2. Epigenetics PI3K/Akt/mTOR Cell Cycle/DNA Damage Autophagy Apoptosis
  3. Epigenetic Reader Domain Akt CDK Autophagy Apoptosis
  4. BRD4/AKT-IN-1

BRD4/AKT-IN-1 是一种 BRD4/AKT1 抑制剂，其 BRD4 IC50 为 66.12 nM，AKT1 IC50 为 143.81 nM。BRD4/AKT-IN-1 可阻断 BRD4 介导的 c-Myc 转录调控，调控 AKT1 信号通路，使 AKT 磷酸化与促存活效应因子解偶联。BRD4/AKT-IN-1 可通过下调磷酸化 RB、cyclin E1 和 CDK2 诱导细胞周期 G0/G1 期阻滞。BRD4/AKT-IN-1 可上调 LC3B 水平以促进自噬 (autophage)。BRD4/AKT-IN-1 可促进癌细胞凋亡 (apoptosis)。BRD4/AKT-IN-1 可用于转移性去势抵抗性前列腺癌的研究。

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BRD4/AKT-IN-1

BRD4/AKT-IN-1 Chemical Structure

CAS No. : 3087270-50-3

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BRD4/AKT-IN-1 相关抗体

Top Publications Citing Use of Products

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Akt Akt1 Akt2 Akt3

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CDK1 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK8 CDK9 CDK11 CDK12 CDK13 CDK14 CDK16 CDK19 CDC CLK Pho85 CDK10 CDK15 CDK17 CDK18 CDK20 PITSLRE

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

BRD4/AKT-IN-1 is a BRD4/AKT inhibitor with BRD4 IC50 66.12 nM and AKT1 IC50 143.81 nM. BRD4/AKT-IN-1 blocks BRD4-mediated c-Myc transcriptional regulation, modulates AKT1 signaling, decouples AKT phosphorylation from pro-survival effectors. BRD4/AKT-IN-1 induces G0/G1 cell cycle arrest via downregulated phosphorylated RB, cyclin E1, CDK2. BRD4/AKT-IN-1 elevates LC3B levels to promote autophagy. BRD4/AKT-IN-1 promotes apoptosis in cancer cells. BRD4/AKT-IN-1 can be used for the research of metastatic castration-resistant prostate cancer[1].

IC50 & Target[1]

BRD4

66.12 nM (IC50)

Akt1

143.81 nM (IC50)

CDK2/cyclin E1

 

体外研究
(In Vitro)

BRD4/AKT-IN-1 (Compound 21d) (300-1000 nM) 可在无细胞生化 HTRF 分析中强效抑制纯化的 BRD4 (IC50 = 66.12 nM) 和 AKT1 (IC50 = 143.81 nM) 蛋白[1]。
BRD4/AKT-IN-1 (0.01-100 μM；72 小时) MTT 抗增殖实验中可强效抑制 22Rv1 (IC50 = 0.51 μM)、VCaP (IC50 = 0.69 μM) 和 PC3 (IC50 = 4.62 μM) 这几种 mCRPC 细胞的增殖[1]。
BRD4/AKT-IN-1 (0.5-2 μM；24 小时) 可通过下调 p-RB、cyclin E1 和 CDK2 的表达，诱导 22Rv1 mCRPC 细胞出现剂量依赖性 G0/G1 期细胞周期阻滞[1]。
BRD4/AKT-IN-1 (0.5-2 μM；48 小时) 划痕愈合实验中呈剂量依赖性抑制 22Rv1 mCRPC 的迁移[1]。
BRD4/AKT-IN-1 (0.5-2 μM；12-14 天) 可剂量依赖性地抑制 22Rv1 mCRPC 细胞的长期克隆增殖能力[1]。
BRD4/AKT-IN-1 (0.5-2 μM；24 小时) 可呈剂量依赖性抑制 BRD4/c-Myc 通路并调控 AKT 磷酸化，且在处理 22Rv1 mCRPC 细胞不会激活下游促存活信号[1]。
BRD4/AKT-IN-1 (0.5-2 μM；24 小时) 可呈剂量依赖性诱导 22Rv1 mCRPC 发生自噬，处理 24 小时后可观察到 MDC 阳性囊泡增多及 LC3B 蛋白水平升高[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

BRD4/AKT-IN-1 相关抗体:

Cell Cycle Analysis[1]

Cell Line: 22Rv1 mCRPC cells
Concentration: 0.5 μM; 1 μM; 2 μM
Incubation Time: 24 h
Result: Induced a dose-dependent accumulation of cells in the G0/G1 phase, with 51.9% of untreated cells in G0/G1 increasing to higher proportions with compound treatment.
Downregulated phosphorylated RB (p-RB), cyclin E1, and CDK2 protein levels in a dose-dependent manner.

Cell Migration Assay [1]

Cell Line: 22Rv1 mCRPC cells
Concentration: 0.5 μM; 1 μM; 2 μM
Incubation Time: 48 h
Result: Demonstrated dose-dependent inhibition of wound closure, with higher concentrations resulting in significantly less migration compared to the control.

Cell Proliferation Assay[1]

Cell Line: 22Rv1 mCRPC cells
Concentration: 0.5 μM; 1 μM; 2 μM
Incubation Time: 12-14 days
Result: Significantly reduced colony formation in a dose-dependent manner, with fewer and smaller colonies observed at higher compound concentrations.

Western Blot Analysis[1]

Cell Line: 22Rv1 mCRPC cells
Concentration: 0.5 μM; 1 μM; 2 μM
Incubation Time: 24 h
Result: Reduced the expression of c-Myc (a BRD4 transcriptional target) in a dose-dependent manner, with efficacy comparable to positive control BRD4 inhibitors.
Induced a dose-dependent increase in p-AKT (Ser473) but did not activate downstream effectors p-PRAS40 and p-S6.

Cell Autophagy Assay[1]

Cell Line: 22Rv1 mCRPC cells
Concentration: 0.5 μM; 1 μM; 2 μM
Incubation Time: 24 h
Result: Increased the number of MDC-positive autophagic vesicles in a dose-dependent manner.
Induced a dose-dependent upregulation of LC3B protein levels, confirming autophagy induction.
药代动力学
(Parmacokinetics)
Species Dose Route T1/2 Tmax Cmax
Mice[1] 40 mg/kg i.p. 6.8 h 0.25 h 16967 ng/mL
体内研究
(In Vivo)

BRD4/AKT-IN-1 (Compound 21d) (40-80 mg/kg；腹腔注射；每日一次；共 18 天) 在 22Rv1 前列腺癌异种移植模型中表现出剂量依赖性抗肿瘤功效，在 80 mg/kg 每日腹腔注射剂量下实现 62.0% 的肿瘤生长抑制率，且耐受性良好[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c nude (male; subcutaneously injected 22Rv1 cells into the right flank to form a xenograft model)[1]
Dosage: 40 mg/kg; 80 mg/kg
Administration: i.p.; daily; 18 days
Result: Achieved a tumor growth inhibition (TGI) rate of 37.7% with no observable body weight loss or treatment-related mortality.
Achieved a TGI rate of 62.0%, which was superior to capivasertib monotherapy, compound 15 monotherapy, and their combination.
Significantly reduced tumor volume and tumor weight compared to controls, with no significant body weight loss or histopathological lesions in major organs (heart, liver, spleen, lung, kidney).
分子量

926.55

Formula

C51H60ClN11O4
CAS 号
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.
纯度 & 产品资料
参考文献

BRD4/AKT-IN-1 相关分类

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Keywords:

BRD4/AKT-IN-13087270-50-3Epigenetic Reader DomainAktCDKAutophagyApoptosisPKBProtein kinase BCyclin dependent kinaseG0/G1 cell cycle arrestc-Mycxenograft mouse modelautophagymetastatic castration-resistant prostate cancerAKT1apoptosisBRD422Rv1LC3BInhibitorinhibitorinhibit

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