-蛋白酶体系统，以浓度和时间依赖性的方式诱导快速、稳定的 AKT 降解。MS143 能抑制癌细胞生长。

MS143

MS143 Chemical Structure

CAS No. : 2376137-41-4

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

MS143 is a potent AKT degrader (DC50=46 nM and GI50=0.8 µM in PC3 cells). MS143 induces rapid and robust AKT degradation in a concentration- and time-dependent manner via hijacking the ubiquitin-proteasome system. MS143 can suppress cancer cell growth[1].

IC50 & Target

AKT
体外研究
(In Vitro)

MS143 (1 nM-10 μM; 24 hours) induces T-AKT degradation with a concentration-dependent manner in PC3 cells[1].
MS143 (0.1-10 µM;14 days, replenish every 2 days) effectively inhibits colony formation in BT474 cells[1].
MS143 (1 µM; 24 hours) promotes AKT degradation in an E3 ligase- and UPS-dependent manner[1].
MS143 (1 nM-10 µM) can inhibit the cell growth of PC3 cells (GI50=0.8 nM) and MDA-MB-468 cells (GI50=1.0 nM)[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay

Cell Line: PC3 cells and MDA-MB-468 cells[1]
Concentration: 1 nM, 10 nM, 100 nM, 1 μM, 10 μM
Incubation Time: 5 days
Result: Inhibited the cell growth of PC3 cells (GI50=0.8 nM) and MDA-MB-468 cells (GI50=1.0 nM).

Western Blot Analysis

Cell Line: PC3 cells[1]
Concentration: 1 μM
Incubation Time: 24 hours
Result: Promoted AKT degradation in an E3 ligase- and UPS-dependent manner.

体内研究
(In Vivo)

MS143 (75 mg/kg; i.p., 22 days) drastically inhibits the tumor growth by 92%, also substantially degrades T-AKT and P-AKT, and effectively inhibits the downstream signaling (PRAS40 phosphorylation) in xenograft mice[1].
Pharmacokinetic Parameters of MS143 in male Swiss Albino mice[1].

IP (75 mg/kg)
Cmax (μM) 7
Tmax (h) 2
AUC0-12 (h·ng/mL) 63600

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male immunocompromised NU/J mice (6 weeks old)[1]
Dosage: 75 mg/kg
Administration: i.p., 22 days
Result: Drastically inhibited the tumor growth by 92%, also substantially degraded T-AKT and P-AKT, and effectively inhibited the downstream signaling (PRAS40 phosphorylation).

分子量

1121.87

Formula

C59H81ClN12O6S
CAS 号

2376137-41-4
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Yu X, et al. Discovery of Potent, Selective, and In Vivo Efficacious AKT Kinase Protein Degraders via Structure-Activity Relationship Studies. J Med Chem. 2022;65(4):3644-3666.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

MS143

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

MS143 

MS143 是一种有效的 AKT 降解剂，在 PC3 细胞中 DC50=46 nM，GI50=0.8 µM。MS143 通过劫持泛素-蛋白酶体系统，以浓度和时间依赖性的方式诱导快速、稳定的 AKT 降解。MS143 能抑制癌细胞生长。

MS143

MS143 Chemical Structure

CAS No. : 2376137-41-4

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

MS143 is a potent AKT degrader (DC50=46 nM and GI50=0.8 µM in PC3 cells). MS143 induces rapid and robust AKT degradation in a concentration- and time-dependent manner via hijacking the ubiquitin-proteasome system. MS143 can suppress cancer cell growth[1].

IC50 & Target

AKT
体外研究
(In Vitro)

MS143 (1 nM-10 μM; 24 hours) induces T-AKT degradation with a concentration-dependent manner in PC3 cells[1].
MS143 (0.1-10 µM;14 days, replenish every 2 days) effectively inhibits colony formation in BT474 cells[1].
MS143 (1 µM; 24 hours) promotes AKT degradation in an E3 ligase- and UPS-dependent manner[1].
MS143 (1 nM-10 µM) can inhibit the cell growth of PC3 cells (GI50=0.8 nM) and MDA-MB-468 cells (GI50=1.0 nM)[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay

Cell Line: PC3 cells and MDA-MB-468 cells[1]
Concentration: 1 nM, 10 nM, 100 nM, 1 μM, 10 μM
Incubation Time: 5 days
Result: Inhibited the cell growth of PC3 cells (GI50=0.8 nM) and MDA-MB-468 cells (GI50=1.0 nM).

Western Blot Analysis

Cell Line: PC3 cells[1]
Concentration: 1 μM
Incubation Time: 24 hours
Result: Promoted AKT degradation in an E3 ligase- and UPS-dependent manner.

体内研究
(In Vivo)

MS143 (75 mg/kg; i.p., 22 days) drastically inhibits the tumor growth by 92%, also substantially degrades T-AKT and P-AKT, and effectively inhibits the downstream signaling (PRAS40 phosphorylation) in xenograft mice[1].
Pharmacokinetic Parameters of MS143 in male Swiss Albino mice[1].

IP (75 mg/kg)
Cmax (μM) 7
Tmax (h) 2
AUC0-12 (h·ng/mL) 63600

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male immunocompromised NU/J mice (6 weeks old)[1]
Dosage: 75 mg/kg
Administration: i.p., 22 days
Result: Drastically inhibited the tumor growth by 92%, also substantially degraded T-AKT and P-AKT, and effectively inhibited the downstream signaling (PRAS40 phosphorylation).

分子量

1121.87

Formula

C59H81ClN12O6S
CAS 号

2376137-41-4
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Yu X, et al. Discovery of Potent, Selective, and In Vivo Efficacious AKT Kinase Protein Degraders via Structure-Activity Relationship Studies. J Med Chem. 2022;65(4):3644-3666.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

MS143

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

MS143 

MS143 是一种有效的 AKT 降解剂，在 PC3 细胞中 DC50=46 nM，GI50=0.8 µM。MS143 通过劫持泛素-蛋白酶体系统，以浓度和时间依赖性的方式诱导快速、稳定的 AKT 降解。MS143 能抑制癌细胞生长。

MS143

MS143 Chemical Structure

CAS No. : 2376137-41-4

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

MS143 is a potent AKT degrader (DC50=46 nM and GI50=0.8 µM in PC3 cells). MS143 induces rapid and robust AKT degradation in a concentration- and time-dependent manner via hijacking the ubiquitin-proteasome system. MS143 can suppress cancer cell growth[1].

IC50 & Target

AKT
体外研究
(In Vitro)

MS143 (1 nM-10 μM; 24 hours) induces T-AKT degradation with a concentration-dependent manner in PC3 cells[1].
MS143 (0.1-10 µM;14 days, replenish every 2 days) effectively inhibits colony formation in BT474 cells[1].
MS143 (1 µM; 24 hours) promotes AKT degradation in an E3 ligase- and UPS-dependent manner[1].
MS143 (1 nM-10 µM) can inhibit the cell growth of PC3 cells (GI50=0.8 nM) and MDA-MB-468 cells (GI50=1.0 nM)[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay

Cell Line: PC3 cells and MDA-MB-468 cells[1]
Concentration: 1 nM, 10 nM, 100 nM, 1 μM, 10 μM
Incubation Time: 5 days
Result: Inhibited the cell growth of PC3 cells (GI50=0.8 nM) and MDA-MB-468 cells (GI50=1.0 nM).

Western Blot Analysis

Cell Line: PC3 cells[1]
Concentration: 1 μM
Incubation Time: 24 hours
Result: Promoted AKT degradation in an E3 ligase- and UPS-dependent manner.

体内研究
(In Vivo)

MS143 (75 mg/kg; i.p., 22 days) drastically inhibits the tumor growth by 92%, also substantially degrades T-AKT and P-AKT, and effectively inhibits the downstream signaling (PRAS40 phosphorylation) in xenograft mice[1].
Pharmacokinetic Parameters of MS143 in male Swiss Albino mice[1].

IP (75 mg/kg)
Cmax (μM) 7
Tmax (h) 2
AUC0-12 (h·ng/mL) 63600

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male immunocompromised NU/J mice (6 weeks old)[1]
Dosage: 75 mg/kg
Administration: i.p., 22 days
Result: Drastically inhibited the tumor growth by 92%, also substantially degraded T-AKT and P-AKT, and effectively inhibited the downstream signaling (PRAS40 phosphorylation).

分子量

1121.87

Formula

C59H81ClN12O6S
CAS 号

2376137-41-4
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Yu X, et al. Discovery of Potent, Selective, and In Vivo Efficacious AKT Kinase Protein Degraders via Structure-Activity Relationship Studies. J Med Chem. 2022;65(4):3644-3666.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

AKT-IN-8

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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

AKT-IN-8 

AKT-IN-8 是一种有效的 AKT 抑制剂，对 AKT1、AKT2 和 AKT3 的IC50 分别为 4.46、2.44 和 9.47 nM。

AKT-IN-8

AKT-IN-8 Chemical Structure

CAS No. : 2654026-13-6

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

AKT-IN-8 is a potent AKT inhibitor with IC50s of 4.46, 2.44, and 9.47 nM for AKT1, AKT2, and AKT3, respectively[1].

IC50 & Target[1]

Akt1

4.46 nM (IC50)

Akt2

2.44 nM (IC50)

Akt3

9.47 nM (IC50)

分子量

456.93

Formula

C22H25ClN6O3
CAS 号

2654026-13-6
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Fused tetracyclic derivative, preparation method therefor, and medical use thereof. WO2021121276A1.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

AKT-IN-7

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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

AKT-IN-7 

AKT-IN-7 (compound 1-P1) 是一种有效的 AKT 抑制剂。AKT-IN-7 具有用于癌症研究的潜力。

AKT-IN-7

AKT-IN-7 Chemical Structure

CAS No. : 2654025-97-3

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

AKT-IN-7 (compound 1-P1) is a potent AKT inhibitor. AKT-IN-7 has the potential for cancer research[1].

IC50 & Target[1]

Akt

 

分子量

454.95

Formula

C23H27ClN6O2
CAS 号

2654025-97-3
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Xin Li, et al. Fused tetracyclic derivatives, their preparation method and their application in medicine. WO2021121276A1.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

AKT-IN-8

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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

AKT-IN-8 

AKT-IN-8 是一种有效的 AKT 抑制剂，对 AKT1、AKT2 和 AKT3 的IC50 分别为 4.46、2.44 和 9.47 nM。

AKT-IN-8

AKT-IN-8 Chemical Structure

CAS No. : 2654026-13-6

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

AKT-IN-8 is a potent AKT inhibitor with IC50s of 4.46, 2.44, and 9.47 nM for AKT1, AKT2, and AKT3, respectively[1].

IC50 & Target[1]

Akt1

4.46 nM (IC50)

Akt2

2.44 nM (IC50)

Akt3

9.47 nM (IC50)

分子量

456.93

Formula

C22H25ClN6O3
CAS 号

2654026-13-6
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Fused tetracyclic derivative, preparation method therefor, and medical use thereof. WO2021121276A1.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

AKT-IN-7

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

AKT-IN-7 

AKT-IN-7 (compound 1-P1) 是一种有效的 AKT 抑制剂。AKT-IN-7 具有用于癌症研究的潜力。

AKT-IN-7

AKT-IN-7 Chemical Structure

CAS No. : 2654025-97-3

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

AKT-IN-7 (compound 1-P1) is a potent AKT inhibitor. AKT-IN-7 has the potential for cancer research[1].

IC50 & Target[1]

Akt

 

分子量

454.95

Formula

C23H27ClN6O2
CAS 号

2654025-97-3
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Xin Li, et al. Fused tetracyclic derivatives, their preparation method and their application in medicine. WO2021121276A1.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

AKT-IN-8

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

AKT-IN-8 

AKT-IN-8 是一种有效的 AKT 抑制剂，对 AKT1、AKT2 和 AKT3 的IC50 分别为 4.46、2.44 和 9.47 nM。

AKT-IN-8

AKT-IN-8 Chemical Structure

CAS No. : 2654026-13-6

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

AKT-IN-8 is a potent AKT inhibitor with IC50s of 4.46, 2.44, and 9.47 nM for AKT1, AKT2, and AKT3, respectively[1].

IC50 & Target[1]

Akt1

4.46 nM (IC50)

Akt2

2.44 nM (IC50)

Akt3

9.47 nM (IC50)

分子量

456.93

Formula

C22H25ClN6O3
CAS 号

2654026-13-6
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Fused tetracyclic derivative, preparation method therefor, and medical use thereof. WO2021121276A1.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

AKT-IN-7

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

AKT-IN-7 

AKT-IN-7 (compound 1-P1) 是一种有效的 AKT 抑制剂。AKT-IN-7 具有用于癌症研究的潜力。

AKT-IN-7

AKT-IN-7 Chemical Structure

CAS No. : 2654025-97-3

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

AKT-IN-7 (compound 1-P1) is a potent AKT inhibitor. AKT-IN-7 has the potential for cancer research[1].

IC50 & Target[1]

Akt

 

分子量

454.95

Formula

C23H27ClN6O2
CAS 号

2654025-97-3
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Xin Li, et al. Fused tetracyclic derivatives, their preparation method and their application in medicine. WO2021121276A1.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

PI3K/Akt/mTOR-IN-2

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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

PI3K/Akt/mTOR-IN-2 

PI3K/Akt/mTOR-IN-2 是一种有效的 PI3K/AKT/mTOR 抑制剂。PI3K/Akt/mTOR-IN-2 具有抗癌作用，并对 MDA-MB-231 细胞具有选择性，IC50 为 2.29 μM。PI3K/Akt/mTOR-IN-2 可诱导癌细胞周期阻滞和细胞凋亡 (apoptosis)。

PI3K/Akt/mTOR-IN-2

PI3K/Akt/mTOR-IN-2 Chemical Structure

CAS No. : 2757804-89-8

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

PI3K/Akt/mTOR-IN-2 is a PI3K/AKT/mTOR pathway inhibitor. PI3K/Akt/mTOR-IN-2 possess anti-cancer effects and selectivity against MDA-MB-231 cells with IC50 value of 2.29 μM. PI3K/Akt/mTOR-IN-2 can induce cancer cell cycle arrest and apoptosis[1].

IC50 & Target

IC50: 2.29 μM (PI3K/AKT/mTOR) in MDA-MB-231[1]
体外研究
(In Vitro)

PI3K/Akt/mTOR-IN-2 (compound 23) (0.5 – 100 μM; 72 hours) exhibits effective anti-cancer activity with IC50s of 2.29 – 24.63 μM, of which, IC50 in MDA-MB-231 is 2.29 μM[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces growth inhibition of MDA-MB-231 cells by cell cycle arrest at G0/G1[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24, 48 and 72 hours) induces apoptosis in MDA-MB-231 cells with both dose- and time-dependent manners[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 48 hours) increases the expression of Bax, and decreases the expression of Bcl-2 in MDA-MB-231 cells[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces mitochondria-dependent apoptosis in MDA-MB-231 cells through disruption of MMP, accumulation of ROS, depletion of GSH and elevation of intracellular Ca2+[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay

Cell Line: PC3, BGC-823, A549, MCF-7, MDA-MB-231 cells and MCF-10A cells[1]
Concentration: 0.5 – 100 μM
Incubation Time: 72 hours
Result: Exhibited effective anti-cancer activity with IC50s of 2.29 – 24.63 μM, of which, IC50 in MDA-MB-231 was 2.29 μM.

Cell Cycle Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 24 hours
Result: Induced growth inhibition of MDA-MB-231 cells by cell cycle arrest at G0/G1.

Apoptosis Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 24, 48 and 72 hours
Result: Induced apoptosis in MDA-MB-231 cells with both dose- and time-dependent manners.

Western Blot Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 48 hours
Result: Increased the expression of Bax, and decreased the expression of Bcl-2

分子量

285.29

Formula

C17H13F2NO
CAS 号

2757804-89-8
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Qin J, Sun X, Ma Y, et al. Design, synthesis and biological evaluation of novel 1,3,4,9-tetrahydropyrano[3,4-b]indoles as potential treatment of triple negative breast cancer by suppressing PI3K/AKT/mTOR pathway [published online ahead of print, 2021 Dec 31]. Bioorg Med Chem. 2021;55:116594.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

PI3K/Akt/mTOR-IN-2

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

PI3K/Akt/mTOR-IN-2 

PI3K/Akt/mTOR-IN-2 是一种有效的 PI3K/AKT/mTOR 抑制剂。PI3K/Akt/mTOR-IN-2 具有抗癌作用，并对 MDA-MB-231 细胞具有选择性，IC50 为 2.29 μM。PI3K/Akt/mTOR-IN-2 可诱导癌细胞周期阻滞和细胞凋亡 (apoptosis)。

PI3K/Akt/mTOR-IN-2

PI3K/Akt/mTOR-IN-2 Chemical Structure

CAS No. : 2757804-89-8

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

PI3K/Akt/mTOR-IN-2 is a PI3K/AKT/mTOR pathway inhibitor. PI3K/Akt/mTOR-IN-2 possess anti-cancer effects and selectivity against MDA-MB-231 cells with IC50 value of 2.29 μM. PI3K/Akt/mTOR-IN-2 can induce cancer cell cycle arrest and apoptosis[1].

IC50 & Target

IC50: 2.29 μM (PI3K/AKT/mTOR) in MDA-MB-231[1]
体外研究
(In Vitro)

PI3K/Akt/mTOR-IN-2 (compound 23) (0.5 – 100 μM; 72 hours) exhibits effective anti-cancer activity with IC50s of 2.29 – 24.63 μM, of which, IC50 in MDA-MB-231 is 2.29 μM[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces growth inhibition of MDA-MB-231 cells by cell cycle arrest at G0/G1[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24, 48 and 72 hours) induces apoptosis in MDA-MB-231 cells with both dose- and time-dependent manners[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 48 hours) increases the expression of Bax, and decreases the expression of Bcl-2 in MDA-MB-231 cells[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces mitochondria-dependent apoptosis in MDA-MB-231 cells through disruption of MMP, accumulation of ROS, depletion of GSH and elevation of intracellular Ca2+[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay

Cell Line: PC3, BGC-823, A549, MCF-7, MDA-MB-231 cells and MCF-10A cells[1]
Concentration: 0.5 – 100 μM
Incubation Time: 72 hours
Result: Exhibited effective anti-cancer activity with IC50s of 2.29 – 24.63 μM, of which, IC50 in MDA-MB-231 was 2.29 μM.

Cell Cycle Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 24 hours
Result: Induced growth inhibition of MDA-MB-231 cells by cell cycle arrest at G0/G1.

Apoptosis Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 24, 48 and 72 hours
Result: Induced apoptosis in MDA-MB-231 cells with both dose- and time-dependent manners.

Western Blot Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 48 hours
Result: Increased the expression of Bax, and decreased the expression of Bcl-2

分子量

285.29

Formula

C17H13F2NO
CAS 号

2757804-89-8
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Qin J, Sun X, Ma Y, et al. Design, synthesis and biological evaluation of novel 1,3,4,9-tetrahydropyrano[3,4-b]indoles as potential treatment of triple negative breast cancer by suppressing PI3K/AKT/mTOR pathway [published online ahead of print, 2021 Dec 31]. Bioorg Med Chem. 2021;55:116594.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

PI3K/Akt/mTOR-IN-2

发表于由
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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

PI3K/Akt/mTOR-IN-2 

PI3K/Akt/mTOR-IN-2 是一种有效的 PI3K/AKT/mTOR 抑制剂。PI3K/Akt/mTOR-IN-2 具有抗癌作用，并对 MDA-MB-231 细胞具有选择性，IC50 为 2.29 μM。PI3K/Akt/mTOR-IN-2 可诱导癌细胞周期阻滞和细胞凋亡 (apoptosis)。

PI3K/Akt/mTOR-IN-2

PI3K/Akt/mTOR-IN-2 Chemical Structure

CAS No. : 2757804-89-8

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

PI3K/Akt/mTOR-IN-2 is a PI3K/AKT/mTOR pathway inhibitor. PI3K/Akt/mTOR-IN-2 possess anti-cancer effects and selectivity against MDA-MB-231 cells with IC50 value of 2.29 μM. PI3K/Akt/mTOR-IN-2 can induce cancer cell cycle arrest and apoptosis[1].

IC50 & Target

IC50: 2.29 μM (PI3K/AKT/mTOR) in MDA-MB-231[1]
体外研究
(In Vitro)

PI3K/Akt/mTOR-IN-2 (compound 23) (0.5 – 100 μM; 72 hours) exhibits effective anti-cancer activity with IC50s of 2.29 – 24.63 μM, of which, IC50 in MDA-MB-231 is 2.29 μM[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces growth inhibition of MDA-MB-231 cells by cell cycle arrest at G0/G1[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24, 48 and 72 hours) induces apoptosis in MDA-MB-231 cells with both dose- and time-dependent manners[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 48 hours) increases the expression of Bax, and decreases the expression of Bcl-2 in MDA-MB-231 cells[1].
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces mitochondria-dependent apoptosis in MDA-MB-231 cells through disruption of MMP, accumulation of ROS, depletion of GSH and elevation of intracellular Ca2+[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay

Cell Line: PC3, BGC-823, A549, MCF-7, MDA-MB-231 cells and MCF-10A cells[1]
Concentration: 0.5 – 100 μM
Incubation Time: 72 hours
Result: Exhibited effective anti-cancer activity with IC50s of 2.29 – 24.63 μM, of which, IC50 in MDA-MB-231 was 2.29 μM.

Cell Cycle Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 24 hours
Result: Induced growth inhibition of MDA-MB-231 cells by cell cycle arrest at G0/G1.

Apoptosis Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 24, 48 and 72 hours
Result: Induced apoptosis in MDA-MB-231 cells with both dose- and time-dependent manners.

Western Blot Analysis

Cell Line: MDA-MB-231[1]
Concentration: 1 μM, 2 μM and 4 μM
Incubation Time: 48 hours
Result: Increased the expression of Bax, and decreased the expression of Bcl-2

分子量

285.29

Formula

C17H13F2NO
CAS 号

2757804-89-8
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Qin J, Sun X, Ma Y, et al. Design, synthesis and biological evaluation of novel 1,3,4,9-tetrahydropyrano[3,4-b]indoles as potential treatment of triple negative breast cancer by suppressing PI3K/AKT/mTOR pathway [published online ahead of print, 2021 Dec 31]. Bioorg Med Chem. 2021;55:116594.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

API-1

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

API-1 

API-1 是一种有效的 Akt/PKB 抑制剂，与 PH 结构域结合并抑制 Akt 膜易位。API-1 有效降低 Akt 的磷酸化水平，IC50 为 ∼0.8 μM。API-1 对 PKB 具有选择性，不抑制 PKC 和 PKA 的激活。API-1 还通过与 TNF 相关的凋亡诱导配体 (TRAIL) 协同作用来诱导细胞凋亡 (apoptosis)。

API-1

API-1 Chemical Structure

CAS No. : 36707-00-3

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

API-1, a potent Akt/PKB inhibitor, binds to the PH domain and inhibits Akt membrane translocation. API-1 efficiently reduces the phosphorylation levels of Akt with an IC50 of ∼0.8 μM. API-1 is selective for PKB and does not inhibit the activation of PKC, and PKA. API-1 also induces apoptosis by synergizing with TNF-related apoptosis-inducing ligand (TRAIL)[1][2].

分子量

337.29

Formula

C13H15N5O6
CAS 号

36707-00-3
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Donghwa Kim, et al. A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation. J Biol Chem. 2016 Oct 21;291(43):22856.

    [2]. Donghwa Kim, et al. A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation. J Biol Chem. 2016 Oct 21;291(43):22856.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

API-1

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

API-1 

API-1 是一种有效的 Akt/PKB 抑制剂，与 PH 结构域结合并抑制 Akt 膜易位。API-1 有效降低 Akt 的磷酸化水平，IC50 为 ∼0.8 μM。API-1 对 PKB 具有选择性，不抑制 PKC 和 PKA 的激活。API-1 还通过与 TNF 相关的凋亡诱导配体 (TRAIL) 协同作用来诱导细胞凋亡 (apoptosis)。

API-1

API-1 Chemical Structure

CAS No. : 36707-00-3

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

API-1, a potent Akt/PKB inhibitor, binds to the PH domain and inhibits Akt membrane translocation. API-1 efficiently reduces the phosphorylation levels of Akt with an IC50 of ∼0.8 μM. API-1 is selective for PKB and does not inhibit the activation of PKC, and PKA. API-1 also induces apoptosis by synergizing with TNF-related apoptosis-inducing ligand (TRAIL)[1][2].

分子量

337.29

Formula

C13H15N5O6
CAS 号

36707-00-3
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Donghwa Kim, et al. A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation. J Biol Chem. 2016 Oct 21;291(43):22856.

    [2]. Donghwa Kim, et al. A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation. J Biol Chem. 2016 Oct 21;291(43):22856.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

API-1

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

API-1 

API-1 是一种有效的 Akt/PKB 抑制剂，与 PH 结构域结合并抑制 Akt 膜易位。API-1 有效降低 Akt 的磷酸化水平，IC50 为 ∼0.8 μM。API-1 对 PKB 具有选择性，不抑制 PKC 和 PKA 的激活。API-1 还通过与 TNF 相关的凋亡诱导配体 (TRAIL) 协同作用来诱导细胞凋亡 (apoptosis)。

API-1

API-1 Chemical Structure

CAS No. : 36707-00-3

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生物活性

API-1, a potent Akt/PKB inhibitor, binds to the PH domain and inhibits Akt membrane translocation. API-1 efficiently reduces the phosphorylation levels of Akt with an IC50 of ∼0.8 μM. API-1 is selective for PKB and does not inhibit the activation of PKC, and PKA. API-1 also induces apoptosis by synergizing with TNF-related apoptosis-inducing ligand (TRAIL)[1][2].

分子量

337.29

Formula

C13H15N5O6
CAS 号

36707-00-3
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Donghwa Kim, et al. A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation. J Biol Chem. 2016 Oct 21;291(43):22856.

    [2]. Donghwa Kim, et al. A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation. J Biol Chem. 2016 Oct 21;291(43):22856.

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AKT-IN-2

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

AKT-IN-2 

AKT-IN-2 是一种有效的，选择性和口服生物可利用的 AKT 抑制剂，抑制 AKT1，IC50 为 5 nM。

AKT-IN-2

AKT-IN-2 Chemical Structure

CAS No. : 1295514-91-8

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生物活性

AKT-IN-2 is a potent, selective and orally bioavailable AKT inhibitor with an IC50 of 5 nM for AKT1[1].

IC50 & Target[1]

Akt1

5 nM (IC50)

P70S6K

399 nM (IC50)

PKA

84 nM (IC50)

PKCβ2

3.98 μM (IC50)

RSK1

568 nM (IC50)

pGSK3β

92 nM (IC50)

体外研究
(In Vitro)

AKT-IN-2 (Compound 8) also inhibits P70S6K, PKA, PKCβ2, RSK1, and pGSK3β with IC50s of 0.399, 0.084, 3.98, 0.568, and 0.092 μM, respectively[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

505.58

Formula

C25H34F3N7O
CAS 号

1295514-91-8
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Parthasarathy S, et al. Discovery of chiral dihydropyridopyrimidinones as potent, selective and orally bioavailable inhibitors of AKT. Bioorg Med Chem Lett. 2018 Jun 1;28(10):1887-1891.

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SC79

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

SC79  纯度: ≥98.0%

SC79，一个特异的、能透过血脑屏障的 Akt 激动剂，可激活胞质中 Akt，并抑制 Akt 膜转位。SC79 特异性结合Akt 的PH 结构域。

SC79

SC79 Chemical Structure

CAS No. : 305834-79-1

规格 价格 是否有货 数量
5 mg ￥600 In-stock
10 mg ￥950 In-stock
50 mg ￥2820 In-stock
100 mg ￥4200 In-stock
200 mg ￥5700 In-stock
500 mg   询价  
1 g   询价  

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SC79 相关产品

•相关化合物库:

  • Bioactive Compound Library Plus

生物活性

SC79, a unique specific and BBB permeable Akt activator, activates Akt in the cytosol and inhibits Akt membrane translocation. SC79 specifically binds to the PH domain of Akt[1][2][3].

IC50 & Target

Akt

 

体外研究
(In Vitro)

SC79 augmentes Akt phosphorylation at both the Thr308 and S473 sites[1].
SC79 (10.96 μM) induces cytosolic phosphorylation of Akt. SC79 enhances IGF1-induced Akt phosphorylation in both serum-starved cells and cells grown in serum-rich medium[1].
SC79 reduces neuronal excitotoxicity and prevents stroke-induced neuronal death. SC79 suppresses PHAKTM-GFP plasma membrane translocation[1].
SC79 restores proliferation of BRAT1 knockdown cells, and reduces the production of superoxide in mitochondria of MitoSox positive cells[2].
SC79 upregulates FLIPL/S expression and consequently suppresses caspase-8 activation[5].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[1]

Cell Line: HeLa cells.
Concentration: 4 μg/mL (10.96 μM).
Incubation Time: 30 min.
Result: Induced cytosolic phosphorylation of Akt.

体内研究
(In Vivo)

SC79 treatment, even at much high dose (0.4 mg/g of body weight), does not induce any detectable changes in body weight, survival rate, appearance, and behavior in mice[1].
SC79 (10 mg/kg, i.p.) Protects C57BL/6 mice from fas-induced fulminant hepatic failure[4].
SC79 protects hepatocytes from TNFα-mediated apoptosis and mice from Gal/LPS-induced liver injury and damage[5].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male, age-matched (6- to 8-weekeold) C57BL/6 or BALB/c mice weighing 16 to 18 g[4].
Dosage: 10 mg/kg.
Administration: Intraperitoneally at 0.5 hour before the i.p. administration of an agonistic anti-Fas Jo2 antibody at a lethal dose of 0.5 and 0.4 mg/kg for C57BL/6 and BALB/c mice, respectively.
Result: Treatment of mice with 10 mg/kg of SC79 at 0.5 hour before Jo2 injection increased mouse survival at 12 hours after Jo2 injection from 0% to 35%, and no additional mortality was observed to the end of the 2-month observation period.
Animal Model: Male, age-matched (6 to 8 weeks old) C57BL/6 mice weighing 16-18 g[5].
Dosage: 10 mg/kg.
Administration: Intraperitoneally at 0.5 h before i.p. administration of 400 mg/kg of D-galactosamine (D-Gal) and 60 µg/kg of lipopolysaccharide (LPS) for C57BL/6 mice.
Result: Gal/LPS challenge there was more bleeding on the liver of the vehicle control-treated mice as compared to that of SC79-treated mice.
A single dose of SC79 significantly reduced Gal/LPS-mediated liver damage but not an infiltration of inflammatory cells in liver sections.

分子量

364.78

Formula

C17H17ClN2O5
CAS 号

305834-79-1
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years

*该产品在溶液状态不稳定，建议您现用现配，即刻使用。
溶解性数据
In Vitro: 

DMSO : ≥ 100 mg/mL (274.14 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.7414 mL 13.7069 mL 27.4138 mL
5 mM 0.5483 mL 2.7414 mL 5.4828 mL
10 mM 0.2741 mL 1.3707 mL 2.7414 mL

*

请根据产品在不同溶剂中的溶解度，选择合适的溶剂配制储备液；该产品在溶液状态不稳定，建议您现用现配，即刻使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: 10 mg/mL (27.41 mM); Suspended solution; Need ultrasonic

    此方案可获得 10 mg/mL (27.41 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

    以 1 mL 工作液为例，取 100 μL 100.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 5% DMSO    40% PEG300    5% Tween-80    50% saline

    Solubility: 5 mg/mL (13.71 mM); Suspended solution; Need ultrasonic

  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (6.85 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (6.85 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献

  • [1]. Jo H, et al. Small molecule-induced cytosolic activation of protein kinase Akt rescues ischemia-elicited neuronal death. Proc Natl Acad Sci U S A. 2012 Jun 26;109(26):10581-10586.

    [2]. So EY, et al. BRAT1 deficiency causes increased glucose metabolism and mitochondrial malfunction. BMC Cancer. 2014 Jul 29;14:548

    [3]. Liu X, et al. Activation of Akt by SC79 decreased cerebral infarct in early cerebral ischemia-reperfusion despite increased BBB disruption. Neurosci Lett. 2018 Aug 10;681:78-82.

    [4]. Liu W, et al. A Novel AKT Activator, SC79, Prevents Acute Hepatic Failure Induced by Fas-Mediated Apoptosis of Hepatocytes. Am J Pathol. 2018 May;188(5):1171-1182.

    [5]. Jing ZT, et al. AKT activator SC79 protects hepatocytes from TNF-α-mediated apoptosis and alleviates d-Gal/LPS-induced liver injury. Am J Physiol Gastrointest Liver Physiol. 2019 Mar 1;316(3):G387-G396.

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