PD-166866 |
Catalog No.GC19279
One-Click Copy Product Info
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PD-166866 is a selective and orally active FGFR1 (fibroblast growth factor receptor 1) tyrosine kinase inhibitor, with an IC₅₀ of 52.4nM.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 192705-79-6
Sample solution is provided at 25 µL, 10mM.
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PD-166866 is a selective and orally active FGFR1 (fibroblast growth factor receptor 1) tyrosine kinase inhibitor, with an IC₅₀ of 52.4nM[1]. FGFR1 is a transmembrane receptor tyrosine kinase that, upon ligand binding, activates downstream signaling cascades regulating cell proliferation, differentiation, and survival[2]. PD-166866 inhibits FGFR1 tyrosine kinase activity through an ATP-competitive mechanism and is widely used to study FGFR-driven signaling in tumor growth, angiogenesis, and related pathophysiological processes[3].
In vitro, treatment of lymphatic endothelial cells with 1μM PD-166866 for 48h significantly inhibited the proliferation, migration, invasion, and tube formation, reduced the phosphorylation levels of FGFR1, PTEN, and AKT, and decreased CXCL9 secretion[4]. PD-166866 (0.1-50μM; 24h) reduced cell viability, increased membrane damage, induced DNA fragmentation, and accumulated PARP in HeLa cells[5].
In vivo, PD-166866 (0.1 or 0.5mg/day; i.p.; 2 weeks) significantly reduced tumor volume and decreased the number of proliferating cell nuclear antigen (PCNA)-positive cells in SYO-1 xenograft tumors in BALB/c nu/nu mice[6]. Combination of PD-166866 (30mg/kg; every 2 days for 14 days; i.p.) and rapamycin significantly inhibited the growth and progression of T-ALL cells and prolonged the survival time of the Jurkat cell-derived xenograft NCG mice[7].
References:
[1] Panek RL, Lu GH, Dahring TK, et al. In vitro biological characterization and antiangiogenic effects of PD 166866, a selective inhibitor of the FGF-1 receptor tyrosine kinase. J Pharmacol Exp Ther. 1998;286(1):569-577.
[2] Kaur N, Gare SR, Shen J, Raja R, Fonseka O, Liu W. Multi-organ FGF21-FGFR1 signaling in metabolic health and disease. Front Cardiovasc Med. 2022;9:962561.
[3] Calandrella N, Risuleo G, Scarsella G, et al. Reduction of cell proliferation induced by PD166866: an inhibitor of the basic fibroblast growth factor. J Exp Clin Cancer Res. 2007;26(3):405-409.
[4] Kang J, Cheng A, Chen G, Zhu L, Han Z, Xu Q. Tumor Cells-Derived FGF-2 Promotes Lymphangiogenesis as a Prognostic Marker in OSCC. J Oral Pathol Med. 2025;54(8):694-705.
[5] Risuleo G, Ciacciarelli M, Castelli M, Galati G. The synthetic inhibitor of fibroblast growth factor receptor PD166866 controls negatively the growth of tumor cells in culture. J Exp Clin Cancer Res. 2009;28(1):151.
[6] Ishibe T, Nakayama T, Okamoto T, et al. Disruption of fibroblast growth factor signal pathway inhibits the growth of synovial sarcomas: potential application of signal inhibitors to molecular target therapy. Clin Cancer Res. 2005;11(7):2702-2712.
[7] Zhang ZJ, Wu QF, Ren AQ, et al. ATF4 renders human T-cell acute lymphoblastic leukemia cell resistance to FGFR1 inhibitors through amino acid metabolic reprogramming. Acta Pharmacol Sin. 2023;44(11):2282-2295.
| Cell experiment [1]: | |
Cell lines | HeLa cells |
Preparation Method | HeLa cells were maintained in DMEM (Dulbecco's Modified Eagle's Medium - high glucose), supplemented with newborn bovine serum [final concentration (f.c.) 10%], penicillin-streptomycin (10000U/ml) and glutamine (2mM); the pH of the medium was 7.2 and incubation was at 37°C in a 5% CO2 atmosphere. Cells were routinely passaged when confluent. Cells were exposed to a relatively broad range of PD-166866 concentrations (0.1-50μM) for 24 hours. Then cell vitality was assessed by the MTT assay. Oxidative stress at membrane level was assessed by commercial kit. DNA damage was assessed by in situ fluorescent staining with Terminal Deoxynucleotidyl Transferase dUTP nick end labeling (TUNEL assay). The expression of PARP, consequent to DNA fragmentation, was evidenced by immunohistochemistry. |
Reaction Conditions | 0.1-50μM; 24h |
Applications | PD-166866 (0.1-50μM; 24h) reduced cell viability, increased membrane damage, induced DNA fragmentation, and accumulated PARP in HeLa cells. |
| Animal experiment [2]: | |
Animal models | male BALB/c nu/nu athymic mice |
Preparation Method | SYO-1 (5×106) cells suspended in 100μl of PBS were s.c. injected into the hind flank region of male BALB/c nu/nu athymic mice at 5 weeks of age. When the tumor volume reached about 50mm3 (usually 11-12 days after inoculation), PD-166866 (0.1 or 0.5mg) suspended in 50μl of DMSO was given i.p. , a treatment which was repeated thereafter once a day, 6 days a week, for 2 weeks. Tumor size was measured with vernier calipers, and the volume was calculated as π/6×length×width×height. |
Dosage form | 0.1 and 0.5mg/day; i.p.; 2 weeks |
Applications | PD-166866 significantly reduced tumor volume in SYO-1 xenograft tumors in BALB/c nu/nu mice. |
References: | |
| Cas No. | 192705-79-6 | SDF | |
| Canonical SMILES | O=C(NC(C)(C)C)NC1=NC2=NC(N)=NC=C2C=C1C3=CC(OC)=CC(OC)=C3 | ||
| Formula | C20H24N6O3 | M.Wt | 396.44 |
| Solubility | DMSO : 10.33 mg/mL (26.06 mM) | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.5224 mL | 12.6122 mL | 25.2245 mL |
| 5 mM | 504.5 μL | 2.5224 mL | 5.0449 mL |
| 10 mM | 252.2 μL | 1.2612 mL | 2.5224 mL |
Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
g
μL
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Quality Control & SDS
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- Purity: >99.50% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 22 reference(s) in Google Scholar.)