Missing content? – Request curation!
Request curation for specific Genes, Variants, or PubMed publications.
Have questions, comments, or suggestions? - Let us know!
Email us at : firstname.lastname@example.org
|Authors||J.Bridgewater, F.Meric-Bernstam, A.Hollebecque, J.W.Valle, C.Morizane, T.Karasic, T.Abrams, J.Furuse, R.K.Kelley, P.Cassier, H-J.Klümpen, N.Uboha, A.Mahipal, E.Mitchell, E.R.Ahn, H-M.Chang, K.Masuda, Y.He, K.Benhadji, L.Goyal|
|Title||Efficacy and safety of futibatinib in intrahepatic cholangiocarcinoma (iCCA) harboring FGFR2 fusions/other rearrangements: Subgroup analyses of a phase II study (FOENIX-CCA2)|
|Abstract Text||Background: FGFR2 fusions occur in 10–20% of pts with iCCA and comutations in tumor suppressor genes may be prognostic. FOENIX-CCA2 is a study of futibatinib (a highly selective irreversible FGFR1–4 inhibitor) in pts with iCCA and FGFR2 fusions/other rearrangements. Methods: Pts enrolled had locally advanced/metastatic iCCA with FGFR2 fusions/other rearrangements, progressive disease (PD) after ≥1 systemic therapy (tx), no prior FGFR inhibitor tx, and ECOG PS 0/1. Pts received oral futibatinib 20 mg 1x/day until PD/intolerance. Objective response rate (ORR; independent review) was the primary endpoint and duration of response (DOR), PFS and safety were secondary endpoints. Subanalyses by pt characteristic, fusion, comutation and prognostic factor were performed. Results: Interim data for 67 pts (58% female; median age 57 y) with ≥6 mo of follow-up are reported. Pts had FGFR2 fusions (82%) or rearrangements (18%). The most frequent fusion was FGFR2-BICC1 (n=15). ORR was 37.3%, median DOR 8.3 mo, and disease control rate 82%. In pts with confirmed FGFR2 alterations, ORR was 36.2% (21/58 fusions) and 44.4% (4/9 rearrangements). ORR was 33.3% in pts with FGFR2-BICC1. Best overall response in pts with comutations of interest is shown in the table below. All baseline characteristic subgroups (eg, age, gender, prior tx) had responding pts, including pts aged ≥65 y (ORR=57%; 8/14). Higher phosphate levels trended in responders vs nonresponders. Grade ≥3 treatment-related hyperphosphatemia resolved in a median of 6 d. Management of special interest AEs will be presented. Conclusions: These interim data demonstrate manageable AEs and efficacy of futibatinib in iCCA with FGFR2 fusions/other rearrangements. Responses were observed across pt subgroups, including those with common FGFR2 fusions, comutations, and poor prognostic factors. Clinical trial identification: NCT02052778; EudraCT: 2013-004810-16.|
|Molecular Profile||Treatment Approach|
|Gene Name||Source||Synonyms||Protein Domains||Gene Description||Gene Role|
|Therapy Name||Drugs||Efficacy Evidence||Clinical Trials|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Gene||Variant||Impact||Protein Effect||Variant Description||Associated with drug Resistance|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|