dPDL1-4
dPDL1-4 is a potent and selective eHSPTAC eHSP90 PD-L1 degrader with DC50s of 7.77 μM and 6.52 μM in HeLa and B16F10 cells. dPDL1-4 bridges eHSP90 with the target protein, inducing lysosomal degradation. dPDL1-4 can degrade PD-L1 significantly and inhibits tumor growth. dPDL1-4 can be used for the study of cervical cancer and melanoma. ((Pink: eHSP90 ligand (HY-174476); Blue: PD-L1 ligand (HY-116274); Black: Linker (HY-W021787); HSP ligand + linker: HY-174799)).
For research use only. We do not sell to patients.
- Formula: C60H74BrN7O10
- Molecular Weight:1133.17
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
dPDL1-4 (5-20 μM, 12-24 h) promotes degradation of membrane PD-L1 in an eHSP90-, ternary complex- and lysosome-dependent manner in HeLa and B16F10 cells[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:HeLa and B16F10 cells
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Concentration:0, 1, 3, 5, 10, 20 μM
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Incubation Time:12 h
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Result:Induced dose- and time-dependent degradation of PD-L1 in HeLa cells (Dmax = 68%) and B16F10 cells (Dmax = 56%).
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Cell Line:B16F10 cells
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Concentration:5 μM
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Incubation Time:12 h
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Result:Inhibited the degradation of membrane-associated PD-L1 by BMS-8 (HY-116274) or HSP90i-Ac.
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Cell Line:HeLa cells
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Concentration:10, 20 μM
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Incubation Time:24 h
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Result:Inhibited the degradation of membrane-associated PD-L1 by Bafilomycin A1 (HY-100558) and Monensin (HY-N4302) but not by MG132 (HY-13259).
Parmacokinetics
| Species | Dose | Route | AUC0-∞ | T1/2 |
|---|---|---|---|---|
| Rat[1] | 50 mg/kg | i.v. | 27866.1 μg/L·h | 1.6 h |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:B16F10 melanoma syngeneic mouse model established by tumor-bearing mice (C57BL/6J, 6-7 weeks, female)[1]
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Dosage:50 mg/kg
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Administration:Intraperitoneal injection (i.p.), once every 2 days for 6 doses.
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Result:Suppressed tumor growth significantly, without causing notable weight loss.
Induced a remarkable decrease in the PD-L1 level among all the treatments.
Increased the percentage of activated cytotoxic T cells (CD8+cells).
Chemical Information
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Molecular Weight 1133.17
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Formula C60H74BrN7O10
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SMILES
CC(C1=C(C=C(C(C2=NN=C(N2C3=CC=C(C=C3)CN4CCN(CC4)C(CCOCCOCCOCCOCCNC(C5CCCCN5CC6=CC=C(OCC7=C(C(C8=CC=CC=C8)=CC=C7)C)C(Br)=C6)=O)=O)O)=C1)O)O)C
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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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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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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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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)