The Green Cross Corporation

Yoshitomi Pharmaceutical Industries, Ltd.

Yasuo Amatsuji

Toshizumi Tanabe

Masaaki Hirose

Hiroshi Matsuda

Yasuo Ikeda

Hirofumi Arimura

Haruhide Kawabe

Kaeko Kamide

Ryuji Hiramatsu

Shusei Uno

Mitsuru Murata

Masanori Nagai

Takashi Imagawa

A complex comprising a lipid and a conjugate of GPIb and lipid having a functional group, and use thereof. The GPIb-lipid complex of the present invention is extremely useful as a platelet substitute, a pharmaceutical agent for the prophylaxis and treatment of angiopathy, vascular damages and thrombosis, a diagnostic for vWF deficiency and the like, a biological or medical reagent, a reagent for screening platelet aggregation suppressant or antithrombosis, and the like. The GPIb-lipid complex of the present invention is also useful as a diagnostic for finding the location of vascular lesion or thrombus formation, or a therapeutic agent therefor, since it accumulates at vascular lesions.

GPIb-lipid complex and uses thereof

A mutant human prourokinase wherein a neutral amino acid in the epidermal growth factor (EGF) region of human prourokinase (human PUK) has been replaced with a basic amino acid, or an acidic amino acid has been replaced with a non-acidic amino acid, and a method for producing a mutant human PUK which comprises expression of mutant human PUK by cultivating a host transformed by a plasmid inserted with a DNA sequence coding for said mutant human PUK. By replacing a neutral amino acid in the EGF region of human PUK which is a fibrinolysin with a basic amino acid, or an acidic amino acid with a non-acidic amino acid, half-life in blood can be prolonged, and affinity for fibrin can be improved.

Mutant human prourokinase

A human prourokinase mutant in which the entire or a partial epidermal growth factor domain of human prourokinase is deleted or a partial epidermal growth factor domain of human prourokinase is replaced by one or more different amino acid residues, said mutant having a longer blood half-life than naturally occurring human prourokinase while retaining prourokinase enzymatic activity. In this human prourokinase mutant the region selected from the group consisting of: (a) from asparagine (10) to cysteine (42); (b) from asparagine (10) to aspartic acid (45); and (c) from asparagine (10) to threonine (49) is missing.

Human prourokinase mutants

Growing community of inventors

Hirakata, Japan

Yasuo Amatsuji