BRD4/AKT-IN-1
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.
For research use only. We do not sell to patients.
- CAS No.: 3087270-50-3
- Formula: C51H60ClN11O4
- Molecular Weight:926.55
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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BRD4 66.12 nM (IC50) |
Akt1 143.81 nM (IC50) |
CDK2/cyclin E1 |
BRD4/AKT-IN-1 (Compound 21d) (300-1000 nM) potently inhibits purified BRD4 (IC50 = 66.12 nM) and AKT1 (IC50 = 143.81 nM) proteins in a cell-free biochemical HTRF assay[1].
BRD4/AKT-IN-1 (0.01-100 μM; 72 h) potently inhibits the proliferation of 22Rv1 (IC50 = 0.51 μM), VCaP (IC50 = 0.69 μM), and PC3 (IC50 = 4.62 μM) mCRPC cells in a MTT antiproliferation assay[1].
BRD4/AKT-IN-1 (0.5-2 μM; 24 h) induces dose-dependent G0/G1 phase cell cycle arrest in 22Rv1 mCRPC cells by downregulating the expression of p-RB, cyclin E1, and CDK2[1].
BRD4/AKT-IN-1 (0.5-2 μM; 48 h) dose-dependently inhibits the migration of 22Rv1 mCRPC cells in a wound healing assay[1].
BRD4/AKT-IN-1 (0.5-2 μM; 12-14 days) dose-dependently suppresses the long-term clonogenic proliferative capacity of 22Rv1 mCRPC cells[1].
BRD4/AKT-IN-1 (0.5-2 μM; 24 h) dose-dependently suppresses the BRD4/c-Myc pathway and modulates AKT phosphorylation without activating downstream pro-survival signaling in 22Rv1 mCRPC cells after 24 h of treatment[1].
BRD4/AKT-IN-1 (0.5-2 μM; 24 h) dose-dependently induces autophagy in 22Rv1 mCRPC cells after 24 h of treatment, as shown by increased MDC-positive vesicles and elevated LC3B protein levels[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:22Rv1 mCRPC cells
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Concentration:0.5 μM; 1 μM; 2 μM
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Incubation Time:24 h
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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.
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Cell Line:22Rv1 mCRPC cells
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Concentration:0.5 μM; 1 μM; 2 μM
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Incubation Time:48 h
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Result:Demonstrated dose-dependent inhibition of wound closure, with higher concentrations resulting in significantly less migration compared to the control.
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Cell Line:22Rv1 mCRPC cells
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Concentration:0.5 μM; 1 μM; 2 μM
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Incubation Time:12-14 days
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Result:Significantly reduced colony formation in a dose-dependent manner, with fewer and smaller colonies observed at higher compound concentrations.
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Cell Line:22Rv1 mCRPC cells
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Concentration:0.5 μM; 1 μM; 2 μM
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Incubation Time:24 h
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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.
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Cell Line:22Rv1 mCRPC cells
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Concentration:0.5 μM; 1 μM; 2 μM
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Incubation Time:24 h
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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.
| Species | Dose | Route | T1/2 | Tmax | Cmax |
|---|---|---|---|---|---|
| Mice[1] | 40 mg/kg | i.p. | 6.8 h | 0.25 h | 16967 ng/mL |
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (male; subcutaneously injected 22Rv1 cells into the right flank to form a xenograft model)[1]
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Dosage:40 mg/kg; 80 mg/kg
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Administration:i.p.; daily; 18 days
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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).
Chemical Information
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CAS No. 3087270-50-3
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Molecular Weight 926.55
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Formula C51H60ClN11O4
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SMILES
CC1=NOC(C)=C1C2=CC=C3C(C(N(C(N3C)=O)CCCCCC(N4CCN(CC4)CC[C@@H](C5=CC=C(C=C5)Cl)NC(C6(CCN(CC6)C7=C8C=CNC8=NC=N7)N)=O)=O)C9=CC=CC=C9)=C2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
BRD4/AKT-IN-1 Related Classifications
HY-183273 Related Classifications
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