Theophylline sodium acetate  (Synonyms: 1,3-Dimethylxanthine sodium acetate; Theo-24 sodium acetate)

Theophylline (1,3-Dimethylxanthine) sodium acetate is a potent phosphodiesterase (PDE) inhibitor, adenosine receptor antagonist, and histone deacetylase (HDAC) activator. Theophylline (1,3-Dimethylxanthine) sodium acetate inhibits PDE3 activity to relax airway smooth muscle. Theophylline (1,3-Dimethylxanthine) sodium acetate has anti-inflammatory activity by increase IL-10 and inhibit NF-κB into the nucleus. Theophylline (1,3-Dimethylxanthine) sodium acetate induces apoptosis. Theophylline (1,3-Dimethylxanthine) sodium acetate can be used for asthma and chronic obstructive pulmonary disease (COPD) research^{[1][2][3][4][5]}.

Theophylline (1,3-Dimethylxanthine) sodium acetate (1-1000 μM) inhibits cAMP hydrolysis by PDE in homogenates of bronchial tissue to relax human bronchus and pulmonary arteries^[1].
Theophylline (1,3-Dimethylxanthine) sodium acetate (10 μg/mL; 24 h; eosinophils) induces apoptosis through a reduction in the antiapoptotic protein Bcl-2^[2].
Theophylline (1,3-Dimethylxanthine) sodium acetate (0-500 μM; 2 h; A549 cells) inhibits NF-κB activation, I kappa B alpha (I-κBα) degradation and decreases the level of IL-6 in a concentration-dependent manner^[3].
Theophylline (1,3-Dimethylxanthine) sodium acetate (0-1000 μM; 30 min; A549 cells) induces histone deacetylase activity to decrease inflammatory gene expression^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Theophylline (1,3-Dimethylxanthine) (100 mg/kg; i.p.; daily, for 9 d; male Swiss mice) has anti-inflammatory activity in mice and increases IL-6 and IL-10 levels and inhibits TNF-α and NO^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

284.18

C₉H₁₀N₄Na₂O₄

8002-89-9

CC(O[Na])=O.O=C(N1C)N(C)C2=C([N-]C=N2)C1=O.[Na+]

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Rabe KF, et, al. Theophylline and selective PDE inhibitors as bronchodilators and smooth muscle relaxants. Eur Respir J. 1995 Apr;8(4):637-42.  [Content Brief]

  [2]. Chung IY, et, al. The downregulation of Bcl-2 expression is necessary for theophylline-induced apoptosis of eosinophil. Cell Immunol. 2000 Aug 1;203(2):95-102.  [Content Brief]

  [3]. Ichiyama T, et, al. Theophylline inhibits NF-kappa B activation and I kappa B alpha degradation in human pulmonary epithelial cells. Naunyn Schmiedebergs Arch Pharmacol. 2001 Dec;364(6):558-61.  [Content Brief]

  [4]. Ito K, et, al, Adcock IM, Barnes PJ. A molecular mechanism of action of theophylline: Induction of histone deacetylase activity to decrease inflammatory gene expression. Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8921-6.  [Content Brief]

  [5]. Barnes PJ. Theophylline. Am J Respir Crit Care Med. 2013 Oct 15;188(8):901-6.  [Content Brief]