{{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}}
Status:
US Approved Rx
(1994)
Source:
ANDA074473
(1994)
Source URL:
First approved in 1976
Source:
TOLECTIN by ORTHO MCNEIL JANSSEN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Tolmetin is a nonsteroidal anti-inflammatory agent. It was marketed as Tolectin in USA. TOLECTIN (tolmetin sodium) is indicated for the relief of signs and symptoms of
rheumatoid arthritis and osteoarthritis. TOLECTIN is indicated in the treatment of
acute flares and the long-term management of the chronic disease.
TOLECTIN is also indicated for treatment of juvenile rheumatoid arthritis. The mode of action of tolmetin is not known. However, studies in laboratory animals and man have demonstrated that the anti-inflammatory action of tolmetin is not due to pituitary-adrenal stimulation. Tolmetin inhibits prostaglandin synthetase in vitro and lowers the plasma level of prostaglandin E in man. This reduction in prostaglandin synthesis may be responsible for the anti-inflammatory action.
Status:
US Approved Rx
(2022)
Source:
ANDA214475
(2022)
Source URL:
First approved in 1976
Source:
NALFON by KEY THERAP
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Fenoprofen is a propionic acid derivative with analgesic, antiinflammatory and antipyretic properties. Fenoprofen inhibits prostaglandin synthesis by decreasing the enzyme needed for biosynthesis. In patients with rheumatoid arthritis, the anti-inflammatory action of fenoprofen has been evidenced by relief of pain, increase in grip strength, and reductions in joint swelling, duration of morning stiffness, and disease activity (as assessed by both the investigator and the patient). In patients with osteoarthritis, the anti-inflammatory and analgesic effects of fenoprofen have been demonstrated by reduction in tenderness as a response to pressure and reductions in night pain, stiffness, swelling, and overall disease activity (as assessed by both the patient and the investigator). These effects have also been demonstrated by relief of pain with motion and at rest and increased range of motion in involved joints. In patients with rheumatoid arthritis and osteoarthritis, clinical studies have shown fenoprofen to be comparable to aspirin in controlling the aforementioned measures of disease activity, but mild gastrointestinal reactions (nausea, dyspepsia) and tinnitus occurred less frequently in patients treated with fenoprofen than in aspirin-treated patients. It is not known whether fenoprofen causes less peptic ulceration than does aspirin. In patients with pain, the analgesic action of fenoprofen has produced a reduction in pain intensity, an increase in pain relief, improvement in total analgesia scores, and a sustained analgesic effect. Indicated for relief of the signs and symptoms of rheumatoid arthritis and osteoarthritis. Also for the relief of mild to moderate pain.
Status:
US Approved Rx
(1994)
Source:
ANDA074473
(1994)
Source URL:
First approved in 1976
Source:
TOLECTIN by ORTHO MCNEIL JANSSEN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Tolmetin is a nonsteroidal anti-inflammatory agent. It was marketed as Tolectin in USA. TOLECTIN (tolmetin sodium) is indicated for the relief of signs and symptoms of
rheumatoid arthritis and osteoarthritis. TOLECTIN is indicated in the treatment of
acute flares and the long-term management of the chronic disease.
TOLECTIN is also indicated for treatment of juvenile rheumatoid arthritis. The mode of action of tolmetin is not known. However, studies in laboratory animals and man have demonstrated that the anti-inflammatory action of tolmetin is not due to pituitary-adrenal stimulation. Tolmetin inhibits prostaglandin synthetase in vitro and lowers the plasma level of prostaglandin E in man. This reduction in prostaglandin synthesis may be responsible for the anti-inflammatory action.
Status:
US Approved Rx
(2022)
Source:
ANDA214475
(2022)
Source URL:
First approved in 1976
Source:
NALFON by KEY THERAP
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Fenoprofen is a propionic acid derivative with analgesic, antiinflammatory and antipyretic properties. Fenoprofen inhibits prostaglandin synthesis by decreasing the enzyme needed for biosynthesis. In patients with rheumatoid arthritis, the anti-inflammatory action of fenoprofen has been evidenced by relief of pain, increase in grip strength, and reductions in joint swelling, duration of morning stiffness, and disease activity (as assessed by both the investigator and the patient). In patients with osteoarthritis, the anti-inflammatory and analgesic effects of fenoprofen have been demonstrated by reduction in tenderness as a response to pressure and reductions in night pain, stiffness, swelling, and overall disease activity (as assessed by both the patient and the investigator). These effects have also been demonstrated by relief of pain with motion and at rest and increased range of motion in involved joints. In patients with rheumatoid arthritis and osteoarthritis, clinical studies have shown fenoprofen to be comparable to aspirin in controlling the aforementioned measures of disease activity, but mild gastrointestinal reactions (nausea, dyspepsia) and tinnitus occurred less frequently in patients treated with fenoprofen than in aspirin-treated patients. It is not known whether fenoprofen causes less peptic ulceration than does aspirin. In patients with pain, the analgesic action of fenoprofen has produced a reduction in pain intensity, an increase in pain relief, improvement in total analgesia scores, and a sustained analgesic effect. Indicated for relief of the signs and symptoms of rheumatoid arthritis and osteoarthritis. Also for the relief of mild to moderate pain.
Status:
US Approved Rx
(1994)
Source:
ANDA074473
(1994)
Source URL:
First approved in 1976
Source:
TOLECTIN by ORTHO MCNEIL JANSSEN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Tolmetin is a nonsteroidal anti-inflammatory agent. It was marketed as Tolectin in USA. TOLECTIN (tolmetin sodium) is indicated for the relief of signs and symptoms of
rheumatoid arthritis and osteoarthritis. TOLECTIN is indicated in the treatment of
acute flares and the long-term management of the chronic disease.
TOLECTIN is also indicated for treatment of juvenile rheumatoid arthritis. The mode of action of tolmetin is not known. However, studies in laboratory animals and man have demonstrated that the anti-inflammatory action of tolmetin is not due to pituitary-adrenal stimulation. Tolmetin inhibits prostaglandin synthetase in vitro and lowers the plasma level of prostaglandin E in man. This reduction in prostaglandin synthesis may be responsible for the anti-inflammatory action.
Status:
US Approved Rx
(1998)
Source:
ANDA075150
(1998)
Source URL:
First approved in 1975
Source:
NDA017533
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clonazepam, a benzodiazepine, is used primarily as an anticonvulsant in the treatment of absence seizures, petit mal variant seizures (Lennox-Gastaut syndrome), akinetic and myoclonic seizures, and nocturnal myoclonus. Klonopin is the brand name for Clonazepam, an anxiolytic and anticonvulsant. The precise mechanism by which clonazepam exerts its antiseizure
and antipanic effects is unknown, although it is believed to be related to its ability to
enhance the activity of gamma aminobutyric acid (GABA), the major inhibitory
neurotransmitter in the central nervous system. Allosteric interactions between central benzodiazepine receptors and gamma-aminobutyric acid (GABA) receptors potentiate the effects of GABA. As GABA is an inhibitory neurotransmitter, this results in increased inhibition of the ascending reticular activating system. Benzodiazepines, in this way, block the cortical and limbic arousal that occurs following stimulation of the reticular pathways.
Status:
US Approved Rx
(1998)
Source:
ANDA075259
(1998)
Source URL:
First approved in 1975
Source:
DTIC-DOME by BAYER HLTHCARE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Dacarbazine (DTIC), also known as imidazole carboxamide, is an antineoplastic agent, which is used in the treatment of metastatic malignant melanoma. In addition, this drug also is indicated for Hodgkin’s disease as a second-line therapy when used in combination with other effective agents. Dacarbazine works by methylating guanine at the O-6 and N-7 positions. Guanine is one of the four nucleotides that makes up DNA. The alkylated DNA strands stick together such that cell division becomes impossible. This affects cancer cells more than healthy cells because cancer cells divide faster. Dacarbazine is bioactivated in liver by demethylation to "MTIC" and then to diazomethane, which is an alkylating agent. Symptoms of anorexia, nausea, and vomiting are the most frequently noted of all toxic reactions. Over 90% of patients are affected with the initial few doses.
Status:
US Approved Rx
(1998)
Source:
ANDA075259
(1998)
Source URL:
First approved in 1975
Source:
DTIC-DOME by BAYER HLTHCARE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Dacarbazine (DTIC), also known as imidazole carboxamide, is an antineoplastic agent, which is used in the treatment of metastatic malignant melanoma. In addition, this drug also is indicated for Hodgkin’s disease as a second-line therapy when used in combination with other effective agents. Dacarbazine works by methylating guanine at the O-6 and N-7 positions. Guanine is one of the four nucleotides that makes up DNA. The alkylated DNA strands stick together such that cell division becomes impossible. This affects cancer cells more than healthy cells because cancer cells divide faster. Dacarbazine is bioactivated in liver by demethylation to "MTIC" and then to diazomethane, which is an alkylating agent. Symptoms of anorexia, nausea, and vomiting are the most frequently noted of all toxic reactions. Over 90% of patients are affected with the initial few doses.
Status:
US Approved Rx
(2018)
Source:
ANDA210125
(2018)
Source URL:
First approved in 1975
Source:
DITROPAN by JANSSEN PHARMS
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Oxybutynin is an antispasmodic, anticholinergic agent indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency. Oxybutynin relaxes bladder smooth muscle. Oxybutynin exhibits only one-fifth of the anticholinergic activity of atropine on the rabbit detrusor muscle, but four to ten times the antispasmodic activity. Antimuscarinic activity resides predominantly in the R-isomer. Oxybutynin exerts a direct antispasmodic effect on smooth muscle and inhibits the muscarinic action of acetylcholine on smooth muscle. No blocking effects occur at skeletal neuromuscular junctions or autonomic ganglia (antinicotinic effects). By inhibiting particularily the M1 and M2 receptors of the bladder, detrusor activity is markedly decreased.
Status:
US Approved Rx
(2018)
Source:
ANDA210125
(2018)
Source URL:
First approved in 1975
Source:
DITROPAN by JANSSEN PHARMS
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Oxybutynin is an antispasmodic, anticholinergic agent indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency. Oxybutynin relaxes bladder smooth muscle. Oxybutynin exhibits only one-fifth of the anticholinergic activity of atropine on the rabbit detrusor muscle, but four to ten times the antispasmodic activity. Antimuscarinic activity resides predominantly in the R-isomer. Oxybutynin exerts a direct antispasmodic effect on smooth muscle and inhibits the muscarinic action of acetylcholine on smooth muscle. No blocking effects occur at skeletal neuromuscular junctions or autonomic ganglia (antinicotinic effects). By inhibiting particularily the M1 and M2 receptors of the bladder, detrusor activity is markedly decreased.