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Search results for m root_references_url in Reference URL (approximate match)
Status:
Possibly Marketed Outside US
Source:
Lebody Fit Body Massager Plus by Gtg Wellness Co., Ltd.
Source URL:
First approved in 1988
Source:
21 CFR 348
Source URL:
Class:
STRUCTURALLY DIVERSE
Status:
Possibly Marketed Outside US
Source:
IZUN Periactive Mouthwash by Izun Pharmaceuticals Corporation
Source URL:
First approved in 1984
Source:
21 CFR 341
Source URL:
Class:
STRUCTURALLY DIVERSE
Status:
Possibly Marketed Outside US
Source:
Blood Care Honzo Seika Chinese Herbal Aroma Oil by Nic Co., Ltd.
Source URL:
First approved in 1961
Source:
ADELGADINA by ProMex LLC
Source URL:
Class:
STRUCTURALLY DIVERSE
Status:
Possibly Marketed Outside US
Class:
STRUCTURALLY DIVERSE
Status:
Other
Class:
G1 SPECIFIED SUBSTANCE
Status:
Other
Class:
CONCEPT
Status:
US Approved Rx
(2015)
Source:
NDA207620
(2015)
Source URL:
First approved in 2015
Source:
NDA207620
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Sacubitril is a prodrug neprilysin inhibitor used in combination with valsartan (sold under the brand name Entresto among others) to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction. It was approved under the FDA's priority review process for use in heart failure on July 7, 2015. Sacubitril's active metabolite, LBQ657 inhibits neprilysin, a neutral endopeptidase that would typically cleave natiuretic peptides such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and c-type natriuretic peptide (CNP). ANP and BNP are released under atrial and ventricle stress, which activate downstream receptors leading to vasodilation, natriuresis and diuresis. Under normal conditions, neprilysin breaks down other vasodilating peptides and also vasoconstrictors such as angiotensin I and II, endothelin-1 and peptide amyloid beta-protein. Inhibition of neprilysin therefore leads to reduced breakdown and increased concentration of endogenous natriuretic peptides in addition to increased levels of vasoconstricting hormones such as angiotensin II.
Status:
US Approved Rx
(2003)
Source:
ANDA040480
(2003)
Source URL:
First marketed in 1931
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Amphetamine is a potent central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity. Amphetamine was discovered in 1887 and exists as two enantiomers: levoamphetamine and dextroamphetamine. The mode of therapeutic action in ADHD is not known. Amphetamines are thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. At higher dosages, they cause release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems. Amphetamine may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). In the periphery, amphetamines are believed to cause the release of noradrenaline by acting on the adrenergic nerve terminals and alpha- and beta-receptors. Modulation of serotonergic pathways may contribute to the calming affect. The drug interacts with VMAT enzymes to enhance release of DA and 5-HT from vesicles. It may also directly cause the reversal of DAT and SERT. Several currently prescribed amphetamine formulations contain both enantiomers, including Adderall, Dyanavel XR, and Evekeo, the last of which is racemic amphetamine sulfate. Amphetamine is also prescribed in enantiopure and prodrug form as dextroamphetamine and lisdexamfetamine respectively. Lisdexamfetamine is structurally different from amphetamine, and is inactive until it metabolizes into dextroamphetamine.