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Status:
US Approved Rx
(2021)
Source:
ANDA214543
(2021)
Source URL:
First approved in 1950
Source:
NDA007513
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Norepinephrine (l-arterenol/Levarterenol or l-norepinephrine) is a sympathomimetic catecholamine with multiple roles including as a hormone and a neurotransmitter. As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. Norepinephrine can also suppress neuroinflammation when released diffusely in the brain from the locus ceruleus. Norepinephrine may be used for blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy, poliomyelitis, spinal anesthesia, myocardial infarction, septicemia, blood transfusion, and drug reactions) and as an adjunct in the treatment of cardiac arrest and profound hypotension. Norepinephrine performs its action by being released into the synaptic cleft, where it acts on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine, or by uptake by surrounding cells. Prolonged administration of any potent vasopressor may result in plasma volume depletion which should be continuously corrected by appropriate fluid and electrolyte replacement therapy.If plasma volumes are not corrected, hypotension may recur when Norepinephrine is discontinued, or blood pressure may be maintained at the risk of severe peripheral and visceral vasoconstriction (e.g., decreased renal perfusion)with diminution in blood flow and tissue perfusion with subsequent tissue hypoxia and lactic acidosis and possible ischemic injury. Gangrene of extremities has been rarely reported. Overdoses or conventional doses in hypersensitive persons (e.g., hyperthyroid patients) cause severe hypertension with violent headache, photophobia, stabbing retrosternal pain, pallor, intense sweating, and vomiting.
Status:
US Approved Rx
(2021)
Source:
ANDA214543
(2021)
Source URL:
First approved in 1950
Source:
NDA007513
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Norepinephrine (l-arterenol/Levarterenol or l-norepinephrine) is a sympathomimetic catecholamine with multiple roles including as a hormone and a neurotransmitter. As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. Norepinephrine can also suppress neuroinflammation when released diffusely in the brain from the locus ceruleus. Norepinephrine may be used for blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy, poliomyelitis, spinal anesthesia, myocardial infarction, septicemia, blood transfusion, and drug reactions) and as an adjunct in the treatment of cardiac arrest and profound hypotension. Norepinephrine performs its action by being released into the synaptic cleft, where it acts on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine, or by uptake by surrounding cells. Prolonged administration of any potent vasopressor may result in plasma volume depletion which should be continuously corrected by appropriate fluid and electrolyte replacement therapy.If plasma volumes are not corrected, hypotension may recur when Norepinephrine is discontinued, or blood pressure may be maintained at the risk of severe peripheral and visceral vasoconstriction (e.g., decreased renal perfusion)with diminution in blood flow and tissue perfusion with subsequent tissue hypoxia and lactic acidosis and possible ischemic injury. Gangrene of extremities has been rarely reported. Overdoses or conventional doses in hypersensitive persons (e.g., hyperthyroid patients) cause severe hypertension with violent headache, photophobia, stabbing retrosternal pain, pallor, intense sweating, and vomiting.
Status:
US Approved Rx
(2022)
Source:
NDA216264
(2022)
Source URL:
First approved in 1950
Source:
NDA022272
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Indigotindisulfonic acid (also known as Indigo carmine) is a synthetic dye discovered in 18th century. It is used in many countiries as a food colorant and a pH indicator. In medicine the dye is used to localize ureteral orifices during cystoscopy and ureteral catheterization. In June 2014 the FDA announced the shortage of indigotindisulfonic acid.
Status:
US Approved Rx
(1999)
Source:
ANDA040319
(1999)
Source URL:
First approved in 1950
Source:
BENTYL by ALLERGAN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Dicyclomine is an anticholinergic tertiary amine used frequently by oral and parenteral route as an effective anti-spasmodic agent. Dicyclomine hydrochloride salt is approved under brand name bentyl for the treatment of functional bowel/irritable bowel syndrome. In addition is known, that dicyclomine is also used in morning and motion sickness, dysmenorrheal, intestinal hypermotility. It was shown, that Dicyclomine is a selective M1 and M3 muscarinic receptors antagonist, but os shown pharmacological activity via the M1 receptor.
Status:
US Approved Rx
(2000)
Source:
NDA021011
(2000)
Source URL:
First approved in 1950
Source:
NDA007337
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).
Status:
US Approved Rx
(2021)
Source:
ANDA214543
(2021)
Source URL:
First approved in 1950
Source:
NDA007513
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Norepinephrine (l-arterenol/Levarterenol or l-norepinephrine) is a sympathomimetic catecholamine with multiple roles including as a hormone and a neurotransmitter. As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. Norepinephrine can also suppress neuroinflammation when released diffusely in the brain from the locus ceruleus. Norepinephrine may be used for blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy, poliomyelitis, spinal anesthesia, myocardial infarction, septicemia, blood transfusion, and drug reactions) and as an adjunct in the treatment of cardiac arrest and profound hypotension. Norepinephrine performs its action by being released into the synaptic cleft, where it acts on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine, or by uptake by surrounding cells. Prolonged administration of any potent vasopressor may result in plasma volume depletion which should be continuously corrected by appropriate fluid and electrolyte replacement therapy.If plasma volumes are not corrected, hypotension may recur when Norepinephrine is discontinued, or blood pressure may be maintained at the risk of severe peripheral and visceral vasoconstriction (e.g., decreased renal perfusion)with diminution in blood flow and tissue perfusion with subsequent tissue hypoxia and lactic acidosis and possible ischemic injury. Gangrene of extremities has been rarely reported. Overdoses or conventional doses in hypersensitive persons (e.g., hyperthyroid patients) cause severe hypertension with violent headache, photophobia, stabbing retrosternal pain, pallor, intense sweating, and vomiting.
Status:
US Approved Rx
(2021)
Source:
ANDA214543
(2021)
Source URL:
First approved in 1950
Source:
NDA007513
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Norepinephrine (l-arterenol/Levarterenol or l-norepinephrine) is a sympathomimetic catecholamine with multiple roles including as a hormone and a neurotransmitter. As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. Norepinephrine can also suppress neuroinflammation when released diffusely in the brain from the locus ceruleus. Norepinephrine may be used for blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy, poliomyelitis, spinal anesthesia, myocardial infarction, septicemia, blood transfusion, and drug reactions) and as an adjunct in the treatment of cardiac arrest and profound hypotension. Norepinephrine performs its action by being released into the synaptic cleft, where it acts on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine, or by uptake by surrounding cells. Prolonged administration of any potent vasopressor may result in plasma volume depletion which should be continuously corrected by appropriate fluid and electrolyte replacement therapy.If plasma volumes are not corrected, hypotension may recur when Norepinephrine is discontinued, or blood pressure may be maintained at the risk of severe peripheral and visceral vasoconstriction (e.g., decreased renal perfusion)with diminution in blood flow and tissue perfusion with subsequent tissue hypoxia and lactic acidosis and possible ischemic injury. Gangrene of extremities has been rarely reported. Overdoses or conventional doses in hypersensitive persons (e.g., hyperthyroid patients) cause severe hypertension with violent headache, photophobia, stabbing retrosternal pain, pallor, intense sweating, and vomiting.
Status:
US Approved Rx
(2000)
Source:
NDA021011
(2000)
Source URL:
First approved in 1950
Source:
NDA007337
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).
Status:
US Approved Rx
(1981)
Source:
ANDA087204
(1981)
Source URL:
First approved in 1949
Source:
EURAX by JOURNEY
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Crotamiton is a scabicidal and antipruritic agent available as a cream or lotion for topical use. The drug was approved by FDA for the treatment of scabies and pruritic skin. Crotamiton is a mixture of the cis and trans isomers of N-ethyl-N-(o-methylphenyl)-2butenamide. Although the activity of crotamiton was shown both in vitro and in vivo, the mechanism of its action is still unknown.
Status:
US Approved Rx
(1974)
Source:
ANDA084364
(1974)
Source URL:
First approved in 1949
Source:
ARTANE by LEDERLE
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Trihexyphenidyl (Artane, Apo-Trihex, Parkin, Pacitane), also known as benzhexol and trihex has been in clinical usage for decades.It is an anticholinergic used in the symptomatic treatment of all etiologic groups of parkinsonism and drug induced extrapyramidal reactions (except tardive dyskinesia). Trihexyphenidyl possesses both anticholinergic and antihistaminic effects, although only the former has been established as therapeutically significant in the management of parkinsonism. Trihexyphenidyl is a selective M1 muscarinic acetylcholine receptor antagonist. It is able to discriminate between the M1 (cortical or neuronal) and the peripheral muscarinic subtypes (cardiac and glandular). Trihexyphenidyl partially blocks cholinergic activity in the CNS, which is responsible for the symptoms of Parkinson's disease. It is also thought to increase the availability of dopamine, a brain chemical that is critical in the initiation and smooth control of voluntary muscle movement. Trihexyphenidyl is indicated for the treatment of parkinson's disease and extrapyramidal reactions caused by drugs.