Biotech Values

[dewophile]

probably
or the sink issue leaving inadequate drug to disrupt the target axis in tissues other than RBCs
or some quirk w the drug where it spares platelets much like TRIL's drug spares RBCs. This is the least likely explanation. The most likely is use of a weaker immunoglobulin since there wasn't a hint of thrombocytopenia in either human or animal data, and stanford clearly chose the weaker IgG subtype due to toxicity concerns (one of which may have been affect on platelets)
you know stanford now is looking at combination with both rituxan and erbitux - i have a feeling they are just not seeing efficacy as monotherapy. I hope the fact we are seeing side effects with the TRIL drug that are not described w the stanford drug is a proxy for efficacy (much like rash with EGFR drugs)