BACKGROUND: Fyn is a kinase that is upregulated in a subset of metastatic 
castration-resistant prostate cancer. Saracatinib potently inhibits Fyn 
activation. We have noted a relationship between Fyn expression and directional 
motility, a cellular process related to metastasis. As such we hypothesized that 
treatment with saracatinib would increase the time required to develop new 
metastatic lesions.
METHODS: Patients with metastatic castration-resistant prostate cancer that had 
progressed after docetaxel were eligible for enrollment. This study was executed 
as a randomized discontinuation trial. During a lead-in phase of two 28-Day 
cycles, all patients received saracatinib. Afterward, patients with 
radiographically stable disease were randomized to either saracatinib or 
placebo. Patients continued treatment until evidence of new metastasis.
RESULTS: Thirty-one patients were treated. Only 26% of patients had stable 
disease after 8 weeks and thus proceeded to randomization. This required early 
termination of the study for futility. The 70% of patients who progressed after 
the lead-in phase exhibited expansion of existing lesions or decompensation due 
to clinical progression without new metastatic lesions. Fatigue was reported in 
more than 25% of patients (all grades) with only two patients experiencing grade 
3 toxicity. Other grade 3 adverse events included dehydration, thrombocytopenia, 
and weakness.
CONCLUSIONS: This study was unable to determine if saracatinib had potential as 
metastasis inhibitor. Metastasis inhibition by saracatinib may still be viable 
in an earlier time in the disease history.