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Rigel Advances Asthma Programs: Two Inhaled Drug Candidates Take Aim at Acute and Chronic Lung Disease
Date:5/16/2012

ajority of the cases are considered allergic asthma, for which there is no known cure.  Acute and severe episodes of the disease make up approximately two million Emergency Room visits each year, accounting for 25% of all visits.

R343, Inhaled SYK Inhibitor
In patients with allergic asthma, allergens, such as pollen, trigger the production of immunoglobulin E (IgE) antibodies, which then bind to mast cells (the body's defense system gatekeepers in the lung) and spark a cascade of intracellular signals to mount an immune response resulting in swelling and inflammation of the airways. SYK is a protein tyrosine kinase that plays a pivotal role in IgE receptor signaling in mast cells. Rigel's R343 is designed to bind to the SYK in mast cells and to interrupt the signal from the IgE receptors. R343's ability to inhibit SYK potentially prevents or stops the immune response to the allergen and may be effective in the short and long-term control of allergic asthma.

Rigel expects to initiate a multi-center, multiple-dose, and placebo-controlled study with R343 in approximately 270 asthma patients this summer.

To view Rigel's R343 Asthma Animation, please go to: http://www.rigel.com/rigel/aa.

R256, Inhaled IL13 Signaling /JAK Inhibitor
In patients with severe or chronic asthma, the cells lining the walls of the respiratory airways and lungs experience persistent inflammation and cellular remodeling resulting in scarring (pulmonary fibrosis) if left untreated.   Inhibition of JAK along the IL13 and IL4 signaling pathways, at the primary cellular level of the airways, may reduce or stop the inflammatory cascade associated with bronchospasms, mucus overproduction, cell wall thickening and other symptoms of chronic lung obstruction.  Rigel has conducted preclinical studies with R256 in a variety of models and expects to initiate preclinical development leading to an I
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SOURCE Rigel Pharmaceuticals, Inc.
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