MD Biosciences Blog

Osteoarthritis (OA) is a widespread condition that affects greater than 70% of the elderly population and poses a heavy cost burden on healthcare. It is a chronic degenerative disease characterized byt the loss of articular cartilage components, which affects the entire joint structure. One of the major complaints by OA patients is the loss of joint function as well as chronic pain. Current therapies are focused on alleviating joint pain, however full pain relief is rarely experienced and significant side affects are commonly present. Research is not only focused disease pathology but also on understanding the mechanisms responsible for induction and maintenance of pain states.

There are currently a large number of well-characterized, ischemic stroke animal models available for pre-clinical research. These models can be categorized into those two groups – those for the study of stroke-associated risk factors and those for the study of stroke pathophysiology. The latter can be further separated into models of focal verses global ischemia and are listed:[1]

Neuroinflammation is a common thread in neuropathic pain (NP), regardless of the conditions under which neuropathic pain develops. This opens up a whole new avenue for investigations into neuropathic pain pathology. Since the primary cell type responsible for immune-like functions in the CNS is microglia, many researchers have turned their attention toward working to better understand microglial physiology and its potential involvement in neuropathic pain.

Cardiovascular disease (CVD) including heart disease, vascular disease and atherosclerosis are the most critical global health threats.

An estimated 26 million people are living with the effects of heart disease and is a major cause of death in western society. Until recently the widely held belief was that the CVD is simply the process as a build up of fat on the surface of artery walls. Eventually, this build up of fat blocks the artery and a heart attack or stroke occurs. However, the process has now been identified as a disease of the inner artery wall (intima) and inflammation is a key factor in its progression.

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that affects approximately 1% of the population, and in 2010 cost the US alone $39.2 billion (1,2).  The disease is characterized by bone erosion, cartilage damage, synovial hyperplasia and cellular infiltration, all of which result in debilitating joint pain and stiffness (1,3,4).  Studying preclinical models such as the collagen-induced arthritis (CIA) model and the anti-collagen antibody induced arthritis (ACAIA) model, which show the above hallmarks of disease has allowed the identification of the cells and cytokines involved in the pathogenesis of the disease (5,6).

Inflammatory Events Associated With Obesity

There is a major unmet need in the treatment of asthma which is growing in incidence and prevalence in industrialized countries. The prevalence of asthma has doubled in the Western world over the previous 20 years. In addition to the estimated 180,000 asthma related deaths per year, there is a substantial economic burden due to lost school/work days and increased medical costs.

The role of T-cells and their actions in rheumatoid arthritis (RA) has been the focus of a great deal of research for some time [1], mainly as a result of many observations in human patients and experimental animal models.  The association of Human Leukocyte Antigen (HLA) DR, a MHC class II cell surface receptor, in RA provides the strongest evidence that CD4+ T-cells are involved in the development of disease [2, 3, 6]. Many other types of T-cells, including CD8+, regulatory T-cells and γδ T-cells have been shown to play different roles in the progression of RA [1, 2, 3, 8]. The mechanisms of disease involved in RA are still unknown; however the main hypothesis theorizes that auto antigens are presented to auto reactive T helper cells, which then orchestrate the inflammatory processes which are characteristic of the disease [3]. The nature of the antigens involved is unknown however several candidates have been suggested, most recently, citrullinated proteins [5, 6].

With the number of blockbuster drugs approaching patent expiration and pharma companies struggling to maintain pipeline and portfolios with in-house programs, companies are increasingly turning to licensing, aquisitions and partnerships. Early-stage licensing deals tend to carry more risk for pharma companies in-licensing. To offset this risk, additional data may be required from the pharma partner to confirm any internal research performed by the biotech/out-licensing company.

Mini-case study. MD Biosciences helps a medium-sized biotech company to develop Rheumatoid Arthritis drug for out-licensing in under two years.