R&D pipeline

For hypertension there are no mouse models. Hypertension is one example of a disease that involves multiple loci.
The rat hypertension models and especially the spontaneously hypertensive rat, the stroke prone rat, the borderline hypertensive rat and the feminized rat parallel the physiological markers of the human disorders. There are some basic differences between the rat and mouse that have an impact on their physiological responses. For instance, the mouse is well adapted to dry and hot environment such as desert areas and consequently has a kidney with high capacity to conserve water. This isn't the case for rat and human species. This difference in the conservatory ability lies in the highly activated renin angiotensin system in the digestive system where it regulates the level of water and sodium. This system is very important in rat and human hypertension.

Neuroanatomical/stereotaxic injections into the CNS are frequently required to study behaviors. Such techniques are very difficult to carry out on mice and are thus poorly defined. (The neuroanatomy/neurochemistry of the rat brain is also much better described than that in the mouse.)
Moreover, the size of the rat is necessary to perform important behavior tests associated with many neurological disorders, especially those tests involving site-specific brain cannulas. Neuro-behavioral tests relevant to Alzheimer's disease are best developed and validated in rats.

The rat model mimics many features of human asthma.
Mice don't show the same biological responses to viral illnesses, and it is unlikely that a relevant model could be developed in mice. One major advantage in rat studies is that we have been able to adapt numerous methods for detailed assessment of lung physiology in rats; most of these can be done repeatedly over time in individual animals.
The rat is an excellent model for silica-induced pulmonary fibrosis and cancer. Human epidemiological data also link silica exposure to lung fibrosis and cancer. The mouse is non-responsive for silica-induced lung cancer and for certain strains of fibrosis. A good deal of mechanistic information has been gathered on the initiation and progression of pneumocinioses using the rat model.

RA is a complex, polygenic disease that afflicts approximately 1% of the population worldwide and shows familial association with several autoimmune diseases. There are several rat models of chronic arthritis that do not occur in mice. Rats are the traditional species for studying acute and chronic arthritis whereas mice, are resistant to most of the classic protocols for arthritis induction. Mice do not develop "Adjuvant Arthritis", a classic T-lymphocyte driven model of chronic peripheral arthritis in rats.
Furthermore, rats (but not mice) are susceptible to get "Bacterial Cell Wall Arthritis" and arthritis induced by systemic infection with viable Mycoplasma arthritidis. Therefore, rat models of these diseases emphasize the possible microbial etiology of human arthritis. Other rat models of arthritis include 6-sulfanilamide imidazole arthritis and an immune complex model of arthritis that results from colon loop isolation.

The rat complement system is robust and stimulates more closely human levels compared to that of most laboratory mouse strains. Activation of the complement system is being implicated in high priority diseases today especially in atherosclerosis and Alzheimer's disease. For diseases in which the complement system is involved, one just cannot obtain a mouse model with predictable efficiency.

The rat phenotype parallels predictions from human epidemiological observations, whereas the same has not been observed in mouse models, as outlined below: The lesions in the rat atherosclerosis model is in the coronary arteries like in humans. However, in transgenic mouse models these lesions appear to be in the root of the aorta at the coronary ostia .
Given the same level of cholesterol and triglycerides, the rat atherosclerosis model demonstrates coronary artery disease and decreased survival in contrast to the mouse model.