CMTTdb

An integrated database for cancer molecular targeted thearpies

Entry Detail


General information
Database:DB00200
Objective:Although durable responses can be achieved with tyrosine kinase inhibitors such as imatinib in melanomas harboring KIT mutations, the efficacy of alternative inhibitors after progression to imatinib and the activity of these agents on brain metastases are unknown.
Authors:Carvajal RD, et al
Title:Phase II Study of Nilotinib in Melanoma Harboring KIT Alterations Following Progression to Prior KIT Inhibition.
Journal:Clin Cancer Res.
Year:2015
PMID:25695690
Trial Design
Clinical Trial Id:NA
Agent:nilotinib
Target:Plateletderived growth factor receptor
Abl
Mast/stem cell growth factor receptor
Cancer Type:melanoma
Cancer Subtype:melanomas harboring KIT mutations or amplification
Therapy Type:mono
Therapeutic Combination Type:NA
Therapeutic Combination Content:NA
Study Type:a phase II study
Key Patients Feature:patients with melanomas harboring KIT mutations or amplification
Biomarker:KIT mutations or amplification
Biomark Analysis:Nilotinib may achieve disease control in patients with melanoma harboring KIT alterations and whose disease progressed after imatinib therapy.
Control Group Info:single arm
Treatment Info:Patients who met eligibility criteria received nilotinib 400 mg by mouth twice daily. Safety evaluations, including clinical and laboratory assessments, were conducted at baseline, every week for 4 weeks, every 2 weeks for 4 weeks, every 4 weeks for 28 weeks, and then every 3 months subsequently.
Primary End Point:the proportion of patients who were alive and without progression of disease 4 months after beginning treatment with nilotinib.
Secondary End Point:best overall response rate (BORR), timetoprogression (TTP), overall survival (OS), and tolerability.
Patients Number:20
Trial Results
DLT_MTD:NA
Objective Response Rate:3 patients on cohort A [27%; 95% confidence interval (CI), 8%-56%] and 1 on cohort B (12.5%; 90% CI, 0.6%-47%) achieved the primary endpoint. 2 partial responses were observed in cohort A (18.2%; 90% CI, 3%-47%); none were observed in cohort B
Disease Control Rate:NA
Median Time to Progression:3.3 (90% CI, 2.1-3.9 months)
Median PFS A vs. C:NA
Median OS A vs. C:9.1 months (90% CI, 4.3-14.2 months)
Adverse Event(agent arm):Although nilotinib was generally well tolerated, 17 of the 19 patients treated reported adverse events, with fatigue (26%) and lowgrade musculoskeletal and gastrointestinal discomfort (32%) most commonly observed. Grade3 toxicities were observed in 4 patients, and included rash (n = 1), elevated pancreatic enzymes (n = 2), and transaminitis and hyponatremia (n = 1). Grade 3 toxicity was managed by dose reduction to 400 mg QD (n = 2) or dose delay follotheyd by reinitiation of treatment at 400 mg twice a day (n = 2). No patient experienced grade4 related adverse events. Toxicity rates and patterns were comparable for cohorts A and B.
Conclusions: Nilotinib may achieve disease control in patients with melanoma harboring KIT alterations and whose disease progressed after imatinib therapy. The efficacy of this agent in KITaltered melanoma with brain metastasis is limited.