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

To: Henry Niman who wrote (12333)	12/9/1997 1:23:00 AM
From: Miljenko Zuanic	Read Replies (1) \| Respond to of 32384

Hanry: I guess you are a right persons (also others are welcome) which can help me clear two questions: 1. SUGN is developing PTPs antagonist for TypeI/II diabetes(in preclinical study). This compounds are intracellular inhibitors of the protein-tyrosine phosphatases and they can increase sensitivity to insulin. But, from current literature, scientist are divided regards which class of the PTPs are responsive for downregulating of the insulin-signal. From SUGN 10K file: >>DIABETES Both Type I and Type II diabetes are characterized by pathologically high levels of blood glucose due to inefficient cellular uptake and metabolism of glucose. Type I diabetes is characterized by insufficient levels of insulin and is thought to be caused by the autoimmune destruction of the pancreatic cells that make insulin. In contrast, Type II diabetics often produce elevated levels of insulin, although this insulin does not seem to have sufficient effect. All Type I and some Type II diabetics are treated with insulin. The long-term side effects of diabetes and of insulin therapy can be severe. Dr. Ullrich was the first to clone the TK receptor to which insulin binds. In a normal state, the body secretes insulin which in turn binds to the insulin TK. These events activate the insulin TK signalling pathway, resulting in cellular uptake of glucose and glucose metabolism. In Type I and Type II diabetes, the TK signalling mechanism is impaired. Certain TPs appear to be involved in down regulating (dephosphorylating) the insulin TK signalling pathway. SUGEN believes that a small molecule which specifically inhibits these TPs may increase insulin TK signalling, thereby increasing glucose uptake and metabolism. SUGEN's animal studies with its lead phosphatase inhibitor compounds have demonstrated the ability of its initial lead compounds to lower blood glucose levels with efficacy comparable to currently available drugs. These compounds will serve as the starting point for medicinal chemistry and drug development with the aim of producing an optimized drug candidate to go forward into clinical development. Based on the mechanism of action of these compounds and their oral availability, the Company believes that it now has the opportunity to develop drug candidates for the treatment of both Type II (non-insulin dependent) and Type I (insulin dependent) diabetes. << To your knowledge and training what are real rule of this TPs in downregulating receptor acrivity for insulin signaling and are there clear evidence that diabetes patients have malfunction in this enzymes? Or this will be addition effects to insulin signaling in d/p which have problems with receptor TKs activity (reduced sensitivity). 2. SQNA recently announced identification of the DNA region with genes which may be responsive for onset and development (pathogenesis) of the type II diabetes. Also, SQNA and GLX announce that they will revised their collaboration on diabetes/obesity where each party will have define right and obligation. Did you have any additional info to which genes (both company are talking about multiple genes) SQNA discovery may be connected? One of join work at SQNA/ARRS (if merge proceed normally) may be on this field, IMO. Thanks in advance. mz