PDGFRβ-IN-1
PDGFRβ-IN-1 is an orally active PDGFRβ inhibitor with an IC50 of 3.9 nM against human PDGFRβ. PDGFRβ-IN-1 selectively inhibits PDGFRβ, blocks its downstream signaling pathways, and promotes its degradation via a non-classical pathway. PDGFRβ-IN-1 inhibits cancer cell proliferation, migration and colony formation, and induces cancer cell apoptosis. PDGFRβ-IN-1 suppresses tumor growth in xenograft models. PDGFRβ-IN-1 can be used for the research of hepatocellular carcinoma.
For research use only. We do not sell to patients.
- Formula: C25H27F2N7O
- Molecular Weight:479.52
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
PDGFRβ 3.9 nM (IC50) |
In Vitro
PDGFRβ-IN-1 inhibits the proliferation of human hepatocellular carcinoma cell lines Huh-7 and Hep3B, with IC50 values of 0.39 μM and 0.75 μM, respectively; meanwhile, it exhibits low toxicity to normal human hepatocyte MIHA, with an IC50 of 10.65 μM[1].
PDGFRβ-IN-1 (0.1-0.4 μM; 48 h) inhibits long-term clonogenic growth of Huh-7 and Hep3B human hepatocellular carcinoma cells in a concentration-dependent manner, reduces DNA replication, induces apoptosis, inhibits adhesion to extracellular matrix components, and suppresses migration[1].
PDGFRβ-IN-1 (0.4 μM; 6 h, 0-48 h) inhibits PDGFRβ-mediated signaling pathways in human hepatocellular carcinoma cell lines Huh-7 and Hep3B by suppressing receptor phosphorylation and promoting PDGFRβ degradation via a non-canonical pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Huh-7 and Hep3B human hepatocellular carcinoma cells
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Concentration:0.1, 0.2, 0.4 μM
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Incubation Time:48 h
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Result:Significantly decreased the number of migrated cells in both cell lines in a dose-dependent manner.
Suppressed invasive capacity of Huh-7 cells in a dose-dependent manner.
Showed inhibition substantially greater than that induced by 0.4 μM Sorafenib (HY-10201).
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Cell Line:Huh-7 and Hep3B human hepatocellular carcinoma cells
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Concentration:0.1, 0.2, 0.4 μM
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Incubation Time:48 h
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Result:Effectively suppressed cell migration.
Resulted in only ~30% of the wound area being covered after 48 h when used at 0.4 μM.
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Cell Line:Huh-7 and Hep3B human hepatocellular carcinoma cells
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Concentration:0.1, 0.2, 0.4 μM
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Incubation Time:48 h
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Result:Effectively suppressed cell apoptosis.
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Cell Line:Huh-7 and Hep3B human hepatocellular carcinoma cells
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Concentration:0.4 μM (treatment for signaling pathway analysis)
100 nM (proteasome inhibitor in combination)
20 μM (lysosomotropic agent in combination)
50 μg/mL (protein synthesis inhibitor in combination) -
Incubation Time:6 h (treatment with proteasome inhibitor or lysosomotropic agent in combination)
0, 1, 2, 4, 8, 12, 24, 48 h (treatment with protein synthesis inhibitor in combination) -
Result:Markedly reduced phosphorylation levels of PDGFRβ, STAT3, AKT, and ERK, with stronger inhibition than Sorafenib.
Decreased total PDGFRβ protein levels.
Showed cotreatment with proteasome inhibitor or lysosomotropic agent did not restore PDGFRβ levels.
Shortened PDGFRβ half-life in protein synthesis inhibitor chase experiments, indicating degradation via a noncanonical pathway independent of proteasomes and autophagy-lysosomes.
Parmacokinetics
In Vivo
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 (6-week-old)[1]
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Dosage:15 mg/kg; 30 mg/kg
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Administration:i.p.; daily; 14 days
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Result:Achieved a tumor growth inhibition (TGI) of 45% at 30 mg/kg dose.
Suppressed phosphorylation of PDGFRβ and its downstream effectors STAT3, AKT, and ERK in tumor tissues.
Increased tumor necrosis via H&E staining.
Substantially reduced proliferating cells compared to controls via Ki67 immunostaining.
Maintained stable body weights across treatment groups.
- Cell migration
- Somatic Cell Culture
- Liver Cancer Modeling
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Apoptosis Solutions
- Soft Agar Colony Formation Assay
- MTT Cell Proliferation Assay
- Annexin V plus membrane-impermeant dye apoptosis staining
- BrdU Incorporation Assay
- CFSE Dye Dilution Proliferation Assay
- Dye-dilution cell tracking and proliferation staining
- Patient-Derived Orthotopic Xenograft (PDOX)
- CCK-8/WST-8 Cell Proliferation Assay
- Protocol for Cell Cycle
- Cell Counting-Based Growth Curve Assay
- Colony Formation (Clonogenic) Assay
- Cell Viability Determination by MTT Colorimetric Assay
- EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
- Ki-67 Immunostaining Proliferation Assay
- PCNA Immunodetection Proliferation Assay
- Protocol for Cell Counting and Cell Density Analysis
- Patient-Derived Xenograft (PDX)
- Splenic/Portal-Vein Liver Metastasis Xenograft
- Subcutaneous Cell-Line-Derived Xenograft
- Orthotopic Cell-Line Xenograft
- Intraperitoneal/Peritoneal Dissemination Xenograft
Chemical Information
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Molecular Weight 479.52
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Formula C25H27F2N7O
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SMILES
FC1=CN=C(N=C1NC2=CC=CC3=C2C=CN3CCO)NC4=CC=C(C(F)=C4)N5CCN(CC5)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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
PDGFRβ-IN-1 Related Classifications
HY-187366 Related Classifications
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