Drug Information

Drug (ID: DG00550) and It's Reported Resistant Information

• Name: Infigratinib
• Synonyms: NVP-BGJ398; Infigratinib; 872511-34-7; BGJ398; BGJ-398; BGJ 398; Infigratinib free base; 3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-(6-((4-(4-ethylpiperazin-1-yl)phenyl)amino)pyrimidin-4-yl)-1-methylurea; UNII-A4055ME1VK; BGJ398 (NVP-BGJ398); MVP-BGJ398; A4055ME1VK; CHEBI:63451; 872511-34-7 (free base); 3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-(6-{[4-(4-ethylpiperazin-1-yl)phenyl]amino}pyrimidin-4-yl)-1-methylurea; 3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-(6-(4-(4-ethylpiperazin-1-yl)phenylamino)pyrimidin-4-yl)-1-methylurea; 3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-[6-[4-(4-ethylpiperazin-1-yl)anilino]pyrimidin-4-yl]-1-methylurea; C26H31Cl2N7O3; Truseltiq; CHEMBL1834657; 3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-(6-((4-(4-ethylpiperazin-1-yl)phenyl)amino)pyrimidin-4-yl)-1-methylurea.; 3-(2,6-Dichloro-3,5-dimethoxyphenyl)-1-[6-[[4-(4-ethylpiperazin-1-yl)phenyl]amino]pyrimidin-4-yl]-1-methylurea; Infigratinib [INN]; Infigratinib [USAN]; Infigratinib (BGJ398); Infigratinib (USAN/INN); Infigratinib [USAN:INN]; NVP-BGJ389; NVP-BGJ398(Infigratinib); MLS006010953; SCHEMBL374435; GTPL7877; QCR-48; CHEMBL1852688; DTXSID70236238; EX-A057; SYN1152; BGJ398, BGJ-398; HMS3295O21; AMY10737; AOB87703; BCP03602; BGJ398 - NVP-BGJ398; BDBM50355393; FD5035; MFCD22123241; NSC764487; s2183; WHO 10032; ZINC72105034; AKOS025149513; AKOS032949944; BCP9000399; CS-0586; DB11886; NSC-764487; SB16612; NCGC00274030-01; NCGC00274030-11; 3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-(6-(4-(4-ethylpiperazin-1-yl)-phenylamino)pyrimidin-4-yl)-1-methylurea; AC-28417; AS-16290; HY-13311; SMR004702757; Urea, N'-(2,6-dichloro-3,5-dimethoxyphenyl)-N-(6-((4-(4-ethyl-1-piperazinyl)phenyl)amino)-4-pyrimidinyl)-N-methyl-; BCP0726000187; FT-0699366; Y0313; D11589; J-510477; BRD-K42728290-001-01-8; Q27075200; 07J; 3-(2,6-Dichloro-3,5-dimethoxy-phenyl)-1-{6-[4-(4-ethyl-piperazin-1-yl)-phenylamino]-pyrimidin-4-yl}-1-methyl-urea
• Indication:
  In total 2 Indication(s)
  Cholangiocarcinoma [ICD-11: 2C12]; Approved; [1]
  Solid tumour/cancer [ICD-11: 2A00-2F9Z]; Approved; [1]
• Drug Resistance Disease(s):
  Disease(s) with Clinically Reported Resistance for This Drug (4 diseases)
  Head and neck cancer [ICD-11: 2D42]; [2]
  Liver cancer [ICD-11: 2C12]; [1]
  Solid tumour/cancer [ICD-11: 2A00-2F9Z]; [3]
  Transitional cell carcinoma [ICD-11: 2C9Z]; [4]
• Target: Fibroblast growth factor receptor (FGFR); NOUNIPROTAC; [1]
• Target: Fibroblast growth factor receptor 1 (FGFR1); FGFR1_HUMAN; [1]
• Formula: C26H31Cl2N7O3
• IsoSMILES: CCN1CCN(CC1)C2=CC=C(C=C2)NC3=CC(=NC=N3)N(C)C(=O)NC4=C(C(=CC(=C4Cl)OC)OC)Cl
• InChI: 1S/C26H31Cl2N7O3/c1-5-34-10-12-35(13-11-34)18-8-6-17(7-9-18)31-21-15-22(30-16-29-21)33(2)26(36)32-25-23(27)19(37-3)14-20(38-4)24(25)28/h6-9,14-16H,5,10-13H2,1-4H3,(H,32,36)(H,29,30,31)
• InChIKey: QADPYRIHXKWUSV-UHFFFAOYSA-N
• PubChem CID: 53235510
• ChEBI ID: CHEBI:63451
• TTD Drug ID: D03LWG
• DrugBank ID: DB11886

Type(s) of Resistant Mechanism of This Drug

  ADTT: Aberration of the Drug's Therapeutic Target

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Their Corresponding Diseases

ICD-02: Benign/in-situ/malignant neoplasm

Solid tumour/cancer [ICD-11: 2A00-2F9Z]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Fibroblast growth factor receptor 2 (FGFR2) [3]

• Molecule Alteration: Missense mutation; p.V564F (c.1690G>T)
• Resistant Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Gallbladder; N.A.
• Experiment for Molecule Alteration: Targeted sequencing of tumor tissue assay
• Mechanism Description: The missense mutation p.V564F (c.1690G>T) in gene FGFR2 cause the resistance of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [3]

• Molecule Alteration: Missense mutation; p.N540K (c.1620C>G)
• Resistant Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Gallbladder; N.A.
• Experiment for Molecule Alteration: Targeted sequencing of tumor tissue assay
• Mechanism Description: The missense mutation p.N540K (c.1620C>G) in gene FGFR3 cause the resistance of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [3]

• Molecule Alteration: Missense mutation; p.V555M (c.1663G>A)
• Resistant Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Gallbladder; N.A.
• Experiment for Molecule Alteration: Targeted sequencing of tumor tissue assay
• Mechanism Description: The missense mutation p.V555M (c.1663G>A) in gene FGFR3 cause the resistance of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [3]

• Molecule Alteration: Missense mutation; p.V555L (c.1663G>C)
• Resistant Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Gallbladder; N.A.
• Experiment for Molecule Alteration: Targeted sequencing of tumor tissue assay
• Mechanism Description: The missense mutation p.V555L (c.1663G>C) in gene FGFR3 cause the resistance of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [3]

• Molecule Alteration: Missense mutation; p.L608V (c.1822T>G)
• Resistant Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Gallbladder; N.A.
• Experiment for Molecule Alteration: Targeted sequencing of tumor tissue assay
• Mechanism Description: The missense mutation p.L608V (c.1822T>G) in gene FGFR3 cause the resistance of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [3]

• Molecule Alteration: Missense mutation; p.K650E (c.1948A>G)
• Resistant Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Gallbladder; N.A.
• Experiment for Molecule Alteration: Targeted sequencing of tumor tissue assay
• Mechanism Description: The missense mutation p.K650E (c.1948A>G) in gene FGFR3 cause the resistance of Infigratinib by aberration of the drug's therapeutic target

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Fibroblast growth factor receptor 2 (FGFR2) [5]

• Molecule Alteration: Missense mutation; p.K660E (c.1978A>G)
• Sensitive Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Ba/F3 cells; Colon; Homo sapiens (Human); CVCL_0161
• In Vitro Model: NIH-3T3 cells; Embryo; Mus musculus (Mouse); CVCL_0594
• In Vivo Model: Mouse xenograft model; Mus musculus
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Soft-agar colony formation assay
• Mechanism Description: The missense mutation p.K660E (c.1978A>G) in gene FGFR2 cause the sensitivity of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 2 (FGFR2) [5]

• Molecule Alteration: Missense mutation; p.K660N (c.1980G>C)
• Sensitive Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Ba/F3 cells; Colon; Homo sapiens (Human); CVCL_0161
• In Vitro Model: NIH-3T3 cells; Embryo; Mus musculus (Mouse); CVCL_0594
• In Vivo Model: Mouse xenograft model; Mus musculus
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Soft-agar colony formation assay
• Mechanism Description: The missense mutation p.K660N (c.1980G>C) in gene FGFR2 cause the sensitivity of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 2 (FGFR2) [5]

• Molecule Alteration: Missense mutation; p.W290C (c.870G>T)
• Sensitive Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Ba/F3 cells; Colon; Homo sapiens (Human); CVCL_0161
• In Vitro Model: NIH-3T3 cells; Embryo; Mus musculus (Mouse); CVCL_0594
• In Vivo Model: Mouse xenograft model; Mus musculus
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Soft-agar colony formation assay
• Mechanism Description: The missense mutation p.W290C (c.870G>T) in gene FGFR2 cause the sensitivity of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [5]

• Molecule Alteration: Missense mutation; p.R248C (c.742C>T)
• Sensitive Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Ba/F3 cells; Colon; Homo sapiens (Human); CVCL_0161
• In Vitro Model: NIH-3T3 cells; Embryo; Mus musculus (Mouse); CVCL_0594
• In Vivo Model: Mouse xenograft model; Mus musculus
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Soft-agar colony formation assay
• Mechanism Description: The missense mutation p.R248C (c.742C>T) in gene FGFR3 cause the sensitivity of Infigratinib by aberration of the drug's therapeutic target

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [5]

• Molecule Alteration: Missense mutation; p.S249C (c.746C>G)
• Sensitive Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Ba/F3 cells; Colon; Homo sapiens (Human); CVCL_0161
• In Vitro Model: NIH-3T3 cells; Embryo; Mus musculus (Mouse); CVCL_0594
• In Vivo Model: Mouse xenograft model; Mus musculus
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Soft-agar colony formation assay
• Mechanism Description: The missense mutation p.S249C (c.746C>G) in gene FGFR3 cause the sensitivity of Infigratinib by aberration of the drug's therapeutic target

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Fibroblast growth factor receptor 2 (FGFR2) [6]

• Molecule Alteration: Duplication; p.S267_D273 (c.799_819)
• Sensitive Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: NIH-3T3 cells; Embryo; Mus musculus (Mouse); CVCL_0594
• In Vivo Model: Nu/Nu mouse xenograft model; Mus musculus
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Soft-agar colony formation assay

Key Molecule: Fibroblast growth factor receptor 2 (FGFR2) [6]

• Molecule Alteration: Complex-indel; p.W290_I291delinsC (c.870_872delGAT)
• Sensitive Disease: Solid tumour/cancer [ICD-11: 2A00-2F9Z]
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: NIH-3T3 cells; Embryo; Mus musculus (Mouse); CVCL_0594
• In Vivo Model: Nu/Nu mouse xenograft model; Mus musculus
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Soft-agar colony formation assay

Liver cancer [ICD-11: 2C12]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Fibroblast growth factor receptor 1 (FGFR1) [1]

• Molecule Alteration: Structural variation; Amplification
• Resistant Disease: Intrahepatic cholangiocarcinoma [ICD-11: 2C12.1]
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: MET signalling pathway; Activation; hsa04020
• Cell Pathway Regulation: ERK/MAPK signaling pathway; Activation; hsa04210
• In Vitro Model: DMS114 cells; Lung; Homo sapiens (Human); CVCL_1174
• Mechanism Description: Upregulation of the MET signalling pathway leading to re-activation of the ERK/MAPK pathway was observed in conjunction with the development of resistance to infigratinib in FGFR1-amplified DMS114 lung cancer cells.

Key Molecule: Fibroblast growth factor receptor 1 (FGFR1) [1]

• Molecule Alteration: Structural variation; Amplification
• Resistant Disease: Intrahepatic cholangiocarcinoma [ICD-11: 2C12.1]
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: MET signalling pathway; Activation; hsa04020
• Cell Pathway Regulation: ERK/MAPK signaling pathway; Activation; hsa04210
• In Vitro Model: DMS114 cells; Lung; Homo sapiens (Human); CVCL_1174
• Mechanism Description: Upregulation of the MET signalling pathway leading to re-activation of the ERK/MAPK pathway was observed in conjunction with the development of resistance to infigratinib in FGFR1-amplified DMS114 lung cancer cells.

Bladder cancer [ICD-11: 2C94]

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [7]

• Molecule Alteration: Missense mutation; p.G370C (c.1108G>T)
• Sensitive Disease: Bladder cancer [ICD-11: 2C94.0]
• Experimental Note: Identified from the Human Clinical Data

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [7]

• Molecule Alteration: Missense mutation; p.Y373C (c.1118A>G)
• Sensitive Disease: Bladder cancer [ICD-11: 2C94.0]
• Experimental Note: Identified from the Human Clinical Data

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [7]

• Molecule Alteration: Missense mutation; p.R248C (c.742C>T)
• Sensitive Disease: Bladder cancer [ICD-11: 2C94.0]
• Experimental Note: Identified from the Human Clinical Data

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [8]

• Molecule Alteration: Missense mutation; p.S371C (c.1111A>T)
• Sensitive Disease: Bladder cancer [ICD-11: 2C94.0]
• Experimental Note: Identified from the Human Clinical Data

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [8]

• Molecule Alteration: Missense mutation; p.G380R (c.1138G>A)
• Sensitive Disease: Bladder cancer [ICD-11: 2C94.0]
• Experimental Note: Identified from the Human Clinical Data

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [7]

• Molecule Alteration: Missense mutation; p.S249C (c.746C>G)
• Sensitive Disease: Bladder cancer [ICD-11: 2C94.0]
• Experimental Note: Identified from the Human Clinical Data

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [8]

• Molecule Alteration: Synonymous; p.K650K (c.1950G>A)
• Sensitive Disease: Bladder cancer [ICD-11: 2C94.0]
• Experimental Note: Identified from the Human Clinical Data

Urinary system cancer [ICD-11: 2C95]

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [9]

• Molecule Alteration: Missense mutation; p.S249C (c.746C>G)
• Sensitive Disease: Urinary system cancer [ICD-11: 2C95.Y]
• Experimental Note: Revealed Based on the Cell Line Data
• Cell Pathway Regulation: FGF/FGFR signaling pathway; Inhibition; hsa01521
• In Vitro Model: NCI-H716 cells; Colon; Homo sapiens (Human); CVCL_1581
• In Vitro Model: NCI-H520 cells; Lung; Homo sapiens (Human); CVCL_1566
• In Vitro Model: RT112 cells; Bladder; Homo sapiens (Human); CVCL_1670
• In Vitro Model: BaF3 cells; Bone; Mus musculus (Mouse); CVCL_0161
• In Vitro Model: KG-1 cells; Bone marrow; Homo sapiens (Human); CVCL_0374
• In Vitro Model: KATO-3 cells; Gastric; Homo sapiens (Human); CVCL_0371
• In Vitro Model: UMUC14 cells; Kidney; Homo sapiens (Human); CVCL_2747
• In Vitro Model: SNU16 cells; Ascites; Homo sapiens (Human); CVCL_0076
• In Vitro Model: OPM2 cells; Peripheral blood; Homo sapiens (Human); CVCL_1625
• In Vitro Model: NCI-H2444 cells; Lung; Homo sapiens (Human); CVCL_1552
• In Vitro Model: NCI-H1581 cells; Lung; Homo sapiens (Human); CVCL_1479
• In Vitro Model: MFM-223 cells; Pleural effusion; Homo sapiens (Human); CVCL_1408
• In Vitro Model: DMS-114 cells; Lung; Homo sapiens (Human); CVCL_1174
• In Vivo Model: BALB/c nude mouse PDX model; Mus musculus
• Mechanism Description: c-Myc functioned as the key downstream effector that preceded FGFR-MEK/ERK signaling in FGFR aberrant cancer. Disruption of c-Myc overrode the cell proliferation driven by constitutively active FGFR. FGFR inhibition in FGFR-addicted cancer facilitated c-Myc degradation via phosphorylating c-Myc at threonine 58. Ectopic expression of undegradable c-Myc mutant conferred resistance to FGFR inhibition both in vitro and in vivo. c-Myc level alteration stringently determined the response to FGFR inhibitors, as demonstrated in FGFR-responsive cancer subset, as well as cancers bearing acquired or de novo resistance to FGFR inhibition.

Transitional cell carcinoma [ICD-11: 2C9Z]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [4]

• Molecule Alteration: Missense mutation; p.V555M (c.1663G>A)
• Resistant Disease: Transitional cell carcinoma [ICD-11: 2C9Z.0]
• Experimental Note: Identified from the Human Clinical Data

Head and neck cancer [ICD-11: 2D42]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Fibroblast growth factor receptor 3 (FGFR3) [2]

• Molecule Alteration: Missense mutation; p.S131L (c.392C>T)
• Resistant Disease: Head and neck squamous cell carcinoma [ICD-11: 2D42.1]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: SCC25 cells; Oral; Homo sapiens (Human); CVCL_1682
• In Vitro Model: HSC3 cells; Tongue; Homo sapiens (Human); CVCL_1288
• In Vitro Model: FaDu cells; Pharynx; Homo sapiens (Human); CVCL_1218
• In Vitro Model: HN cells; Cervical lymph node; Homo sapiens (Human); CVCL_1283
• In Vitro Model: Detroit 562 cells; Pleural effusion; Homo sapiens (Human); CVCL_1171
• In Vitro Model: 584-A2 cells; Larynx; Homo sapiens (Human); CVCL_V278
• Experiment for Molecule Alteration: Immunohistochemical staining assay; qRT-PCR
• Experiment for Drug Resistance: MTT assay
• Mechanism Description: In vitro, FGFR3 overexpression led to increased proliferation, whereas migration was not altered. Moreover, FGFR3-overexpressing cells were more sensitive to BGJ398. Cells overexpressing FGFR3 mutant versions showed increased proliferation compared to wild-type FGFR3 under serum-reduced conditions and were largely as sensitive as the wild-type protein to BGJ398.

References

• Ref 1: Fibroblast growth factor receptors in cancer: genetic alterations, diagnostics, therapeutic targets and mechanisms of resistance .Br J Cancer. 2021 Mar;124(5):880-892. doi: 10.1038/s41416-020-01157-0. Epub 2020 Dec 3. 10.1038/s41416-020-01157-0
• Ref 2: Evaluation of FGFR3 as a Therapeutic Target in Head and Neck Squamous Cell CarcinomaTarget Oncol. 2016 Oct;11(5):631-642. doi: 10.1007/s11523-016-0431-z.
• Ref 3: Polyclonal Secondary FGFR2 Mutations Drive Acquired Resistance to FGFR Inhibition in Patients with FGFR2 Fusion-Positive CholangiocarcinomaCancer Discov. 2017 Mar;7(3):252-263. doi: 10.1158/2159-8290.CD-16-1000. Epub 2016 Dec 29.
• Ref 4: Efficacy of BGJ398, a Fibroblast Growth Factor Receptor 1-3 Inhibitor, in Patients with Previously Treated Advanced Urothelial Carcinoma with FGFR3 AlterationsCancer Discov. 2018 Jul;8(7):812-821. doi: 10.1158/2159-8290.CD-18-0229. Epub 2018 May 30.
• Ref 5: Inhibitor-sensitive FGFR2 and FGFR3 mutations in lung squamous cell carcinomaCancer Res. 2013 Aug 15;73(16):5195-205. doi: 10.1158/0008-5472.CAN-12-3950. Epub 2013 Jun 20.
• Ref 6: Identification of Oncogenic and Drug-Sensitizing Mutations in the Extracellular Domain of FGFR2Cancer Res. 2015 Aug 1;75(15):3139-46. doi: 10.1158/0008-5472.CAN-14-3771. Epub 2015 Jun 5.
• Ref 7: A Phase I, Open-Label, Multicenter, Dose-escalation Study of the Oral Selective FGFR Inhibitor Debio 1347 in Patients with Advanced Solid Tumors Harboring FGFR Gene AlterationsClin Cancer Res. 2019 May 1;25(9):2699-2707. doi: 10.1158/1078-0432.CCR-18-1959. Epub 2019 Feb 11.
• Ref 8: Small molecule FGF receptor inhibitors block FGFR-dependent urothelial carcinoma growth in vitro and in vivoBr J Cancer. 2011 Jan 4;104(1):75-82. doi: 10.1038/sj.bjc.6606016. Epub 2010 Nov 30.
• Ref 9: c-Myc Alteration Determines the Therapeutic Response to FGFR InhibitorsClin Cancer Res. 2017 Feb 15;23(4):974-984. doi: 10.1158/1078-0432.CCR-15-2448. Epub 2016 Jul 11.