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Search results for norethindrone root_notes_note in Note (approximate match)
Status:
Investigational
Source:
NCT01661634: Phase 3 Interventional Completed Acute Decompensated Heart Failure
(2012)
Source URL:
Class:
PROTEIN
Ularitide is a recombinant form of urodilatin, a natriuretic peptide synthesized in the distal tubular cells of the kidney. It regulates renal sodium and water excretion through binding to natriuretic peptide type A receptors, increasing intracellular cyclic guanosine monophosphate (cGMP) levels. While these effects, as well as others such as vasodilation, are also exhibited by other natriuretic peptides, urodilatin has a terminal extension that brings resistance to biological inactivation by neutral endopeptidase, whose activity is increased in decompensated heart failure. Animal studies have demonstrated enhanced diuresis and natriuresis and reduced PCWP (pulmonary capillary wedge pressure) and systemic vascular resistance relative to atrial natriuretic peptide (ANP [99-126], the active circulating isoform). When injected into the blood, ularitide appears to cause diuresis (urine output) and natriuresis (sodium excretion), as well as vasodilation. Ularitide is currently in Phase 3 development as a potential treatment for patients with acute decompensated heart failure (ADHF).
Class:
PROTEIN
FERTIRELIN is an analog of luteinizing hormone releasing factor. The drug has been used since 1981 in Japan to treat various types of reproductive failure in cattle.
Status:
Investigational
Source:
NCT02359227: Phase 2 Interventional Completed Heart Failure
(2015)
Source URL:
Class:
PROTEIN
Cenderitide, is a novel chimeric natriuretic peptide(NP) developed by the Mayo Clinic as a potential treatment for heart failure. As a chimeric peptide, cenderitide is a single-chemical entity that possesses two separate functions. Specifically, this novel peptide was engineered unlike native NPs to uniquely co-activate the two particulate guanylyl cyclase (pGC) receptors (pGC-A and pGC-B) so as to take advantage of distinct receptor mediated actions through 3′5′ cyclic guanosine monophosphate (cGMP). The rationale for its design was to achieve the renal-enhancing and antifibrotic properties of dual receptor activation, but without clinically significant hypotension.