Sulfacytine

294.33000

294.33

T795873AJP

356717

DTXSID6023606

C47734

Crystals from butyl alcohol, methanol|Crystalline

2935009090

115.46000

2.38120

1.45g/cm3

166.5-168 °C

496.8ºC at 760mmHg

254.2ºC

1.664

175 mg sol in 100 mL buffer at pH 5 at 37 °C|Insoluble in water; soluble in alkali|Solubility increases with increasing pH.|In water, 1,750 mg/L at 37 °C (est)|4.68e-01 g/L

5.25E-10mmHg at 25°C

Henry's Law constant = 6.06X10-15 atm-cu m/mol at 25 °C (est)

pK'= 6.9 /as per source/

Hydroxyl radical reaction rate constant = 6.19X10-11 cu cm/molec-sec at 25 °C (est)

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products. Sulfacytine is included on this list.

Briggs GG et al; Drugs Preg Lactation 324-377 1984. Drugs in pregnancy and lactation: A reference guide to fetal and neonatal risk (drugs S-Z).

These medications /coumarin- or indandione-derivative anticoagulants; hydantoin anticonvulsants or oral antidiabetic agents/ may be displaced from protein binding sites and/or their metabolism may be inhibited by some sulfonamides, resulting in increased or prolonged effects and/or toxicity; dosage adjustments may be necessary during and after sulfonamide therapy. /Sulfonamides/|Concurrent use of bone marrow depressants with sulfonamides may increase the leukopenic and/or thrombocytopenic effects; if concurrent use is required, close observation for myelotoxic effects should be considered. /Sulfonamides/|Concurrent long-term use of sulfonamides /with estrogen-containing, oral contraceptives/ may result in increased incidence of breakthrough bleeding and pregnancy. /Sulfonamides/|Concurrent use /of cyclosporine/ with sulfonamides may increase the metabolism of cyclosporine, resulting in decreased plasma concentration and potential transplant rejection, and additive nephrotoxicity; plasma cyclosporine concentrations and renal function should be monitored. /Sulfonamides/|For more Interactions (Complete) data for SULFACYTINE (13 total), please visit the HSDB record page.

Acute hemolytic anemia may occur during the first week of therapy as a result of sensitization or glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. This reaction may also occur in the fetus or premature infant in whom G-6-PD is normally deficient. /Sulfonamides/|Patients with acquired immunodeficiency syndrome (AIDS) may have a greater incidence of side/adverse effects, especially rash, fever, and leukopenia, than do non-AIDS patients. /Sulfonamides/|Except as concurrent adjunctive therapy with pyrimethamine in the treatment of congenital toxoplasmosis, use of sulfonamides is contraindicated in infants up to 2 months of age. Sulfonamides compete for bilirubin binding sites on plasma albumin, increasing the risk of kernicterus in the newborn. Also, because the acetyltransferase system is not fully developed in the newborn, increased blood concentrations of the free sulfonamide can further increase the risk of kernicterus. /Sulfonamides/|Elderly patients may be at increased risk of severe side/adverse effects. Severe skin reactions, generalized bone marrow depression, and decreased platelet count (with or without purpura) are the most frequently reported severe side/adverse effects in the elderly. An increased incidence of thrombocytopenia with purpura has been reported in elderly patients who are receiving diuretics, primarily thiazides, concurrently with sulfamethoxazole. The potential for these problems should also be considered for elderly patients taking other sulfonamide medications. /Sulfonamides/

Sulfonamides are distributed into milk. /Sulfonamides/

Used orally in the treatment of acute urinary tract infections.

Anti-Infective Agents /SRP: Antibacterial/|Sulfacytine is used to treat acute urinary tract infections caused by susceptible strains of Escherichia coli, the Klebsiella-Enterobacter group, Staphylococcus aureus, Proteus mirabilis, & less frequently, Proteus vulgaris.|Sulfonamides are indicated in the treatment of chancroid caused by Hemophilus ducreyi. However, other agents such as erythromycin and ceftriaxone, are considered to be first line agents. /Sulfonamides; Included in US product labeling/|Sulfonamides are indicated in the treatment of endocervical and urethral infections caused by Chlamydia trachomatis. However, other agents, such as doxycycline and azithromycin, are considered to be first line agents. /Sulfonamides; Included in US product labeling/|For more Therapeutic Uses (Complete) data for SULFACYTINE (15 total), please visit the HSDB record page.

The number of conditions for which the sulfonamides are therapeutically useful and constitute drugs of first choice has been reduced sharply by the development of more effective antimicrobial agents and by the gradual increase in the resistance of a number of bacterial species to this class of drugs. /Sulfonamides/|Although the risk of crystalluria apparently is minimal, fluid intake should be increased when this drug is prescribed. Sulfacytine should be used with caution in patients with impaired renal function.|...Because no well-controlled clinical studies exist.../sulfacytine/ should not be used during pregnancy unless the expected benefits outweigh the possible adverse effects of the drug.|Sulfacytine is contraindicated in individuals allergic to sulfonamides.|For more Drug Warnings (Complete) data for SULFACYTINE (26 total), please visit the HSDB record page.

Both chromosomal and R-factor-mediated resistance to sulfonamides have been attributed to altered forms of dihydropterate synthetase (for which sulfonamides have a lowered affinity). Another mechanism of resistance is the overproduction of PABA, which overcomes the metabolic block imposed by the inhibition of dihydropterate synthetase. Cross-resistance between sulfonamides is the general rule. Resistance does emerge gradually and is widespread in many animal populations; continued use of sulfonamides increases the incidence. Plasmid-mediated sulfonamide resistance in intestinal gram-negative bacteria is often linked with ampicillin and tetracycline resistance.

Sulfacytine is a short-acting sulfonamide. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of p-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus.

Well absorbed following oral administration.|Sulfacytine...is rapidly absorded following oral administration. More than 90% is excreted by kidneys almost entirely in the free, active form. ...86% is bound to serum proteins. ...The drug crosses the placenta & is excreted in milk...|By comparison to sulfisoxazole urine levels, 1 g/day of sulfacytine appears to be appropriate therapeutic dose & produces urine concn at least 10 times highest min inhibitory concentration found for sensitive microorganisms.|Sulfacytine is highly soluble in urine within the normal acidic pH range.|Thirty-four subjects were divided into 3 groups of 12, 12, and 10 respectively. The first group received 250 mg /sulfacytine/ 4 times a day, the second, 500 mg 4 times a day, and the third group received placebo. The renal function was not altered during the 84 days of the trial. Creatinine clearance, urea nitrogen, urinalysis, and phenosulfophthalein excretion tests were performed to evaluate kidney function.|For more Absorption, Distribution and Excretion (Complete) data for SULFACYTINE (11 total), please visit the HSDB record page.

Sulfonamides undergo metabolic alterations to varying extent in tissues, especially in liver. Both acetylation & oxidation occur. ... In nearly all species, major metabolic derivative is N4-acetylated sulfonamide. /Sulfonamides/|Although the liver is the major site of metabolism, sulfonamides may also be metabolized in other body tissues. Most sulfonamides are metabolized mainly by N4-acetylation. The degree of acetylation, which is a function of time, varies from less than 5% for sulfamethizole to up to 40% for sulfadiazine. The N4-acetyl metabolites, which do not possess antibacterial activity, have greater affinity for plasma albumin than does the nonacetylated drug and are usually less soluble than the parent sulfonamide, particularly in acidic urine. Like acetyl derivatives, glucuronide derivatives do not possess antibacterial activity; however, glucuronide derivatives are water soluble, appear to resemble the nonacetylated sulfonamide in plasma binding capacity, and have not been associated with adverse effects. /Sulfonamides/

Sulfacytine has a biological half-life of approximately 4 hrs...

Sulfacytine is a competitive inhibitor of the enzyme dihydropteroate synthetase. It inhibits bacterial synthesis of of dihydrofolic acid by preventing the condensation of the pteridine with para-aminobenzoic acid (PABA), a substrate of the enzyme dihydropteroate synthetase. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.|Sulfonamides are usually bacteriostatic in action. Sulfonamides interfere with the utilization of p-aminobenzoic acid (PABA) in the biosynthesis of tetrahydrofolic acid (the reduced form of folic acid) cofactors in susceptible bacteria. Sulfonamides are structural analogs of PABA and appear to interfere with PABA utilization by competitively inhibiting the enzyme dihydropteroate synthase, which catalyzes the formation of dihydropteroic acid (a precursor of tetrahydrofolic acid) from PABA and pteridine; however, other mechanism(s) affecting the biosynthetic pathway also may be involved. Compounds such as pyrimethamine and trimethoprim, which block later stages in the synthesis of folic acid, act synergistically with sulfonamides. Only microorganisms that synthesize their own folic acid are inhibited by sulfonamides; animal cells and bacteria which are capable of utilizing folic acid precursors or preformed folic acid are not affected by these drugs. The antibacterial activity of the sulfonamides is reportedly decreased in the presence of blood or purulent body exudates. /Sulfonamides/|The sulfonamides are structural analogs of para-aminobenzoic acid (PABA) and competitively inhibit an enzymatic step (dihydropterate synthetase) during which PABA is incorporated into the synthesis of dihydrofolic acid (folic acid). Because dihydrofolate synthesis is reduced, the levels of tetrahydrofolate (folinic acid) formed from dihydrofolate diminish. Tetrahydrofolate is an essential component of the coenzymes responsible for single carbon metabolism in cells. Acting as antimetabolites to PABA, sulfonamides eventually block, in a complex fashion, several enzymes. These enzymes include those needed for the biogenesis of purine bases; for the transfer of desoxyuridine to thymidine; and for the biosynthesis of methionine, glycine, and formylmethionyl-transfer-RNA. This results in suppression of protein synthesis, impairment of metabolic processes, and inhibition of growth and multiplication of those organisms that cannot use preformed folate. The effect is bacteriostatic, although a bactericidal action is evident at the high concentrations that may be found in urine.

Maintain an open airway and assist ventilation if necessary. Treat coma, seizures, hypotension, anaphylaxis, and hemolysis if they occur. Replace fluid losses resulting from gastroenteritis with intravenous crystalloids. Maintain steady urine flow with fluids to alleviate crystalluria ... Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. Most antibiotics are excreted unchanged in the urine, so maintenance of adequate urine flow is important. The role of forced diuresis is unclear. Hemodialysis is not usually indicated, except perhaps in patients with renal dysfunction and a high level of a toxic agent. /Antibacterial agents/

/SIGNS AND SYMPTOMS/ Sulfacytine...is capable of causing any of the toxic manifestations produced by the sulfonamides, including serious reactions like kernicterus or Stevens-Johnson syndrome... Common adverse reactions associated with sulfacytine therapy are headache, GI disturbances, and allergic rash. ...Risk of crystalluria /is/ minimal...

N(1)-(1-ethyl-1,2-dihydro-2-oxo-4-pyrimidinyl)sulfanilamide

Renoquid (Parke-Davis).

The holders of the application ... /has/ informed EPA that /Renoquid/ is no longer marketed and /has/ requested that FDA withdraw approval of ... application ... May 23, 2006.

BLOOD OR URINE, SPECTROPHOTOMETRY. /SULFONAMIDES/|Analyte: sulfacytine; matrix: blood (serum), urine; procedure: disc-agar diffusion microbiological assay; limit of quantitation: 3 ug/mL|Analyte: sulfacytine; matrix: blood (serum); procedure: broth dilution method or agar diffusion assay

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