In a first aspect, the invention provides a polymeric nanoparticle comprising at least one polycationic polymer; at least one polyanionic polymer; and a therapeutically effective amount of at least one therapeutic agent.

In a second aspect, the invention provides a method for the preparation of a polymeric nanoparticle according to the first aspect; the method comprising the steps of: (i)admixing the at least one polyanionic polymer with the at least one therapeutic agent; and (ii) introducing to the mixture of (i), to the at least one polycationic polymer.

In a third aspect, the invention provides a polymeric nanoparticle according to the first aspect of the present invention, or a polymeric nanoparticle prepared according to the second aspect of the present invention; for use in the treatment of an inflammatory and/or arthritic disorder caused by or associated with dysfunctional nuclear receptor signalling.

A method for treating, remedying, or preventing inflammatory skin disorders by administering a therapeutically effective dose of at least one an antagonist of a calcitonin gene-related peptide receptor in a pharmaceutically acceptable formulation. The method for treating, remedying, or preventing an inflammatory skin disorder by administering topically and to the prepsoriatic rim a therapeutically effective dose of at least one an antagonist of a calcitonin gene-related peptide receptor in a pharmaceutically acceptable formulation.

A method for treating, remedying, or preventing inflammatory skin disorders by administering a therapeutically effective dose of at least one an antagonist of a calcitonin gene-related peptide receptor in a pharmaceutically acceptable formulation. The method for treating, remedying, or preventing an inflammatory skin disorder by administering topically and to the prepsoriatic rim a therapeutically effective dose of at least one an antagonist of a calcitonin gene-related peptide receptor in a pharmaceutically acceptable formulation.

The present invention relates to pharmacogenetics, more specifically to strategies involving biomarkers associated with the clinical response to a compound before or during treatment of a cartilage disorder, such as osteoarthritis. The present invention more particularly relates to the combination of JSW measurements and level of specific proteins present in the blood, serum, synovial fluid or in the urine, which can be used in strategies such as patients' enrichment in clinical trials, patients' selection strategy before or during treatment or for adapting the treatment of a patient in the frame of treatments for cartilage disorder, such as osteoarthritis.

The object of the present invention is novel release systems comprising specific hyaluronic acid amides combined with therapeutically and/or biologically active proteins with a mainly hydrophobic nature, for sustained, slow release over time which increases the efficacy of the medicament and the patient's compliance.

The present invention relates to compositions forming a low viscosity mixture of: a) at least one diacyl glycerol; b) at least one phosphatidyl choline; c) at least one oxygen containing organic solvent; d) at least one GnRH analog; Wherein the pre-formulation forms, or is capable of forming, at least one liquid crystalline phase structure upon contact with an aqueous fluid. The invention further relates to methods of treatment comprising administration of such compositions, pre-filled administration devices and kits containing the formulations.

The present invention relates to compositions forming a low viscosity mixture of: a) at least one diacyl glycerol; b) at least one phosphatidyl choline; c) at least one oxygen containing organic solvent; d) at least one GnRH analog; Wherein the pre-formulation forms, or is capable of forming, at least one liquid crystalline phase structure upon contact with an aqueous fluid. The invention further relates to methods of treatment comprising administration of such compositions, pre-filled administration devices and kits containing the formulations.

The invention provides novel compositions of bioactive polypeptides and proteins with improved stability and shelf-life. The compositions are based on liquid vehicles selected from semifluorinated alkanes. These vehicles are remarkably effective in protecting polypeptides and proteins from degradation and/or aggregation. The compositions are useful for topical administration, e.g. into an eye, or by parenteral injection, e.g. via the subcutaneous or intramuscular route.

The invention provides novel compositions of bioactive polypeptides and proteins with improved stability and shelf-life. The compositions are based on liquid vehicles selected from semifluorinated alkanes. These vehicles are remarkably effective in protecting polypeptides and proteins from degradation and/or aggregation. The compositions are useful for topical administration, e.g. into an eye, or by parenteral injection, e.g. via the subcutaneous or intramuscular route.

The present invention provides novel compositions and methods based on the discovery of the mechanisms and gene expression programs associated with homeostatic ILC2s and proinflammatory ILC2s that drive tissue inflammation. Immune signaling abnormalities in the small intestine can trigger chronic type 2 inflammation. Applicants analyzed 58,067 immune cells from the mouse small intestine by single-cell RNA-seq at steady state and after induction of a type 2 inflammatory reaction to ovalbumin. Cell type composition and cell programs shifted in response to inflammation, especially in ILC2s. A key transcript in the inflammation-induced program in intestinal KLRG1+ILC2s was exon 5 of Calca, encoding the alpha-calcitonin gene-related peptide (a-CGRP). a-CGRP antagonized IL-25-induced activation of intestinal ILC2s and reduced their frequency in an ovalbumin reaction model. α-CGRP activated a cAMP response, which suppressed ILC2 proliferation. In homeostasis, α-CGRP was expressed by two subsets of ChAT+ enteric neurons, and genetic perturbation of α-CGRP increased the proportion of intestinal ILC2s and of Tuft cells. The results demonstrate that a-CGRP-mediated neuronal signaling suppresses ILC2 expansion and maintains type 2 immunity homeostasis.