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  • Brand : BIOFRON

  • Catalogue Number : AV-S00553

  • Specification : 98%

  • CAS number : 317-34-0

  • Formula : C16H24N10O4

  • Molecular Weight : 420.43

  • PUBCHEM ID : 9433

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Botanical Source

Structure Type


Standards;Natural Pytochemical;API




1,3-Dimethyl-3,7-dihydro-1H-purin-2,6-dion-ethan-1,2-diamin(2:1)/1,3-dimethyl-3,7-dihydro-1H-purine-2,6-dione - ethane-1,2-diamine (2:1)/Cidophylline/Theophylline ethylenediamine/Aminophylline/Etilen-Xantisan/lasodex/1H-Purine-2,6-dione, 3,7-dihydro-1,3-dimethyl-, compd. with 1,2-ethanediamine (2:1)/aminodur/euufilin/Novophyllin/Variaphylline LA/cariomin/tefamin/1,3-Dimethyl-3,7-dihydro-1H-purine-2,6-dione - 1,2-ethanediamine (2:1)/th/100/CaRine/Ethylenediamine compd. with Theophylline (1:2)/1,3-Dimethyl-3,7-dihydro-1H-purine-2,6-dione - ethane-1,2-diamine (2:1)/1H-purine-2,6-dione, 3,9-dihydro-1,3-dimethyl-, compd. with 1,2-ethanediamine (2:1)/Pecram/Novphyllin/dobo/carena/theomin/eufilina/1,3-Dimethyl-3,9-dihydro-1H-purine-2,6-dione - ethane-1,2-diamine (2:1)/Aminophylline ethylenediamine/1,2-Ethanediamine compd. with 3,7-Dihydro-1,3-dimethyl-1H-purine-2,6-dione (1:2)





Flash Point

Boiling Point

454.1ºC at 760mmHg

Melting Point

269-270 °C


InChl Key

WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:317-34-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Aminophylline therapy has undergone change in the past decade. With the changes in usage and dosage forms, the frequency of toxicity in the pediatric population, especially in adolescents, has increased dramatically. Two distinct patterns, chronic and acute, have been recognized and treatment methods for both are changing. Table 4 summarizes the emerging state-of-the-art therapy for aminophylline toxicity. Judging from the activity seen in the literature, investigation into aminophylline toxicity will continue to be a priority. We will see a greater understanding of the disease process and a refining of the therapeutic process. The ultimate goal is the elimination of mortality and the minimization of morbidity from aminophylline toxicity.


Aminophylline toxicity.


Albert S.

Publish date

1987 Feb




Aminophylline is routinely recommended as a basic part of the emergency treatment of asthma. A comprehensive search found 13 reports of controlled trials of intravenous aminophylline therapy in severe, acute asthma. These studies compared aminophylline therapy with treatment with either albuterol (salbutamol), epinephrine, or other bronchodilators. The 13 reports did not agree. Seven reported no difference in spirometric values between aminophylline treatment and the control regimens. Three found aminophylline treatment superior. Three favored the control regimen. The results of the 13 trials were reanalyzed and pooled. Overall, there was no difference between the aminophylline-treated groups and the control groups. Sensitivity analysis suggests that aminophylline therapy is ineffective alone but may be more effective than single-drug therapy when combined with an injected beta-agonist. Despite widespread practice, available trials do not provide adequate evidence to support or reject the use of aminophylline in the treatment of severe, acute asthma.


Aminophylline treatment in severe, acute asthma. A meta-analysis.


Littenberg B1.

Publish date

1988 Mar 18




Objective: Our study evaluates the effects of aminophylline in the reduction of NGAL levels in perinatal asphyxia.Methods: Term neonates with hypoxic ischaemic encephalopathy who were divided into two groups, the treatment and placebo. Urine NGAL levels were measured on day one and four of the treatment using BIOPORTO kits in both the groups.Results: Day 1 NGAL levels were not statistically different in either group irrespective of the age, gender and the mode of delivery. on 4th day, NGAL in treatment group significantly decreased as compared to day 1 levels and placebo day-4 levels. significant differences were seen between first and fourth day NGAL levels among children with normal and caesarean birth and among female and male neonates.Conclusions: Following the treatment with aminophylline, NGAL levels in asphyxiated neonates are likely to reduce. Further studies based on other kidney dysfunction parameters can lead to the better and accurate conclusions.


NGAL; aminophylline; asphyxiated neonates; renal failure


Effects of aminophylline on the levels of neutrophil gelatinase-associated lipocalin (NGAL) in asphyxiated term neonates.


Maleki-Sadeghi N1, Rahmani P2, Aghsaeifard Z3,4, Heidari G1.

Publish date

2020 Apr 17

Description :

Aminophylline is a competitive nonselective phosphodiesterase inhibitor that is used to treat airway obstruction from asthma or COPD.Target: PhosphodiesteraseAminophylline is a compound of the bronchodilator theophylline with ethylenediamine in 2:1 ratio. The ethylenediamine improves solubility, and the aminophylline is usually found as a dihydrate. Aminophylline is less potent and shorter-acting than theophylline. Its most common use is in the treatment of airway obstruction from asthma or COPD. It is used off-label as a reversal agent during nuclear stress testing. Aminophylline is a nonselective adenosine receptor antagonist and phosphodiesterase inhibitor.Adenosine is an endogenous extracellular messenger that can regulate myocardial oxygen needs. It acts through cellular surface receptors which effect intracellular signalling pathways to increase coronary artery blood flow, slow heart rate, block atrioventricular node conduction, suppress cardiac automaticity, and decrease β-adrenergic effects on contractility. Adenosine also antagonizes chronotropic and ionotropic effects of circulating catecholamines. Overall, adenosine decreases the heart's rate and force of contraction, which increases blood supply to the cardiac muscle. Given specific circumstances this mechanism (which is intended to protect the heart) may cause atropine-resistant refractory bradyasystole. Adenosine's effects are concentration-dependent. Adenosine's receptors are competitively antagonized by methylxanthines such as aminophylline. Aminophylline competitively antagonizes the cardiac actions of adenosine at the cell surface receptors. Thus, it increases heart rate and contractility.