Tag: M.W=200-350

Saboo, Sugandha published the artcileCongruent release of drug and polymer: A “”sweet spot”” in the dissolution of amorphous solid dispersions, Synthetic Route of 21829-25-4, the main research area is amorphous solid dispersion liquid phase separation drug congruent release; Amorphous solid dispersion; Congruent release; Dissolution; Liquid-liquid phase separation.

Liquid-liquid phase separation (LLPS) occurs following amorphous solid dispersion (ASD) dissolution when the drug concentration exceeds the “”amorphous solubility””, and is emerging as an important characteristic of formulations that may enhance the oral bioavailability of poorly soluble drugs. The purpose of this research was to identify criteria that impact the rate and extent of drug release and hence the occurrence or not of LLPS upon ASD dissolution The model polymer was poly (vinylpyrrolidone-co-vinyl acetate) (PVPVA). Nil-PVPVA and Cil-PVPVA ASDs with different drug loadings were prepared Surface area normalized dissolution rates of both the drug and the polymer from ASD tablets were studied. At a similar and relatively low drug loading (<20% weight/weight drug), dissolution of both Nil-PVPVA and Cil-PVPVA ASDs was found to switch from rapid, congruent (i.e., simultaneous) release of drug and polymer to incongruent release with slow release of drug. SEM (SEM) and micro-computed tomog. (micro-CT) showed the presence of characteristic ""pits"" on the surface of partially dissolved, incongruently releasing ASD tablets. This study demonstrates two important findings, firstly, a link between congruent release of drug and polymer and the occurrence of LLPS and secondly, the switch between congruent and incongruent release of drug and polymer is a result of competitive kinetics between phase separation and the release rate of ASD components with minimal influence from drug hydrophobicity for two structural analogs. Journal of Controlled Release published new progress about Crystals. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Synthetic Route of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Yang, Tingting published the artcileL- and T-type calcium channels control aldosterone production from human adrenals, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is TTAP2 nifedipine calcium aldosterone human adrenal; L-type calcium channels; T-type calcium channels; aldosterone secretion; primary aldosteronism.

Aldosterone, which plays a key role in the regulation of blood pressure, is produced by zona glomerulosa (ZG) cells of the adrenal cortex. Exaggerated overproduction of aldosterone from ZG cells causes primary hyperaldosteronism. In ZG cells, calcium entry through voltage-gated calcium channels plays a central role in the regulation of aldosterone secretion. Previous studies in animal adrenals and human adrenal adrenocortical cell lines suggest that the T-type but not the L-type calcium channel activity drives aldosterone production However, recent clin. studies show that somatic mutations in L-type calcium channels are the second most prevalent cause of aldosterone-producing adenoma. Our objective was to define the roles of T and L-type calcium channels in regulating aldosterone secretion from human adrenals. We find that human adrenal ZG cells mainly express T-type CaV3.2/3.3 and L-type CaV1.2/1.3 calcium channels. TTA-P2, a specific inhibitor of T-type calcium channel subtypes, reduced basal aldosterone secretion from acutely prepared slices of human adrenals. Surprisingly, nifedipine, the prototypic inhibitor of L-type calcium channels, also decreased basal aldosterone secretion, suggesting that L-type calcium channels are active under basal conditions. In addition, TTA-P2 or nifedipine also inhibited aldosterone secretion stimulated by angiotensin II- or elevations in extracellular K+. Remarkably, blockade of either L- or T-type calcium channels inhibits basal and stimulated aldosterone production to a similar extent. Low concentrations of TTA-P2 and nifedipine showed additive inhibitory effect on aldosterone secretion. We conclude that T- and L-type calcium channels play equally important roles in controlling aldosterone production from human adrenals.

Journal of Endocrinology published new progress about Adenoma. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Mary, Sheon published the artcileSalt loading decreases urinary excretion and increases intracellular accumulation of uromodulin in stroke-prone spontaneously hypertensive rats, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is SHRSP salt urinary excretion uromodulin intracellular accumulation; Salt; Tamm Horsfall protein; blood pressure; renal physiology; salt-sensitive hypertension.

Uromodulin (UMOD) is the most abundant renal protein secreted into urine by the thick ascending limb (TAL) epithelial cells of the loop of Henle. Genetic studies have demonstrated an association between UMOD risk variants and hypertension. We aimed to dissect the role of dietary salt in renal UMOD excretion in normotension and chronic hypertension. Normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) (n = 8/sex/strain) were maintained on 1% NaCl for 3 wk. A subset of salt-loaded SHRSP was treated with nifedipine. Salt-loading in SHRSP increased blood pressure (δSBP 35 ± 5 mmHg, P<0.0001) and kidney injury markers such as kidney injury marker-1 (KIM-1; fold change, FC 3.4; P = 0.003), neutrophil gelatinase-associated lipocalin (NGAL; FC, 2.0; P = 0.012) and proteinuria. After salt-loading there was a reduction in urinary UMOD excretion in WKY and SHRSP by 26 and 55% resp., compared with baseline. Nifedipine treatment reduced blood pressure (BP) in SHRSP, however, did not prevent salt-induced reduction in urinary UMOD excretion. In all experiments, changes in urinary UMOD excretion were dissociated from kidney UMOD protein and mRNA levels. Colocalization and ex-vivo studies showed that salt-loading increased intracellular UMOD retention in both WKY and SHRSP. Our study provides novel insights into the interplay among salt, UMOD, and BP. The role of UMOD as a cardiovascular risk marker deserves mechanistic reappraisal and further investigations based on our findings. Clinical Science published new progress about Alleles. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Hemati, Tahereh published the artcileActivation of L-type calcium channels and attenuation of oxidative stress are involved in the improving effect of methyl jasmonate on learning and memory and its anxiolytic property in rats, Related Products of pyridine-derivatives, the main research area is anxiety learning oxidative stress calcium channel methyl jasmonate.

The present study was designed to evaluate the effect of plant bioactive compound Me jasmonate on learning and memory, anxiety-like behaviors, and brain oxidative stress in rats. Therefore, we investigated the potential role of L-type calcium channel on Me jasmonate effects. The animals were intracerebroventriculary (i.c.v.) injected with different doses of Me jasmonate (0.5, 2.5, and 5μg/rat). L-type calcium channel blocker (nifedipine 5μg/rat, i.c.v.) was injected 30 min before Me jasmonate (5μg/rat). Shuttle box apparatus was used to evaluate passive avoidance memory. Anxiety-like behaviors were assessed by open field and elevated plus maze tests. Lastly, oxidative stress-related indexes were assessed in hippocampus and prefrontal cortex. The data showed that Me jasmonate dose-dependently could improve passive avoidance learning and memory and reduce anxiogenic behaviors. The Me jasmonate effects were significantly prevented by nifedipine. Furthermore, central microinjection of Me jasmonate significantly decreased hydrogen peroxide concentration, and increased reactive oxygen species scavenger activity (catalase and peroxide enzymes) in rats’ hippocampus as well as prefrontal cortex. Indeed, the results indicated that the beneficial effects of Me jasmonate on learning and memory and anxiety might be partly associated with L-type calcium channel and partly on the inhibition of oxidant indexes.

Behavioural Pharmacology published new progress about Anxiety. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Related Products of pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Hayashi, Tokumasa published the artcileProperties of SK3 channel-expressing PDGFRα (+) cells in the rodent urinary bladder, COA of Formula: C17H18N2O6, the main research area is PDGFRalpha vimentin channelDSM contraction membrane hyperpolarization; Interstitial cell; P2Y receptor; Platelet-derived growth factor receptor-α (PDGFRα); Small-conductance calcium-activated potassium (SK3) channel; Urinary bladder.

Localisation of platelet-derived growth factor receptor-α (PDGFRα) (+) cells expressing small-conductance Ca2+-activated K+ (SK3) channels in the urinary bladder was investigated, while putative roles of SK3 (+) PDGFRα (+) cells in suppressing detrusor smooth muscle (DSM) spontaneous activity were explored. In guinea-pig bladder, immunohistochem. for SK3 channels, PDGFRα or vimentin was examined, as were the effects of purinergic agonists on spontaneous phasic contractions (SPCs). In bladder of PDGFRα-GFP mice, the effects of purinergic agonists on intracellular Ca2+ signaling in PDGFRα (+) cells or DSM cells in situ and SPCs were investigated. SK3 (+) cells co-expressing PDGFRα or vimentin were distributed in DSM bundles but not inter-bundle spaces or lamina propria. SK3 (+) cells had a stellate- or spindle-shape cell body extending processes. MRS2365 (100 nM or 1μM), a P2Y1 agonist, caused a transient contraction without inhibiting SPCs in both DSM and lamina propria. In PDGFRα-GFP mice bladder, MRS2365, (100 nM), ADP (100μM) or ATP (100μM) increased the Ca2+ level of PDGFRα (+) cells without suppressing spontaneous Ca2+ transients in neighboring DSM cells, and also failed to suppress SPCs. Preferential localisation of SK3 pos. PDGFRα (+) cells in DSM bundles appears to indicate their functional interaction with DSM cells. However, increases in Ca2+ level of PDGFRα (+) cells upon purinergic stimulation are not associated with the inhibition of Ca2+ or contractile activity in DSM cells. Thus, it is unlikely that the SK3-dependent hyperpolarization generated in SK3 expressing PDGFRα (+) cells is transmitted to DSMs to suppress their excitability.

European Journal of Pharmacology published new progress about Bladder. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, COA of Formula: C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Bhunia, Sudeshna published the artcileNew approaches suggest term and preterm human fetal membranes may have distinct biomechanical properties, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is term preterm human fetal membrane biomech property.

Preterm prelabour rupture of membranes is the leading cause of preterm birth and its associated infant mortality and morbidity. However, its underlying mechanism remains unknown. We utilized two novel biomech. assessment techniques, ball indentation and Optical Coherence Elastog. (OCE), to compare the mech. properties and behaviors of term (≥ 37 wk) and preterm (33-36 wk) human fetal membranes from ruptured and non-ruptured regions. We defined the expression levels of collagen, sulfated glycosaminoglycans (sGAG), matrix metalloproteinase (MMP-9, MMP-13), fibronectin, and interleukin-1β (IL-1β) within membranes by biochem. anal., immunohistochem. staining and Western blotting, both with and without simulated fetal movement forces on membrane rupture with a new loading system. Preterm membranes showed greater heterogeneity in mech. properties/behaviors between ruptured and non-ruptured regions compared with their term counterparts (displacement rate: 36% vs. 15%; modulus: 125% vs. 34%; thickness: 93% vs. 30%; collagen content: 98% vs. 29%; sGAG: 85% vs 25%). Furthermore, simulated fetal movement forces triggered higher MMP-9, MMP-13 and IL-1β expression in preterm than term membranes, while nifedipine attenuated the observed increases in expression. In conclusion, the distinct biomech. profiles of term and preterm membranes and the abnormal biochem. expression and activation by external forces in preterm membranes may provide insights into mechanisms of preterm rupture of membranes.

Scientific Reports published new progress about Amnion. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Amssayef, Ayoub published the artcileAqueous extract of oakmoss produces antihypertensive activity in L-NAME-induced hypertensive rats through sGC-cGMP pathway, Product Details of C17H18N2O6, the main research area is norepinephrine oakmoss antihypertensive agent hypertension; Hypertension; lichens; oakmoss; pathways; vasorelaxant.

BackgroundLichens are a symbiotic association of a fungus with a green alga or cyanobacterium. They are widely used in traditional medicine as a treatment against skin disorders, diabetes and hypertension. The Aim of the StudyThe goal of this paper was to assess the possible antihypertensive and vasorelaxant capacity of the aqueous extract of a lichen species called Oakmoss or Evernia prunastri (L.). Material and MethodsIn the present study, the aqueous extract of Oakmoss was prepared, its antihypertensive activity was examined in N(ω)-nitro-L-arginine Me ester (L-NAME)-induced hypertensive rats, and its vasorelaxant ability was performed in rat isolated thoracic aorta. ResultsThe results proved that Oakmoss reduced the systolic, diastolic, mean arterial blood pressure, and heart rate in hypertensive rats but not in normotensive rats. Besides, the data showed that Oakmoss exerts its antihypertensive effect through vasorelaxant ability. ConclusionThe present study presents the favorable action of Oakmoss as an antihypertensive agent.

Clinical and Experimental Hypertension published new progress about Antihypertensives. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Product Details of C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Jhanwar, Anshul published the artcilePharmacoeconomic analysis of various brands of commonly prescribed oral antihypertensive medicines in Indian market, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is nifedipine antihypertensive agent pharmacoeconomic hypertension.

Objectives: The objective of the study was to analyze the percentage cost variations among various brands of the commonly prescribed antihypertensive medicines in India. Cost of a particular medicine (cost per 10 tablets) in the same strength and dosage forms being produced by various pharmaceutical companies was taken from Current Index of Medical specialties and Drug Today. Difference between the highest and lowest cost of the same drug manufactured by various pharmaceutical industries was obtained and percentage cost variation was calculated The percentage variation in the price was above 100% with almost all of the commonly prescribed antihypertensive medicines. The cost of a total of 23 drugs (14 single and nine combination preparations), available in forty nine different formulations were studied. Overall, Amlodipine (5 mg) shows highest price difference of 982.3%, while Nifedipine (5 mg) shows lowest price difference of 39%. Telmisartan + Hydrochlorthiazide (80 + 12.5 mg) combinations shows highest price variation of 318.9%, while Amlodipine + Losartan (5 + 50 mg) shows lowest price difference of 50%. Conclusion: The average percentage price difference of the same antihypertensive medicine manufactured by various pharmaceuticals company in India is very huge. Hence, Government, Pharmaceutical companies, prescribing health care workers should educate themselves about huge variation in price of brand drugs in comparison with their cheap generic counterpart to provide maximum benefits with min. financial burden to the patients receiving antihypertensive drugs.

Asian Journal of Pharmaceutical and Clinical Research published new progress about Antihypertensives. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Doris, Ursula published the artcileA sexy approach to pacemaking: differences in function and molecular make up of the sinoatrial node, Application In Synthesis of 21829-25-4, the main research area is pacemaking sinoatrial node human.

Functional properties of the sinoatrial node (SAN) are known to differ between sexes. Women have higher resting and intrinsic heart rates. Sex determines the risk of developing certain arrhythmias such as sick sinus syndrome, which occur more often in women. We believe that a major contributor to these differences is in gender specific ion channel expression. QPCR was used to compare ion channel gene expression in the SAN and right atrium (RA) between male and female rats. Histol., immunohistochem. and signal intensity anal. were used to locate the SAN and determine abundance of ion channels. The effect of nifedipine on extracellular potential recording was used to determine differences in beating rate between sexes. MRNAs for Cav1.3, Kir3.1, and Nkx2-5, as well as expression of the L-Type Ca2+ channel protein, were higher in the female SAN. Females had significantly higher intrinsic heart rates and the effect of nifedipine on isolated SAN preparations was significantly greater in male SAN. Computer modeling using a SAN cell model demonstrated a higher propensity of pacemaker-related arrhythmias in females. This study has identified key differences in the expression of Cav1.3, Kir3.1 and Nkx2-5 at mRNA and/or protein levels between male and female SAN. Cav1.3 plays an important role in the pacemaker function of the SAN, therefore the higher intrinsic heart rate of the female SAN could be caused by the higher expression of Cav1.3. The differences identified in this study advance our understanding of sex differences in cardiac electrophysiol. and arrhythmias.

Histology and Histopathology published new progress about Atrial arrhythmia. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Application In Synthesis of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Hamada, Teruki published the artcileMicrominipig: A suitable animal model to estimate oral absorption of sustained-release formulation in humans, Computed Properties of 21829-25-4, the main research area is pharmaceutical oral sustained release formulation gastrointestinal absorption simulation microminipig; Deconvolution analysis; Gastrointestinal absorption; Microminipig; Non-compartmental analysis; Sustained-release formulation.

We investigated the gastrointestinal absorption characteristics of oral sustained-release formulations in microminipigs, dogs, and monkeys in order to clarify the similarities in absorption properties between these animals and humans. Time profiles of oral absorption of nifedipine and valproic acid were calculated from the plasma concentration-time profiles of the drugs by a deconvolution method. The curves for both drugs in microminipigs were close to or slightly higher than those in humans, whereas those in monkeys were lower. Furthermore, the plasma concentration-time profiles of the drugs were subjected to non-compartmental anal. The fractions of a dose absorbed into the portal vein (FaFg) in microminipigs ranged from 50 to 100% of the human values, whereas those in monkeys were less than half the human values. In addition, the other absorption-related parameters for the sustained-release formulation in microminipigs, as well as monkeys, were comparable to those in humans. In conclusion, the oral absorption properties of microminipigs and humans were similar regarding the sustained-release formulations. Therefore, microminipig is a suitable animal model to estimate the oral absorption of sustained-release formulations in humans.

International Journal of Pharmaceutics (Amsterdam, Netherlands) published new progress about Biological uptake. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Computed Properties of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem