Cell Therapeutics, Inc.

Fred Hutchinson Cancer Center

Jack W Singer

James A Bianco

David J Porubek

Paul Woodson

Stuart L Bursten

Glenn C Rice

David W Leung

Paul A Brown

J Peter Klein

Marc Besman

John E Tulinsky

Rama Bhatt

Stewart D Chipman

Peter De Vries

Robert A Lewis

Gail E Underiner

William J Novick, Jr

Edward Abraham

Elisa Eiseman

Emer Clarke

Disclosed are biologically active protein conjugates that comprise a biologically active polypeptide coupled via a peptide bond to a polypeptide comprising from 2 to about 500 units of a repeating peptide motif, wherein the biologically active protein conjugate exhibits a modified plasma half-life compared to the intrinsic half-life of the unconjugated biologically active polypeptide or protein. Also disclosed are methods of making and using the conjugated proteins, as well as methods for determining whether a given conjugate exhibits a modified half life relative to the intrinsic half life of the unconjugated polypeptide.

Conjugates of biologically active polypeptides having an increased in vivo half-life

Conjugates of biologically active proteins having a modified in vivo half-life

The invention provides polyglutamic acid-therapeutic agent conjugates and methods for their preparation and use.

Polyglutamic acid-camptothecin conjugates and methods of preparation

There is disclosed a method for preventing tissue injury caused by tissue hypoxia and reoxygenation, comprising administering a compound that inhibits signal transduction by inhibiting cellular accumulation of linoleoyl phosphatidic acid (PA) through an inhibition of the enzyme LPAAT (lysophosphatidic acyltransferase).

Method for preventing tissue injury from hypoxia

Use of xanthines as immunosuppressants and to inhibit allograft reactions

Disclosed are methods for treating conditions resulting from hyperoxia or mechanical ventilation comprising the administration of a compound of the formula: ##STR1## wherein R.sub.1 is a substantially pure resolved R enantiomer .omega.-1, secondary alcohol-substituted (C.sub.5-8) alkyl; and R.sub.2 and R.sub.3 are independently hydrogen atom or a (C.sub.1-12) alkyl optionally containing one or two oxygen atoms in place of non-adjacent carbon atoms.

Method for treating hyperoxia

There is disclosed a method of preventing or delaying the occurrence of acquired immunodeficiency syndrome (AIDS) in human immunodeficiency virus (HIV) seropositive humans by administering an effective amount of a compound that inhibits cellular signaling through a specific phospholipid-based cellular signaling and signal amplification pathway. The invention further provides a method for preventing or delaying clinical symptoms of a group of viral diseases wherein the viral disease is mediated by host cell viral replication. The invention provides an advantage by attacking host cellular signaling mechanisms to prevent the development of drug resistance from rapidly mutating viruses.

Method for inhibiting intracellular viral replication

There is disclosed compounds and pharmaceutical compositions that are a resolved R or S (preferably R) enantiomer of an .omega.-1 alcohol of a straight chain alkyl (C.sub.5-8) substituted at the 1-position of 3,7-disubstituted xanthine. The inventive compounds are effective in modulating cellular response to external or in situ primary stimuli, as well as to specific modes of administration of such compounds in effective amounts.

Enantiomerically pure hydroxylated xanthine compounds

Method for treating diseases mediated by cellular proliferation in

In a method for treating or preventing allergy or allergic disorders an effective amount of a compound that inhibits intracellular generation of phosphatidic acid and diacylglycerol is administered. The intracellular generation of phosphatidic acid and diacylglycerol results from allergen presentation or mast cell/basophil activation.

Method for inhibiting mast cell and basophil activation

There is disclosed a method for screening for inhibitors of cellular second messenger signaling regulated by lysophosphatidic acid acyl transferase (LPAAT) and phosphatidic acid phosphohydrolase (PAPH), which method comprises contacting target cells or appropriate subcullular elements under appropriate conditions of stimulation with a candidate drug and assessing the levels of the relevant subsets of phosphatidic acid (PA) and diacylglycerol (DAG) in the presence and absence of the candidate drug.

Assay for identification therapeutic agents

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Seattle, WA, United States of America

Jack W Singer