Brivanib (BMS-582664) in advanced solid tumors (AST): Results of a phase II randomized discontinuation trial (RDT).

Ratain, Mark J.; Schwartz, G. K.; Oza, Amit M.; Rudin, Charles M.; Kaye, S.B.; Jonge, Maja J. De; Khayat, David; Awada, Ahmad; Sawyer, Michael B.; Obel, Jennifer; Médioni, Jacques; Evans, T. R. J.; Grève, Jacques De; Soetekouw, Patricia M.M.B.; Baurain, Jean‐François; O’Dwyer, P. J.; Hartman, Christine M.; Poulart, Valerie; Walters, Ian

doi:10.1200/jco.2011.29.15_suppl.3079

Cited by 22 publications

(9 citation statements)

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“…All patients discontinued treatment, mainly due to disease progression, no FGFR3 status-related responses were recorded and the trial was terminated. Brivanib, a VEGFR2 and FGFR1 inhibitor similarly showed disappointing results in patients with advanced bladder cancer [127]. Reports of Phase I trials of nintedanib (BIBF 1120), lenvatinib (E7080) and lucitanib (E-3810) did not describe any bladder cancer patients, but these drugs have progressed for other indications.…”

Section: Umuc3 and Umuc13; High Fgfr1 Expressionmentioning

confidence: 99%

A Place for Precision Medicine in Bladder Cancer: Targeting the Fgfrs

Martino

Tomlinson

et al. 2016

Future Oncol.

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Section: Umuc3 and Umuc13; High Fgfr1 Expressionmentioning

confidence: 99%

A Place for Precision Medicine in Bladder Cancer: Targeting the Fgfrs

Martino

Tomlinson

et al. 2016

Future Oncol.

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“…These small molecule inhibitors, including BGJ398 (Novartis), TKI258/CHIR258 (Dovitinib, Novartis) (12-14), AZD4547 (Astra Zeneca) PD173074 (Pfizer, Groton, CT), and BMS-582664 (Brivanib, Bristol Myers Squibb) (15), generally target all members of the FGFR family, VEGFR2 and other tyrosine kinases (11, 12). This general FGF and VEGF pathway inhibition is associated with significant diarrhea, nausea, fatigue (16, 17), dyspnea (18), and abdominal pain (16-18), as well as thrombocytopenia and thromboembolic events (16). Hyperphosphatemia-mediated soft tissue calcification has been a further hurdle impeding preclinical development of pan-FGFR inhibitors (11).…”

Section: Introductionmentioning

confidence: 99%

Fibroblast Growth Factor Receptor 3 Is a Rational Therapeutic Target in Bladder Cancer

Gust

McConkey

Awrey

et al. 2013

Molecular Cancer Therapeutics

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Activating mutations of Fibroblast growth factor receptor-3 (FGFR3) have been described in approximately 75% of low-grade papillary bladder tumors. In muscle invasive disease, FGFR3 mutations are found in 20% of tumors, but overexpression of FGFR3 is observed in about half of cases. Therefore, FGFR3 is a particularly promising target for therapy in bladder cancer. Up to now most drugs tested for inhibition of FGFR3 have been small molecule, multi-tyrosine kinase inhibitors. More recently, a specific inhibitory monoclonal antibody targeting FGFR3 (R3Mab) has been described and tested pre-clinically. In this study, we have evaluated mutation and expression status of FGFR3 in 19 urothelial cancer cell lines and a cohort of 170 American bladder cancer patients. We demonstrated inhibitory activity of R3Mab on tumor growth and corresponding cell signaling in three different orthotopic xenografts of bladder cancer. Our results provide the pre-clinical proof of principle necessary to translate FGFR3 inhibition with R3Mab into clinical trials in patients with bladder cancer.

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“…Although no phase II FGFR1-specific trials are mature, brivanib has been evaluated in a randomized discontinuation trial that enrolled 396 patients with five different tumor types. 127 While SD was seen in 24 of the 42 NSCLC patients in the trial, none of the unselected NSCLC patients had a response of PR or better. Activating mutations in the FGFR2/3 genes that are oncogenic and drug sensitive have recently been described in lung squamous cell cancers.…”

Section: Fgfrmentioning

confidence: 92%

Targeted Therapies in Non-Small Cell Lung Cancer: Emerging Oncogene Targets Following the Success of Epidermal Growth Factor Receptor

Berge¹,

Doebele²

2014

Seminars in Oncology

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The diagnostic testing, treatment and prognosis of non-small cell lung cancer (NSCLC) has undergone a paradigm shift since the discovery of sensitizing mutations in the epidermal growth factor receptor (EGFR) gene in a subset of NSCLC patients. Several additional oncogenic mutations, including gene fusions and amplifications have since been discovered, with a number of drugs that target each specific oncogene. This review focuses on oncogenes in NSCLC other than EGFR and their companion ‘targeted therapies’. Particular emphasis is placed on the role of ALK, ROS1, RET, MET, BRAF, and HER2 in NSCLC.

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Brivanib (BMS-582664) in advanced solid tumors (AST): Results of a phase II randomized discontinuation trial (RDT).

Cited by 22 publications

References 0 publications

A Place for Precision Medicine in Bladder Cancer: Targeting the Fgfrs

A Place for Precision Medicine in Bladder Cancer: Targeting the Fgfrs

Fibroblast Growth Factor Receptor 3 Is a Rational Therapeutic Target in Bladder Cancer

Targeted Therapies in Non-Small Cell Lung Cancer: Emerging Oncogene Targets Following the Success of Epidermal Growth Factor Receptor

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