The present invention relates to a new coating system useful for coating particles, which comprise an active ingredient. Such coated particles, when consumed, do show a controlled release in the human or animal body.

The present invention relates to a method for manufacturing acrylated epoxidised plant oil particles comprising the following steps: a) mixing acrylated epoxidised plant oil with at least one solvent and in the presence of at least one photoinitiator; b) optionally mixing the solution after step a) with a solution S1; c) mixing the solution obtained after step a) or after optional step b) with an aqueous solution comprising at least one surfactant in order to obtain droplets; d) exposing said droplets to a UV light; e) retrieving the acrylated epoxidised plant oil particles obtained after step d).

A one-pot procedure to extract a dispersible exine shell. The shell can be used as a protection and/or delivery vehicle for immunocontraceptive active substances or as an antioxidant. The invention provides a formulation containing the dispersible exine shell together with an immunocontraceptive active substance; and a method for preparing the shell by isolating a dispersible exine shell from a naturally occurring spore or pollen grain by treating the spore or pollen grain with a base or surfactant or both with or without a catalyst in the same reaction vessel.

Encapsulated particles comprising one or more particle cores of silicon-containing material, wherein the one or more particle cores are encapsulated in a waxy lipid shell comprising: a) two lipidic components present at from 55% to 95% of the total encapsulated particle weight; b) a surfactant present at from 0.1% to 5% by weight of the total encapsulated particle weight; c) a co-surfactant present at from 0.01% to 1% by weight of the total encapsulated particle weight; d) a regulator of metastable state present at from 0.1% to 5% by weight of the total encapsulated particle, wherein the regulator of metastable state is selected from one or more of: the terpenes; the terpenoids; fatty acids, from myristic to docosanoic, pegylated by methyl ether of polyethylene glycol (PEG. Me M. W. 750-2000); diacylphosphatidylethanolamines pegylated with PEG; poloxamers (Pluronics); and derivatives thereof. Also related compositions and methods.

The present invention relates to a new delivery system for PUFAs.

The present disclosure relates to a taste-masking microcapsule composition. The composition comprises a core portion encapsulated by a shell portion. The core portion comprises an active pharmaceutical ingredient (API) and one or more excipients. The shell portion comprises a hydrophobic matrix and a pH-responsive material. The microcapsule compositions prevent API release at the more neutral pH levels in the oral cavity, but upon exposure to pH levels of the stomach, the pH-responsive material becomes soluble thereby permitting release of the API.

Described herein are milk exosomes and uses thereof. In some embodiments, the milk exosomes are capable of targeting an injury site or a cancer cell or population thereof. The milk exosomes can contain an exogenous cargo. Described herein are formulations containing the milk exosomes, and optionally, a targeting agent, such as IgG or stimulation of ATP concentration, and/or ADP. Also described herein are methods of delivering a cargo to a target.

This application relates to the technical field of biological products, and provides an application, extraction method and composition of TGL-ELNs in the treatment of glioma. The TGL-ELNs are applied in any one or more of the following aspects: a) Preparation of products for promoting apoptosis of glioma cells; b) Preparation of products for inhibiting proliferation of glioma cells; c) Preparation of products for inhibiting autophagy of glioma cells; d) Preparation of products for treating glioma. Verified through cell and animal experiments, the TGL-ELNs in this application can effectively induce apoptosis of glioma cells and inhibit autophagy of glioma cells to induce glioma cell death, and act on glioma cells through the AKT/mTOR signaling pathway and by inhibiting the production of autophagosomes in glioma cells.