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Search results for nonoxynol root_codes_CAS in CAS (approximate match)
Status:
US Approved Rx
(1988)
Source:
NDA019357
(1988)
Source URL:
First approved in 1988
Source:
NDA019357
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Ethanolamine oleate is a salt of ethanolamine, a basic substance, and oleic acid. It is marketed under a trade name of Ethamoline as a sclerotic agent for the treatment of patients with esophageal varices that have recently bled, to prevent rebleeding. In vitro studies revealed that ethanolamine oleate inhibits fibrin clot formation because of the Ca2+-chelating ability of its constituent ethanolamine. Nevertheless, from in vivo studies it was suggested that intravascular injection of ethamoline activates the local coagulation system. The activation may be accelerated by an acute inflammatory process provoked by oleate, which is supported by such clinical manifestations as mild fever, retrosternal pain leukocytosis and an increase in plasma fibrinogen level.
Status:
US Approved Rx
(2002)
Source:
ANDA076078
(2002)
Source URL:
First approved in 1987
Source:
IFEX by BAXTER HLTHCARE
Source URL:
Class (Stereo):
CHEMICAL (UNKNOWN)
Targets:
Conditions:
Ifosfamide (IF) is a widely used antitumor prodrug. It is in the oxazaphosphorine class of alkylating agents, and it is effective against solid tumors. Ifosfamide mechanism of crosslinking DNA plays a major role in preventing cancer cells from proliferating. Ifosfamide is approved by FDA for the treatment of germ cell testicular cancer.
Status:
US Approved Rx
(2006)
Source:
ANDA076871
(2006)
Source URL:
First approved in 1987
Source:
NOVANTRONE by EMD SERONO
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Mitoxantrone (NOVANTRONE) is a synthetic antineoplastic
anthracenedione. Mitoxantrone, a DNA-reactive agent that intercalates into deoxyribonucleic acid (DNA)
through hydrogen bonding, causes crosslinks and strand breaks. Mitoxantrone also interferes with ribonucleic acid (RNA) and is a potent inhibitor of topoisomerase II, an
enzyme responsible for uncoiling and repairing damaged DNA. It has a cytocidal effect
on both proliferating and nonproliferating cultured human cells, suggesting lack of cell
cycle phase specificity.
Mitoxantrone has been shown in vitro to inhibit B cell, T cell, and macrophage
proliferation and impair antigen pre sentation, as well as the secretion of interferon
gamma, TNFα, and IL-2. NOVANTRONE is indicated for reducing neurologic disability and/or the frequency of
clinical relapses in patients with secondary (chronic) progressive, progressive relapsing,
or worsening relapsing-remitting multiple sclerosis (i.e., patients whose neurologic status
is significantly abnormal between relapses). NOVANTRONE in combination with corticosteroids is indicated as initial chemotherapy
for the treatment of patients with pain related to advanced hormone-refractory prostate
cancer.
NOVANTRONE in combination with other approved drug(s) is indicated in the initial
therapy of acute nonlymphocytic leukemia (ANLL) in adults. This category includes
myelogenous, promyelocytic, monocytic, and erythroid acute leukemias.
Status:
US Approved Rx
(2009)
Source:
NDA022314
(2009)
Source URL:
First approved in 1987
Source:
NDA019787
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. Experimental data suggest that amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular mooth muscle cells than on cardiac muscle cells. Amlodipine is indicated for the treatment of hypertension and coronary artery disease.
Status:
US Approved Rx
(1999)
Source:
ANDA075221
(1999)
Source URL:
First approved in 1986
Source:
NDA019353
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Alfentanil is an opioid analgesic with a rapid onset of action. Alfentanil interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, alfentanil exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Alfentanil may increase the patient's tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Alfentanil depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Alfentanil, marketed under the trade name Alfenta, Rapifen in Australia is indicated for the management of postoperative pain and the maintenance of general anesthesia.
Status:
US Approved Rx
(1985)
Source:
NDA018738
(1985)
Source URL:
First approved in 1985
Source:
NDA018738
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Sulconazole (trade name Exelderm) is an antifungal medication of the imidazole class. Sulconazole has a broad spectrum of antifungal activity in vitro and has been shown to be an effective topical antifungal agent for the management of superficial fungal infections of the skin, particularly dermatophytosis and tinea versicolor. Sulconazole inhibits the cytochrome P-450 isoenzyme, C-14-alpha-demethylase by binding to the heme iron of the enzyme. This results in a largely fungistatic effect. The selectivity of azole antifungal agents for pathogenic organisms compared with mammalian cells appears to depend on a preferred affinity of these drugs for fungal versus mammalian cytochrome P-450 sterol demethylases. Enzyme inhibition by sulconazole prevents the synthesis of ergosterol, a sterol found in fungal cell membranes but, in general, not in mammalian cell membranes. Additionally, lanosterol accumulates, which changes membrane permeability, cell volume, secondary metabolic effects, and causes defective cell division and growth inhibition. As sulconazole is primarily fungistatic, an intact immune system may be needed for infection resolution.In selected situations, sulconazole may have growth phase-dependent fungicidal activity against very susceptible organisms. The 1% concentration of sulconazole may greatly exceed the minimum inhibitory concentration and exert a direct physiochemical effect on the fungal cell membrane. The fungicidal effect may be due to hydrophobic interactions between sulconazole and unsaturated fatty acids in the membrane. Mammalian cells generally have little or no unsaturated fatty acids. Sulconazole may also prevent DNA and RNA synthesis and increase their degradation.Sulconazole has activity against many dermatophytes and yeast. One measure of the drug's antifungal activity is the relative inhibition factor (RIF). The RIF approaches 0% for a drug to which a fungus is highly sensitive and 100% for a drug that is non-inhibitory. The RIF values of sulconazole for Candida species, Aspergillus species, and dermatophytes are broadly similar to those of clotrimazole, econazole, ketoconazole, miconazole, and tioconazole. The mean RIF values were 69% (30—98%) for Candida species, 71% (61—82%) for Aspergillus species, and 12% (5—18%) for dermatophytes. Sulconazole is available as a cream or solution to treat skin infections such as athlete's foot, ringworm, jock itch, and sun fungus.
Status:
US Approved Rx
(2000)
Source:
ANDA075479
(2000)
Source URL:
First approved in 1985
Source:
NDA018998
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Enalapril (marketed as Vasotec in the US, Enaladex and Renitec in some other countries) is an angiotensin-converting-enzyme (ACE) inhibitor used in the treatment of hypertension, diabetic nephropathy, and some types of chronic heart failure. Enalapril, after hydrolysis to enalaprilat, inhibits angiotensin-converting enzyme (ACE) in human subjects and animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. The beneficial effects of enalapril in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decrease aldosterone secretion.
Status:
US Approved Rx
(2019)
Source:
ANDA207594
(2019)
Source URL:
First approved in 1985
Source:
NDA050587
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Imipenem is a beta-lactam antibiotic belongings to the subgroup of carbapenems. Imipenem has a broad spectrum of activity against aerobic and anaerobic Gram positive as well as Gram negative bacteria. It is particularly important for its activity against Pseudomonas aeruginosa and the Enterococcus species. Imipenem is rapidly degraded by the renal enzyme dehydropeptidase when administered alone, and is always co-administered with cilastatin to prevent this inactivation. The bactericidal activity of imipenem results from the inhibition of cell wall synthesis. Its greatest affinity is for
penicillin binding proteins (PBPs) 1A, 1B, 2, 4, 5 and 6 of Escherichia coli, and 1A, 1B, 2, 4 and 5 of
Pseudomonas aeruginosa. The lethal effect is related to binding to PBP 2 and PBP 1B. Imipenem is marketed under the brand name Primaxin. PRIMAXIN I.M. (Imipenem and Cilastatin for Injectable Suspension) is a formulation of imipenem (a
thienamycin antibiotic) and cilastatin sodium (the inhibitor of the renal dipeptidase, dehydropeptidase I).
PRIMAXIN I.M. is a potent broad spectrum antibacterial agent for intramuscular administration.
Status:
US Approved Rx
(1995)
Source:
ANDA074007
(1995)
Source URL:
First approved in 1984
Source:
SECTRAL by PROMIUS PHARMA
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Acebutolol is a cardioselective, beta-adrenoreceptor blocking agent, which possesses mild intrinsic sympathomimetic activity (ISA) in its therapeutically effective dose range. Acebutolol is marketed under the trade names Sectral, Prent. Acebutolol is indicated for the management of hypertension in adults. It may be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics. Acebutolol is also indicated in the management of ventricular premature beats; it reduces the total number of premature beats, as well as the number of paired and multiform ventricular ectopic beats, and R-on-T beats. Acebutolol is a selective β1-receptor antagonist. Activation of β1-receptors by epinephrine increases the heart rate and the blood pressure, and the heart consumes more oxygen. Acebutolol blocks these receptors, lowering the heart rate and blood pressure. This drug then has the reverse effect of epinephrine. In addition, beta blockers prevent the release of renin, which is a hormone produced by the kidneys which leads to constriction of blood vessels.
Status:
US Approved Rx
(2005)
Source:
ANDA077507
(2005)
Source URL:
First approved in 1984
Source:
GLUCOTROL by PFIZER
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Glipizide, a second-generation sulfonylurea, is used with diet to lower blood glucose in patients with diabetes mellitus type II. The primary mode of action of glipizide in experimental animals appears to be the stimulation of insulin secretion from the beta cells of pancreatic islet tissue and is thus dependent on functioning beta cells in the pancreatic islets. In humans glipizide appears to lower the blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. In man, stimulation of insulin secretion by glipizide in response to a meal is undoubtedly of major importance. Fasting insulin levels are not elevated even on long-term glipizide administration, but the postprandial insulin response continues to be enhanced after at least 6 months of treatment. Some patients fail to respond initially, or gradually lose their responsiveness to sulfonylurea drugs, including glipizide. Sulfonylureas likely bind to ATP-sensitive potassium-channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin. Glipizide is used as an adjunct to diet for the control of hyperglycemia and its associated symptomatology in patients with non-insulin-dependent diabetes mellitus (NIDDM; type II), formerly known as maturity-onset diabetes, after an adequate trial of dietary therapy has proved unsatisfactory. Glipizide is marketed by Pfizer under the brand name Glucotrol in the USA, where Pfizer sells Glucotrol in doses of 5 and 10 milligrams and Glucotrol XL (an extended release form of glipizide) in doses of 2.5, 5, and 10 milligrams. Other companies also market glipizide, most commonly extended release tablets of 5 and 10 milligrams.