b) HLA-2 is an immune system effector and the MOA of ipi is unambiguously immune based.
I haven't followed ipi's development, but I was having trouble understanding why ipi's efficacy, as a CTLA-4 blocker, is dependent on HLA typing when there's no drug specificity against any TAA. Then I saw this in the NEJM article. It's an interesting labeling conundrum. Surely BMY would submit this data in the BLA to try to avoid HLA restrictions, though I don't know how the FDA would consider it.
The eligibility criteria for patients in this study included HLA-A*0201–positive status, on the basis of the mechanism of action of gp100. However, CTLA-4 blockade by ipilimumab is independent of HLA status, as indicated by efficacy and safety outcomes in earlier clinical trials that were similar between HLA-A*0201–positive and HLA-A*0201–negative patients21 (and unpublished data).
In the NEJM article there's also a link to the trial protocol and SAP.
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