FGFR-IN-26
FGFR-IN-26 is an orally active FGFR inhibitor. FGFR-IN-26 inhibits FGFR2 wild-type and clinically relevant resistance mutations. FGFR-IN-26 inhibits tumor growth in FGFR2-amplified xenograft mouse models. FGFR-IN-26 can be used for the research of cancer, suah as gastric carcinoma.
For research use only. We do not sell to patients.
- CAS No.: 2823290-68-0
- Formula: C22H23N7O
- Molecular Weight:401.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
FGFR3 0.2 nM (IC50) |
FGFR2 2.1 nM (IC50) |
FGFR1 3.8 nM (IC50) |
FGFR4 49 nM (IC50) |
In Vitro
FGFR-IN-26 (Compound 13) (dose-response series) potently inhibits proliferation of Ba/F3 cells expressing FGFR1, FGFR2 (wild-type and clinically relevant resistance mutations), FGFR3, and FGFR4, with highest potency against FGFR2K660E (IC50 = 0.6 nM) and FGFR3 (IC50 = 0.2 nM) and 23-fold selectivity for FGFR2 over FGFR4[1].
FGFR-IN-26 binds potently to FGFR2 (Kd = 2.7 nM), FGFR2(N550K) (Kd = 10 nM), FGFR1 (Kd = 21 nM), and FGFR3 (Kd = 3.5 nM), with 85-fold selectivity for FGFR2 over FGFR4, and shows weak reversible binding to FGFR2(C491F) (Kd = 956 nM) consistent with a covalent mechanism[1].
FGFR-IN-26 (72-120 h) potently inhibits viability of FGFR2-driven SNU-16 gastric cancer cells (IC50 = 7.5 nM) and AN3CA endometrial cancer cells harboring FGFR2N550K (IC50 = 13 nM)[1].
FGFR-IN-26 (1 μM) shows high selectivity against the human kinome, inhibiting only 13 wild-type kinases by >90%[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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:FGFR2-amplified SNU-16 gastric carcinoma xenograft model in nude mice (female, 6-8-week-old)[1]
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Dosage:10 mg/kg
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Administration:p.o.; twice daily; 21 days
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Result:Achieved 152% tumor growth inhibition (TGI) over 21 days.
Reached a terminal day 21 plasma level of 192 ng/mL (480 nM) 4 h after the final dose.
Caused no significant body weight loss after 21 days.
Chemical Information
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CAS No. 2823290-68-0
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Molecular Weight 401.46
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Formula C22H23N7O
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SMILES
C=CC(NC1=CC2=C(C=C1)C(C3=NC(NC4=CN(C(C)C)N=C4)=NC=C3)=CN2C)=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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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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Splenic/Portal-Vein Liver Metastasis Xenograft
Splenic and portal-vein liver metastasis xenograft models deliver tumor cells into the portal circulation so that cells reach the liver first and form hepatic metastatic lesions; splenic injection uses the spleen as an access route to the portal system, while direct portal-vein injection introduces cells into the portal vein without requiring splenectomy. The assay detects liver colonization, intrahepatic tumor growth, tumor distribution, treatment response, survival, and liver-metastasis microenvironment changes; readouts include bioluminescence or fluorescence imaging, gross liver nodule counts, liver weight or tumor burden, histology, and survival.
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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
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Intraperitoneal/Peritoneal Dissemination Xenograft
Intraperitoneal (IP) or peritoneal dissemination xenograft models are based on the introduction of human cancer cells into the peritoneal cavity of immunodeficient mice, where they attach to peritoneal surfaces, form multicellular aggregates or spheroids, and progressively generate disseminated tumor nodules that mimic advanced peritoneal metastatic disease. These models are widely used to study ovarian cancer progression, tumor-microenvironment interactions, and intraperitoneal therapeutic responses, often incorporating bioluminescence or fluorescence imaging to longitudinally monitor tumor burden in vivo. The biological principle relies on the capacity of tumor cells such as SKOV3 or related ovarian carcinoma lines to survive in suspension, aggregate within ascites-like fluid, adhere to mesothelial surfaces, and invade peritoneal organs, thereby recapitulating human peritoneal carcinomatosis patterns observed in advanced disease.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)