TITLE: 20-HETE receptor (GPR75 antagonism for the treatment of hypertension, vascular
diseases, inflammatory conditions, sepsis, neovascularization, tumor growth, and
ischemic renal/cardiovascular diseases.
INVENTORS: JR Falck
TECHNOLOGY: Biologicals
UTSD: 3003
SUMMARY: A receptor (GPR75) for 20-hydroxyeicosatetraenoic acid (20-HETE) has been
identified as well as chemical agonists and antagonists for the receptor. 20-HETE's synthesis is
increased in tissues and biological fluids in cardiovascular, cerebral and renal diseases
including pathologies such as hypertension, stroke, coronary artery diseases, myocardial
infarction, acute kidney failure, chronic kidney disease, polycystic kidney disease as well as
conditions that are associated with hypertrophy and hyperplasia including tumor growth and
metastasis, end-organ damage, and fibrosis.
20-HETE is a potent vascular constrictor, proinflammatory, pro-oxidative, pro-growth mediator
and pro-angiogenic factor, except in the lung. The invention includes the characterization of the
20-HETE receptor (GPR75) and molecular antagonistic compounds which interfere with the
biological actions of 20-HETE and functioning as antihypertensive and/or anti-inflammatory
and/or anti-growth agents in hypertension and cardiovascular complications including vascular
stiffening, artherosclerosis, and in disorders of abnormal blood vessels growth including diabetic
retinopathy and tumor growth cancer. This technology also includes the agonistic compounds
targeted at the 20-HETE receptor (GPR75) and their use alone or in combination with other
angiogenic factors such as VEGF, EGF and FGF for growing blood vessels in
ischemic cardiovascular diseases including ischemic heart disease, peripheral vascular disease,
reinforcement of ischemic anastomoses, acceleration of wound healing as well as in conditions
associated with hypotension such as sepsis.
Please contact the Office for Technology Development for more details:
Phone: 214-648-1888
Email: TechnologyDevelopment@utsouthwestern.edu
Please reference UT Southwestern Case Number: 3003