A method of inhibiting and/or reducing the activity, signaling, and/or function of leukocyte-common antigen related (LAR) family of phosphatases in a cell of a subject induced by proteoglycans includes administering to the cell a therapeutic agent that inhibits one or more of catalytic activity, signaling, and function of the LAR family phosphatases without inhibiting binding to or activation the LAR family phosphatases by the proteoglycans.

Immunogen enhancers for admixture with an antigen of interest are described herein. The enhancers generally comprise a steroid acid and/or a steroid acid-peptide conjugate in an amount sufficient to improve or modify the adaptive immune response to antigens admixed therewith. In embodiments, the steroid acid may be a bile acid and the peptide may comprise one or more functional domains, such as a nuclear localization signal, which may facilitate antigen-presentation and/or antigen cross-presentation, thereby triggering improved cellular immunity, or improved cellular and humoral immunity, against the antigen.

In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.

The present invention relates to a gas-generating micelle for reducing localized fat. In the present invention, by forming a micelle using a material having high biocompatibility and also introducing a cell-targeting ligand (peptide) onto the surface of the micelle, delivery to surrounding cells and tissues other than adipocytes can be minimized, and delivery into adipocytes can be maximized. The gas-generating micelle for reducing localized fat according to the present invention can be produced as an injectable preparation, and can be applied to local lipolysis supplements or diet beauty products that break down localized fat.

Provided herein are Taxol transporter compounds, pharmaceutical compositions, methods of their preparation, and methods of their use in treatment or prevention of a proliferative, dermatological, or ophthalmological disease or disorder.

Infection with obligatory intracellular bacteria is difficult to treat as intracellular targets and delivery methods of therapeutics are not well-known. Ehrlichia translocated factor-1 (Etf-1), a type IV secretion system (T4SS) effector, is a primary virulence factor for an obligatory intracellular bacterium, Ehrlichia chaffeensis. Disclosed herein are Etf-1-specific nanobodies (Nbs) that block Etf-1 functions and Ehrlichia infection. Also disclosed is a method for treating human monocytic ehrlichiosis (HME) in a subject with the disclosed nanobodies.

The present invention relates to polypeptides which are covalently bound to molecular scaffolds such that two or more peptide loops are subtended between attachment points to the scaffold. In particular, the invention describes peptides which bind to OX40. The invention also relates to multimeric binding complexes of polypeptides which are covalently bound to molecular scaffolds such that two or more peptide loops are subtended between attachment points to the scaffold that are functional agonists of OX40. The invention also includes drug conjugates comprising said peptides and complexes, conjugated to one or more effector and/or functional groups, to pharmaceutical compositions comprising said peptide ligands, complexes and drug conjugates and to the use of said peptide ligands and drug conjugates in preventing, suppressing or treating a disease or disorder mediated by OX40.

The present invention relates to compositions and methods for the delivery of agents to a subject, particularly to the central nervous system (CNS).

Immunogen enhancers for admixture with an antigen of interest are described herein. The enhancers generally comprise a steroid acid and/or a steroid acid-peptide conjugate in an amount sufficient to improve or modify the adaptive immune response to antigens admixed therewith. In embodiments, the steroid acid may be a bile acid and the peptide may comprise one or more functional domains, such as a nuclear localization signal, which may facilitate antigen-presentation and/or antigen cross-presentation, thereby triggering improved cellular immunity, or improved cellular and humoral immunity, against the antigen.

Described herein are methods and compositions for the targeted delivery of selective delivery molecule therapeutic agents and imaging agents.