bucladesine (dibutyryl cAMP, db cAMP) - also a phosphodiesterase inhibitor. *pertussis toxin, which increases cAMP levels by ...
"Effects of pentoxifylline and H-89 on epileptogenic activity of bucladesine in pentylenetetrazol-treated mice". European ...
In in vitro studies, the compound has demonstrated concentration-dependent enhancement of bucladesine and staurosporine-induced ...
... combinations C01CE01 Amrinone C01CE02 Milrinone C01CE03 Enoximone C01CE04 Bucladesine QC01CE90 Pimobendane C01CX06 ...
... dihydrate Amipizone Apremilast Arofylline Atizoram Befuraline Bemarinone hydrochloride Bemoradan Benafentrine Bucladesine ...
... bucladesine (INN) Bucladin-S buclizine (INN) buclosamide (INN) bucloxic acid (INN) bucolome (INN) bucricaine (INN) bucrilate ( ...
... bucladesine MeSH D13.695.462.250 - cyclic cmp MeSH D13.695.462.275 - cyclic gmp MeSH D13.695.462.275.325 - dibutyryl cyclic gmp ... bucladesine MeSH D13.695.827.068.506 - flavin-adenine dinucleotide MeSH D13.695.827.068.694 - nad MeSH D13.695.827.068.749 - ... bucladesine MeSH D13.695.667.138.410 - deoxyadenine nucleotides MeSH D13.695.667.138.506 - flavin-adenine dinucleotide MeSH ...
The effect of bucladesine as a cAMP analog has been studied on the pentylenetetrazol-induced seizure in the wild-type mice. The ... Bucladesine is a cell permeable cAMP analog. The compound is used in a wide variety of research applications because it mimics ... Bucladesine is a cyclic nucleotide derivative which mimics the action of endogenous cAMP and is a phosphodiesterase inhibitor. ... Bucladesine (50-100nM/mouse) showed significant attenuation in the morphine withdrawal syndrome in the wild-type mice. In ...
... (trade names Daxas, Daliresp) is a drug that acts as a selective, long-acting inhibitor of the enzyme phosphodiesterase-4 (PDE-4). It has anti-inflammatory effects and is used as an orally administered drug for the treatment of inflammatory conditions of the lungs such as chronic obstructive pulmonary disease (COPD).[5][6][7][8] In June 2010, it was approved in the EU for severe COPD associated with chronic bronchitis.[9] In March 2011, it gained FDA approval in the US for reducing COPD exacerbations.[10] ...
HCl): InChI=1S/C31H29N5O7.ClH/c1-18-13-19(7-11-32-18)16-36-27(31(38)42-5)25(20-14-22(39-2)28(41-4)23(15-20)40-3)21-8-12-35-29(26(21)30(36)37)43-17-24-33-9-6-10-34-24;/h6-15H,16-17H2,1-5H3; ...
... is not produced by plants[citation needed] and is only observed in nature as a metabolite of caffeine in animals. Paraxanthine is also a natural metabolite of caffeine in some species of bacteria.[1] After intake, roughly 84% of caffeine is demethylated at the 3-position to yield paraxanthine, making it the chief metabolite of caffeine in the body.[2] Paraxanthine is also a major metabolite of caffeine in humans and other animals, such as mice.[3] Shortly after ingestion, caffeine is metabolized into paraxanthine by hepatic cytochrome P450,[4] which removes a methyl group from the N3 position of caffeine.[5] After formation, paraxanthine can be broken down to 7-methylxanthine by demethylation of the N1 position,[6] which is subsequently demethylated into xanthine or oxidized by CYP2A6 and CYP1A2 into 1,7-dimethylaric acid.[5] In another pathway, paraxanthine is broken down into 5-acetylamino-6-formylamino-3-methyluracil through N-acetyl-transferase 2, which is then broken down into ...
Molostvov G, Morris A, Rose P, Basu S, Muller G (February 2004). "The effects of selective cytokine inhibitory drugs (CC-10004 and CC-1088) on VEGF and IL-6 expression and apoptosis in myeloma and endothelial cell co-cultures". British Journal of Haematology. 124 (3): 366-75. doi:10.1046/j.1365-2141.2003.04777.x. PMID 14717786 ...
... has been shown to inhibit TGF-beta-mediated conversion of pulmonary fibroblasts into myofibroblasts in COPD and asthma via cAMP-PKA pathway and suppresses COL1 mRNA, which codes for the protein collagen.[24] It has been shown that theophylline may reverse the clinical observations of steroid insensitivity in patients with COPD and asthmatics who are active smokers (a condition resulting in oxidative stress) via a distinctly separate mechanism. Theophylline in vitro can restore the reduced HDAC (histone deacetylase) activity that is induced by oxidative stress (i.e., in smokers), returning steroid responsiveness toward normal.[25] Furthermore, theophylline has been shown to directly activate HDAC2.[25] (Corticosteroids switch off the inflammatory response by blocking the expression of inflammatory mediators through deacetylation of histones, an effect mediated via histone deacetylase-2 (HDAC2). Once deacetylated, DNA is repackaged so that the promoter regions of inflammatory genes ...
Reports of recreational use of glaucine have recently been published, and effects include dissociative-type symptoms; feeling detached and 'in another world', as well as nausea, vomiting and dilated pupils. These reports mirror those about the effects of clinical use, which state dissociative-type symptoms as well as lethargy, fatigue, hallucinations.[8][9] Investigation of side effects in a clinical setting also reports that the hallucinatory effects manifest as bright and colorful visualizations. They also report that patients perceive their environments clearly yet feel detached from it; "the patient sees and understands everything and is oriented well enough, but cannot take a clear and adequate action".[8]. One particular report of recreational use gone awry described the form of distribution as tablets being marketed as a 1-benzylpiperazine (BZP)-free "herbal high" which the patient referred to as "head candy".[9]. ...
The common, adverse drug reactions (side effects) are the same as with other PDE5 inhibitors. The frequent vardenafil-specific side-effect is nausea; the infrequent side effects are abdominal pain, back pain, photosensitivity, abnormal vision, eye pain, facial edema, hypotension, palpitation, tachycardia, arthralgia, myalgia, rash, itch, and priapism. One possibly serious, but rare, side effect with vardenafil is heart attack. Also, in rare cases, vardenafil use may cause priapism, a very painful emergency condition that can cause impotence if left untreated.[4] On 18 October 2007, the U.S. Food and Drug Administration (FDA) announced that a warning about possible deafness (sudden hearing loss) would be added to the drug labels of vardenafil, and other PDE5 inhibitors.[5] ...
Lunell E, Svedmyr N, Andersson KE, Persson CG (1982). "Effects of enprofylline, a xanthine lacking adenosine receptor antagonism, in patients with chronic obstructive lung disease". European Journal of Clinical Pharmacology. 22 (5): 395-402. doi:10.1007/bf00542541. PMID 6288396 ...
Animals that metabolize theobromine (found in chocolate) more slowly, such as dogs,[26] can succumb to theobromine poisoning from as little as 50 grams (1.8 oz) of milk chocolate for a smaller dog and 400 grams (14 oz), or around nine 44-gram (1.55 oz) small milk chocolate bars, for an average-sized dog. The concentration of theobromine in dark chocolates (approximately 10 g/kg (0.16 oz/lb)) is up to 10 times that of milk chocolate (1 to 5 g/kg (0.016 to 0.080 oz/lb)) - meaning dark chocolate is far more toxic to dogs per unit weight or volume than milk chocolate. The same risk is reported for cats as well,[27] although cats are less likely to ingest sweet food, with most cats having no sweet taste receptors.[28] Complications include digestive issues, dehydration, excitability, and a slow heart rate. Later stages of theobromine poisoning include epileptic-like seizures and death. If caught early on, theobromine poisoning is treatable.[29] Although not common, the effects of theobromine ...
The FDA's approval of sildenafil in 1998[16] was a ground-breaking commercial event for the treatment of ED, with sales exceeding US$1 billion. Subsequently, the FDA approved vardenafil in 2003,[17] and tadalafil in 2003. It initially was developed by the biotechnology company ICOS, and then again developed and marketed worldwide by Lilly ICOS, LLC, the joint venture of ICOS Corporation and Eli Lilly and Company. Tadalafil was approved in 2009 in the United States for the treatment of pulmonary arterial hypertension[18] and is under regulatory review in other regions for this condition. In late November 2008, Eli Lilly sold the exclusive rights to commercialize tadalafil for pulmonary arterial hypertension in the United States to United Therapeutics for an upfront payment of $150 million. Tadalafil was discovered by Glaxo Wellcome (now GlaxoSmithKline) under a partnership between Glaxo and ICOS to develop new drugs that began in August 1991.[19][20] In 1993, the Bothell, Washington biotechnology ...
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Kindling models in rats has shown vinpocetine to exhibit anticonvulsant properties. The most pronounced anticonvulsant effects were observed in Pentylenetetrazole (PTZ)-kindled rats although there was also an effect on amygdala-kindled and neocortically-kindled rats.[8] Vinpocetine has also been shown to abolish [3H]Glu release after in vivo exposure to 4-aminopyridine (4-AP) which suggests an important mechanism for vinpocetine anticonvulsant activity.[9] Vinpocetine has been investigated in animal models as a potential anti-inflammatory agent.[10] [11] Vinpocetine inhibits the up-regulation of NF-κB by TNFα in various cell tests. Reverse transcription polymerase chain reaction also shows that it reduced the TNFα-induced expression of the mRNA of proinflammatory molecules such as interleukin-1 beta, monocyte chemoattractant protein-1 (MCP-1), and vascular cell adhesion molecule-1 (VCAM-1). In mice, vinpocetine reduced lipopolysaccharide inoculation induced polymorphonuclear neutrophil ...