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Restrict the search for
droxidopa
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There is one exact (name or code) match for droxidopa
Status:
US Approved Rx
(2018)
Source:
ANDA210839
(2018)
Source URL:
First approved in 1950
Source:
NDA007513
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Droxidopa (Northera, Chelsea Therapeutics) is a synthetic catecholamino acid precursor of norepinephrine indicated for the treatment of orthostatic dizziness or lightheadedness in adult patients with symptomatic neurogenic orthostatic hypotension (NOH) caused by primary autonomic failure, dopamine beta-hydroxylase deficiency, and non-diabetic autonomic neuropathy. Droxidopa was approved as oral therapy in February 2014 under the FDA’s accelerated approval program. Droxidopa is directly metabolized to norepinephrine by dopadecarboxylase. The specific mechanism of action of the drug is not known completely, but it is supposed to exert the pharmacological effects through norepinephrine and not through the parent molecule or other metabolites. It increases blood flow to the brain by stimulating peripheral arterial and venous vasoconstriction.
Status:
US Approved Rx
(2018)
Source:
ANDA210839
(2018)
Source URL:
First approved in 1950
Source:
NDA007513
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Droxidopa (Northera, Chelsea Therapeutics) is a synthetic catecholamino acid precursor of norepinephrine indicated for the treatment of orthostatic dizziness or lightheadedness in adult patients with symptomatic neurogenic orthostatic hypotension (NOH) caused by primary autonomic failure, dopamine beta-hydroxylase deficiency, and non-diabetic autonomic neuropathy. Droxidopa was approved as oral therapy in February 2014 under the FDA’s accelerated approval program. Droxidopa is directly metabolized to norepinephrine by dopadecarboxylase. The specific mechanism of action of the drug is not known completely, but it is supposed to exert the pharmacological effects through norepinephrine and not through the parent molecule or other metabolites. It increases blood flow to the brain by stimulating peripheral arterial and venous vasoconstriction.
Status:
US Approved Rx
(2018)
Source:
ANDA210839
(2018)
Source URL:
First approved in 1950
Source:
NDA007513
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Droxidopa (Northera, Chelsea Therapeutics) is a synthetic catecholamino acid precursor of norepinephrine indicated for the treatment of orthostatic dizziness or lightheadedness in adult patients with symptomatic neurogenic orthostatic hypotension (NOH) caused by primary autonomic failure, dopamine beta-hydroxylase deficiency, and non-diabetic autonomic neuropathy. Droxidopa was approved as oral therapy in February 2014 under the FDA’s accelerated approval program. Droxidopa is directly metabolized to norepinephrine by dopadecarboxylase. The specific mechanism of action of the drug is not known completely, but it is supposed to exert the pharmacological effects through norepinephrine and not through the parent molecule or other metabolites. It increases blood flow to the brain by stimulating peripheral arterial and venous vasoconstriction.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Protocatechuic acid (3,4-dihydroxybenzoic acid, PCA) is a simple phenolic acid. It is found in a large variety of edible plants and possesses various pharmacological activities. This bioactive compound is famous for its biological properties and pharmacological activities such as: antioxidant, antibacterial, anticancer, antiulcer, antidiabetic, antiaging, antifibrotic, antiviral, anti-inflammatory, analgesic, antiatherosclerotic, cardiac, hepatoprotective,
neurological and nephroprotective. The neuroprotective effects of PCA, extracted from Alpinia oxyphylla, on H2O2 resulted in apoptosis and oxidative stress in cultured PC12 cells. Apoptotic cell death by H2O2 was dose-dependent. Enhanced effect of PCA on protecting PC12 cells
against apoptosis, augmented glutathione (GSH)
level and an increase in catalytic activity was investigated
by flow cytometric analysis. In cytotoxic assays, PCA causes cell death in
HepG2 cancerous cell line of liver showing that
PCA stimulates the c-Jun N-terminal kinase (JNK)
and p38 subgroups of the mitogen-activated protein
kinase (MAPK) family. Treatment with
PCA decreased OVA-induced airway hyper-responsiveness
to inhaled methacholine. Cell inflammation
and mucus hypersecretion was also decreased by
PCA. Thus, PCA can be useful for treating asthma. Experimental studies strongly support the role of protocatechuic acid in the prevention of neurodegenerative processes, including Alzheimer's and Parkinson's diseases, due to its favorable influence on processes underlying cognitive and behavioral impairment, namely accumulation of the β-amyloid plaques in brain tissues, hyperphosphorylation of tau protein in neurons, excessive formation of reactive oxygen species and neuroinflammation.