Disclosed herein are methods of treatment for an intraocular pressure (IOP)-associated condition in a subject, that include administering to the subject an effective amount of a tissue plasminogen activator (tPA) therapeutic agent. In one embodiment, the IOP-associated condition is glaucoma. The administration of a tPA therapeutic agent can be an extended administration intended to cause a reduction in IOP in the subject for a period of at least one day to a year or more, relative to IOP levels in the subject prior to administration of the tPA therapeutic agent. The tPA therapeutic agent can be, for example, tPA, a tPA derivative, a small molecule direct or indirect tPA agonist, or a gene therapy vector.

The invention relates to molecular biology, biotechnology, medicine, veterinary science. A group of inventions is proposed: a fusion protein comprising a ligand to MATN1 protein, and a growth factor of EGF, TGF, FGF, IGF, the construct components are connected via a flexible link, characterized by the amino acid sequence of FIG. 1; such fusion protein further comprising the Fc-fragment of an antibody or a polypeptide binding with FcRn and/or transferrin or a fragment thereof, the construct components connected via a flexible link, characterized by the amino acid sequence of FIG. 1; encoding polynucleotide, codon-optimized for expression in the producer cells or a target organism, a genetic construct for the synthesis of the fusion protein in producer cells, or cells of a target organism, the fusion protein producer, a producer of a genetic construct based on a bacterial cell, a preparation for the regeneration of cartilage containing at least 1 fusion protein or genetic construct as the active agent, in an effective amount, and a physiologically acceptable carrier or buffer solution, for parenteral or, in the case of the preparation based on at least 1 fusion protein containing the transport domain, oral administration, in the latter case the preparation is enclosed in an enteric coating, all variants

The present invention provides therapeutic products with decreased fibrinolytic activity of t-PA-deficient and/or plasminogen-deficient blood products, as well as compositions, kits and methods using the same in treating bleeding associated with hereditary or acquired bleeding disorders. The invention further provides extracorporeal apparatus for blood or blood products Plasmapheresis aimed to prevent or treat bleeding disorders.

The present disclosure provides various molecular constructs having a targeting element and an effector element. Methods for treating various diseases using such molecular constructs are also disclosed.

The present disclosure provides various molecular constructs having a targeting element and an effector element. Methods for treating various diseases using such molecular constructs are also disclosed.

The invention relates to an anti fibrinolytic composition comprising at least one tPA mutant that carries at least one point mutation substituting Ser.sup.481 to Ala on tPA, said mutant inhibits the fibrinolytic activity of at least one of tPA and uPA and therefore may be used for treating disorders associated with fibrinolytic processes, specifically, coagulopathies, thrombocytopenia and bleeding. The invention further provides methods and uses of the mutants of the invention.

A fusion protein includes the SARS-COV-2 receptor binding domain (RBD) of the SARS-COV-2 spike protein or a fragment, and a N-terminal signal peptide, and at least one of the following: a polyhistidine tag, linker, an oligomerization tag, a region in spike protein outside RBD, a horseradish peroxidase binding domain or a protease cleavage site.

The present invention is directed to methods of treatment of airway obstruction associated with fibrin-containing cast formation by administering a fibrinolytic agent.

The present invention relates to a novel process of isolating and purifying tissue plasminogen activator and its variants more specifically TNK-tPA from CHO cells and describes an industrially applicable, simple, cost effective, robust and highly efficient process of TNK-tPA purification.

This disclosure relates to a method of generating conditionally active biologic proteins from wild type proteins, in particular therapeutic proteins, which are reversibly or irreversibly inactivated at the wild type normal physiological conditions. For example, evolved proteins are virtually inactive at body temperature, but are active at lower temperatures.