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Biotech / Medical : Incyte (INCY) -- Ignore unavailable to you. Want to Upgrade?

To: former_pgs who wrote (3155)	1/4/2018 7:13:53 PM
From: Miljenko Zuanic	Respond to of 3202

Thanks, we agree Indo is not an INDO-1 inhibitor. <Thus, indoximod acts as a high-potency tryptophan mimetic in reversing mTORC1 inhibition and the accompanying autophagy that is induced by tryptophan depletion in cells.> Can this explain synergy with IO path and added activity, seen for other INDO-1 inhibitor? Should re-activation of the mTORC1 bring "survival" benefit to cancer cells?

To: former_pgs who wrote (3155)	1/9/2018 1:59:18 PM
From: Miljenko Zuanic	Read Replies (2) \| Respond to of 3202

At JPM, INCY was cautious on IDO1, so...PFE exiting IDO-target may (after hearing their and BMY presentation) sound as diversification from BMY-overlapping programs. IF PFE can afford (at least) 40% premium to current BMY MC, they would go after it. Sorry to pollute INCY tread with PFE/BMY thoughts!

To: former_pgs who wrote (3155)	1/9/2018 3:29:40 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 3202

These findings are important translationally, because they suggest broader clinical uses for D-1MT against cancers that overexpress any tryptophan catabolic enzyme (IDO1, IDO2 or TDO). ncbi.nlm.nih.gov >> does suggest one would make a mistake by extrapolating heavily based on the indoximod data << Yeah, but a mistake in which direction?? Isn't downstream inhibition of IDO1, IDO2 and TDO better than IDO1 alone?? The Incyte rationale for IOD1 selective agents is given here, third paragraph..... ncbi.nlm.nih.gov So they would say "no".