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Last updated on April 17, 2014 at 7:39 EDT

New Drug To Treat Anemia

November 30, 2010

(Ivanhoe Newswire) — The name of the drug is FG-2216, and it’s designed to stimulate production of the hormone erythropoietin (EPO) in dialysis patients.  In fact, it’s the world’s first oral drug for the treatment of kidney disease-related anemia; it’s a hypoxia inducible factor prolyl hydroxylase inhibitor (HIF-PHI) that stabilizes the “master switch,” which normally tells the body to produce EPO in response to low oxygen levels.

Anemia, one of the more common blood disorders, is caused by low production of EPO, which has been assumed to result from damage to the kidney cells that produce EPO.

“Our study clearly shows that this may not be the case, and that the kidneys of patients on dialysis retain significant ability to produce erythropoietin,” which Wanja M. Bernhardt, MD, Department of Nephrology, University hospital Erlangen, Germany, was quoted as saying.  “Renal anemia seems to result from disturbed regulation rather than lost production capacity of the hormone.

Treatment with FG-2216 considerably increased EPO production in dialysis patients, in addition to healthy people with normal kidneys.  The utmost increase in EPO production occurred in dialysis patients whose kidneys were still present, but no longer functioning.

FG-2216 additionally stimulated EPO production in dialysis patients with no kidneys.  These are individuals whose kidneys had been removed at surgery for cancer or other diseases.  The significant increase in EPO production in patients devoid of kidneys was approximately as high as in people with normally functioning kidneys.  In patients with no kidneys, FG-2216 in fact stimulated production of EPO by the liver.

The study’s outcome questions the standard knowledge that dialysis-related anemia occurs for the reason that patients with advanced kidney disease can no longer make their own EPO.  “Our results confirm that both the liver and the kidneys retain a significant production capacity for erythropoietin in end-stage renal disease patients,” adds Bernhardt.

Presently, patients with dialysis-related anemia are given EPO replacement therapy with drugs called erythropoiesis-stimulating agents (ESAs).  Regardless of nearly two decades of use, there remains a constant debate related to the safety, appropriate clinical use, and in due course high costs of ESAs.  If the latest results are borne out by future studies, then use of prolyl-hydroxylase inhibitors ““ such as FG-2216 to help the body make its own EPO ““ might provide a new-fangled alternative to ESAs.

The groundwork has been set with this study, which moreover evaluated merely the response to a single dose of FG-2216.  Although there were no harmful effects, the results and long-term safety of activation of HIF by prolyl-hydroxylase inhibitors remain uncertain.  Additional research will furthermore be required to find out why HIF is evidently not stabilized in response to decreased oxygen concentrations in patients with kidney disease but responds to treatment with prolyl-hydroxylase inhibitors.

SOURCE: Journal of the American Society of Nephrology, November 29, 2010