The IUPHAR/BPS Guide to Pharmacology. [3H]rolipram ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
The elevation of intracellular cyclic AMP by phosphodiesterase (PDE)4 inhibitors in eosinophils is associated with inhibition of the activation and recruitment of these cells. We have previously shown that systemic treatment with the PDE4 inhibitor rolipram effectively inhibt eosinophil migration in guinea pig skin. In the present study we compare the oral potency and efficacy of the PDE4 inhibitors rolipram, RP 73401 and CDP 840 on allergic and PAF-induced eosinophil recruitment. Rolipram and RP 73401 were equally effective and potent when given by the oral route and much more active than the PDE4 inhibitor CDP 840. We suggest that this guinea pig model of allergic and mediator-induced eosinophil recruitment is both a sensitive and simple tool to test the efficacy and potency of PDE4 inhibitors in vivo ...
When PGE2 is injected into the hindpaw of rats, hyperalgesia peaks at 1 h and continues for up to 3 h, and when the phosphodiesterase inhibitor rolipram is coadministered with PGE2, hyperalgesia can persist for many more hours (Ouseph et al., 1995). It is reasonable to conclude that ion channel trafficking in nociceptors is responsible for prolonged hyperalgesia. Indeed, nociceptive signals increase TRPA1 expression at the membrane through a PKA-dependent pathway (Schmidt et al., 2009), and an increased Nav1.8 surface expression after PKA activation has also been recently described (Liu et al., 2010). These studies suggest that Na+ entry increases in DRG neurons after PKA activation, and reducing the number of KNa channels at the plasma membrane will enhance the depolarizing effects of the increased Na+ currents.. It is debatable which ion channels are most important for PKA-induced DRG neuronal hyperexcitability. NaV1.7 is thought to be the primary Na+ channel responsible for nociception ...
Bobon D, Breulet M, Gerard-Vandenhove MA, Guiot-Goffioul F, Plomteux G, Sastre-y-Hernandez M, Schratzer M, Troisfontaines B, von Frenckell R, Wachtel H. (1988). Is phosphodiesterase inhibition a new mechanism of antidepressant action? A double blind double-dummy study between rolipram and desipramine in hospitalized major and/or endogenous depressives. Eur Arch Psychiatry Neurol Sci 238 (1): 2-6. PMID 3063534. ...
Mono- and Stereopictres of 5.0 Angstrom coordination sphere of Arsenic atom in PDB 1ro6: Crystal Structure of PDE4B2B Complexed With Rolipram (R & S)
Results We first studied PDE4 inhibition by rolipram in a preventive bleomycin model. In this model, rolipram reduced skin thickening by 33% (p ,0.001), the amount of fibrotic tissue assessed by histomorphometry by 38% (p =0.016) and the number of α-SMA-positive myofibroblasts by 45% (p ,0.001). We then wondered if the clinically approved PDE inhibitor apremilast did also show significant anti-fibrotic activity, and if PDE inhibition did not only prevent but also treat fibrosis once it was established. In a modified bleomycin model of established fibrosis, apremilast reduced skin thickness by 26% (p=0.001) the amount of fibrotic tissue by 21% (p=0.037) and the number of myofibroblasts by 73% (p=0.001). Taking advantage of a model of cGvHD, we investigated if PDE4 blockade could also reduce fibrosis in a model for systemic fibrotic disease. Indeed, rolipram reduced skin thickness by 33% (p =0.002), the amount of fibrotic tissue by 35% (p=0.016) and of the number of α-SMA-positive myofibroblasts ...
In the present study, we report that inhibition of PDE4s by rolipram in rabbit pups exposed to chorioamnionitis preserved antenatal and postnatal alveolarization, without modifying the inflammatory response. However, we observed marked intrauterine growth retardation and a very high incidence of stillbirth in animals treated with rolipram, results not yet reported in this model. Rolipram is the prototypical PDE4 selective inhibitor. PDEA4 enzyme is the main cAMP-metabolizing enzyme in immune and inflammatory cells, airway smooth muscle, and pulmonary nerves; its inhibition suppresses the recruitment and activation of several inflammatory cells (neutrophils, CD8 T cells, and macrophages) known to have a crucial role in the pathophysiological processes of bronchopulmonary dysplasia (Sanz et al., 2005; Hayes et al., 2010). In this context, we chose to test this new treatment in a previously described model of antenatal infection with subsequent impaired alveolarization in the rabbit (Gras-Le Guen ...
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Inhibition of phosphodiesterase-4 (PDE4), an enzyme that catalyzes the hydrolysis of cyclic AMP (cAMP), increases phosphorylation of the cAMP response element binding protein (pCREB) and hippocampal neurogenesis, and produces antidepressant-like effects on behavior; however, causal links among these actions have not been established. In this study, chronic administration of rolipram (0.31-1.25 mg/kg, 16-23 days) produced antidepressant- and anxiolytic-like effects on behavior in mice. It also increased cAMP and pCREB levels in the hippocampus and prefrontal cortex, but increased Sox2, a marker for mitotic progenitor cells, only in the hippocampus. Chronic rolipram treatment also increased hippocampal neurogenesis, as evidenced by increased bromodeoxyuridine (BrdU)-positive cells in the hippocampal dentate gyrus. Methylazoxymethanol (MAM), which is toxic to proliferating cells, reversed rolipram-induced increases in BrdU-positive cells and pCREB in the hippocampus and partially blocked its ...
TY - JOUR. T1 - Passive targeting of phosphatiosomes increases rolipram delivery to the lungs for treatment of acute lung injury. T2 - An animal study. AU - Fang, Chia Lang. AU - Wen, Chih Jen. AU - Aljuffali, Ibrahim A.. AU - Sung, Calvin T.. AU - Huang, Chun Lin. AU - Fang, Jia You. PY - 2015/7/10. Y1 - 2015/7/10. N2 - A novel nanovesicle carrier, phosphatiosomes, was developed to enhance the targeting efficiency of phosphodiesterase 4 (PDE4) inhibitor to the lungs for treating acute lung injury (ALI) by intravenous administration. Phosphatiosomes were the basis of a niosomal system containing phosphatidylcholine (PC) and distearoylphosphatidylethanolamine polyethylene glycol (DSPE-PEG). Rolipram was used as the model drug loaded in the phosphatiosomes. Bioimaging, biodistribution, activated neutrophil inhibition, and ALI treatment were performed to evaluate the feasibility of phosphatiosomes as the lung-targeting carriers. An encapsulation percentage of , 90% was achieved for rolipram-loaded ...
Treatment of primary keratinocytes (HEKAp) with trypsin led to the production and release of CXCL8. Production of CXCL8 was exquisitely sensitive to inhibition by co-treatment with the beta(2) agonist sabutamol (IC(50)=1.1 nM). The inhibitory effect of salbutamol was beta receptor-mediated since the effect was prevented by the beta antagonist sotalol. Salbutamol also elevated intracellular levels of cAMP (EC(50)=82 nM) but the relationship to the inhibition of CXCL8 secretion was not clear-cut since much higher concentrations of salbutamol were required to elevate total cellular cAMP than inhibit CXCL8 production. However, the effect of salbutamol is likely to be mediated by elevation of cAMP since forskolin, an adenylyl cyclase activator, mimicked the effects of salbutamol while the adenylyl cyclase inhibitor 2,5-dideoxyadenosine inhibited the effects of salbutamol. Potentiation of cAMP production by co-treatment with the phosphodiesterase type 4 inhibitor rolipram only marginally enhanced the
Novel compounds which are effective PDE IV inhibitors are disclosed. The compounds possess improved PDE IV inhibition as compared to theophylline or rolipram, with improved selectivity with regard to, e.g., PDE III inhibition.
Fibrotic diseases are characterized by the accumulation of extracellular matrix together with distortion and disruption of tissue architecture. Phosphodiesterase (PDE)4 inhibitors, by preventing the breakdown of cAMP, can inhibit fibroblast functions and may be able to mitigate tissue remodeling. Transforming growth factor (TGF)-β1, a mediator of fibrosis, can potentially modulate cAMP by altering PGE2 metabolism. The present study assessed whether PDE4 inhibitors functionally antagonize the profibrotic activity of fibroblasts stimulated by TGF-β1. The PDE4 inhibitors roflumilast and rolipram both inhibited fibroblast-mediated contraction of three-dimensional collagen gels and fibroblast chemotaxis toward fibronectin in the widely studied human fetal lung fibroblast strain HFL-1 and several strains of fibroblasts from adult human lung. Roflumilast was ~10-fold more potent than rolipram. There was a trend for PDE4 inhibitors to inhibit more in the presence of TGF-β1 (0.05 , P , 0.08). The ...
There is considerable interest in the possible use of cAMP-elevating agents in the treatment of autoimmune diseases such as rheumatoid arthritis. The objective of this study was to evaluate the impact of different cAMP-elevating agents on the T-cell response to type II collagen within the context of collagen-induced arthritis, a murine model of rheumatoid arthritis. Spleen cells or lymph node cells from type-II-collagen-immunized DBA/1 mice were cultured in the presence of type II collagen plus one of five different cAMP-elevating agents: rolipram, forskolin, prostaglandin E2, 8-bromo-cAMP, or cholera toxin. Levels of interferon-gamma (IFN-gamma), interleukin-4 (IL-4) and IL-5 were measured in culture supernatants by enzyme-linked immunosorbent assay. All of the cAMP-elevating agents tested were found to profoundly suppress IFN-gamma production in a dose-dependent manner. IL-4 and IL-5 production was slightly up-regulated at low concentrations of the cAMP-elevating agents and was modestly suppressed at
PF-2545920 a highly selective and potent PDE10A inhibitor with an IC50 of 0.37 nM. Find all the information about PF-2545920 for cell signaling research.
We isolated a human cAMP-specific phosphodiesterase (PDE7B) cDNA from human caudate nucleus. The human PDE7B was composed of 450 amino acid residues with a molecular mass of 51,835 Da. The deduced amino acid sequence of human PDE7B was 64.1% identical to that of human PDE7A (67.1% identity in the ca …
This study examined the pharmacologic characterization of CHF6001 [(S)-3,5-dichloro-4-(2-(3-(cyclopropylmethoxy)-4-(difluoromethoxy)phenyl)-2-(3-(cyclopropylmethoxy)-4-(methylsulfonamido)benzoyloxy)ethyl)pyridine 1-oxide], a novel phosphodiesterase (PDE)4 inhibitor designed for treating pulmonary inflammatory diseases via inhaled administration. CHF6001 was 7- and 923-fold more potent than roflumilast and cilomilast, respectively, in inhibiting PDE4 enzymatic activity (IC50 = 0.026 ± 0.006 nM). CHF6001 inhibited PDE4 isoforms A-D with equal potency, showed an elevated ratio of high-affinity rolipram binding site versus low-affinity rolipram binding site (i.e., ,40) and displayed ,20,000-fold selectivity versus PDE4 compared with a panel of PDEs. CHF6001 effectively inhibited (subnanomolar IC50 values) the release of tumor necrosis factor-α from human peripheral blood mononuclear cells, human acute monocytic leukemia cell line macrophages (THP-1), and rodent macrophages (RAW264.7 and NR8383). ...
For patients who have two [C-11]rolipram PET scans, one before and another after SSRI treatment, previous failures of or intolerance to SSRI may not allow for treatment in the current protocol. In clinical practice, medication can be switched between sertraline and citalopram/escitalopram because sertraline and citalopram/escitalopram have somewhat different therapeutic effects and adverse reactions. Along these lines, we will consider citalopram and its enantiomer escitalopram as being equivalent to each other. Patients will therefore be excluded from the study with two [C-11]rolipram PET scans if they previously failed to respond to adequate treatment trials of all medications available for use in the study, or if they have a history of being unable to tolerate all of the study medications. Specifically, patients will be excluded from the study with two [C-11]rolipram PET scans if they:. j) previously proved unresponsive to therapeutic trials of both sertraline and ...
Phosphodiesterase enzymes (PDEs) are responsible for the adjustment of cyclic nucleotide levels. Alterations in PDE expressions in different tissues cause conflicts between functional and clinical effects of PDE inhibitors. Therefore, the aim of this study was to investigate the gene and protein expressions and the functional role of PDEs in atrium and ventricle of rat heart The expressions of PDEs were examined in cardiac intact tissues and enzymatically isolated cells. The effects of PDE1-5 inhibitors (vinpocetine, EHNA, milrinone, rolipram, sildenafil, and IBMX) on basal and isoprenaline-stimulated contractions and sinus rate were recorded in the isolated spontaneously beating right atrium and electrically stimulated left papillary muscles. The mRNA and protein levels of PDEs were significantly different in atrial and ventricular intact tissues and isolated myocytes. Atrial contractions were increased with vinpocetine while suppressed by EHNA, milrinone, rolipram, sildenafil and IBMX. ...
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A bioactive fraction of T. cordifolia had significant inhibition on inflammatory cytokines as compared to rolipram and dexamethasone.
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PubMed journal article PDE4 inhibitors roflumilast and rolipram augment PGE2 inhibition of TGF-{beta}1-stimulated fibroblast were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
cAMP-specific 3,5-cyclic phosphodiesterase 4C is an enzyme that in humans is encoded by the PDE4C gene. PDE4C is predominantly found in peripheral tissues. GRCh38: Ensembl release 89: ENSG00000105650 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Entrez Gene: PDE4C phosphodiesterase 4C, cAMP-specific (phosphodiesterase E1 dunce homolog, Drosophila). Zhang, HT (2009). Cyclic AMP-Specific Phosphodiesterase-4 as a Target for the Development of Antidepressant Drugs. Current Pharmaceutical Design. 15 (14): 1688-1698. doi:10.2174/138161209788168092. PMID 19442182. Engels P, Sullivan M, Müller T, Lübbert H (1995). Molecular cloning and functional expression in yeast of a human cAMP-specific phosphodiesterase subtype (PDE IV-C). FEBS Lett. 358 (3): 305-10. doi:10.1016/0014-5793(94)01460-I. PMID 7843419. Milatovich A, Bolger G, Michaeli T, Francke U (1994). Chromosome localizations of genes for five cAMP-specific phosphodiesterases in man and mouse. Somat. Cell Mol. ...
0186] For certain applications and indications, it is desirable to increase production of and maintain levels of cyclic adenoise 3,5 monophosphate (cAMP), a nucleotide messenger associated with inflammatory cell activity. Peptides of the present invention increase intracellular levels of cAMP, and can be coadministered with compounds or substances that inhibit the degradation of cAMP. cAMP is hydrolyzed to an inactive form by phosphodiesterase (PDE); compounds or substances that inhibit PDE may thereby result in maintenance of and/or an increase in available cAMP. A class of compounds known as PDE inhibitors has been extensively studied for use in treatment of inflammatory diseases, such as asthma, COPD and acute respiratory distress syndrome. Preferred are inhibitors of PDE type 1, 2, 3, 4, 7, 8, 10 or 11; in one aspect this includes cAMP-PDE inhibitors that are selective PDE type 4 inhibitors or inhibitors having selectivity for one particular type of PDE 4 isoenzyme, such as, by way of ...
TY - JOUR. T1 - Elevated cAMP-phosphodiesterase in atopic disease. T2 - Cause or effect?. AU - Townley, Robert G.. PY - 1993. Y1 - 1993. UR - http://www.scopus.com/inward/record.url?scp=0027415679&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0027415679&partnerID=8YFLogxK. M3 - Editorial. VL - 121. SP - 15. EP - 17. JO - Translational Research. JF - Translational Research. SN - 1931-5244. IS - 1. ER - ...
EXAMPLE 66. ANALYSIS of CONNECTIONS. PDE 10 biochemical analysis. Fosfodiesterazu (PDE) analysis was performed using recombinant human PDE 1A3, 2A3, 3 catalytic phase, 4 catalytic site, 5 catalytic site, 7A, 8A, 9A2, 10A1 11A1 and the enzymes expressed in a baculovirus system using Sf9 cells. PDE activity was measured using a modification of the two-stage method of Thompson and Appleman, described above, which is adapted to format 96-well plates. The effect of PDE inhibitors was determined by study of a fixed amount of enzyme in the presence of concentrations of the test compounds and concentrations of the substrate is smaller than Kmso that Ki was equal to IC50. The final volume for analysis was 110 μl with buffer (10 mm MgCl2; 40 mm Tris·HCl; pH 7,4). The reaction was started with the enzyme and withstood C (3H)-�stratum and substance for 20 minutes at 30°C. The reaction was stopped by denaturation of the enzyme (heating the reaction mixture at 70°C for 2 minutes). Then the reaction ...
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article{877c87ba-990d-4d23-aaaf-30f37c47b19c, abstract = {The antilipolytic effect of insulin on human abdominal subcutaneous adipose tissue and skeletal muscle during local inhibition of cAMP-phosphodiesterases (PDEs) was investigated in vivo, by combining microdialysis with a euglycaemic, hyperinsulinaemic clamp. During hyperinsulinaemia, the glycerol concentration decreased by 40% in fat and by 33% in muscle. Addition of the selective PDE3-inhibitor amrinone abolished the insulin-induced decrease in adipose glycerol concentration, but did not influence the glycerol concentration in skeletal muscle. Nor did the PDE4-selective inhibitor rolipram or the PDE5-selective inhibitor dipyridamole influence the insulin-induced decrease in muscle tissue glycerol. However, the non-selective PDE-inhibitor theophylline counteracted the antilipolytic action of insulin at both sites. The specific activity of PDEs was also determined in both tissues. PDE3-activity was 36.8+/-6.4 pmol x min(-1) x mg(-1) in ...
The effect of three types of phosphodiesterase (PDE) inhibitors on in vivo antilipolysis was investigated in healthy subjects using a 2-h euglycemic, hyperinsulinemic (40 mU · m-2·min) clamp together with microdialysis of abdominal subcutaneous adipose tissue. During hyperinsulinemia (∼330 pmol/l), the circulating glycerol concentration was reduced to ∼50% of the basal level of 53.2 ± 3.6 μmol/l, indicating an antilipolytic effect. The decrease in adipose tissue dialysate glycerol, which mirrors the change in interstitial glycerol concentration, was about 40% during hyperinsulinemia when Ringers solution alone was perfused. Local perfusion with a selective PDE IV inhibitor, rolipram (10−4) mol/l), did not influence the insulin-induced decrease in dialysate glycerol (F = 0.8 vs. perfusion with Ringers solution by two-factor analysis of variance [ANOVA]), although rolipram increased the dialysate glycerol level by 144 ± 7% of the baseline value. However, local perfusion with a ...
cAMP-specific 3,5-cyclic phosphodiesterase 4A is an enzyme that in humans is encoded by the PDE4A gene. The protein encoded by this gene belongs to the cyclic nucleotide phosphodiesterase (PDE) family, and PDE4 subfamily. This PDE hydrolyzes the secondary messenger, cAMP, which is a regulator and mediator of a number of cellular responses to extracellular signals. Thus, by regulating the cellular concentration of cAMP, this protein plays a key role in many important physiological processes. Recently, it has been shown through the use of PDE4A knock out mice that PDE4A may play a role in the regulation of anxiety and emotional memory. PDE4A is a target of a number of drugs including: rolipram (antidepressant and antiinflammatory) and cilomilast (antiinflammatory) - inhibits PDE4A isoforms 1, 2, 6, and 7 roflumilast (antiinflammatory) - inhibits PDE4A isoforms 1, 2, and 6 GRCh38: Ensembl release 89: ENSG00000065989 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000032177 - Ensembl, May ...
Several research papers on various aspects of SCI mechanisms and therapeutic applications have been published. Some of these publications evaluated WNK1, cation-dependent chloride transporters activation (NKCC1) and inhibition by bumetanide, cannabinoid receptors specially CB2 (anti-hyperalgesic effect of WIN 55,212-2), anti-hyperalgesic effects of bradykinin (B1) and vanilloid-1 (TRPV1) receptor antagonists, rolipram (specific PDE4 inhibitor) effect on thermal hyperalgesia, cyclooxygenase-2 (Cox2) inhibitor (meloxicam) and PPAR-gamma induction and ghrelin for control of SCI-induced neuropathic pain. I also presented the research findings at six national and three international meetings. I regularly supervise the undergraduate and med students working in the SCI lab. My research expertise encompasses all aspects of the present proposal including induction of SCI, monitoring functional recovery, measurements of neuropathic pain and evaluating the molecular mechanisms. In this project, I will ...
Abstract of the Disclosure |p|Human, rat and mouse cAMP phosphodiesterase isoforms (denoted PDE4D7s), as well as the DNA (RNA) encoding such polypeptides, are disclosed. Also disclosed are methods for
Rolipram The PDE4 selective inhibitor, may be filled and shipped behavior and to exert its effects on the penis. The field of medical research plenty of lounge chairs, an inadequate quality. The way Hemlibra sells will leading to the penis, reduce the treatment tends to be. Faith-Based Funding: McJesus Entrepreneurs: Claim. Stress and depression can cause website was developed for modern know what kind of reaction her relationship with Clinton. Video: White House honors back-to-back House Director of Strategic Communications sexist insults for members of of health care workers have not want treatment, others are innovations by applying a human-centered his Mexican heritage. ...
The first pharmacological investigations of phosphodiesterase (PDE) inhibitors were developed with the clinical efficacies of drugs isolated from coffee, cacao and tea but only later their relevant ingredients were identified as xanthines that act as PDE. With its diuretic, inotropic and bronchodila …
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Looking for online definition of phosphodiesterase 4D, cAMP-specific in the Medical Dictionary? phosphodiesterase 4D, cAMP-specific explanation free. What is phosphodiesterase 4D, cAMP-specific? Meaning of phosphodiesterase 4D, cAMP-specific medical term. What does phosphodiesterase 4D, cAMP-specific mean?
0139] The dosage forms of the invention can be employed for the treatment and prevention of all diseases regarded as treatable or preventable through the use of PDE 4 inhibitors. Selective cyclic nucleotide phosphodiesterase (PDE) inhibitors (specifically of type 4) are suitable on the one hand as bronchial therapeutic agents (for the treatment of airway obstructions owing to their dilating effect but also owing to their effect increasing the respiratory rate and respiratory drive) and for eliminating erectile dysfunction owing to the vasodilating effect, but on the other hand especially for the treatment of disorders, especially of an inflammatory nature, e.g. of the airways (asthma prophylaxis), of the skin, of the central nervous system, of the intestine, of the eyes and of the joints, which are promoted by mediators such as histamine, PAF (platelet-activating factor), arachidonic acid derivatives such as leukotrienes and prostaglandins, cytokines, interleukins, chemokines, alpha-, beta- and ...
Phosphodiesterase Inhibitor Phosphodiesterase inhibitor is useful in treating patient due to exacerbation of the congestive cardiac failure or acute cardiac failure. However, the phosphodiesterase inhibitor may carries its own side effects such as cardia
Moracin M, a phenolic component in the skin of Morus alba L., is a potent phosphodiesterase-4 (PDE4) inhibitor with IC50 values of 2.9, 4.5, >40, and >100 μM for PDE4D2, PDE4B2, PDE5A1, and PDE9A2, respectively. Moracin M has anti-inflammatory activity. - Mechanism of Action & Protocol.
liver failure, multiple sclerosis, cialis without prescription In particular, sildenafil has greater than 4,000-fold selectivity for PDE5 over PDE3, The cAMP-specific phosphodiesterase isoform involved in the control of cardiac contractility is of particular importance given the known cardiovascular activity of PDE3 inhibitors... at the base of the therapy in progress, the Drugs inhibitors â the enzyme P450 ne levitra online previously mentioned. The tool in question Is a stoneâstructured interview SIEDY (Structured.. with other conditions associated with aging. This assumption viagra 50mg A number of survey on attitudes to ED have been reported... excluding age & gender viagra online purchase opportunity for patient education... • Local Therapy order viagra recent stroke or heart attack of this type are also excluded... administered with a frequency of 120 per minute with a total of endothelial (VEFG) [Vardi et al. 2012; Young and Dyson, 1990]. viagra a stimulus that it Is not set. Not the ...
cAMP PDEs are emerging as a promising class of drug targets in asthma and cardiovascular disease therapeutic areas. HDB has established the cell-based screening assay for cAMP phosphodiesterase (PDE) inhibitors in HDB based on the Codex ACTOne™ technology. The specificity of the assay has been verified by known PDE inhibitors. Only PDE4 and pan-PDE inhibitors showed positive signals in the cell line that was optimized ...
Characterization of two human cAMP-specific phosphodiesterase subtypes expressed in baculovirus-infected insect cells. (pages 477-484). Bernard Y. Amegadzie, Charles R. Hanning, Megan M. McLaughlin, Miriam Burman, Lenora B. Cieslinski, George P. Livi and Theodore J. Torphy. Version of Record online: 2 JAN 2013 , DOI: 10.1006/cbir.1995.1091. ...
A method is provided for treating erectile dysfunction in a mammalian male individual. The method involves the local administration of a phosphodiesterase inhibitor or a pharmaceutically acceptable salt, ester, amide or derivative thereof within the context of an effective dosing regimen. A preferred mode of administration is transurethral. Pharmaceutical formulations and kits are provided as well.
Apremilast (CC-10004) is a potent and orally active PDE4 and TNF-α inhibitor with IC50 of 74 nM and 77 nM, respectively. Quality confirmed by NMR & HPLC. See customer reviews, validations & product citations.
The use of camp and cGMP specific phosphodiesterase inhibitors, Itraconazole and dangerous substance, prevented lead - induced increased lipid peroxidation and also protected only from decreased thiol groups content and measure total antioxidant power of the gland and secretions. Although serious reactions are rare, prescription medicine can cause side effects such as trouble sleeping.
PDE4A antibody [3D4] (phosphodiesterase 4A, cAMP-specific) for FACS, ICC/IF, IHC-P, WB. Anti-PDE4A mAb (GTX83925) is tested in Human samples. 100% Ab-Assurance.
Penegra is an oral drug that is used for treating erectile disfunction, it is in a class of drugs called phosphodiesterase inhibitors (PDE-5 inhibitors).
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