BGJ-398 - CAS 872511-34-7
Catalog number: 872511-34-7
Category: Inhibitor
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BGJ398, also known as NVP-BGJ398, is a pan FGFR kinase inhibitor, and is an orally bioavailable pan inhibitor of human fibroblast growth factor receptors (FGFRs) with potential antiangiogenic and antineoplastic activities. BGJ398 selectively binds to and inhibits the activities of FGFRs, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death.
Related CAS:
1310746-10-1 (phosphate); 1310746-11-2 (monohydrate)
Solid powder
3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-(6-((4-(4-ethylpiperazin-1-yl)phenyl)amino)pyrimidin-4-yl)-1-methylurea; NVPBGJ398; NVPBGJ 398; NVPBGJ-398; BGJ398; BGJ-398; BG J398; Infigratinib
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Current Developer:
Novartis Oncology.
1.Signature program: a platform of basket trials.
Slosberg ED;Kang BP;Peguero J;Taylor M;Bauer TM;Berry DA;Braiteh F;Spira A;Meric-Bernstam F;Stein S;Piha-Paul SA;Salvado A Oncotarget. 2018 Apr 20;9(30):21383-21395. doi: 10.18632/oncotarget.25109. eCollection 2018 Apr 20.
Investigating targeted therapies can be challenging due to diverse tumor mutations and slow patient accrual for clinical studies. The Signature Program is a series of 8 phase 2, agent-specific basket protocols using a rapid study start-up approach involving no predetermined study sites. Each protocol evaluated 1 agent (buparlisib, dovitinib, binimetinib, encorafenib, sonidegib, BGJ398, ceritinib, or ribociclib) in patients with solid or hematologic malignancies and an actionable mutation. The primary endpoint of each study was the clinical benefit rate (ie, complete or partial response, or stable disease) at 16 weeks. A total of 192 individual sites were opened in the United States, with a median start-up time of 3.6 weeks. The most common tumor types among the 595 treated patients were colorectal (9.2%), non-small cell lung adenocarcinoma (9.1%), and ovarian (8.4%). Frequent genetic alterations were in ;PIK3CA;, ;RAS;, ;p16;, and ;PTEN;. Overall, 30 partial or complete responses were observed with 6 compounds in 16 tumor types. The Signature Program presents a unique and successful approach for rapid signal finding across multiple tumors and allowed various agents to be evaluated in patients with rare alterations.
2.Upregulation of EGFR signaling is correlated with tumor stroma remodeling and tumor recurrence in FGFR1-driven breast cancer.
Holdman XB;Welte T;Rajapakshe K;Pond A;Coarfa C;Mo Q;Huang S;Hilsenbeck SG;Edwards DP;Zhang X;Rosen JM Breast Cancer Res. 2015 Nov 18;17:141. doi: 10.1186/s13058-015-0649-1.
INTRODUCTION: ;Despite advances in early detection and adjuvant targeted therapies, breast cancer is still the second most common cause of cancer mortality among women. Tumor recurrence is one of the major contributors to breast cancer mortality. However, the mechanisms underlying this process are not completely understood. In this study, we investigated the mechanisms of tumor dormancy and recurrence in a preclinical mouse model of breast cancer.;METHODS: ;To elucidate the mechanisms driving tumor recurrence, we employed a transplantable Wnt1/inducible fibroblast growth factor receptor (FGFR) 1 mouse mammary tumor model and utilized an FGFR specific inhibitor, BGJ398, to study the recurrence after treatment. Histological staining was performed to analyze the residual tumor cells and tumor stroma. Reverse phase protein array was performed to compare primary and recurrent tumors to investigate the molecular mechanisms leading to tumor recurrence.;RESULTS: ;Treatment with BGJ398 resulted in rapid tumor regression, leaving a nonpalpable mass of dormant tumor cells organized into a luminal and basal epithelial layer similar to the normal mammary gland, but surrounded by dense stroma with markedly reduced levels of myeloid-derived tumor suppressor cells (MDSCs) and decreased tumor vasculature.
3.Targeting Fibroblast Growth Factor Receptor 1 for Treatment of Soft-Tissue Sarcoma.
Chudasama P;Renner M;Straub M;Mughal SS;Hutter B;Kosaloglu Z;Schweßinger R;Scheffler M;Alldinger I;Schimmack S;Persigehl T;Kobe C;Jäger D;von Kalle C;Schirmacher P;Beckhaus MK;Wolf S;Heining C;Gröschel S;Wolf J;Brors B;Weichert W;Glimm H;Scholl C;Mechtersheimer G;Specht K;Fröhling S Clin Cancer Res. 2017 Feb 15;23(4):962-973. doi: 10.1158/1078-0432.CCR-16-0860. Epub 2016 Aug 17.
Purpose:; Altered FGFR1 signaling has emerged as a therapeutic target in epithelial malignancies. In contrast, the role of FGFR1 in soft-tissue sarcoma (STS) has not been established. Prompted by the detection and subsequent therapeutic inhibition of amplified FGFR1 in a patient with metastatic leiomyosarcoma, we investigated the oncogenic properties of FGFR1 and its potential as a drug target in patients with STS.;Experimental Design:; The frequency of ;FGFR1; amplification and overexpression, as assessed by FISH, microarray-based comparative genomic hybridization and mRNA expression profiling, SNP array profiling, and RNA sequencing, was determined in three patient cohorts. The sensitivity of STS cell lines with or without FGFR1 alterations to genetic and pharmacologic FGFR1 inhibition and the signaling pathways engaged by FGFR1 were investigated using viability assays, colony formation assays, and biochemical analysis.;Results:; Increased ;FGFR1; copy number was detected in 74 of 190 (38.9%; cohort 1), 13 of 79 (16.5%; cohort 2), and 80 of 254 (31.5%; cohort 3) patients. ;FGFR1; overexpression occurred in 16 of 79 (20.2%, cohort 2) and 39 of 254 (15.4%; cohort 3) patients. Targeting of FGFR1 by RNA interference and small-molecule inhibitors (PD173074, AZD4547, BGJ398) revealed that the requirement for FGFR1 signaling in STS cells is dictated by FGFR1 expression levels, and identified the MAPK-ERK1/2 axis as critical FGFR1 effector pathway.
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CAS 872511-34-7 BGJ-398

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