Replies to post #111375 on Biotech Values

[DewDiligence]

Teva’s low-volume Copaxone is not Copaxone—it’s a distinct drug that required Teva to submit an NDA under the 505b2 pathway.

I’m surprised that you were hoodwinked by the spin in Teva’s PR that posits a linkage between Teva’s low-volume Copaxone NDA and NVS/MNTA’s Copaxone ANDA. In fact, no such linkage exists because these are two different drugs.

That the FDA rejected Teva’s NDA for low-volume Copaxone was fully expected by those who have done a modicum of DD on this matter. The reason rejection was expected has nothing to do with Copaxone per se; rather, rejection was expected because Teva’s data package, consisting of a single open-label trial, was pathetically weak.

Please see #msg-50939364 and #msg-51123550 for additional background info.

[dewophile]

jbog
teva supporters agree with you as the stock is up significantly. interestingly so is mnta. i think this can be reconciled by the fact many teva longs must not listen to mnta ccs, while mnta longs listen to every mnta cc. on the latest mnta cc wheeler addressed the very issue of not fully understanding the moa of copaxone. i alluded to it in post # 110950, where he went into some detail on how the moa of lovenox is also not fully understood yet they were able to get approval based on analytics (although lovenox is better understood mechanistically than copaxone, the active moiety is definitely not "fully described" by simple Xa/IIa activity assays)

i look forward to wheeler clearing this up at JPM conference in a couple weeks (just like he did in the last presentation)

actually imo very few drugs' MOA are "fully understood", not to mention as dew pointed out that unlike LV cop, mnta's application is NOT a formulation change (or any change for that matter)