Johns Hopkins University is seeking licensees for Hypoxia-Induced Mitogenic Factor (HIMF/ FIZZ1/RELM), a cell line expressing tagged HIMF, antibodies to HIMF and receptor. HIMF provides a wide array of novel biomarkers and therapeutic targets for lung, vascular, cardiac and inflammatory diseases, as well as cancer and wound-healing. Key HIMF findings: • Highly upregulated during hypoxia-induced pulmonary hypertension • Angiogenic and pro-inflammatory effect on pulmonary vasculature • May contribute to growth of lung, breast and other cancers
Technical Details:
JHU researchers have discovered a novel cytokine named Hypoxia- Induced Mitogenic Factor (HIMF; also known as FIZZ/RELM) a secreted protein that is highly up regulated in the lungs as a result of hypoxia-induced pulmonary hypertension. HIMF profoundly constricts the pulmonary vasculature and participates in angiogenesis and vascular remodeling by promoting smooth muscle cell proliferation and endothelial cell migration. HIMF is also a key mediator of inflammation, having proinflammatory effects in the lung. HIMF is implicated in a number of diseases, such as pulmonary arterial hypertension, pulmonary fibrosis, inflammatory lung disease (adult respiratory distress syndrome, sepsis, bronchodysplasia), asthma and pulmonary vascular disease related to AIDS. Due to pro-angiogenic effects, there is evidence for a role of the FIZZ/RELM family proteins in the growth of lung, breast and other forms of cancer. In the heart, the FIZZ/RELM proteins initiate cardiac hypertrophy and mediate cardiac hypertrophic conditions related to pulmonary and arterial hypertension, congestive heart failure, and ischemic heart disease. JHU researchers have developed novel methods of inhibiting HIMF and anti-HIMF antibodies that may be used to measure HIMF in body fluids as a potential predictive/diagnostic of disease.
Looking for Partners:
HIMF provides a novel biomarker and therapeutic target for a wide array of lung, vascular, cardiac and inflammatory diseases, as well as cancer and wound-healing. Inhibition of HIMF will provide receptor antagonists that block activation of HIMF pathways.
