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Biotech / Medical : Ligand (LGND) Breakout! -- Ignore unavailable to you. Want to Upgrade?


To: WTDEC who wrote (30118)1/11/2000 10:24:00 AM
From: Wallace Rivers  Read Replies (1) | Respond to of 32384
 
What time is LGND's presentation?



To: WTDEC who wrote (30118)1/12/2000 6:32:00 AM
From: Henry Niman  Respond to of 32384
 
Walter, As you know, Biotechs have been hot recently. I think that LGND's move, based in part on their ability to make McCamants board on CNBC, suggests that retail is also looking for those beaten down biotechs on the verge of "Internet-like" moves.

I was on the road, and knew that there was no press release, so I was rather surprised at LGND's jump to 17. I think that McCamant had to have been a factor. Last night, CNBC again mention LGND (along with ICOS - called I Coast on tv-eyes) as stocks that McCamant likes.

LGND's chart is amazing, and momentum players should be jumping in also. A correction is due, but a continued sharp rise would not be a major surprise.

Clinical data could easily fuel a move to an all time high at this time.



To: WTDEC who wrote (30118)1/12/2000 7:22:00 AM
From: Henry Niman  Read Replies (1) | Respond to of 32384
 
Walter, Very significant paper in Nature on diabetes, obesity, and cardiovascular implications. Shows that PPAR gamma involved, but more importantly, study uses LGD1268 as part of proof of PPARgamma involvement in human diseases. LLY deal will be VERY big:

Nature 402, 880 - 883 (1999) © Macmillan Publishers Ltd.

Dominant negative mutations in human PPAR associated with severe
insulin resistance, diabetes mellitus and hypertension

I. BARROSO, M. GURNELL, V. E. F. CROWLEY, M. AGOSTINI, J. W. SCHWABE, M. A. SOOS, G. LI MASLEN, T. D. M. WILLIAMS, H. LEWIS, A. J. SCHAFER, V. K. K. CHATTERJEE & S. O'RAHILLY

Thiazolidinediones are a new class of antidiabetic agent that improve insulin sensitivity and reduce plasma glucose and blood pressure in subjects with type 2 diabetes. Although these agents can bind and activate an orphan nuclear receptor, peroxisome proliferator-activated receptor gamma (PPAR), there is no direct evidence to conclusively implicate this receptor in the regulation of mammalian glucose homeostasis. Here we report two different heterozygous mutations in the ligand-binding domain of PPAR in three subjects with severe insulin resistance. In the PPAR crystal structure, the mutations destabilize helix 12 which mediates transactivation. Consistent with this, both receptor mutants are markedly transcriptionally impaired and, moreover, are able to inhibit the action of coexpressed wild-type PPAR in a dominant negative manner. In addition to insulin resistance, all three subjects developed type 2 diabetes mellitus and hypertension at an unusually early age. Our findings represent the first germline loss-of-function mutations in PPAR and provide compelling genetic evidence that this receptor is important in the control of insulin sensitivity, glucose homeostasis and blood pressure in man.