Empros Pharma has developed a revolutionary drug – EMP16. The main mechanism of action for EMP16 is to delay normal food digestion and absorption processes towards the end of the small intestine. EMP16 is based on a proprietary advanced drug delivery technology, designed to have features that optimizes its effect throughout the gastrointestinal system. EMP16 is an oral product with a local effect in the gastrointestinal systems. It is a fixed dose combination of two locally active, safe and established active drugs (orlistat and acarbose). The advanced multiple unit, modified release formulation is designed to maximize the effect of the drugs as well as improving tolerability.

The mechanism of action of EMP16 is supporting and increasing the natural satiety response present in the gastrointestinal system to regulate food intake.
An important distinction to other, often hormone based satiety regulating pharmaceuticals (that will act on one or a few of the hormone signalling pathways) is that EMP16 enhances the entire endogenous hormone response in a physiological way. Empros Pharma expects this to be a safer and more potent method to address the medical need of obese patients. The design is also expected to significantly reduce local side-effects and to increase tolerability.

Satiety is triggered by a complex interplay between hormones, nutrients and transmitter substances in the body. Undigested food reaching the end of small intestine leads to an increased secretion of several gut hormones that act locally on the motility of the gastrointestinal tract and on the brain centre regulating satiety. The gastric motility is down-regulated, resulting in reduced stomach emptying rate and food transit rate through the upper part of the gastrointestinal system.

The main mechanism is local enzyme inhibition of various amylases and lipases responsible for carbohydrate and lipid digestion in the gastrointestinal tract.

The gastrointestinal tract is an organ for enzyme mediated digestion and absorption of ingested food as well as it is largest endocrine (hormone secretion) organ in the body.

Satiety is triggered by a complex interplay between hormones, nutrients and transmitter substances in the body.

Digested food reaching the end of small intestine leads to an increased secretion of several gut hormones that act locally through receptor in specialized enteroendocrine cells on the motility of the gastrointestinal tract and on the brain centre regulating satiety.

The gastric motility is regulated so that stomach emptying rate and food transit rate through the upper part of the gastrointestinal system slows down. This effect is commonly known as the ileal brake and is mediated by locally released gut hormones when digestion and absorption of free fatty acids and hexoses (i.e. glucose) act via specialized receptors in ileum. The shift on gastrointestinal digestion induced by EMP16 is expected to increase satiety by increasing the local hormone response, once the digested carbohydrates and lipids are absorbed by the intestinal enteroendocrine cells where these specific receptors are located.

EMP16 acts locally in the gastrointestinal system through re-routing digestion and the exposure of natural dietary derived ligands (i.e. digested carbohydrates and lipids) to important satiety and eating behaviour regulating mechanisms.

  • Acarbose inhibits amylases

    Acarbose inhibits amylases

    Delayed, extended release of acarbose protects complex carbohydrates.

  • Acarbose and orlsitat inhibit amylases and lipases

    Acarbose and orlsitat inhibit amylases and lipases

    Gastroresistant coating and rapid release protects fat and carbohydrates from “enzyme-shower” in duodenum.

  • Orlistat inhibits lipases

    Orlistat inhibits lipases

    Delayed extended release provides prolonged protection of fat.

EMP16