The invention refers to genetic engineering and can be used in biotechnology, medicine, and agriculture for the manufacture of gene therapy products. A gene therapy DNA vector based on the VTvaf1V gene therapy DNA vector is proposed that carries a target gene selected from the group of genes ANG, ANGPT1, VEGFA, FGF1, HIF1a, HGF, SDF1, KFK4, PDGFC, PROK1, PROK2, to increase the expression level of this target gene in humans and animals. Gene therapy DNA vector VTvaf17-ANG or VTvaf 17-AN GPT 1 or VTvaf17-VEGFA or VTvaf17-FGF1 or VTvaf17-HIF1a or VTvaf17-HGF or VTvaf17-SDF1 or VTvaf 17-KFK4 or VTvaf 17-PDGFC, or VTvaf 17-PDKFC or VTvaf17 has the nucleotide sequence of SEQ ID No. 1 or SEQ ID No. 2 or SEQ ID No. 3 or SEQ ID No. 4 or SEQ ID No. 5 or SEQ ID No. 6 or SEQ ID No. 7 or SEQ ID No. 8 or SEQ ID No. 9 or SEQ ID No. 10 or SEQ ID No. 11, respectively. Also provided are a method of producing said vector, the use of a vector, a strain of Escherichia coli carrying said vector, as well as a method of industrial production of said vector.

Provided are preparations of tissue kallikrein-1 (KLK1) glycoforms having a defined number of oligosaccharide units per KLK1 molecule. Also provided are mixtures of such glycoforms, pharmaceutical compositions containing such glycoforms or mixtures thereof, methods of obtaining the rhKLK1 glycoforms, and therapeutic uses thereof.

Provided are high concentration compositions of tissue kallikrein-1 (KLK1) and methods of parenterally administering such compositions to a subject in need thereof, where absorption into the circulation via, for example, intravenous or subcutaneous administration improves systemic pharmacokinetics, bioavailability, safety, and/or convenience relative to intravenous or other forms of administration. Also provided are recombinant human KLK1 (rhKLK1) polypeptides that can be readily concentrated to high protein concentrations, and substantially pure compositions thereof.

This document provides methods and materials involved in modulating a cell's ability to be resistant to apoptosis. For example, methods and materials for exposing cells to KLK6 polypeptides, or increased KLK6 polypeptide activity, to promote resistance to apoptosis are provided. In addition, methods and materials for reducing the ability of KLK6 polypeptides to promote resistance to apoptosis are provided.

The present invention relates antidotes to anticoagulants targeting factor Xa. The antidotes are factor X and factor Xa protein derivatives that bind to the factor Xa inhibitors thereby substantially neutralizing them but do not assemble into the prothrombinase complex. The derivatives describe herein lack or have reduced intrinsic coagulant activity. Disclosed herein are methods of reversing anticoagulation, stopping or preventing bleeding in a patient that is currently undergoing anticoagulant therapy with a factor Xa inhibitor.

Compositions and methods for therapeutic delivery are disclosed. More particularly, the present disclosure relates to nanoparticle compositions that sequester the activity of a target molecule while leaving other domains accessible to bind targeted tissues of interest. Methods for thrombus dissolution include administering a nanoparticle reversibly coupled to a target molecule that can dissolve a blood clot. Compositions and methods for inducing blood clotting are also disclosed. Methods for inducing blood clotting include administering a nanoparticle reversibly coupled to a target molecule that can induce the formation of a blood clot. Methods for sequestering a target molecule are also disclosed. The method includes reversibly coupling a target molecule to a nanoparticle having an affinity ligand that reversibly couples the target molecule, and thus, sequesters the target molecule activity until the target molecule interacts with its substrate resulting in the release of the target molecule.

This document provides methods and materials involved in modulating a cell's ability to be resistant to apoptosis. For example, methods and materials for exposing cells to KLK6 polypeptides, or increased KLK6 polypeptide activity, to promote resistance to apoptosis are provided. In addition, methods and materials for reducing the ability of KLK6 polypeptides to promote resistance to apoptosis are provided.

Provided are preparations of tissue kallikrein-1 (KLK1) glycoforms having a defined number of oligosaccharide units per KLK1 molecule. Also provided are mixtures of such glycoforms, pharmaceutical compositions containing such glycoforms or mixtures thereof, methods of obtaining the rhKLK1 glycoforms, and therapeutic uses thereof.

Provided are high concentration compositions of tissue kallikrein-1 (KLK1) and methods of parenterally administering such compositions to a subject in need thereof, where absorption into the circulation via, for example, intravenous or subcutaneous administration improves systemic pharmacokinetics, bioavailability, safety, and/or convenience relative to intravenous or other forms of administration. Also provided are recombinant human KLK1 (rhKLK1) polypeptides that can be readily concentrated to high protein concentrations, and substantially pure compositions thereof.

The present invention relates antidotes to anticoagulants targeting factor Xa. The antidotes are factor X and factor Xa protein derivatives that bind to the factor Xa inhibitors thereby substantially neutralizing them but do not assemble into the prothrombinase complex. The derivatives describe herein lack or have reduced intrinsic coagulant activity. Disclosed herein are methods of reversing anticoagulation, stopping or preventing bleeding in a patient that is currently undergoing anticoagulant therapy with a factor Xa inhibitor.