{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Restrict the search for
fludrocortisone acetate
to a specific field?
Class:
PROTEIN
Aspartocin, an antibiotic, possesses antimicrobial properties
Status:
Investigational
Source:
NCT03427151: Phase 3 Interventional Completed Lupus Erythematosus, Systemic
(2018)
Source URL:
Class:
PROTEIN
Forigerimod (also known as IPP-201101) a phosphopeptide is being investigated for the treatment of Lupus Erythematosus, Systemic. This drug is completed phase III clinical trials and is ready for licensing.
Class:
PROTEIN
Dumorelin is a 27-L-Leu-44a-Gly peptide. It is a stimulator of human growth hormone release.
Status:
Investigational
Source:
NCT00869986: Phase 2/Phase 3 Interventional Completed Relapsing Remitting Multiple Sclerosis
(2006)
Source URL:
Class:
PROTEIN
Dirucotide (MBP 8298) is a synthetic myelin basic protein (MBP) peptide designed to decrease type 2 helper T cells (TH2)-mediated B-cell signalling of auto-reactive T-cells thereby reducing the production of specific antibodies that target endogenous MBP. MBP is the dominant site of attack in patients with multiple sclerosis and haplotype (HLA) DR2 or DR4. Dirucotide did not meet the primary endpoint of delaying disease progression, as measured by the Expanded Disability Status Scale (EDSS), during the two-year MAESTRO-01 Phase III trial in patients with secondary progressive multiple sclerosis (SPMS). In addition, there were no statistically significant differences between dirucotide and placebo on the secondary endpoints of the study. After disappointing trial results, development of the drug was ended in 2009.
Status:
Investigational
Source:
NCT00785954: Phase 2 Interventional Completed Myocardial Infarction
(2008)
Source URL:
Class:
PROTEIN
Delcasertib is a peptide inhibitor of protein kinase C-delta, developed by KAI Pharmaceuticals. Delcasertib disrupts binding of delta-PKC to its receptor for activated C kinase, thereby preventing localization of delta-PKC to the mitochondria during periods of myocardial ischemia and reperfusion. In preclinical studies, when given as a single intracoronary dose, delcasertib reduced infarct size, enhanced early recovery of regional left ventricular contractility, and improved microvascular patency and function in animal models of acute myocardial infarction. The compound diminished myocardial necrosis and improved reperfusion in a pilot study during the primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI). In a larger clinical trial, however, intravenous infusion of delcasertib during PCI for acute STEMI in a population of patients treated according to the contemporary standard of care did not reduce biomarkers of myocardial injury.
Status:
Investigational
Source:
NCT00537420: Phase 2 Interventional Completed Obesity
(2007)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT00785408: Phase 2 Interventional Completed Obesity
(2008)
Source URL:
Class:
PROTEIN
Davalintide (AC-2307) is a second-generation mimetic of a pancreatic peptide hormone amylin, developed by Amylin Pharmaceuticals. In preclinical models, davalintide possessed enhanced pharmacological properties and was able to reduce food intake. Safety, tolerability, and effect on body weight of subcutaneous davalintide were investigated in obese or overweight subjects. The results of the clinical trial were not reported, but Amylin decided to discontinue davalintide in 2010.
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.
