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Restrict the search for
amphotericin b
to a specific field?
Status:
US Approved Rx
(2023)
Source:
ANDA217272
(2023)
Source URL:
First approved in 1953
Source:
NDA009175
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Furadantin (nitrofurantoin), a synthetic chemical, is a stable, yellow, crystalline compound. Furadantin is an antibacterial agent for specific urinary tract infections. Orally administered Furadantin is readily absorbed and rapidly excreted in urine. Blood concentrations at therapeutic dosage are usually low. Unlike many drugs, the presence of food or agents delaying gastric emptying can increase the bioavailability of Furadantin, presumably by allowing better dissolution in gastric juices. Nitrofurantoin is active against some gram positive organisms such as S. aureus, S. epidermidis, S. saprophyticus, Enterococcus faecalis, S. agalactiae, group D streptococci, viridians streptococci and Corynebacterium. Its spectrum of activity against gram negative organisms includes E. coli, Enterobacter, Neisseria, Salmonella and Shigella. It may be used as an alternative to trimethoprim/sulfamethoxazole for treating urinary tract infections though it may be less effective at eradicating vaginal bacteria. May also be used in females as prophylaxis against recurrent cystitis related to coitus. Nitrofurantoin is highly stable to the development of bacterial resistance, a property thought to be due to its multiplicity of mechanisms of action. Nitrofurantoin is activated by bacterial flavoproteins (nitrofuran reductase) to active reduced reactive intermediates that are thought to modulate and damage ribosomal proteins or other macromolecules, especially DNA, causing inhibition of DNA, RNA, protein, and cell wall synthesis. The overall effect is inhibition of bacterial growth or cell death.
Status:
US Approved Rx
(2022)
Source:
ANDA216983
(2022)
Source URL:
First approved in 1953
Source:
NDA008578
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Pyrimethamine, sold under the trade name Daraprim, is one of the folic acid antagonists that is used as an antimalarial or with a sulfonamide to treat toxoplasmosis. In addition it was approved in Chemoprophylaxis of Malaria. However, resistance to pyrimethamine is prevalent worldwide. It is not suitable as a prophylactic agent for travelers to most areas. Pyrimethamine is well absorbed with peak levels occurring between 2 to 6 hours following administration. It is eliminated slowly and has a plasma half-life of approximately 96 hours. Pyrimethamine is 87% bound to human plasma proteins. Pyrimethamine acts by selectively inhibiting malarial dihydrofolate reductase-thymidylate synthase and the rationale for its therapeutic action is based on the differential requirement between host and parasite for nucleic acid precursors involved in growth. This activity is highly selective against plasmodia and Toxoplasma gondii. Pyrimethamine possesses blood schizonticidal and some tissue schizonticidal activity against malaria parasites of humans. The action of pyrimethamine against Toxoplasma gondii is greatly enhanced when used in conjunction with sulfonamides.
Status:
US Approved Rx
(2001)
Source:
NDA021265
(2001)
Source URL:
First approved in 1953
Source:
M.V.I.-12 ADULT by HOSPIRA
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Riboflavin (vitamin B2) is part of the vitamin B group. Riboflavin 5’-phosphate is the precursor of two coenzymes, flavin adenine dinucleotide and flavin mononucleotide, which catalyze oxidation/reduction reactions involved in a number of metabolic pathways. FAD and riboflavin phosphate in foods are hydrolyzed in the intestinal lumen by nucleotide diphosphatase and a variety of nonspecific phosphatases to yield free riboflavin, which is absorbed in the upper small intestines by a sodium-dependent saturable mechanism. Riboflavin has been used in several clinical and therapeutic situations. For over 30 years, riboflavin supplements have been used as part of the phototherapy treatment of neonatal jaundice. Corneal ectasia is a progressive thinning of the cornea; the most common form of this condition is keratoconus. Collagen cross-linking is a non-surgical treatment intended to slow progression of corneal ectasia by strengthening corneal tissue. The standard protocol calls for application directly to the eye of a 0.1% riboflavin solution for 30 minutes followed by 30 minutes of ultraviolet-A irradiation with a wavelength of 370 nm and power of 3 mW/cm2. Under the conditions used for corneal collagen cross-linking, riboflavin 5‘-phosphate functions as a photo enhancer and generates singlet oxygen which is responsible for the cross-linking.
Status:
US Approved Rx
(2023)
Source:
ANDA216435
(2023)
Source URL:
First approved in 1953
Source:
CALCIUM DISODIUM VERSENATE by BAUSCH
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Edetic acid (EDTA) is a chelating agent. The U.S. Food and Drug Administration (FDA) approved edetic acid chelation therapy as a treatment for lead and heavy metal poisoning. Edetic acid in form of disodium salt was withdrawn from the market due to death resulting from hypocalcemia during chelation.
Status:
US Approved Rx
(1972)
Source:
ANDA061621
(1972)
Source URL:
First approved in 1952
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Erythromycin cyclocarbonate (Davercin) is a first generation semi-synthetic erythromycin. It is active against Gram-positive and some Gram-negative microorganisms. Davercin shows comparable or better in vitro potency, low host toxicity and improved pharmacokinetics compared with erythromycin. It is approved for the treatment of acne, atypical pneumonia (caused by Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila), whooping cough (treatment and prevention), urethritis (caused by Ureaplasma urealyticum and Chlamydia trachomatis), gastrointestinal infection caused by Campylobacter spp., short-term infections of the skin and soft tissues (e.g. acne, staphylococcal dermatitis). In streptococcal infections, diphtheria, gonorrhea, early syphilis in patients who are allergic to penicillin, and in the prevention of bacterial endocarditis before the planned dental procedures. Adverse effects are: nausea, vomiting, abdominal pain, diarrhea, skin allergic reactions.
Status:
US Approved Rx
(2019)
Source:
NDA210660
(2019)
Source URL:
First approved in 1952
Source:
NDA008372
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Cysteine (cysteine hydrochloride is a salt) is a thiol-containing amino acid that is oxidized to form cystine. Cysteine is synthesized from methionine via the trans-sulfuration pathway in the adult, but newborn infants lack the enzyme, cystathionase, necessary to effect this conversion. Therefore, cysteine is generally considered to be an essential amino acid in infants.
Status:
US Approved Rx
(1983)
Source:
ANDA088235
(1983)
Source URL:
First approved in 1952
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Isoniazid is a bactericidal agent active against organisms of the genus Mycobacterium, specifically M. tuberculosis, M. bovis and M. kansasii. Isoniazid is recommended for all forms of tuberculosis in which organisms are susceptible. Isoniazid is a prodrug and must be activated by bacterial catalase. Isoniazid inhibits InhA, the enoyl reductase from Mycobacterium tuberculosis, by forming a covalent adduct with the NAD cofactor. The most frequent adverse reactions to isoniazid are those affecting the nervous system and the liver.
Status:
US Approved Rx
(2000)
Source:
ANDA040335
(2000)
Source URL:
First approved in 1952
Source:
LEUCOVORIN CALCIUM by HOSPIRA
Source URL:
Class (Stereo):
CHEMICAL (EPIMERIC)
Leucovorin is a compound similar to folic acid, which is a necessary vitamin. It has been around and in use for many decades. Leucovorin is a medication frequently used in combination with the chemotherapy drugs fluoruracil and methotrexate. Leucovorin is not a chemotherapy drug itself, however it is used in addition to these chemotherapy drugs to enhance anticancer effects (with fluorouracil) or to help prevent or lessen side effects (with methotrexate). Leucovorin is also used by itself to treat certain anemia problems when folic acid deficiency is present.
Status:
US Approved Rx
(1998)
Source:
NDA020805
(1998)
Source URL:
First approved in 1951
Source:
HYDROCORTONE by MERCK
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Hydrocortisone is the main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). Hydrocortisone is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.
Status:
US Approved Rx
(2023)
Source:
ANDA217030
(2023)
Source URL:
First approved in 1951
Source:
BENEMID by MERCK
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Probenecid is the prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy. Probenecid is used for treatment of the hyperuricemia associated with gout and gouty arthritis. Probenecid is a uricosuric and renal tubular blocking agent. It inhibits the tubular reabsorption of urate, thus increasing the urinary excretion of uric acid and decreasing serum urate levels. Effective uricosuria reduces the miscible urate pool, retards urate deposition, and promotes resorption of urate deposits. Probenecid inhibits the tubular secretion of penicillin and usually increases penicillin plasma levels by any route the antibiotic is given. A 2-fold to 4-fold elevation has been demonstrated for various penicillins. Probenecid decreases both hepatic and renal excretion of sulfobromophthalein (BSP). The tubular reabsorption of phosphorus is inhibited in hypoparathyroid but not in euparathyroid individuals. Probenecid does not influence plasma concentrations of salicylates, nor the excretion of streptomycin, chloramphenicol, chlortetracycline, oxytetracycline, or neomycin.
