Journal: International forum of allergy & rhinology

Article Title: Inhibition of fibroblast growth factor receptor with AZD4547 mitigates juvenile nasopharyngeal angiofibroma

doi: 10.1002/alr.21987

Figure Lengend Snippet: FGFR inhibition mitigates JNA fibroblast proliferation and MAPK activation. (A) JNA fibroblast lines were treated in triplicate with the indicated concentrations of AZD4547 for 72 hours and assessed for viability. Experiments were repeated 3 times and cumulative data were used to generate dose-response curves and determine the IC50 values for each line. (B) Levels of total and phosphorylated p44/42 MAPK were assessed by immunoblotting. (C) Cumulative densitometric values from 3 independent experiments of phosphorylated and total levels were graphed. FGFR = fibroblast growth factor receptor; IC50 = the dose that is cytotoxic to 50% of the cells treated in vitro; JNA = juvenile nasopharyngeal angiofibroma; MAPK = mitogen-activated protein kinase.

Article Snippet: Pan FGFR inhibitor AZD4547 was obtained from Chemietek (Indianapolis, IN), and VEGFR inhibitor SU5416 was obtained from Selleckchem (Houston, TX).

Techniques: Inhibition, Activation Assay, Western Blot, In Vitro

Journal: International forum of allergy & rhinology

Article Title: Inhibition of fibroblast growth factor receptor with AZD4547 mitigates juvenile nasopharyngeal angiofibroma

doi: 10.1002/alr.21987

Figure Lengend Snippet: FGFR inhibition mitigates migration and invasion of JNA fibroblasts. JNA fibroblast (A) migration and (B) invasion was measured in vitro in the presence of IC50 values of AZD4547 or DMSO. The number of migrating cells were normalized to the cell viability and represented graphically. All experiments performed in duplicate with 3 experimental repeats. DMSO = dimethylsulfoxide; FGFR = fibroblast growth factor receptor; IC50 = the dose that is cytotoxic to 50% of the cells treated in vitro; JNA = juvenile nasopharyngeal angiofibroma.

Article Snippet: Pan FGFR inhibitor AZD4547 was obtained from Chemietek (Indianapolis, IN), and VEGFR inhibitor SU5416 was obtained from Selleckchem (Houston, TX).

Techniques: Inhibition, Migration, In Vitro

Journal: The International journal of developmental biology

Article Title: FGF signaling mediates definitive endoderm formation by regulating epithelial-to-mesenchymal transition and cell proliferation.

doi: 10.1387/ijdb.190372ql

Figure Lengend Snippet: Fig. 2. Definitive endoderm induc tion is disturbed by BGJ398, as well as gene expression of FGF family members. (A,B) RT-qPCR analysis for the indicated genes expressed in Activin A-induced cells in the absence and presence of BGJ398. Data represent means ± s.d. from three biological repeats. *p<0.05; **p<0.01, compared to Activin A-induced cells in the absence of BGJ398.

Article Snippet: To blocking the FGF signaling pathway in DE differentiation, an effective and selective FGFR1/2/3 inhibitor BGJ398 (50 nM, Selleck Chemicals, USA) or AZD4547 (50 nM, Selleck Chemicals, USA) was added during the whole induction process.

Techniques: Gene Expression, Quantitative RT-PCR

Journal: The International journal of developmental biology

Article Title: FGF signaling mediates definitive endoderm formation by regulating epithelial-to-mesenchymal transition and cell proliferation.

doi: 10.1387/ijdb.190372ql

Figure Lengend Snippet: Fig. 3. An epithelial-to-mesenchymal transition (EMT) during definitive endoderm differentiation is blocked by BGJ398. (A) Immunofluorescence images of undifferentiated hESCs and Activin A-induced cells with or without BGJ398 treatment. The scale bar indicates 20 mm. (B) Time-course RT- qPCR analysis for EMT associated genes expressed in hESCs and Activin A-induced cells with or without BGJ398 treatment. Shown are the means ± s.d. of three replicates. *p<0.05; **p<0.01, compared to Activin A-induced cells in the absence of BGJ398. (C) Western blot analysis for EMT and DE associated markers at day 0, day 1, day 2 and day 3.

Article Snippet: To blocking the FGF signaling pathway in DE differentiation, an effective and selective FGFR1/2/3 inhibitor BGJ398 (50 nM, Selleck Chemicals, USA) or AZD4547 (50 nM, Selleck Chemicals, USA) was added during the whole induction process.

Techniques: Immunofluorescence, Quantitative RT-PCR, Western Blot

Journal: BMC Biology

Article Title: FGF-independent MEK1/2 signalling in the developing foetal testis is essential for male germline differentiation in mice

doi: 10.1186/s12915-023-01777-x

Figure Lengend Snippet: Summary of treatments and doses used in gonad cultures

Article Snippet: Additional inhibitors for FGFR (AZD4547; SelleckChem, S2801 and SU5402; MedChem Express, HY-10407), p38 (Ralimetinib dimesylate; MedChem Express, HY-13241) and PI3K (PF-04691502; MedChem Express, HY-15177) signalling were also used (Table ) to ensure consistency of outcomes with each of the primary inhibitors used.

Techniques: Control, Recombinant

Journal: bioRxiv

Article Title: FGFR1-phosphate sensing and crystal-induced gasdermin D signaling in neutrophils drive vascular calcification in CKD

doi: 10.64898/2026.05.23.725305

Figure Lengend Snippet: (A) Neutrophils pretreated with a 20 μM FGFR1 inhibitor (FGFR1-I, SU5402) were cultured under high phosphate conditions for 6 hours, subsequently stained by SYTOX green. (B) The quantification of SYTOX-positive area. n=4. (C) HL-60 cells were differentiated into neutrophils by incubation with ATRA for 24 hours. The cells were then transfected with FGFR1-specific siRNA via electroporation, performed twice at 24-hours intervals. As a control, HL-60 cells were electroporated under the same conditions with non-targeting control siRNA. At 24 hours after the second transfection, both control and FGFR1 knockdown HL-60 cells were cultured under high phosphate conditions for 10 hours. (D) The expression of FGFR1 mRNA in differentiated HL-60 cells transfected with control or FGFR1-targeting siRNA, assessed by qPCR (n=3). (E-H) FGFR1 knockdown HL-60 cells and control HL-60 cells were incubated under 0.9mM or 4.8mM phosphate conditions for 10 hours. NET formation was assessed by (E and F) SYTOX green (green) (n=6) and (G and H) CitH3 staining (red), with MPO (green) serving as a neutrophil marker (n=8). (I) Immunoblotting was performed using antibodies against ERK and pERK on lysates derived from FGFR1 knockdown or control HL-60 cells under low or high phosphate conditions. As a positive control (posi con), human kidney-2 (HK2) cells exposed by FGF2, one of the FGFR ligands, were used. (J) The ratio of pERK/ERK expression. n=3. Data represent mean ± SEM. Statistical analysis was performed using one-way ANOVA followed by post hoc Tukey’s test (B, F and H) or Student’s unpaired t test (D and J). *P <0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ns: not significant. The insets are higher magnification images of the black and yellow boxes. Scale bars: 200 μm (A, E, and G).

Article Snippet: FGFR inhibitor (AZD4547, 6 mg/kg; MedChemExpress) ( ) or vehicle was administered via intraperitoneal injection beginning at 15 weeks of age.

Techniques: Cell Culture, Staining, Incubation, Transfection, Electroporation, Control, Knockdown, Expressing, Marker, Western Blot, Derivative Assay, Positive Control

Journal: bioRxiv

Article Title: FGFR1-phosphate sensing and crystal-induced gasdermin D signaling in neutrophils drive vascular calcification in CKD

doi: 10.64898/2026.05.23.725305

Figure Lengend Snippet: (A) Illustration of the experimental design. Eight-week-old C57BL/6 male mice were randomly divided into three groups: the high phosphate (HP) group (N=6), the CKD vascular calcification model (CKD + HP) group (N=8) and the FGFR inhibitor-treated CKD vascular calcification model (CKD + HP + FGFR-I) group (N=6). For phosphate loading, mice were administered a high-phosphate diet (1.25% phosphate). CKD was induced by feeding an adenine-rich diet (0.15-0.2% adenine). AZD4547 (FGFR inhibitor, 6mg/kg) or vehicle control was administered via intraperitoneal injection. (B) The serum levels of creatinine (Cr), blood urea nitrogen (BUN), calcium (Ca) and phosphate (P) were measured at the end of the experimental period. (C) The panels show the representative images of Elastica Masson staining and von Kossa staining of kidneys. Scale bars: 1000 μm (low magnification) and 100 μm (high magnification). (D) The graphs show the percentage of fibrosis area and von Kossa-positive area per section. (E) The representative images of von Kossa, Ly6b (brown), and CitH3 (brown) staining of the aortic valve. The black arrows indicate Ly6b- and CitH3-positive cells, respectively. The insets are higher magnification images of the yellow boxes. Scale bars: 200 μm (low magnification) and 50 μm (high magnification). (F) The graphs show the percentage of von Kossa-positive area calcified area in the aortic valve annulus (HP: n=6, CKD + HP: n=8, CKD + HP + FGFR-I: n=6) and the ratio of CitH3-positive area to Ly6b-positive area within the aortic valve, reflecting NET-forming neutrophils (HP: n=3, CKD + HP: n=4, CKD + HP + FGFR-I: n=4). Data represent mean ± SEM. Statistical analysis was performed using Kruskal-Wallis test (B, D and F). *P <0.05, **P < 0.01, ***P < 0.001. ns: not significant.

Article Snippet: FGFR inhibitor (AZD4547, 6 mg/kg; MedChemExpress) ( ) or vehicle was administered via intraperitoneal injection beginning at 15 weeks of age.

Techniques: Control, Injection, Staining

Journal: Experimental and Therapeutic Medicine

Article Title: Fibroblast growth factor 2 suppresses the expression of C-C motif chemokine 11 through the c-Jun N-terminal kinase pathway in human dental pulp-derived mesenchymal stem cells

doi: 10.3892/etm.2021.10791

Figure Lengend Snippet: The AZD4547 FGFR inhibitor abolishes the suppression in the expression of CCL11. SDP11 cells were cultured in the presence of 10 µM AZD4547 with or without 20 ng/ml FGF2 for 24 h, and the expression of CCL11 was analyzed by reverse transcription-quantitative PCR. AZD4547 attenuated the FGF2-mediated suppression of CCL11 expression. Data are presented as the mean ± SEM. ** P<0.01. FGFR, FGF receptor; FGF2, fibroblast growth factor 2; CCL11, C-C motif ligand 11; n.s., not significant.

Article Snippet: FGF2 and AZD4547 (FGFR inhibitor) were purchased from R&D Systems, Inc. and Santa Cruz Biotechnology, Inc., respectively.

Techniques: Expressing, Cell Culture, Reverse Transcription, Real-time Polymerase Chain Reaction

Journal: Oncotarget

Article Title: Fibroblast growth factor receptor 2 expression, but not its genetic amplification, is associated with tumor growth and worse survival in esophagogastric junction adenocarcinoma

doi: 10.18632/oncotarget.7782

Figure Lengend Snippet: ( A ) Proliferation assay of tumor cells exposed to AZD4547 with and without FGF7 stimulation; ( B ) De-phosphorylation of AKT and ERK by AZD4547, with and without FGF7 stimulation; ( C ) Proliferation assay using siRNAs targeted against FGFR2 (si-FGFR2), with and without FGF7 stimulation; ( D ) De-phosphorylation of AKT and ERK after FGFR2 knockdown by si-FGFR2, with and without FGF7 stimulation. * P < 0.05.

Article Snippet: A pan-FGFR inhibitor AZD4547 was purchased from AdooQ BioScience (Irvine, Carlsbad, CA, USA).

Techniques: Proliferation Assay, De-Phosphorylation Assay, Knockdown

Journal: British Journal of Cancer

Article Title: Fibroblast growth factor signalling influences homologous recombination-mediated DNA damage repair to promote drug resistance in ovarian cancer

doi: 10.1038/s41416-022-01899-z

Figure Lengend Snippet: Immunoblot analysis was used to assess blockade of the FGF signalling pathway in A2780DPP cells in response to a AZD4547 (0–10 µM) and b SU5402 (0–10 µM). MTT assays were used to investigate the viability of A2780DPP cells following co-treatment with 10 µM AZD4547 or 10 µM SU5402 and c , d cisplatin (0–25.33 µM) and e , f carboplatin (0–85.12 µM). Results represent three independent experiments. Pairwise comparisons of mean IC 50 values were calculated by Student’s t -tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Ns not significant.

Article Snippet: 2.5 × 10 5 cells were seeded in six-well plates and incubated for 24 h prior to harvest or treatment with either an acute cisplatin challenge (3 μM) (Sigma Aldrich, prepared as a 2 mg/mL stock in sterile water), the FGFR inhibitors AZD4547 (ApexBio, Cambridge, UK, prepared as a 10 mM stock in DMSO) or SU5402 (Sigma Aldrich, Dorset, UK, prepared as a 10 mM stock in DMSO), or transfection as described above.

Techniques: Western Blot

Journal: British Journal of Cancer

Article Title: Fibroblast growth factor signalling influences homologous recombination-mediated DNA damage repair to promote drug resistance in ovarian cancer

doi: 10.1038/s41416-022-01899-z

Figure Lengend Snippet: a The Dundee Ovarian Cancer Study; ‘A1’ sample = chemonaïve, ‘A2’ sample = disease relapse. b FGF1 and FGFR2 gene expression in chemoresistant ovarian cancer patient-derived cells was assessed by qRT-PCR analysis. MTT assays were used to compare viability of chemonaive cells, and cells from drug-resistant relapse samples from two patients in the presence or absence of combination treatments with 10 µM AZD4547 and c , e cisplatin (0–25.33 µM) or d , f carboplatin (0–85.12 µM). Pairwise comparisons of mean IC 50 values and relative gene expression were calculated by Student’s t -tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Ns not significant.

Article Snippet: 2.5 × 10 5 cells were seeded in six-well plates and incubated for 24 h prior to harvest or treatment with either an acute cisplatin challenge (3 μM) (Sigma Aldrich, prepared as a 2 mg/mL stock in sterile water), the FGFR inhibitors AZD4547 (ApexBio, Cambridge, UK, prepared as a 10 mM stock in DMSO) or SU5402 (Sigma Aldrich, Dorset, UK, prepared as a 10 mM stock in DMSO), or transfection as described above.

Techniques: Gene Expression, Derivative Assay, Quantitative RT-PCR

Journal: Oncology Letters

Article Title: In vivo acquired sorafenib-resistant patient-derived tumor model displays alternative angiogenic pathways, multi-drug resistance and chromosome instability

doi: 10.3892/ol.2018.9078

Figure Lengend Snippet: LIXC-004SR activates an alternative angiogenic pathway. (A) Reverse transcription-quantitative polymerase chain reaction analyses of selected differentially expressed genes; MMP-1, FGF-5 and VEGF-A. *P<0.05, ***P<0.0001; two-way ANOVA with Bonferroni post tests. (B) HUVEC proliferation. ***P<0.001, one-way ANOVA. (C) HUVEC Akt and ERK phosphorylation determination by western blot analysis. (D) Western blot analyses of 004SR supernatant-induced HUVEC Akt and ERK phosphorylation in the presence of sorafenib and AZD4547 (upper panel) and quantification of the western blot analyses (lower panel, data represent two separate experiments). (E) 004SR tumor-bearing mice were treated with vehicle, sorafenib, AZD4547, or the combination of AZD4547 and sorafenib. (F) AZD4547 inhibited tumor progression (***P<0.001 vs. the vehicle control group on day 27; two-way ANOVA with Bonferroni post hoc tests). The study was repeated once with similar results. 004SR, LIXC-004SR; MMP-1, matrix metalloproteinase 1; FGF-5, fibroblast growth factor 5; VEGF-A, vascular endothelial growth factor A; ANOVA, analysis of variance; HUVEC, human umbilical vein endothelial cells; ERK, extracellular-signal-regulated kinase; CM, conditioned medium.

Article Snippet: Sorafenib was purchased from LC Laboratories (Woburn, MA, USA) and AZD4547 [a selective inhibitor for fibroblast growth factor (FGF) receptor 1] was purchased from Shanghai Biochempartner Co., Ltd. (Shanghai, China).

Techniques: Reverse Transcription, Real-time Polymerase Chain Reaction, Phospho-proteomics, Western Blot, Control