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 SEATTLE, Dec. 8 /PRNewswire/ -- Cell Therapeutics, Inc., today reported data indicating that its compound, CT-2576, not only may have significant use in defining mechanisms involved in IL-2 intracellular signaling, but may lead to a new class of clinically effective immunosuppressive agents. Cell Therapeutics reported the findings, which were based on data obtained from an IL-2 stimulated murine cytotoxic cell line, CT-6, in a presentation to The American Society of Hematology's Annual Meeting in St. Louis.
 CT-2576 has a unique mechanism of action that is distinct from other immunosuppressive agents such as rapamycin, FK-506 and cyclosporin A.
 CT-2576 is member of a novel class of small molecule synthetic compounds developed by Cell Therapeutics scientists to potently inhibit IL-2 signal transduction. CT-2576 does not affect signaling pathways generally believed to be associated with IL-2 signaling, including MAP kinase, p70S6 kinase and the induction of nuclear oncogenes such as c-myc, c-jun and c-fos.
 In contrast to these systems, Cell Therapeutics scientists found that the phospholipid inositol phosphate-glycan (gly-PI), a previously not well understood lipid, may be an earlier and possibly upstream signaling molecule involved in IL-2 signal transduction.
 In the paper presented by Dr. Glenn Rice, director of the Cell Biology Division of Cell Therapeutics, the proprietary compound CT-2576 was described as blocking breakdown of gly-PI and subsequent formation of a unique myristylated phosphatic acid (mPA) species in IL-2 induced mouse cytotoxic T-cell clone CT6, suggesting that mPA is a necessary signaling lipid involved in IL-2 activation of T cells.
 Moreover, the data indicated that CT-2576 inhibits IL-2 induced proliferation in CT6, as well as inhibiting proliferation of conA or anti-CD3 primed mouse thymocytes in response to IL-2 (50% inhibitory concentration (IC50) in the range of 200-850 nanomolar). Dr. Rice also reported that CT-2576 inhibited a human mixed leukocyte reaction between HLA disparate individuals with an IC50 of approximately 500 nM.
 Dr. James A. Bianco, president and chief executive officer of Cell Therapeutics, noted: "The conclusions reached through analysis of the data presented in St. Louis -- namely, that the inhibition of IL-2 induced proliferation in CT6 is not a result of blocking previously identified kinase and nuclear oncogene-related signals; rather the mechanism of immunosuppression of CT-2576 is distinct from that of the calcineurin inhibitors cyclosporin A and FK-506 -- are quite significant and in marked contrast to other data presented at the ASH annual meeting.
 "We believe that in addition to understanding the mode of action of the cellular pathway responsible for signaling IL-2, we have designed a compound that may be effective in inhibiting cell activation and abnormal immune responses," continued Dr. Bianco.
 "In in vitro models of immune and antigenic challenge, CT-2576 potently inhibits T cell activation at low concentrations yet was not toxic to a variety of cell types at concentrations 1,000 to 10,000 fold higher. Dr. David Leung of Cell Therapeutics, and Dr. Phil Peterson of the University of Minnesota, reported that CT-2576 also transcriptally inhibits the replication of HIV and human cytomegalovirus, suggesting that inhibitors of mPA may have a role in the therapy of AIDS. Overall, these findings suggest that CT-2576 is a unique and non-toxic immunosuppressive compound that may prove clinically useful in treatment of immune disorders such as rheumatoid arthritis, multiple sclerosis, psoriasis, and organ transplant rejection."
 Cell Therapeutics, Inc., is a biopharmaceutical company focused on the development and commercialization of proprietary small molecule pharmaceuticals targeting oncologic and immune diseases.
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 /CONTACT: James A. Bianco, M.D., of Cell Therapeutics, Inc., 206-284-5774; or Todd Fogarty of Kekst and Company, 212-593-2655/

CO: Cell Therapeutics, Inc. ST: Washington IN: MTC SU:

TW -- NY031 -- 1676 12/08/93 10:13 EST
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Publication:PR Newswire
Date:Dec 8, 1993

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