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How does Vectibix® (panitumumab) work?
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  • How does Vectibix® (panitumumab) work?

  • How did RAS testing evolve?

  • Why don’t anti-EGFRs work in the presence of RAS mutations?

  • What is the PRIME study, and how was it conducted?

  • How was the analysis of outcomes among patients with wild-type RAS mCRC conducted in PRIME?

  • What proportion of patients with mCRC have RAS wild-type status?

  • What were the results of the prospective-retrospective analysis of outcomes in patients with RAS wild-type mCRC in PRIME?

  • What were the outcomes in PRIME for the patients with wild-type KRAS (exon 2) mCRC but with additional RAS mutations?

  • How did mutation in BRAF influence the results of the RAS wild-type prospective-retrospective analysis in PRIME?

  • Did RAS status have any impact on safety in the prospective-retrospective analysis in PRIME?

  • What can we conclude from the RAS wild-type prospective-retrospective analysis in PRIME?

  • What is the PEAK study?

  • What was the distribution of RAS mutations in the PEAK study?

  • What were the PFS results in PEAK for patients with wild-type KRAS (exon 2) and those with wild-type RAS mCRC?

  • What were the OS results in PEAK for patients with wild-type KRAS (exon 2) and those with wild-type RAS mCRC?

  • What were the safety findings from PEAK in patients with wild-type RAS mCRC?

  • What are the outstanding issues in the management of mCRC?

  • Why should Vectibix® + FOLFOX be considered in the 1st line setting in patients with RAS wild-type mCRC?

  • How should patients be managed until RAS testing results become available?

  • Will it be more difficult or take longer to obtain RAS results than KRAS results?