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

To: scaram(o)uche who wrote (3030)	6/18/2014 3:12:59 PM
From: Biotech Jim	Respond to of 3202

I did substantially increase my GILD position, but lost out on INCY and TGTX, a couple of others that I keep following. I do plan to pick up some TGTX. In some not so related stocks, I did manage to sell and reload my RIGL in a couple of accounts, and did the same with CCXI. I now have sold out of CCXI completely. I did get some MGNX, but some 15% or so off the low. I do think that the GILD play in checkpoint inhibition is a very good one. I know several very smart people at GILD. But as Barry Bloom, who was head of Pfizer Central Research during the glory days, once said to me: "there is a lot of luck involved in this drug discovery game". NOT kinda like when I was back in college, in the days where the harder I studied, the luckier I was with my exams.

To: scaram(o)uche who wrote (3030)	9/17/2014 6:30:16 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 3202

GILD - Idelalisib INCY - INCB40093 TGTX - TGR-1202 INFI - IPI-145 and IPI-443 Updated....... GILD - Idelalisib INCY - INCB40093 and INCB050465 TGTX - TGR-1202 INFI - IPI-145 and IPI-443 (IPI-145 licensed to AbbVie, $275M upfront, INFI retains rights to IPI-443) Any others??

To: scaram(o)uche who wrote (3030)	10/23/2014 6:04:27 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 3202

Interesting. Don't think I ever put this abstract up, as it didn't hone in on delta (perhaps the manuscript did, don't know). But Dr. Khleif appears to be a driver behind the anti-PD-1 that Medivation just licensed. His group is immersed in stuff that is of interest..... (edit: inhibitors included triciribine, MK-2206, wortmannin and IC87114, the latter being PI3Kdelta selective) Cancer Immunol Res. 2014 Jul 30. [Epub ahead of print] Selective Inhibition of Regulatory T Cells by Targeting the PI3K-Akt Pathway. Abu-Eid R1, Samara RN2, Ozbun L2, Abdalla MY2, Berzofsky JA2, Friedman KM3, Mkrtichyan M1, Khleif SN4. 1Georgia Regents University Cancer Center, Augusta, Georgia. 2National Cancer Institute, National Institutes of Health, Bethesda, Maryland. 3bluebird bio, Cambridge, Massachusetts. 4Georgia Regents University Cancer Center, Augusta, Georgia. SKhleif@gru.edu. Despite the strides that immunotherapy has made in mediating tumor regression, the clinical effects are often transient, and therefore more durable responses are still needed. The temporary nature of the therapy-induced immune response can be attributed to tumor immune evasion mechanisms, mainly the effect of suppressive immune cells and, in particular, regulatory T cells (Treg). Although the depletion of Tregs has been shown to be effective in enhancing immune responses, selective depletion of these suppressive cells without affecting other immune cells has not been very successful, and new agents are sought. We found that PI3K-Akt pathway inhibitors selectively inhibit Tregs with minimal effect on conventional T cells (Tconv). Our results clearly show selective in vitro inhibition of activation (as represented by a decrease in downstream signaling) and proliferation of Tregs in comparison with Tconvs when treated with different Akt and PI3K inhibitors. This effect has been observed in both human and murine CD4 T cells. In vivo treatment with these inhibitors resulted in a significant and selective reduction in Tregs in both naïve and tumor-bearing mice. Furthermore, these PI3K-Akt inhibitors led to a significant therapeutic antitumor effect, which was shown to be Treg dependent. Here, we report the use of PI3K-Akt pathway inhibitors as potent agents for the selective depletion of suppressive Tregs. We show that these inhibitors are able to enhance the antitumor immune response and are therefore promising clinical reagents for Treg depletion.