Pfizer has finalised its collaboration with fellow big pharma firm Bristol-Myers Squibb (BMS).
The deal was originally announced back in April but now more details have emerged.
The alliance centres on generating inhibitors against diacylglycerol acyltransferase 1( DGAT-1 ), one of two known DGAT enzymes that catalyses the final step in triglyceride synthesis.
Triglycerides are the principal component of fat, and so this target could be utilised to create potential anti-obesity drugs.
Overweight and obese individuals have significantly greater triglyceride levels, making them more prone to diabetes and its associated metabolic complications.
In animal tests, lower triglyceride levels have been shown to increase sensitivity to insulin and leptin and so the same molecules could prove useful in treating diabetes.
As well as developing new compounds, the programme also includes DGAT-1 inhibitors in-licensed by Pfizer from Bayer Pharmaceuticals in June 2006, such as the pre-clinical compound PF-04415060 (BAY 74-4113).
BMS will pay Pfizer $50m (€36.6m) and Pfizer has agreed to fund the early stage R&D before sharing costs at Phase III development.
Both these later costs and any profits will be shared 40-60 with Pfizer getting the larger share.
"The worldwide incidence of metabolic disorders is increasing rapidly, and complications from diabetes and obesity are leading causes of disability and mortality globally.
DGAT-1 inhibitors have shown promise in pre-clinical testing, and this research program has potential to yield several compounds that may improve treatment options for patients," said Elliott Sigal, chief scientific officer and head of R&D at BMS.
GlaxoSmithKline (GSK) is clearly keen on Exelixis ' Mesenchymal epithelial transition factor ( MET ) inhibitor, XL880, and has asked its collaborator to review the compound early - before it reaches proof-of-concept.
The small, yet prolific cancer specialist believes its MET inhibitor is the most advanced in clinical development.
One rival is Arqule's ARQ 197, which is currently in a Phase I clinical trial.
XL880 is currently in Phase II clinical trials and, in preclinical tests, reduced tumour growth in kidney cancer, breast cancer, colorectal cancer, non-small cell lung cancer, and brain cancer.
Significantly, said Exelixis, a single dose of XL880 completely inhibited tumour growth for 21 days in a glioblastoma model.
Takeda Pharmaceutical has published details of the mechanism of action of TAK-242 (Ethyl (6R)-6-[N-(2-chloro-4-fluorophenyl)sulfamoyl]cyclohex-1-ene-1-carboxylate), which is designed to inhibit Toll-like receptor 4 ( TLR-4 ) signalling and thus treat severe sepsis.
There are 10 known TLRs in the human immune system, which enable the body to sense threats from pathogens (i.e. viruses and bacteria) that cause disease.
In a recent article in the European Journal of Pharmacology, Takeda said its molecule inhibits various kinds of inflammatory mediators such as nitric oxide (NO), tumour necrosis factor (TNF)-alpha, interleukin (IL)-1, IL-6, IL-10, macrophage inhibitory protein (MIP)-2 and prostaglandin E2 (PGE2).
The tests were carried out on a mouse model of endotoxin shock.
Scientists at the University of Leeds have made what they describe as a "big breakthrough" in the treatment of Huntington's disease.
They discovered that in Huntington's patients, the repressor element 1-silencing transcription factor ( REST ) - usually found only in certain regions of the brain - enters the nucleus of the neuron and decreases the expression of brain derived neurotrophic factor (BDNF).
This prevents 57 genes from operating normally, according to Dr Lezanne Ooi, who has also been studying some of the enzymes which assist the function of REST.
It is these enzymes that provide the mechanism for the protein to wreak havoc in the brains of Huntington's sufferers, and that are already being targeted in certain cancer drugs.
"This breakthrough is particularly exciting as it opens up an avenue for researching a possible treatment using drugs that are already available, rather than starting from scratch," she said.