Guanine therapy

I shows that uric acid was almost completely absent from or urine, confirming the severity of the enz3mie defect in either direction. No significant increment was noted until guanine therapy commenced. Table I also shows the gross purine overproduction characteristic of this defect with a total purine end product of 2.4-3.8 mmol/mmol creatinine compared with <1.0 for controls. 

J.D., Garcia, G.A., Reuter, K., Klebe, G. From hit to lead de novo design based on virtual screening hits of inhibitors of tRNA-guanine transglycosylase, a putative target of shigellosis therapy. Helv. Chim. Acta 2003, 86, 1435-1452. 

Treatment the drug that most effectively inhibits the formation of uric acid is allopurinol, a competitive inhibitor of xanthine oxidase. Hypoxanthine and xanthine are excreted during allopurinol therapy. Allopurinol, as with guanine and hypoxanthine, can be converted to its ribonucleotide form by HGPRT. Reducing the formation of uric acid with allopurinol relieves the symptoms of gout and decreases the possibility that uric acid kidney stones will form. 

Broxson EH, Dole M, Wong R, Laya BF, Stork L. Portal hypertension develops in a subset of children with standard risk acute lymphoblastic leukemia treated with oral 6-thio-guanine during maintenance therapy. Pediatr Blood Cancer 2005 44(3) 226-31. 

Mycophenolate mofetil, a semisynthetic morpholinoester of my-cophenolic acid, initially was used to prevent acute rejection after renal and cardiac transplantation, but it is now used as part of combination therapy in moderate to severe psoriasis and other autoimmune dermatoses. It reversibly blocks de novo synthesis of guanine nucleotides required for DNA and RNA synthesis. The drug has been shown to have a speciflc lymphocyte antiproliferative effect. Oral mycophenolate mofetil, as well as topical mycophenolic acid, may undergo further clinical studies to establish efficacy in the treatment of patients with severe psoriasis. " ... 

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