Sodium theophylline glycinate

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

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Signaling Pathways >> Immunology/Inflammation >> Interleukin Related

Signaling Pathways >> Cell Cycle/DNA Damage >> HDAC

Signaling Pathways >> GPCR/G Protein >> Adenosine Receptor

Signaling Pathways >> Epigenetics >> HDAC

Theophylline sodium glycinate (1-1000 µM) inhibits cAMP hydrolysis by PDE in homogenates of bronchial tissue to relax human bronchus and pulmonary arteries[1]. Theophylline sodium glycinate (10 µg/mL; 24 h) induces apoptosis through a reduction in the antiapoptotic protein Bcl-2 in eosinophils[2]. Theophylline sodium glycinate (0-500 µM; 2 h) 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 sodium glycinate (0-1000 µM; 30 min; A549 cells) induces histone deacetylase activity to decrease inflammatory gene expression[4]. Western Blot Analysis[3] Cell Line: A549 cells Concentration: 0, 20, 100 and 500 µM Incubation Time: 2 hours Result: Decreased the expression of NF-κB p65 and I-κBα degradation in a dose-dependent manner.

Theophylline sodium glycinate (100 mg/kg; i.p.; daily, for 9 d) has anti-inflammatory activity in mice and increases IL-6 and IL-10 levels and inhibits TNF-α and NO in male Swiss mice[1]. Animal Model: Male Swiss mice[1] Dosage: 100 mg/kg Administration: Intraperitoneal injection; daily; for 9 days Result: Increased IL-6 and IL-10 levels and inhibited TNF-α and NO.

[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.

[2]. Németh ZH, et, al. Amrinone and theophylline differentially regulate cytokine and nitric oxide production in endotoxemic mice. Shock. 1997 May;7(5):371-5.

[3]. 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.

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