"It's possible that the Genentech/Xoma drug could be preferred even if it is second to market because it doesn't have the T-cell-depleting effect," Reddoch says.
Agree with the sentiment, but it may be a superficial analysis. LFA3TIP can be depleting, but.... does Biogen say that it is, under conditions being tested? Anti-CD11a appears to be relatively non-depleting, but will there be systemic immunosuppression that would be a no-no for chronic diseases?
(I don't know the answers)
"If one drug works in this T-cell-mediated disease, it could work well in other T-cell-mediated diseases," Reddoch notes.
Duh!
Let's see if MEDI transitions to subcutaneous phase II, and, if so, at what dose. Two mechanisms have been described for 507 (Fc-independent apoptosis from Dumont et al., and Fc-dependent NK- or monocyte-mediated depletion as described at MEDI). Both indicate that only activated cells are removed.
Been like pulling teeth. If that Carson Group analyst is correct, we will soon know if the MEDI project looks hot. It would create an interesting situation...... wildest dreams, there'd be a dilemma for virtually every pharma with an interest in inflammation. Lilly, Merck, Pfizer..... there would be sudden interest. Novartis has probably been keeping an eye out for some time.
If this one hits, MEDI is a different creature. |
