FD1-C10-CB
FD1-C10-CB is a PROTAC degrader targeting the BRD4 protein. FD1-C10-CB binds to FEM1B to form a ternary complex with BRD4, achieving FEM1B-dependent degradation of BRD4 via the ubiquitin-proteasome system. FD1-C10-CB binds to CD36 to mediate endocytic cellular delivery, thereby enhancing its degrading activity. FD1-C10-CB mediates protein degradation through the Cullin-dependent ubiquitin-proteasome pathway, rather than the lysosomal autophagy pathway. FD1-C10-CB induces a decrease in BRD4 protein levels, and its degrading activity is competitively inhibited by FL47 or JQ1. FD1-C10-CB can be used in the research of breast cancer and osteosarcoma.
(Pink: BRD4 ligand (HY-78695); Blue: FEM1B E3 ligase ligand; Black: linker).
For research use only. We do not sell to patients.
- Formula: C64H85Cl2N9O9S
- Molecular Weight:1227.39
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All PROTACs Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
BRD4 |
In Vitro
FD1-C10-CB (10 μM; unspecified time course) mediates FEM1B-dependent BRD4 degradation in HEK293T cells via the ubiquitin-proteasome system, with enhanced activity relative to FD1 that relies on CD36-mediated endocytosis[1].
FD1-C10-CB effectively degrades BRD4 in MDA-MB-231 and HOS cells with greater efficacy than FD1[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HEK293T cells, FEM1B-knockout HEK293T cells
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Concentration:10 μM (inhibitor/competitor experiments); multiple concentrations (dose-dependent analysis)
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Incubation Time:1-24 h
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Result:Induced concentration- and time-dependent degradation of BRD4, with significantly improved DC50 and Dₘₐₓ values compared to the parent compound FD1.
Abrogated BRD4 degradation in FEM1B-knockout cells.
Inhibited BRD4 degradation when co-administered with proteasome inhibitor MG132, neddylation inhibitor MLN4924, CD36 inhibitor SMS121, and excess FL47 or JQ1.
Left BRD4 degradation unaffected by lysosomal inhibitors bafilomycin A1 or chloroquine.
Chemical Information
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Molecular Weight 1227.39
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Formula C64H85Cl2N9O9S
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SMILES
ClCC(N1CCN(CCCNC([C@]23C[C@@H]4C[C@@H](C[C@@](C(NC5=CC(OCCNC(C[C@H]6C7=NN=C(C)N7C(SC(C)=C8C)=C8C(C9=CC=C(Cl)C=C9)=N6)=O)=CC(OC(CCCCCCCCCCC(OC(C)(C)C)=O)=O)=C5)=O)(C4)C3)C2)=O)CC1)=O
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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.
Protocols
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Autophagy
Autophagy is a process in which eukaryotic cells use lysosomes to degrade their own cytoplasmic proteins and damaged organelles under the regulation of autophagy related gene (Atg). Microtubule-associated proteins light chain 3 (LC3) is recognized as autophagy marker, which transfers from cytoplasmic LC3 (LC3-I) to membrane type (LC3-II). LC3-II/I ratio could be detected by Western Blot and fluorescence microscopy.
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Lysosome and acidic-vesicle live-cell staining
Lysosome and acidic-vesicle live-cell staining detects acidic intracellular compartments by using membrane-permeant acidotropic probes that accumulate in low-pH vesicles, including lysosomes, late endosomes, autolysosomes, and acidic phagosomes. LysoTracker staining is commonly used as an intensity-based readout of acidic lysosomal compartment abundance or enlargement, while acridine orange produces green fluorescence in less concentrated compartments and red fluorescence after concentration-dependent accumulation in acidic vesicular organelles. Loss or reduction of acridine-orange red signal can be used as a readout of lysosomal membrane permeabilization or reduced acidic-vesicle integrity. This protocol is designed for live cultured cells and can be adapted for fluorescence microscopy, high-content imaging, plate-reader readout, or flow cytometry when the selected literature supports the readout. Because these dyes report acidotropic accumulation rather than lysosome identity alone,
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Macroautophagy Solutions
Macroautophagy is a conserved lysosome-dependent degradation pathway in which cytoplasmic material is sequestered into double-membrane autophagosomes and delivered to lysosomes for degradation and recycling. The pathway supports cellular homeostasis during nutrient limitation, organelle stress, protein-aggregate accumulation, infection, differentiation, and tissue remodeling by coupling cargo sequestration, autophagosome maturation, lysosomal fusion, and degradation of cargo-derived macromolecules. The core molecular sequence includes initiation by nutrient- and stress-regulated autophagy machinery, autophagosome nucleation, LC3/ATG8-family conjugation to autophagosomal membranes, cargo selection through receptors such as SQSTM1/p62, autophagosome-lysosome fusion, and lysosomal degradation. LC3 was identified as a mammalian homolog of yeast Atg8 that localizes to autophagosomal membranes after processing, and p62/SQSTM1 was shown to connect ubiquitinated cargo with autophagic degradati
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)