For poorly soluble bRo5 and BCS Class II/IV APls, exposure is driven by the combined effects of solubility, dissolution rate, and permeability-related barriers.
Traditional formulation methods, such as ASDs, typically address only one of these elements.
THE PROBLEM
Poor oral bioavailability is often treated as a solubility problem, but in vivo exposure is rarely determined by solubility alone. Once an API enters the gastrointestinal environment, it must dissolve fast enough, remain available for absorption, and overcome biological barriers such as the aqueous boundary layer, mucus, and efflux transporters.
A formulation that improves only one of these steps may still fail to deliver meaningful systemic exposure.
3 LEVERS OF BIOAVAILABILITY
SOLUBILITY
NanoGlass™ formulations generate amorphous nanoparticles of API in situ, maximising solubility by maintaining the API in a high-energy amorphous state.
DISSOLUTION RATE
Amorphous nanoparticles provide a high surface area of API. As solubilised API is absorbed, these nanoparticles can rapidly dissolve to replenish the solubilised fraction.
PERMEABILITY
Amorphous nanoparticles facilitate transport through the aqueous boundary layer and mucus, while formulation components address efflux-related barriers.
Note: NanoGlass™ does not change the intrinsic permeability of the API across a biological membrane.
HOW NANOGLASS™ PULLS ALL THREE LEVERS
NanoGlass™ formulations are designed to generate amorphous API nanoparticles in situ, creating a colloidal reservoir of drug within the gastrointestinal environment. As dissolved API is absorbed, this reservoir continuously replenishes the solubilised fraction, helping maintain elevated apparent solubility and the concentration gradient that drives absorption.
This mechanism links solubility enhancement, rapid dissolution, and permeability enhancement, thus NanoGlass™ is designed to maximise total oral exposure.
