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Restrict the search for
valproic acid
to a specific field?
Status:
US Approved Rx
(1999)
Source:
ANDA075089
(1999)
Source URL:
First approved in 1991
Source:
TICLID by ROCHE PALO
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Ticlopidine (trade name Ticlid) is an antiplatelet drug in the thienopyridine family which is an adenosine diphosphate (ADP) receptor inhibitor. Ticlopidine is a prodrug that is metabolized to an as yet undetermined metabolite that acts as a platelet aggregation inhibitor. Inhibition of platelet aggregation causes a prolongation of bleeding time. In its prodrug form, ticlopidine has no significance in vitro activity at the concentrations attained in vivo. The active metabolite of ticlopidine prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. It is proposed that the inhibition involves a defect in the mobilization from the storage sites of the platelet granules to the outer membrane. No direct interference occurs with the GPIIb/IIIa receptor. As the glycoprotein GPIIb/IIIa complex is the major receptor for fibrinogen, its impaired activation prevents fibrinogen binding to platelets and inhibits platelet aggregation. Ticlopidine is FDA approved for the prevention of strokes and, when combined with aspirin, for patients with a new coronary stent to prevent closure. There are also several off-label uses, including acute treatment of myocardial infarction and unstable angina, peripheral vascular disease, prevention of myocardial infarctions, diabetic retinopathy, and sickle cell disease. The most serious side effects associated with ticlopidine are those that affect the blood cells, although these life-threatening complications are relatively rare.
Status:
US Approved Rx
(1991)
Source:
NDA020122
(1991)
Source URL:
First approved in 1991
Source:
NDA020122
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Pentostatin, also known as 2’-deoxycoformycin (DCF) under the trade name Nipent, is a potent inhibitor of the enzyme adenosine deaminase and is isolated from fermentation cultures of Streptomyces antibioticus. It was developed by Parke-Davis (now Pfizer) and the National Cancer Institute in the US. Nipent is indicated as single-agent treatment for both untreated and alpha-interferon-refractory hairy cell leukemia patients with active disease as defined by clinically significant anemia, neutropenia, thrombocytopenia, or disease-related symptoms. Pentostatin is a potent transition state inhibitor of the enzyme adenosine deaminase (ADA). The greatest activity of ADA is found in cells of the lymphoid system with T-cells having higher activity than B-cells, and T-cell malignancies having higher ADA activity than B-cell malignancies. Pentostatin inhibition of ADA, particularly in the presence of adenosine or deoxyadenosine, leads to cytotoxicity, and this is believed to be due to elevated intracellular levels of dATP, which can block DNA synthesis through inhibition of ribonucleotide reductase. Pentostatin can also inhibit RNA synthesis as well as cause increased DNA damage. In addition to elevated dATP, these mechanisms may also contribute to the overall cytotoxic effect of pentostatin. The precise mechanism of pentostatin’s antitumor effect, however, in hairy cell leukemia is not known. In several instances, hepatic toxicity from pentostatin appeared to be somewhat dose related, suggesting that the liver injury is a direct effect of the purine analogue. Because pentostatin is a potent immunosuppressive agent, the possibility exists that some cases of hepatic injury are due to reactivation of hepatitis B or other opportunistic infections. While pentostatin has not been shown to cause reactivation of hepatitis B, there is a strong possibility that it might induce this syndrome, and several cases of hepatic injury during pentostatin therapy were described as due to concurrent hepatitis B.
Status:
US Approved Rx
(2004)
Source:
ANDA076787
(2004)
Source URL:
First approved in 1991
Source:
ROMAZICON by HOFFMANN LA ROCHE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Fumazenil is an imidazobenzodiazepine derivative and a potent benzodiazepine receptor antagonist that competitively inhibits the activity at the benzodiazepine recognition site on the GABA/benzodiazepine receptor complex, thereby reversing the effects of benzodiazepine on the central nervous system. Fumazenil is used for the complete or partial reversal of the sedative effects of benzodiazepines in cases where general anesthesia has been induced and/or maintained with benzodiazepines, and where sedation has been produced with benzodiazepines for diagnostic and therapeutic procedures. Also for the management of benzodiazepine overdose as an adjunct for appropriate supportive and symptomatic measures. Flumazenil went off patent in 2008 so at present generic formulations of this drug are available.
Status:
US Approved Rx
(2018)
Source:
ANDA210847
(2018)
Source URL:
First approved in 1991
Source:
PLENDIL by ASTRAZENECA
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Felodipine is a long-acting 1,4-dihydropyridine calcium channel blocker (CCB)b. It acts primarily on vascular smooth muscle cells by stabilizing voltage-gated L-type calcium channels in their inactive conformation. By inhibiting the influx of calcium in smooth muscle cells, felodipine prevents calcium-dependent myocyte contraction and vasoconstriction. Felodipine is the most potent CCB in use and is unique in that it exhibits fluorescent activity. In addition to binding to L-type calcium channels, felodipine binds to a number of calcium-binding proteins, exhibits competitive antagonism of the mineralcorticoid receptor, inhibits the activity of calmodulin-dependent cyclic nucleotide phosphodiesterase, and blocks calcium influx through voltage-gated T-type calcium channels. Felodipine is used to treat mild to moderate essential hypertension.
Status:
US Approved Rx
(2007)
Source:
ANDA065288
(2007)
Source URL:
First approved in 1990
Source:
IDAMYCIN by PFIZER
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Idarubicin is an antineoplastic in the anthracycline class.Idarubicin hydrochloride is a DNA-intercalating analog of daunorubicin which has an inhibitory effect on nucleic acid synthesis and interacts with the enzyme topoisomerase II. The absence of a methoxy group at position 4 of the anthracycline structure gives the compound a high lipophilicity which results in an increased rate of cellular uptake compared with other anthracyclines.Idarubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. Idarubicin in combination with other approved antileukemic drugs is indicated for the treatment of acute myeloid leukemia (AML) in adults.
Status:
US Approved Rx
(2022)
Source:
ANDA216130
(2022)
Source URL:
First approved in 1990
Source:
FLOXIN by JANSSEN PHARMS
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Ofloxacin is one of a new generation of fluorinated quinolones structurally related to nalidixic acid, primary mechanism of action is inhibition of bacterial DNA gyrase. It is an orally administered broad spectrum antibacterial drug active against most Gram-negative bacteria, many Gram-positive bacteria and some anaerobes. Clinical trials to date have demonstrated the efficacy of ofloxacin in the treatment of lower respiratory tract infections, urinary tract infections, and sexually transmitted diseases. Adverse effects to ofloxacin are usually mild and include gastrointestinal, central nervous system, and hypersensitivity reactions. Also available in solution for treatment of otic and ophthalmic bacterial infections.
Status:
US Approved Rx
(2006)
Source:
ANDA077169
(2006)
Source URL:
First approved in 1990
Source:
DYNACIRC by SMITHKLINE BEECHAM
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Isradipine (tradenames DynaCirc, Prescal) is a calcium channel blocker of the dihydropyridine class. It is usually prescribed for the treatment of high blood pressure in order to reduce the risk of stroke and heart attack. Except for diuretic activity, the mechanism of which is not clearly understood, the pharmacodynamics effects of isradipine observed in whole animals can also be explained by calcium channel blocking activity, especially dilating effects in arterioles, which reduce systemic resistance and lower blood pressure, with a small increase in resting heart rate. Isradipine binds to calcium channels with high affinity and specificity and inhibits calcium flux into cardiac and arterial smooth muscle cells. It exhibits greater selectivity towards arterial smooth muscle cells owing to alternative splicing of the alpha-1 subunit of the channel and increased prevalence of inactive channels in smooth muscle cells. Although like other dihydropyridine calcium channel blockers, isradipine has negative inotropic effects in vitro; studies conducted in intact anesthetized animals have shown that the vasodilating effect occurs at doses lower than those do which affect contractility. In patients with normal ventricular function, isradipine's afterload reducing properties lead to some increase in cardiac output. Effects in patients with impaired ventricular function have not been fully studied. Most adverse reactions were mild and related to the vasodilatory effects of isradipine (dizziness, edema, palpitations, flushing, tachycardia), and many were transient. About 5% of isradipine patients left studies prematurely because of adverse reactions (vs. 3% of placebo patients and 6% of active control patients), principally due to headache, edema, dizziness, palpitations, and gastrointestinal disturbances.
Status:
US Approved Rx
(1990)
Source:
NDA019481
(1990)
Source URL:
First approved in 1990
Source:
NDA019481
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Gluconolactone, a lactone of D-glucuronic acid, is a food additive with the E number E575. Gluconolactone is commonly found in honey, fruit juices, wine. In medcine, gluconolactone is used as a component of irrigation solution Renacidin for dissolution of bladder calculi of the struvite or apatite variety, and to prevent or minimize encrustations of indwelling urinary tract catheters.
Status:
US Approved Rx
(1990)
Source:
NDA019715
(1990)
Source URL:
First approved in 1990
Source:
NDA019715
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Olsalazine is an anti-inflammatory drug used in the treatment of inflammatory bowel disease such as ulcerative colitis. Orally administered olsalazine is converted to mesalamine which is thought to be the therapeutically active agent in the treatment of ulcerative colitis. The mechanism of action of mesalamine (and sulfasalazine) is unknown but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes (LTs) and hydroxyelcosatetraenoic acids (HETEs) is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon. After oral administration, olsalazine has limited systemic bioavailability. Based on oral and intravenous dosing studies, approximately 2.4% of a single 1.0 g oral dose is absorbed. Less than 1% of olsalazine is recovered in the urine. The remaining 98 to 99% of an oral dose will reach the colon, where each molecule is rapidly converted into two molecules of 5¬ aminosalicylic acid (5-ASA) by colonic bacteria and the low prevailing redox potential found in this environment. The liberated 5-ASA is absorbed slowly resulting in very high local concentrations in the colon. Olsalazine has been evaluated in ulcerative colitis patients in remission, as well as those with acute disease. Both sulfasalazine-tolerant and intolerant patients have been studied in controlled clinical trials. Overall, 10.4% of patients discontinued olsalazine because of an adverse experience compared with 6.7% of placebo patients. The most commonly reported adverse reactions leading to treatment withdrawal were diarrhea or loose stools (olsalazine 5.9%; placebo 4.8%), abdominal pain, and rash or itching (slightly more than 1% of patients receiving olsalazine).
Status:
US Approved Rx
(2017)
Source:
NDA208799
(2017)
Source URL:
First approved in 1990
Source:
CUTIVATE by FOUGERA PHARMS
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Fluticasone propionate, a medium-potency synthetic corticosteroid, is used topically to relieve inflammatory and pruritic symptoms of dermatoses and psoriasis, intranasally to manage symptoms of allergic and non-allergic rhinitis, and orally for the treatment of asthma. Fluticasone proprionate is marketed under several different brand names such as Flonase®. Fluticasone propionate is also available as a combination product of azelastine hydrochloride and fluticasone propionate called Dymista™. Dymista™ is indicated in patients over 12 years old for symptomatic relief of seasonal allergic rhinitis. Fluticasone propionate binds to the glucocorticoid receptor. Unbound corticosteroids cross the membranes of cells such as mast cells and eosinophils, binding with high affinity to glucocorticoid receptors (GR). The results include alteration of transcription and protein synthesis, a decreased release of leukocytic acid hydrolases, reduction in fibroblast proliferation, prevention of macrophage accumulation at inflamed sites, reduction of collagen deposition, interference with leukocyte adhesion to the capillary wall, reduction of capillary membrane permeability and subsequent edema, reduction of complement components, inhibition of histamine and kinin release, and interference with the formation of scar tissue. In the management of asthma, the glucocorticoid receptor complexes down-regulates proinflammatory mediators such as interleukin-(IL)-1, 3, and 5, and up-regulates anti-inflammatory mediators such as IkappaB [inhibitory molecule for nuclear factor kappaB1], IL-10, and IL-12. The antiinflammatory actions of corticosteroids are also thought to involve inhibition of cytosolic phospholipase A2 (through activation of lipocortin-1 (annexin)) which controls the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.
