Disease relevance of TRIAZOLOPYRIMIDINE

• We also report a novel strategy for prevention of parathyroid bone disease using triazolopyrimidine (trapidil) [1].
• Herein, we provide evidence that triazolopyrimidine, a chemical compound primarily developed for the prevention of arterial thrombosis, strongly inhibits the response of human monocytes to CD40 ligation [2].
• Selected analogs bearing this triazolotriazine or the related triazolopyrimidine core structure have been found to be orally active in a mouse catalepsy model of Parkinson's disease [3].
• Suppression of fibroblast proliferation in vitro and of myointimal hyperplasia in vivo by the triazolopyrimidine, Trapidil [4].

High impact information on TRIAZOLOPYRIMIDINE

• Trapidil (triazolopyrimidine) possesses activity against platelet-derived growth factor-induced cellular proliferation in vitro and intimal proliferation in vivo [5].
• The triazolopyrimidine trapidil has been found in controlled clinical trials to prevent restenosis after vascular injury [6].
• In order to pharmacologically characterize this model further, the effects on neointima formation of trapidil (triazolopyrimidine), a platelet-derived growth factor (PDGF) antagonist, and captopril, an angiotensin converting enzyme inhibitor, were investigated [7].
• We conclude that triazolopyrimidine strongly inhibits the CD40 pathway of monocyte activation at least in part by downregulating the gene expression of CD40 [2].
• First, we found that triazolopyrimidine inhibits the production of IL-12, TNF-alpha, and IL-6 by monocytes activated by coculture with fibroblasts transfected with the CD40L gene as well as the induction of procoagulant activity at their membrane [2].

Biological context of TRIAZOLOPYRIMIDINE

• Effects of triazolopyrimidine on lipid peroxidation and nitric oxide levels in the corticosteroid-impaired healing of rat tracheal anastomoses [8].

Anatomical context of TRIAZOLOPYRIMIDINE

• Inhibition of the CD40 pathway of monocyte activation by triazolopyrimidine [2].
• A randomized comparison of trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, versus aspirin in prevention of angiographic restenosis after coronary artery Palmaz-Schatz stent implantation [9].

Associations of TRIAZOLOPYRIMIDINE with other chemical compounds

• The dominant csr1-1 allele encodes an ALS resistant to chlorsulfuron and triazolopyrimidine sulfonamide while the dominant csr1-2 allele encodes an ALS resistant to imazapyr and pyrimidyl-oxy-benzoate [10].
• A chemical profiling technique for sub-lethal acetolactate synthase (ALS)-inhibitor herbicides (e.g., sulfonylureas, imidazolines, triazolopyrimidine sulfonanilides, and pyrimidyloxy salicylic) was developed using 2-aminobutyric acid, and was found to be directly proportional to application rates in field studies on two varieties of potato plants [11].

Gene context of TRIAZOLOPYRIMIDINE

• Triamino derivatives of triazolotriazine and triazolopyrimidine as adenosine A2a receptor antagonists [3].
• In accordance with the EPPO guideline for the efficacy evaluation of plant protection products, resistance risk analysis PP 1/213(1), a method was established to determine the baseline sensitivity of key weed species to florasulam, a new triazolopyrimidine sulfonanilide herbicide for post-emergence control of dicotyledonous weeds in cereals [12].

Analytical, diagnostic and therapeutic context of TRIAZOLOPYRIMIDINE

• Effects of trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, in preventing restenosis after percutaneous transluminal coronary angioplasty [13].
• Analysis of triazolopyrimidine herbicides in soils using field-enhanced sample injection-coelectroosmotic capillary electrophoresis combined with solid-phase extraction [14].
• Trapidil (triazolopyrimidine) (T), is a potent PDGF inhibitor that has been efficacious in preventing restenosis after balloon angioplasty in the experimental animal and after PTCA in a limited clinical trial [15].

References