Biodegradable film with sustained drug delivery

Long-term, localized delivery of small molecules from a biodegradable thin film is challenging owing to their low molecular weight and poor charge density. While MIT researchers recently developed a thin-film drug delivery system enabling steady, sustained release of medication for about 14 months, a scientific advancement with major commercial implications.

This sustained release formulation for small molecules is based on a soluble charged polymer–drug conjugate that is immobilized into nanoscale, conformal, layer-by-layer assembled films applicable to a variety of substrate surfaces. They measured a highly predictable sustained drug release from a polymer thin film coating of 0.5–2.7?m that continued for more than 14 moths with physiologically relevant drug concentrations, providing an important drug delivery advance. They demonstrated this effect with a potent small molecule nonsteroidal anti-inflammatory drug, diclofenac, because this drug can be used to address chronic pain, osteoarthritis, and a range of other critical medical issues. In addition, the quantity of the drug being delivered can be controlled by adding additional layers of the thin-film coating.

The scientific challenge that was overcome, at least experimentally, involved limiting hydrolysis (by which water severs the drug molecule's bonds) while allowing some degradation in order to ensure steady and sustained release.

Polymer nanomaterials are crucial for many types of drug delivery applications, offering the flexibility and durability needed to engineer specific shapes and sizes for particular delivery solutions. Recently, researchers have developed a new technique for creating self-assembling fibers for this purpose, taking a cue from the natural fibers in living cells.

The team used a green fluorescent protein, its molecules linked to one another to form fibers. But although these molecules do not normally link together, the scientists had to do some tinkering to get them to assemble in such a way. By adding PEO-dialkyne linkers to the proteins, they joined together to form long chains.

Nevertheless, the evidence of aspirin's anti-cancer benefits is incidental. These are not the results of randomized trials which can provide the best evidence for us to answer this question. However, there are no studies comparing the effects of not taking aspirin or taking aspirin on cancer. In addition, aspirin-related gastrointestinal bleeding is the most serious side effects, which might lead to stomach bleeding. So the researchers noted that 70 years or older people do not need to start taking aspirin to prevent cancer, which is due to a sharp increase in the risk of serious bleeding.

The researchers also indicated that there are several potential mechanisms of aspirin in cancer prevention. It is known that aspirin disturbs blood coagulation by reducing blood platelets. Platelets are thought to contribute to cancer metastasis, thus limiting the platelets may make cancer cells more difficult to spread. Another theory is that aspirin can stop cell division, which reduces the probability of mutations during cell division. Thus will unlikely to lead to cancer related mutations.

Importantly, the linked GFP structures retained their fluorescence, which indicates that the molecules held on to their original shapes even when linked together. This is the key for the structural integrity of the overall compound.