Abstract: The present invention relates to TWEAK-receptor agonists for use in the treatment of a cancer, wherein the TWEAK-receptor agonist is combined with immunotherapy of the cancer. The TWEAK-receptor agonist preferably is a multivalent ligand that causes clustering of TWEAK-receptors at the cell surface. A suitable TWEAK-receptor agonist is an agonistic anti-Fn14 antibody. The TWEAK-receptor agonist and immunotherapy be can further be combined with a SMAC mimetic in the treatment of cancer. The TWEAK-receptor agonist is useful, optionally in combination with a SMAC mimetic, to prevent resistance of a cancer to immunotherapy and/or to treat a cancer comprising tumor cells that are resistant to immunotherapy.

Abstract: Provided herein are compositions including peptides, pharmaceutical preparations thereof, and methods of preventing photoreceptor death therewith and protecting of retinal cells, including, but not limited to, photoreceptors and retinal pigment epithelium, from Fas- or TRAIL-mediated apoptosis.

Abstract: A peptide is disclosed that has an amino acid sequence selected from X1-X2-X3-Gln-Leu-Met-Leu-Cys-Val-Leu-X4-X5-X6 (SEQ ID NO: 3), X1-X2-X3-Gln-X7-Met-X10-Cys-Val-X11-X4-X5-X6 (SEQ ID NO: 4), Ile-Ser-Phe-Gln-Leu-Met-Leu (SEQ ID NO: 5), Leu-Cys-Val-Leu-Asp-Tyr-Phe (SEQ ID NO: 6), X1-X2-X3-Gln-Leu-X8-Leu-X9-Val-Leu-X4-X5-X6 (SEQ ID NO: 7), X1-X2-X3-Gln-Leu-X8-Leu-X9-Val-Leu-X4-X5-X6 (SEQ ID NO: 7), X1-X2-X3-X12-Leu-Met-Leu-Cys-X13-Leu-X4-X5-X6 (SEQ ID NO: 10), Gln-X7-Met-X10-Cys-Val-X11 (SEQ ID NO: 11), Gln-Leu-X8-Leu-X9-Val-Leu (SEQ ID NO: 12), X12-Leu-Met-Leu-Cys-X13-Leu (SEQ ID NO: 13), Asp-Leu-Val-Ile-Ser-Phe-Gln-Leu-Met-Leu-Cys-Val-Leu-Asp-Tyr-Phe-Ile-Lys (SEQ ID NO: 14) and retro-inverso peptides thereof. The peptides disclosed herein may be used to treat liver cancer, lung cancer, breast cancer, pancreatic cancer, or brain cancer.

Abstract: Provided are methods for sensitizing gastrin-associated tumors and/or cancers in subjects to inducers of humoral and cellular immune responses. In some embodiments, the methods relate to administering compositions that have anti-gastrin antibodies, gastrin peptides, and/or nucleic acids that inhibit expression of gastrin gene products to subjects. Also provided are methods for preventing, reducing, and/or eliminating the formation of fibroses associated with tumors and/or cancers, and methods for treating gastrin-associated tumors and/or cancers that include administering to subjects in need thereof a first agent that provides and/or induces an anti-gastrin humoral or cellular immune response in the subject and a second agent that includes one or more stimulators of cellular immune responses against the tumors and/or cancers.

Abstract: Disclosed are a novel therapeutic means effective and practical against cancer, and a novel substance useful as such a therapeutic means. Provided are novel peptides derived from a partial region of HMGN1, HMGN2, HMGN4 or HMGN5, and anti-cancer agents and anti-cancer effect enhancers containing the peptide as an active ingredient. The peptide of the present invention has an anti-tumor effect even independently, and exerts a remarkably excellent anti-tumor effect particularly when used in combination with an immune checkpoint regulator, or an anti-CD4 antibody or antigen-binding fragment thereof.

Abstract: The present invention provides modified von Willebrand Factor molecules, methods for their preparation and uses thereof. The invention further provides pharmaceutical compositions for treating coagulation disorders.

Abstract: Disclosed are methods of treating obesity or an obesity-related condition comprising administering an effective amount of soluble (pro)renin receptor (sPRR) to a subject that is obese or having an obesity-related condition. In some instances, obesity-related conditions can be, but are not limited to, steatosis, hyperglycemia, insulin resistance, chronic renal disease. Disclosed are methods of reducing body weight comprising administering an effective amount of sPRR to a subject in need thereof. Disclosed are methods of treating fatty liver in a subject comprising administering an effective amount of sPRR to a subject in need thereof. Disclosed are methods of treating a fluid and electrolyte disorder comprising administering an effective amount of sPRR to a subject diagnosed with a fluid and electrolyte disorder.

Abstract: Dithioamine reducing agents useful for the reduction of disulfide bonds. The reducing agents of this invention are useful, for example, to reduce disulfide bonds, particularly in proteins, or to prevent the formation of disulfide bonds, particularly in proteins and other biological molecules. Reducing agents of this invention can be employed to regulate protein function in proteins in which a sulfhydryl group is associated with biological activity. Reducing agents of this invention can prevent inactivation of a given protein or enhance activation of a given protein or other biological molecule in vitro and/or in vivo. Reducing agents of this invention can prevent or reduce oxidation of cysteine residues in proteins and prevent the formation of reduced activity protein dimers (or other oligomers). Reducing agents of this invention are useful and suitable for application in a variety of biological applications, particularly as research and synthetic reagents.

Abstract: The present invention relates to compositions and methods for treating cancer, particularly to agents that inhibit the expression and/or activity of the protein second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI (SMAC/Diablo). The inhibiting agents include RNA interference molecules silencing the expression of SMAC/Diablo and peptides modulating its interactions within the cell nucleus and mitochondria. The methods and agents of the present invention are useful in treating cancers associated with overexpression of SMAC/Diablo.

Abstract: Disclosed herein are conjugates including a fatty acid, a self-assembly domain, and a polypeptide having phase transition behavior. Further disclosed are methods of using the conjugates to treat disease, methods of delivering an agent, and methods of preparing the conjugates.

Abstract: The present invention relates to a method of purifying albumin-fusion proteins to reduce the level of oxidation of susceptible amino acid residues. The method comprises an affinity matrix chromatography step and an anion exchange chromatography step. The purified albumin-fusion proteins have low levels of oxidation and retain their enhanced half-life in vivo and its bioactivity. In some embodiments, the albumin-fusion protein comprises a scaffold, such as human Tenascin C scaffold. Compositions comprising the albumin-fusion protein are further disclosed.

Abstract: The present disclosure provides use of chemokine receptor CXCR5, wherein CAR-T cells with enhanced chemotaxis are obtained by modifying chimeric antigen receptor T cells (CAR-T cells) utilizing the chemotactic signal between CXCR5 and its ligand CXCL13. The chemokine receptor CXCR5 can guide CAR-T cells to migrate to tumors. It has an excellent ability to enhance the chemotaxis of CAR-T cells, can specifically clear tumor cells, and effectively solve the problem of poor efficacy of the existing CAR-T therapy for solid tumors, thereby exhibiting broad application prospects and great market value.

Abstract: The present invention provides modulators of complement activity. Also provided are methods of utilizing such modulators as therapeutics.

Abstract: A method for purifying a target peptide may include mixing a peptide product obtained through a peptide synthesis with a solvent in the presence of a sulfonic acid compound to obtain a solid; and performing a solid-liquid separation to collect the solid.

Abstract: The present invention relates to a method for treating gastrointestinal bleeding in a subject with severe von Willebrand Disease comprising administering to the subject at least one dose of recombinant von Willebrand Factor (rVWF) ranging from about 40 IU/kg to about 100 IU/kg, wherein the first dose further comprises recombinant Factor VIII (rFVIII).

Abstract: Disclosed herein are fusion proteins for use in treating an inflammatory or immune disorder and methods of use. In some examples, the fusion proteins include an anchor domain and a therapeutic polypeptide. In some examples, the fusion proteins and methods herein can be used to treat inflammatory or immune disorders.

Abstract: Methods are disclosed for producing highly purified recombinant human insulin (RHI) having a purity of 99.0% (w/w) or greater, a Total Impurity (not including the related substance desamido AsnA21-RHI, as specified by USP) of 0.8% (w/w) or less, and an impurity C of 0.1% (w/w) or less. Also disclosed are API compositions of highly purified RHI having a purity of 99.0% (w/w) or greater, a Total Impurity of 0.8% (w/w) or less, and an impurity C of 0.1% (w/w) or less.

Abstract: The present disclosure relates to a third generation tubulysin analogues and process of preparation thereof. The present disclosure also relates to a method of using these third generation tubulysin analogues for treatment of various diseases including cancer.

Abstract: A method is provided for extraction of fine silk fibroin powder from Bombyx mori silk cocoons. The conventional method of silk processing includes dissolution of the degummed silk fibers in some strong salt solutions followed by a dialysis step. The earlier reported strong salt solutions have either associated environment issues or lower dissolution ability for silk. However, the provided method includes degumming silk cocoons, drying and cutting the degummed silk fibers, mixing the fibers with an ionic liquid, stirring the mixture, regeneration of silk from the mixture with the help of an anti-solvent followed by centrifugation, drying the precipitated silk and finally obtaining a fine powder of silk.

Abstract: The present disclosure relates to a method for increasing the stability of a Factor VIII molecule after purification, lyophilization and reconstitution, comprising preventing proteolytic cleavage of the Factor VIII molecule into a first fragment comprising essentially the A1 domain and the A2 domain and a second fragment comprising essentially the A3 domain, the C1 domain and the C2 domain throughout manufacturing the Factor VIII molecule. The disclosure further pertains to a method for improving the bioavailability of Factor VIII after intravenous and non-intravenous injection.