adenosine 3’-monophosphate

Cyclic AMP (cAMP) (Adenosine 3',5'-cyclophosphate) combined with vitamin C treatment of children with viral myocarditis has exact curative effect, and it can improve cardiac function of patients and improve immune function.

Adenosine 3’-monophosphate is a nucleotide and metabolite formedviahydrolysis of 2’,3’-cAMP by metal-dependent phosphodiesterases.1It reduces proliferation of rat preglomerular vascular smooth muscles cells (PGVSMCs) and glomerular mesangial cells (GMCs) in a concentration-dependent manner, an effect that is abolished by the adenosine A2Breceptor antagonist MRS1754.2Adenosine 3’-monophosphate is also a metabolic intermediate in the biosynthesis of adenosine .

Roflumilast (APTA 2217) is an orally available, long-acting inhibitor of phosphodiesterase (PDE) type 4 (PDE4), with anti-inflammatory and potential antineoplastic activities. Upon administration, roflumilast and its active metabolite roflumilast N-oxide selectively and competitively bind to and inhibit PDE4, which leads to an increase of both intracellular levels of cyclic-3', 5'-adenosine monophosphate (cAMP) and cAMP-mediated signaling.

Salbutamol (Albuterol) stimulates beta2-adrenergic receptors in the lungs, thereby activating the enzyme adenylate cyclase that catalyzes the conversion of ATP to cyclic-3', 5'-adenosine monophosphate (cAMP). Salbutamol Sulfate is the sulfate salt of the short-acting sympathomimetic agent albuterol, a 1:1 racemic mixture of (R)-albuterol and (S)-albuterol with bronchodilator activity. Increased cAMP concentrations relax the bronchial smooth muscle, relieve bronchospasms, and reduce inflammatory cell mediator release, especially from mast cells. To a lesser extent, Salbutamol stimulates beta1-adrenergic receptors, thereby increasing the force and rate of myocardial contraction.

Gizzerosine 2HCl, a substance produced during the heat treatment of fishmeal, induces histopathological lesions in broiler chicks and increases intracellular cyclic adenosine-3',5'-monophosphate levels in isolated chickens of origin.

Adenosine 5’-methylenediphosphate is an inhibitor of ecto-5’-nucleotidase, also known as CD73, with a Kivalue of 37 nM.1It inhibits cAMP accumulation induced by adenosine 5’-monophosphate , adenosine 5’-diphosphate , or adenosine 5’-triphosphate but not adenosine in VA-13 human fibroblasts when used at a concentration of 100 μM. Adenosine 5’-methylenediphosphate reduces proliferation of U138MG glioma cells, as well as inhibits the invasion and migration of MHCC97H hepatocellular carcinoma (HCC) cells in a migration assay.2,3It increases tumor infiltration of CD3+CD8+T cells and reduces tumor growth in a K1735 murine melanoma model when administered at a dose of 400 μg/mouse.4 1.Bruns, R.F.Adenosine receptor activation by adenine nucleotides requires conversion of the nucleotides to adenosineNaunyn Schmiedebergs Arch. Pharmacol.315(1)5-13(1980) 2.Braganhol, E., Tamajusuku, A.S.K., Bernardi, A., et al.Ecto-5′-nucleotidase/CD73 inhibition by quercetin in the human U138MG glioma cell lineBiochim. Biophys. Acta1770(9)1352-1359(2007) 3.Shali, S., Yu, J., Zhang, X., et al.Ecto\5′\nucleotidase (CD73) is a potential target of hepatocellular carcinomaJ. Cell Physiol.234(7)10248-10259(2018) 4.Forte, G., Sorrentino, R., Montinaro, A., et al.Inhibition of CD73 improves B cell-mediated anti-tumor immunity in a mouse model of melanomaJ. Immunol.189(5)2226-2233(2021)

Indimilast is used to inhibit phosphodiesterase IV that regulates lung inflammation and causes bronchiectasis by increasing intracellular cyclic adenosine 3', 5'-monophosphate in airway smooth muscle and inflammatory cells. Potential to treat chronic obst

Licoarylcoumarin is a strong inhibitor of adenosine 3',5'-cyclic monophosphate (cAMP) phosphodiesterase. Licoarylcoumarin has antibacterial effects on the VRE strains; it has anti-HIV activity, and it has inhibitory effects on xanthine oxidase.

PDE1-IN-4 is a potent and selective inhibitor of PDE1 (phosphodiesterase-1), acting on PDE1C (IC50: 10 nM), PDE1A (IC50: 145 nM) and PDE1B (IC50: 354 nM). PDE1-IN-4 regulates cAMP (3′,5′-cyclic adenosine monophosphate) and cGMP (3′,5′-cyclic guanosine monophosphate) and exhibits antifibrotic effects. PDE1-IN-4 can inhibit TGF-β1-induced differentiation of human lung fibroblasts, and can be used to study idiopathic pulmonary fibrosis (IPF).

Salbutamol-d9 is a deuterated compound of Salbutamol. Salbutamol has a CAS number of 18559-94-9. Albuterol stimulates beta2-adrenergic receptors in the lungs, thereby activating the enzyme adenylate cyclase that catalyzes the conversion of ATP to cyclic-3', 5'-adenosine monophosphate (cAMP). Albuterol Sulfate is the sulfate salt of the short-acting sympathomimetic agent albuterol, a 1:1 racemic mixture of (R)-albuterol and (S)-albuterol with bronchodilator activity. Increased cAMP concentrations relax the bronchial smooth muscle, relieve bronchospasms, and reduce inflammatory cell mediator release, especially from mast cells. To a lesser extent, albuterol stimulates beta1-adrenergic receptors, thereby increasing the force and rate of myocardial contraction.

Kushenol A is a kind of Adenosine 3', 5'-cyclic monophosphate(cAMP)phosphodiesterase inhibitiors, it shows selective alpha-glucosidase inhibitory activity. Kushenol A and kushenol C exhibit inhibitory activity against Sodium-dependent glucose cotransporter 2(SGLT2).

Salbutamol-d3 is a deuterated compound of Salbutamol. Salbutamol has a CAS number of 18559-94-9. Albuterol stimulates beta2-adrenergic receptors in the lungs, thereby activating the enzyme adenylate cyclase that catalyzes the conversion of ATP to cyclic-3', 5'-adenosine monophosphate (cAMP). Albuterol Sulfate is the sulfate salt of the short-acting sympathomimetic agent albuterol, a 1:1 racemic mixture of (R)-albuterol and (S)-albuterol with bronchodilator activity. Increased cAMP concentrations relax the bronchial smooth muscle, relieve bronchospasms, and reduce inflammatory cell mediator release, especially from mast cells. To a lesser extent, albuterol stimulates beta1-adrenergic receptors, thereby increasing the force and rate of myocardial contraction.

Cefminox (Sodium) is a new cephamycin antibiotic possessing a D-amino acid moiety derived from D-cysteine at the C-7B side chain. Cefminox is active against a wide range of bacteria, especially Gram-negative and anaerobic bacteria. Cefminox shows excellent in vivo efficacy (ED50) which is higher than would be expected from its in vitro activity (MIC). Moreover, cefminox possesses more potent activity in suppression of bacterial regrowth than other cephems[1]. Cefminox (Sodium) was the most active beta-lactam, with an MIC at which 50% of isolates are inhibited (MIC50) of 1.0 microg/ml and an MIC90 of 16.0 microg/ml. Cefminox was especially active against Bacteroides fragilis (MIC90, 2.0 microg/ml), Bacteroides thetaiotaomicron (MIC90, 4.0 microg/ml), fusobacteria (MIC90, 1.0 microg/ml), peptostreptococci (MIC90, 2.0 microg/ml), and clostridia, including Clostridium difficile (MIC90, 2.0 microg/ml)[2]. The use of a single preoperative dose of cefminox was similar in efficacy to 3 doses of cefoxitin administered every 4 hours, and that the serum and tissue concentrations attained provide adequate antibiotic coverage[3]. Moreover, cefminox as a dual agonist of IP (Prostacyclin receptor) and PPARγ (peroxisome proliferator-activated receptor-gamma) that significantly inhibits PASMC proliferation by up-regulation of PTEN (phosphatase and tensin homolog) and cAMP ( cyclic adenosine monophosphate), suggesting that it has potential for treatment of PAH(pulmonary arterial hypertension)[4].

Griseolic acid is a cyclic adenosine 3',5'-monophosphate phosphodiesterase II inhibitor.