The study (GICS abstract #642) showed that patients with wild-type KRAS (exon 2) mCRC treated with Vectibix and BSC achieved a median OS of 10 months compared to 7.4 months for patients treated with BSC alone (hazard ratio [HR]=0.73, 95 percent confidence interval [CI]=0.57-0.93, p=0.0096).
Data from a key secondary endpoint showed that patients with wild-type RAS (absence of mutations in exons 2, 3 and 4 of KRAS and NRAS) mCRC treated with Vectibix and BSC achieved a median OS of 10 months compared to 6.9 months for patients treated with BSC alone (n=270; HR=0.70, 95 percent CI=0.53-0.93, p=0.0135).
Key secondary endpoints included progression-free survival (PFS) in patients with wild-type KRAS mCRC, as well as OS and PFS in patients with wild-type RAS (absence of mutations in exons 2, 3 and 4 of KRAS and NRAS) mCRC, objective response rate (ORR) and safety in both wild-type KRAS (exon 2) and wild-type RAS groups.
For patients with wild-type KRAS, ORRs were 27.0 percent with Vectibix versus 1.6 percent with BSC (HR=24.9, 95 percent CI=7.5-123.8, p RAS, ORRs were 31.0 percent with Vectibix versus 2.3 percent for BSC (ODDS Ratio=20.0, 95 percent CI=5.9-101.6, p
Patients with mutant RAS mCRC did not benefit from Vectibix treatment (OS HR=0.99, 95 percent CI=0.49-2.00).