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Art. -Nr.: HY-181152

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FGFR3-IN-11

FGFR3-IN-11(compound B11) is a Fibroblast growth factor receptor 3 (FGFR3) inhibitor with a K_a value of 4.8 μM. FGFR3-IN-11 induces apoptosis, suppresses colony formation, and causes dose-dependent G0/G1 cell cycle arrest in cancer cells. FGFR3-IN-11 exerts anticancer activity against cancer cells with minimal toxicity toward normal hepatocytes and demonstrates tumor growth suppression in xenograft mouse models. FGFR3-IN-11 can be used for the research of hepatocellular carcinoma.

Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.

Formel: C₂₇H₃₅N₃OS
Molecular Weight:449.65

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (276 KB)

FGFR3-IN-11 Chemical Structure

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Preis

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Menge

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target^[1]

FGFR3

In Vitro

FGFR3-IN-11 (B10) (48 h) potently inhibits the proliferation of Huh-7, HepG2, and MHCC97-H hepatocellular carcinoma cell lines with IC₅₀ values of 4.13, 4.76, and 5.79 μM, respectively, and has minimal toxicity to L02 normal hepatocytes^[1].
FGFR3-IN-11 (B10) (1.25-5 μM; 48 h initial treatment, 14 days medium replacement) suppresses colony formation in Huh-7 hepatocellular carcinoma cells in a dose-dependent manner^[1].
FGFR3-IN-11 (B10) (1.25-5 μM; 48 h) induces dose-dependent G0/G1 phase arrest in Huh-7 hepatocellular carcinoma cells^[1].
FGFR3-IN-11 (B10) (1.25-5 μM; 24 h) induces dose-dependent apoptosis in Huh-7 hepatocellular carcinoma cells, with corresponding changes in Bcl-2 and Bax protein levels^[1].
FGFR3-IN-11 (B10) (1.25-5 μM; 24 h) inhibits the PI3K/AKT signaling pathway in Huh-7 hepatocellular carcinoma cells by dose-dependently reducing total and phosphorylated PI3K and AKT levels^[1].
FGFR3-IN-11 (B10) (serial dilutions, 40 μM, 10-40 μM; 1 h DARTS pre-incubation) stably binds to FGFR3 protein with a K_D of 4.8 μM, as validated by molecular docking, SPR, CETSA, and DARTS assays^[1].

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

Cell Proliferation Assay^[1]

Cell Line:

Huh-7
Concentration:

1.25-5 μM
Incubation Time:

48 h (initial treatment); 14 days (medium replacement)
Result:

Significantly suppressed colony formation in Huh-7 cells in a dose-dependent manner.

Cell Cycle Analysis^[1]

Cell Line:

Huh-7
Concentration:

1.25-5 μM
Incubation Time:

48 h
Result:

Induced dose-dependent G0/G1 phase arrest in Huh-7 cells.

Apoptosis Analysis^[1]

Cell Line:

Huh-7
Concentration:

1.25-5 μM
Incubation Time:

24 h
Result:

Induced dose-dependent apoptosis in Huh-7 cells. Downregulated anti-apoptotic protein Bcl-2 and upregulated pro-apoptotic protein Bax in a dose-dependent manner (Western blot).

Western Blot Analysis^[1]

Cell Line:

Huh-7
Concentration:

1.25-5 μM
Incubation Time:

24 h
Result:

Reduced the levels of total and phosphorylated PI3K and AKT in a dose-dependent manner.

In Vivo

B10 (20-60 mg/kg; i.p.; every other day; 28 days) exhibits potent in vivo antitumor efficacy in a Huh-7 xenograft model, with a 64.18% TGI rate at 40 mg/kg, and maintains a favorable safety profile^[1].

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

Animal Model:

Balb/c nude mice (female, 4-6 weeks old, 18-19 g average weight)^[1]
Dosage:

20, 40, 60 mg/kg; 40 mg/kg (TGI assessment)
Administration:

i.p.; every other day; 28 days
Result:

Achieved a tumor growth inhibition (TGI) rate of 64.18% at 40 mg/kg; Induced a dose-dependent decrease in phospho-FGFR3 (p-FGFR3) in tumor tissues; Caused a pronounced decrease in Ki-67-positive cells in tumors; Showed no significant weight loss compared to the control group.

Chemical Information

Molecular Weight 449.65
Formel C₂₇H₃₅N₃OS
SMILES

O=C(C1=CC2=C(N3C[C@@]4(CCCN5CCC[C@@]([C@@]54[H])([C@]3(CC2)[H])[H])[H])S1)NC6=CC=C(C(C)C)C=C6
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (276 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Wang X, et al. A novel matrine derivative B10 exerts its anti-liver cancer activity in vitro and in vivo via targeting FGFR3/PI3K/AKT signaling pathway. Mol Divers. Published online January 14, 2026. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Bioz

Keywords

MOQ

Minimum order quantity

100 mg

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