{{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}}
Search results for "LOINC|ACTIVE|CHEM" in comments (approximate match)
Status:
Possibly Marketed Outside US
Source:
NCT02639637: Phase 4 Interventional Completed Type 2 Diabetes Mellitus
(2015)
Source URL:
Class:
PROTEIN
Neuropeptide Y (NPY) is a 36 amino acid peptide neurotransmitter, which is widely expressed in the central and peripheral nervous systems of mammals. Neuropeptide Y has an important role in the stimulation of the appetite and is relevant to the pathophysiology of anxiety and depressionNeuropeptide Y is one of the most potent stimulators of feeding. At least five distinct G-protein coupled receptors (Y1, Y2, Y4, Y5, and Y6) mediate the actions of NPY. In rodents, repeated administration of Neuropeptide Y leads to hyperphagia and obesity associated with decreased thermogenesis in brown adipose tissue, hyperinsulinemia, hypercorticosteronaemia, reduced plasma testosterone concentrations, and insulin resistance in skeletal muscle. In the cardiovascular system Neuropeptide Y is found in neurons supplying the vasculature, cardiomyocytes, and endocardium, and is involved in physiological processes including vasoconstriction, cardiac remodeling, and angiogenesis. It is increasingly also implicated in cardiovascular disease pathogenesis, including hypertension, atherosclerosis, ischemia/infarction, arrhythmia, and heart failure. Neuropeptide Y is considered to be an anxiolytic endogenous peptide and its levels can be modulated by stress and it may also play a role in the etiology and pathophysiology of posttraumatic stress disorder.
Class:
PROTEIN
Status:
Possibly Marketed Outside US
Source:
M020
(2022)
Source URL:
First approved in 2022
Source:
M020
Source URL:
Class:
POLYMER
Status:
Possibly Marketed Outside US
Source:
NCT04702776: Phase 4 Interventional Completed Dry Eye
(2021)
Source URL:
First approved in 1997
Source:
NaturVet ArthriSoothe by The Garmon Corporation
Source URL:
Class:
POLYMER
Status:
US Approved Rx
(2013)
First approved in 1942
Class:
STRUCTURALLY DIVERSE
Status:
Investigational
Source:
NCT01483287: Early Phase 1 Interventional Completed Irritable Bowel Syndrome
(2011)
Source URL:
Class:
STRUCTURALLY DIVERSE
Status:
Possibly Marketed Outside US
Source:
NCT03431337: Phase 4 Interventional Terminated Sinusitis, Acute
(2018)
Source URL:
Class:
STRUCTURALLY DIVERSE
Status:
US Approved Rx
(2016)
Source:
NDA208470
(2016)
Source URL:
First approved in 2014
Source:
Prasterone by Health Science Funding, LLC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Dehydroepiandrosterone (INTRAROSA™, prasterone) is a major C19 steroid produced from cholesterol by the adrenal cortex. It is also produced in small quantities in the testis and the ovary. Dehydroepiandrosterone (INTRAROSA, prasterone) is structurally similar to, and is a precursor of, androstenedione, testosterone, estradiol, estrone and estrogen. It indicated for the treatment of moderate to severe dyspareunia, a symptom of vulvar and vaginal atrophy, due to menopause. The mechanism of action of dehydroepiandrosterone (INTRAROSA, prasterone) in postmenopausal women with vulvar and vaginal atrophy is not fully established.
Status:
US Approved Rx
(2025)
Source:
NDA219488
(2025)
Source URL:
First approved in 1983
Source:
CHENIX by LEADIANT BIOSCI INC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Approved Rx
(1983)
First approved in 1983
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Hemin (trade name Panhematin) is a protoporphyrin IX containing a ferric iron ion (heme B) with a chloride ligand, which is is indicated for the amelioration of recurrent attacks of acute intermittent porphyria temporally related to the menstrual cycle in susceptible women. Manifestations such as pain, hypertension, tachycardia, abnormal mental status and mild to progressive neurologic signs may be controlled in selected patients with this disorder. the therapy for the acute porphyrias is not curative. Heme acts to limit the hepatic and/or marrow synthesis of porphyrin. This action is likely due to the inhibition of δ-aminolevulinic acid synthetase, the enzyme which limits the rate of the porphyrin/heme biosynthetic pathway. The exact mechanism by which hematin produces symptomatic improvement in patients with acute episodes of the hepatic porphyrias has not been elucidated.