Tag: M.W=200-350

Aali, Ehsan published the artcileCardioprotective Effects of Mebudipine in a Rat Model of Doxorubicin-Induced Heart Failure., Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is Amlodipine ; Doxorubicin; Endothelin-1 ; Heart failure ; Mebudipine.

Background: Mebudipine, a dihydropyridine calcium-channel blocker (CCB), shows greater time- and voltage-dependent inhibitory effects than nifedipine. Its significant negative chronotropic effects without having considerable negative inotropic properties may make it a suitable candidate for the pharmacotherapy of heart failure (HF). This study aimed to investigate the possible beneficial action of mebudipine in a rat model of HF. Methods: The present study carried out in the Department of Pharmacology at the Iran University of Medical Sciences during the years of 2009-2011. An experimental model of HF was induced in male Wistar rats using doxorubicin (DOX). The rats were divided into five groups with seven animals in each group: normal control group, DOX-induced HF control groups, and treatment groups. The animals were administered DOX for 15 days. A consistent deterioration occurred after a four-week rest period. The animals were then treated with intraperitoneal mebudipine (0.5 mg/kg) and intraperitoneal amlodipine (0.35 mg/kg), as well as an equal volume of distilled water for 15 days. The plasma levels of big endothelin-1 (BET-1), creatine kinase-myocardial band (CK-MB), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine aminotransferase (ALT), as well as the clinical status (heart rate and blood pressure), were assessed before and after treatment. Statistical analysis was performed with SPSS software using parametric and nonparametric ANOVA. Results: Mebudipine and amlodipine reversed the increased plasma BET-1 values in the treated animals when compared with the HF control group (0.103 and 0.112 vs 0.231 pg/mL, respectively). The increased plasma levels of AST, ALT, CK-MB, and LDH were also reversed in the HF animals that received mebudipine or amlodipine. Conclusion: The administration of mebudipine to HF animals, akin to amlodipine, palliated the clinical and biochemical signs of the disease in the present study. The abstract was presented in the Iranian Congress of Physiology and Pharmacology as a poster and published in the Scientific Information Database as a supplement (2015; Vol 22).

Iranian journal of medical sciences published new progress about Amlodipine ; Doxorubicin; Endothelin-1 ; Heart failure ; Mebudipine. 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

Eroglu, Talip E published the artcileDifferential effects on out-of-hospital cardiac arrest of dihydropyridines: real-world data from population-based cohorts across two European countries., SDS of cas: 21829-25-4, the main research area is Amlodipine; Epidemiology; Nifedipine; Sudden cardiac arrest.

AIMS: Various drugs increase the risk of out-of-hospital cardiac arrest (OHCA) in the general population by impacting cardiac ion channels, thereby causing ventricular tachycardia/fibrillation (VT/VF). Dihydropyridines block L-type calcium channels, but their association with OHCA risk is unknown. We aimed to study whether nifedipine and/or amlodipine, often-used dihydropyridines, are associated with increased OHCA risk, and how these drugs impact on cardiac electrophysiology. METHODS AND RESULTS: We conducted a case-control study with VT/VF-documented OHCA cases with presumed cardiac cause from ongoing population-based OHCA registries in the Netherlands and Denmark, and age/sex/index date-matched non-OHCA controls (Netherlands: PHARMO Database Network, Denmark: Danish Civil Registration System). We included 2503 OHCA cases, 10 543 non-OHCA controls in Netherlands, and 8101 OHCA cases, 40 505 non-OHCA controls in Denmark. To examine drug effects on cardiac electrophysiology, we performed single-cell patch-clamp studies in human-induced pluripotent stem cell-derived cardiomyocytes. Use of high-dose nifedipine (â‰?0 mg/day), but not low-dose nifedipine (<60 mg/day) or amlodipine (any-dose), was associated with higher OHCA risk than non-use of dihydropyridines [Netherlands: adjusted odds ratios (ORadj) 1.45 (95% confidence interval 1.02-2.07), Denmark: 1.96 (1.18-3.25)] or use of amlodipine [Netherlands: 2.31 (1.54-3.47), Denmark: 2.20 (1.32-3.67)]. Out-of-hospital cardiac arrest risk of (high-dose) nifedipine use was not further increased in patients using nitrates, or with a history of ischaemic heart disease. Nifedipine and amlodipine blocked L-type calcium channels at similar concentrations, but, at clinically used concentrations, nifedipine caused more L-type calcium current block, resulting in more action potential shortening. CONCLUSION: High-dose nifedipine, but not low-dose nifedipine or any-dose amlodipine, is associated with increased OHCA risk in the general population. Careful titration of nifedipine dose should be considered. European heart journal. Cardiovascular pharmacotherapy published new progress about Amlodipine; Epidemiology; Nifedipine; Sudden cardiac arrest. 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, SDS of cas: 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Lee, Hao-Wei published the artcileComparative efficacy of generic nifedipine versus brand-name amlodipine for hypertension management in Taiwan, Safety of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is amlodipine; generic; hypertension; nifedipine; outcome.

The control rate of hypertension remains concerning, indicating the requirement for better management strategies. The calcium channel blockers brand-name amlodipine and nifedipine with extended-release formulations demonstrate similar clin. efficacy. However, the efficacy of generic nifedipine remains obscure. We compared the efficacy of generic nifedipine and brand-name amlodipine in terms of cardiovascular (CV) outcomes. Patients prescribed generic nifedipine (SRFC CYH) or brand-name amlodipine besylate (Norvasc, Pfizer) between August 1, 2017, and July 31, 2018, were enrolled; patients with CV events within 3 mo were excluded. CV outcomes included CV death, nonfatal myocardial infarction (MI), nonfatal ischemic stroke, hospitalization for heart failure, and composite endpoints of 3P- and 4P-major adverse cardiac events (MACE). A total of 1625 patients treated with nifedipine (SRFC CYH) and 16 587 patients treated with Norvasc were included. After propensity score matching, there were 995 and 4975 patients in the nifedipine CYH and Norvasc groups, resp. At a mean follow-up period of 30.3 ± 6.4 mo, nifedipine CYH was comparable to Norvasc in terms of CV death (P = .107), nonfatal MI (P = .121), nonfatal ischemic stroke (P = .453), hospitalization for heart failure (P = .330), 3P-MACE (P = .584), and 4P-MACE (P = .274). Cox regression anal. revealed that nifedipine CYH and Norvasc had similar efficacy in terms of 3P-MACE (hazard ratio, 0.970; 95% confidence interval, 0.601-1.565, P = .900) and 4P-MACE (hazard ratio, 0.880; 95% confidence interval, 0.628-1.233, P = .459). In conclusion, Nifedipine SRFC CYH and Norvasc have comparable clin. efficacy for hypertension management.

Journal of Clinical Hypertension (Hoboken, NJ, United States) published new progress about amlodipine; generic; hypertension; nifedipine; outcome. 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, Safety of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Sakamoto, Aoi published the artcileDissolution Kinetics of Nifedipine-Ionizable Polymer Amorphous Solid Dispersion: Comparison Between Bicarbonate and Phosphate Buffers, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is amorphous solid dispersion; bicarbonate; dissolution test; floating lid; phosphate; supersaturation.

Abstract: Purpose: The intestinal fluid pH is maintained by the bicarbonate buffer system that shows unique properties regarding drug dissolution Nevertheless, current compendial dissolution tests use phosphate buffers. The purpose of the present study was to investigate the effect of bicarbonate and phosphate buffers on the dissolution profiles of amorphous solid dispersions (ASD) composed of ionizable polymers. Methods: Hydroxypropylmethylcellulose acetate succinate (HPMCAS), amino methacrylate copolymer (AMC), and hydroxypropylmethylcellulose (HPMC) were employed as acidic, basic, and neutral polymers, resp. Nifedipine (NIF) was used as a model drug. Dissolution profiles were measured in pH 6.5 bicarbonate and phosphate buffers by a mini-scale paddle dissolution test. The pH of bicarbonate buffers was maintained by the floating lid method. Results: The pH change of the bicarbonate buffer was suppressed to less than + 0.25 pH for 3 h by the floating lid method. In all cases, the NIF concentration was supersaturated against the solubility of crystalline NIF. The dissolution rates of HPMCAS and AMC ASDs were 1.5 to 2.0-fold slower in the bicarbonate buffer than in the phosphate buffer when compared at the same buffer capacity. The dissolution profile of HPMC ASD was not affected by the buffer species. The higher the buffer capacity and ionic strength, the faster the dissolution rate of HPMCAS ASD. Conclusion: The dissolution rate of ASDs with ionizable polymers would be overestimated by using unphysiol. phosphate buffer solutions It is important to use a biorelevant bicarbonate buffer solution for dissolution testing.

Pharmaceutical Research published new progress about amorphous solid dispersion; bicarbonate; dissolution test; floating lid; phosphate; supersaturation. 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

D’Orazio, Beatrice published the artcileSurgical Sphincter Saving Approach and Topical Nifedipine for Chronic Anal Fissure with Hypertonic Internal Anal Sphincter., HPLC of Formula: 21829-25-4, the main research area is analfissure; anoplasty; fissurectomy; lidocaine; nifedipine; proctology.

PURPOSE: The role of augmented internal anal sphincter (IAS) tone in the genesis of posterior chronic anal fissure (CAPF) is still unknown. Lateral internal sphincterotomy is the most employed surgical procedure, nevertheless it is burdened by high risk post-operative anal incontinence. The aim of our study is to evaluate results of sphincter saving procedure with post-operative pharmacological sphincterotomy for patients affected by CAPF with IAS hypertonia. Methods: We enrolled 30 patients, undergone fissurectomy and anoplasty with V-Y cutaneous flap advancement; all patients received topical administration of nifedipine 0.3% and lidocaine 1.5% ointment-based therapy before and for 15 days after surgery. The primary goal was patient’s complete healing and the evaluation of incontinence and recurrence rate; the secondary goal included the evaluation of manometry parameters, symptom relief and complications related to nifedipine and lidocaine administration. Results: All wounds healed within 40 days after surgery. We didn’t observe any de novo postoperative anal incontinence case. We reported 2 cases of recurrences, healed after conservative therapy. We didn’t report any local complications related to the administration of the ointment therapy; with whom all patients reported a good compliance. Conclusions: Fissurectomy and anoplasty with V-Y cutaneous advancement flap and topical administration of nifedipine and lidocaine, is an effective treatment for CAPF with IAS hypertonia.

Chirurgia (Bucharest, Romania : 1990) published new progress about analfissure; anoplasty; fissurectomy; lidocaine; nifedipine; proctology. 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, HPLC of Formula: 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Dong, Wenping published the artcileHighly efficient UV/H2O2 technology for the removal of nifedipine antibiotics: Kinetics, co-existing anions and degradation pathways, Computed Properties of 21829-25-4, the main research area is nifedipine hydrogen peroxide UV technol.

This study investigates the degradation of nifedipine (NIF) by using a novel and highly efficient UV light combined with hydrogen peroxide (UV/H2O2). The degradation rate and degradation kinetics of NIF first increased and then remained constant as the H2O2 dose increased, and the quasi-percolation threshold was an H2O2 dose of 0.378 mmol/L. An increase in the initial pH and divalent anions (SO42- and CO32-) resulted in a linear decrease of NIF (the R2 of the initial pH, SO42- and CO32- was 0.6884, 0.9939 and 0.8589, resp.). The effect of monovalent anions was complex; Cl- and NO3- had opposite effects: low Cl- or high NO3- promoted degradation, and high Cl- or low NO3- inhibited the degradation of NIF. The degradation rate and kinetics constant of NIF via UV/H2O2 were 99.94% and 1.45569 min-1, resp., and the NIF concentration = 5 mg/L, pH = 7, the H2O2 dose = 0.52 mmol/L, T = 20°C and the reaction time = 5 min. The ·OH was the primary key reactive oxygen species (ROS) and ·O2- was the secondary key ROS. There were 11 intermediate products (P345, P329, P329-2, P315, P301, P274, P271, P241, P200, P181 and P158) and 2 degradation pathways (dehydrogenation of NIF â†?P345 â†?P274 and dehydration of NIF â†?P329 â†?P315).

PLoS One published new progress about Anions. 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

Chen, Chunfa published the artcileRelaxant action of diclofenac sodium on mouse airway smooth muscle, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is diclofenac sodium antibronchospasmic agent muscle cell relaxation respiratory disease; BK channels; airway smooth muscle; diclofenac sodium; relaxation; tracheal rings; voltage-dependent Ca2+ channels.

Diclofenac sodium (DCF) is a nonsteroidal anti-inflammatory drug (NSAID) and is widely used as an analgesic and anti-inflammatory agent. Herein, we found that DCF could relax high K+ (80 mM K+)-/ACh-precontracted tracheal rings (TRs) in mice. This study aimed to elucidate the underlying mechanisms of DCF-induced relaxations. The effects of DCF on airway smooth muscle (ASM) cells were explored using multiple biophysiol. techniques, such as isometric tension measurement and patch-clamping experiments Both high K+- and ACh-evoked contraction of TRs in mice were relaxed by DCF in a dose-dependent manner. The results of isometric tension and patch-clamping experiments demonstrated that DCFinduced relaxation in ASM cells was mediated by cytosolic free Ca2+, which was decreased via inhibition of voltage-dependent L-type Ca2+ channels (VDLCCs), nonselective cation channels (NSCCs), and Na+/Ca2+ exchange. Meanwhile, DCF also enhanced large conductance Ca2+ activated K+ (BK) channels, which led to the relaxation of ASMs. Our data demonstrated that DCF relaxed ASMs by decreasing the intracellular Ca2+ concentration via inhibition of Ca2+ influx and Na+/Ca2+ exchange. Meanwhile, the enhanced BK channels also played a role in DCF-induced relaxation in ASMs. These results suggest that DCF is a potential candidate for antibronchospasmic drugs used in treating respiratory diseases such as asthma and chronic obstructive pulmonary disease.

Frontiers in Pharmacology published new progress about Asthma. 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, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Romano, Sonia published the artcileDrug shortages in community pharmacies: Impact on patients and on the health system, COA of Formula: C17H18N2O6, the main research area is community pharmacy drug shortage health system.

Worldwide, drug shortages are a critical public health concern. Consequences range from inconvenience and distress to more serious concerns related to neg. clin., humanistic and economic outcomes. This study aimed to investigate the impact of drug shortages at the community pharmacies on patients and on the health system in Portugal. A national, cross-sectional, multicenter study was conducted in Portuguese community pharmacies during Apr. 2019. The proportion of patients reporting drug shortages, types of drugs affected and consequent economic burden to patients and the health system were estimated Regional and urban setting stratification was performed.A total of 71.1% of pharmacies participated in the study and 22,830 patient surveys were retrieved. About 52.2% of patients experienced a drug shortage in the past 12 mo; 21.5% had to see a physician to change the prescription and 5.7% declared treatment discontinuation because of this shortage. The estimated economic impact of shortages related to addnl. physician appointments varied between euro2.1-euro4.4 million for patients and euro35.3-euro43.8 million for the National Health Service. Drug shortages were mostly felt in rural and inner regions and least felt in the islands. This national study showed that community pharmacy drug shortages are a national problem with neg. consequences on patients and the health system, which need to be tackled and mitigated.

Journal of the American Pharmacists Association published new progress about Asthma. 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

Ding, Shengang published the artcileInflammatory cytokines tumour necrosis factor-α and interleukin-8 enhance airway smooth muscle contraction by increasing L-type Ca2+ channel expression, Quality Control of 21829-25-4, the main research area is TNFalpha IL8 airway smooth muscle contraction LVDCC asthma; IL-8; L-type Ca2+ channel; TNF-α; airway smooth muscle; asthma; inflammation.

Inflammation elevates intracellular calcium concentrations ([Ca2+]i) in airway smooth muscle (ASM). The L-type Ca2+ channel (L-VDCC) plays an important role in regulating Ca2+ influx in ASM. However, the role of L-VDCC in the inflammatory cytokine-induced pathol. of ASM remains unclear. In the present study, we used calcium imaging and isometric tension measurements to assess the role of L-VDCC in agonist-induced [Ca2+]i rise and the associated contractions in mouse ASM, and we used immunoblotting to identify L-VDCC protein expression levels in mouse ASM after exposure to tumor necrosis factor alpha (TNF-a) or interleukin-8 (IL-8). Our results showed that high-K+- or carbachol-induced contractions of mouse ASM were significantly greater after pretreatment with TNF-α or IL-8 for 24 h. Both verapamil and nifedipine, L-VDCC inhibitors, abolished this increased contraction induced by TNF-α or IL-8 pretreatment. Moreover, TNF-α treatment enhanced carbachol-induced Ca2+ influx in ASM cells, and this effect was abrogated by verapamil. Addnl., immunoblotting results showed that preincubation of mouse ASM with TNF-α or IL-8 also enhanced L-VDCC protein expression. On the basis of these findings, we concluded that proinflammatory cytokines, such as TNF-α and IL-8, increase the expression level of L-VDCC, which in turn contributes to augmented agonist-induced ASM contractions. This effect of inflammation on L-VDCC expression in ASM may be associated with airway hyper-responsiveness and involved in the development of asthma.

Clinical and Experimental Pharmacology and Physiology published new progress about Asthma. 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, Quality Control of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Tingle, Samuel J. published the artcileCalcium channel blockers in pancreatic cancer: increased overall survival in a retrospective cohort study, Related Products of pyridine-derivatives, the main research area is pancreatic cancer hypertension Iercanidipine amlodipine calcium channel blocker.

This retrospective cohort study aimed to translate this into the clinic by investigating the effect of CCBs on survival in pancreatic cancer. One hundred sixty-four patients with unresectable pancreatic ductal adenocarcinoma were included. Data were collected on CCB prescription, and for a range of other potentially important prognostic factors: ECOG performance status, AJCC cancer stage, chemotherapy regimen, radiotherapy, age, hypertension and sex. Participants prescribed CCB (n = 30) were more likely to be older (P = 0.004) and have hypertension (P < 0.0005); baseline demographics were otherwise similar between groups. On adjusted cox regression patients prescribed CCBs demonstrated significantly improved overall survival; hazard ratio -0.496 (0.297-0.827; P = 0.007). Performance status (P < 0.0005), tumor stage (P < 0.0005), chemotherapy regimen (P < 0.0005), radiotherapy (0.002) and age (P = 0.012) were also independent predictors of survival. The Kaplan-Meier estimated median survival was 15.3 mo for patients prescribed CCBs vs. 10.1 mo for patients not prescribed CCBs (P = 0.131). This study supports previous work suggesting CCBs may be beneficial in pancreatic cancer. Further work on larger datasets will allow for subgroup anal. delineating the effects of specific CCBs in combination with different forms of chemotherapy, paving the way for future prospective studies. Anti-Cancer Drugs published new progress about Biopsy. 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