Month: December 2022

El Sayed, Mira published the artcileImpact of Simulated Intestinal Fluids on Dissolution, Solution Chemistry, and Membrane Transport of Amorphous Multidrug Formulations, Application In Synthesis of 72509-76-3, the main research area is multidrug formulation dissolution solubility membrane transport simulated intestinal fluid; FaSSIF; amorphous; fixed dose combination; flux; membrane transport; multidrug formulations; solubility; supersaturation.

The solution behavior and membrane transport of multidrug formulations were herein investigated in a biorelevant medium simulating fasted conditions. Amorphous multidrug formulations were prepared by the solvent evaporation method. Combinations of atazanavir (ATV) and ritonavir (RTV) and felodipine (FDN) and indapamide (IPM) were prepared and stabilized by a polymer for studying their dissolution (under non-sink conditions) and membrane transport in fasted state simulated intestinal fluid (FaSSIF). The micellar solubilization by FaSSIF enhanced the amorphous solubility of the drugs to different extents. Similar to buffer, the maximum achievable concentration of drugs in combination was reduced in FaSSIF, but the extent of reduction was affected by the degree of FaSSIF solubilization. Dissolution studies of ATV and IPM revealed that the amorphous solubility of these two drugs was not affected by FaSSIF solubilization. In contrast, RTV was significantly affected by FaSSIF solubilization with a 30% reduction in the maximum achievable concentration upon combination to ATV, compared to 50% reduction in buffer. This pos. deviation by FaSSIF solubilization was not reflected in the mass transport-time profiles. Interestingly, FDN concentrations remain constant until the amount of IPM added was over 1000 μg/mL. No decrease in the membrane transport of FDN was observed for a 1:1 M ratio of FDN-IPM combination. This study demonstrates the importance of studying amorphous multidrug formulations under physiol. relevant conditions to obtain insights into the performance of these formulations after oral administration.

Molecular Pharmaceutics published new progress about Amorphization. 72509-76-3 belongs to class pyridine-derivatives, name is 3-Ethyl 5-methyl 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C18H19Cl2NO4, Application In Synthesis of 72509-76-3.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Zhao, Xiao-Heng published the artcileTopical application of phenytoin or nifedipine-loaded PLGA microspheres promotes periodontal regeneration in vivo, Product Details of C17H18N2O6, the main research area is phenytoin nifedipine loaded PLGA microsphere topical application periodontal regeneration; Alveolar bone loss; Anti-epileptics; Bone remodeling; Drug delivery; Gingival overgrowth.

Gingival recession and alveolar bone loss are common manifestations of periodontitis. Periodontal regeneration is the ideal strategy for rehabilitating periodontal tissue defects and preventing tooth loss. The present study examined whether localized, topical application of gingival overgrowth-inducing drugs, phenytoin, nifedipine or cyclosporine, induces periodontal regeneration. Polylactic-co-glycolic acid (PLGA) was used as the carrier for preparation of phenytoin, nifedipine or cyclosporine-loaded PLGA microspheres, using an oil-in-water emulsification technique. The drug-loaded microspheres were delivered to periodontal defects created on alveolar ridges mesial to the first maxillary molars of Sprague-Dawley rats. After eight weeks, the operation area in each rat, including the maxillary molars and periodontal tissues, was harvested and evaluated by micro-computed tomog., histochem. and immunohistochem. analyzes. Phys. parameters representative of periodontal regeneration, including the length of new alveolar bone (p < 0.01) and the area of new alveolar bone (p < 0.01) were significantly improved in the phenytoin group. Compared to other groups, the phenytoin group demonstrated increased expression of COL-1, VEGF-A, osteoblast and osteoclast markers (BMP-2, TGF-β1, OCN and TRAP staining), as well as decreased expression of MMP-8. Results of the present study provided new evidence that localized, controlled release of phenytoin confers therapeutic benefits toward gingival recession and alveolar bone loss. Phenytoin appears to be a promising drug that promotes periodontal regeneration. Archives of Oral Biology published new progress about Alveolar bone. 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

Lee, Minjin published the artcileProminence of the tropics in the recent rise of global nitrogen pollution, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is nitrogen air pollution tropics.

Nitrogen (N) pollution is shaped by multiple processes, the combined effects of which remain uncertain, particularly in the tropics. We use a global land biosphere model to analyze historical terrestrial-freshwater N budgets, considering the effects of anthropogenic N inputs, atm. CO2, land use, and climate. We estimate that globally, land currently sequesters 11 (10-13)% of annual N inputs. Some river basins, however, sequester >50% of their N inputs, buffering coastal waters against eutrophication and society against greenhouse gas-induced warming. Other basins, releasing >25% more than they receive, are mostly located in the tropics, where recent deforestation, agricultural intensification, and/or exports of land N storage can create large N pollution sources. The tropics produce 56 ± 6% of global land N pollution despite covering only 34% of global land area and receiving far lower amounts of fertilizers than the extratropics. Tropical land use should thus be thoroughly considered in managing global N pollution.

Nature Communications published new progress about Air pollution. 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

Kang, Shenghong published the artcileDesign, synthesis and insecticidal activities of novel acetamido derivatives containing N-pyridylpyrazole carboxamides, Recommanded Product: 2-Chloro-4-methylpyridin-3-amine, the main research area is pyridylpyrazole derivative insecticide; (1)H NMR; (13)C NMR; ADGUQHZGKCFXFF-UHFFFAOYSA-N; AXTBANQNGCQWIH-UHFFFAOYSA-N; Acetamido derivatives; BGRHXOCUOGKOFF-UHFFFAOYSA-N; CCAIWWICQJIRNT-UHFFFAOYSA-N; FVDHIDBTYNAYHU-UHFFFAOYSA-N; HKMJJZJSINSUJI-UHFFFAOYSA-N; HODOGMBBFHOUOU-UHFFFAOYSA-N; HWFBXXMWALNJFJ-UHFFFAOYSA-N; IR; Insecticidal activity; JUCFHZIFBCHESQ-UHFFFAOYSA-N; KBIDVIJRCFEWPJ-UHFFFAOYSA-N; LC(50); LHDALURNYHPVBP-UHFFFAOYSA-N; MESJBVRMCYELSC-UHFFFAOYSA-N; N-pyridylpyrazole carboxamides; P. xylostella; PZPPOKUDKNZEPN-UHFFFAOYSA-N; Plutella xylostella; QIGAGLVKQMVUIW-UHFFFAOYSA-N; RUYMOGKRZCUDBX-UHFFFAOYSA-N; SAR; SMDGKMMSFKFABF-UHFFFAOYSA-N; Synthesis; UUQTUDLAQCJRLR-UHFFFAOYSA-N; WAQJLNODBHIJBL-UHFFFAOYSA-N; WFPFPTZXYSLGKU-UHFFFAOYSA-N; WNIMVUTWILZLSB-UHFFFAOYSA-N; WSFNQGLZXUQPCR-UHFFFAOYSA-N; YUTGLCZQUUBWPD-UHFFFAOYSA-N; ZGBYCDKJPMXJQG-UHFFFAOYSA-N; carbon nuclear magnetic resonance; infrared; median lethal concentration; melting point; mp; proton nuclear magnetic resonance; structure–activity relationship.

A series of novel acetamido derivatives containing N-pyridylpyrazole carboxamides was designed and synthesized by increasing the amide bridge of chlorantraniliprole using acetamido moieties and introducing different aryl substitutions. The target compounds were characterized by 1H NMR, 13C NMR, IR, and elemental anal. Bioassays indicated that some of the synthesized compounds exhibited strong insecticidal activity against Plutella xylostella. Compounds I (R = 2,6-Cl2-4-CF3Ph, 2-NO2Ph or 2-Cl-4-Me-pyridin-3-yl) were the most potent, with LC50 values of 23.72, 2.04, and 20.01 mg/L, resp. The insecticidal activity of compound I (R- 2-NO2Ph) was higher than that of chlorpyrifos (LC50 = 7.25 mg/L), a commonly used insecticide. These results indicate that novel acetamido derivatives containing N-pyridylpyrazole carboxamides can effectively control P. xylostella.

European Journal of Medicinal Chemistry published new progress about Agrochemicals. 133627-45-9 belongs to class pyridine-derivatives, name is 2-Chloro-4-methylpyridin-3-amine, and the molecular formula is C6H7ClN2, Recommanded Product: 2-Chloro-4-methylpyridin-3-amine.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Kashanian, Maryam published the artcileA comparative study on the efficacy of nifedipine and indomethacin for prevention of preterm birth as monotherapy and combination therapy: a randomized clinical trial, Product Details of C17H18N2O6, the main research area is preterm birth nifedipine indomethacin monotherapy combination therapy; Indomethacin; nifedipine; pregnancy; preterm delivery; preterm labor.

Preterm delivery is an important issue in obstetrics, which is the most common cause of neonatal mortality and morbidity. Therefore, finding a way to prevent it is always under serious concern. The study aimed to compare the efficacy of two tocolytic agents, nifedipine and indomethacin, for inhibiting preterm uterine contractions as monotherapy and combination therapy. A double-blind randomized clin. trial was performed on pregnant women with gestational age of 26-34 wk of pregnancy who referred to hospital for preterm labor. They were randomly assigned to three groups. Indomethacin plus placebo, nifedipine plus placebo, and a combination of indomethacin and nifedipine were administered to the three groups. Inhibiting contractions for 2 h and prevention of delivery for 48 h and 7 days were evaluated. Also, duration of pregnancy, the number of preterm births, and the interval between entering the study and delivery were compared between three groups. One hundred fifty women were eligible for the study. Two women in the nifedipine group and one woman in the combined group were excluded from the study because of hypotension. The women of the three groups did not have significant difference according to age, BMI, gravidity, parity, Bishop score, gestational age, and the number of contractions at entering the study. Thirty-six women (72%) in the indomethacin group, 36 women (72%) in the nifedipine group, and 41 women (89.4%) in the combination group had stopped contractions within the first 2 h of intervention (p = .002). Inhibiting contractions for 48 h (p = .003), inhibiting contractions for 7 days (p = .021), gestational age at birth (p = .001), number of pregnancies more than 37 wk (p = .007), and neonatal weight (p = .020) were significantly more in the combination group. Combination therapy with nifedipine and indomethacin was more effective than monotherapy with either of these two medications for inhibiting preterm labor, delaying delivery, and prolongation of the duration of pregnancy.

Journal of Maternal-Fetal & Neonatal Medicine published new progress about Aging, animal. 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

Arias-Cavieres, Alejandra published the artcileIntermittent Hypoxia causes targeted disruption to NMDA receptor dependent synaptic plasticity in area CA1 of the hippocampus, Formula: C17H18N2O6, the main research area is intermittent hypoxia NMDA receptor synaptic plasticity CA1 hippocampus; Hippocampus; Long term depression; Long term potentiation; Oxidative stress; Sleep apnea.

Changed NMDA receptor (NMDAr) physiol. is implicated with cognitive deficit resulting from conditions ranging from normal aging to neurol. disease. Using intermittent hypoxia (IH) to exptl. model untreated sleep apnea, a clin. condition whose comorbidities include neurocognitive impairment, we recently demonstrated that IH causes a pro-oxidant condition that contributes to deficits in spatial memory and in NMDAr-dependent long-term potentiation (LTP). However, the impact of IH on addnl. forms of synaptic plasticity remains ill-defined. Here we show that IH prevents the induction of NMDAr-dependent LTP and long-term depression (LTD) in hippocampal brain slices from mice exposed to ten days of IH (IH10) yet spares NMDAr-independent forms of synaptic plasticity. Deficits in synaptic plasticity were accompanied by a reduction in hippocampal GluN1 expression. Acute manipulation of redox state using the reducing agent, Dithiothreitol (DTT) stimulated the NMDAr-dependent fEPSP following IH10. However, acute use of either DTT or MnTMPyP did not restore NMDAr-dependent synaptic plasticity after IH10 or prevent the IH-dependent reduction in GluN1, the obligatory subunit of the NMDAr. In contrast, MnTMPyP during IH10 (10-MnTMPyP), prevented the suppressive effects of IH on both NMDAr-dependent synaptic plasticity and GluN1 expression. These findings indicate that while the IH-dependent pro-oxidant state causes reversible oxidative neuromodulation of NMDAr activity, acute manipulation of redox state is ineffective in rescuing two key effects of IH related to the NMDAr within the hippocampus. These IH-dependent changes associated with the NMDAr may be a primary avenue by which IH enhances the vulnerability to impaired learning and memory when sleep apnea is left untreated in normal aging and in disease.

Experimental Neurology published new progress about Aging, animal. 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, Formula: C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Wang, Yangui published the artcileEffects of metoprolol, methyldopa, and nifedipine on endothelial progenitor cells in patients with gestational hypertension and preeclampsia, Computed Properties of 21829-25-4, the main research area is gestational hypertension preeclampsia endothelial progenitor cell metoprolol methyldopa nifedipine; antihypertensive drugs; endothelial progenitor cells; gestational hypertension; preeclampsia.

We aimed to determine the possible effects of antihypertensive drugs, such as metoprolol, methyldopa, and nifedipine, on EPC number and functions in patients with gestational hypertension and preeclampsia. We collected blood samples from 30 normal pregnant women, 67 patients with gestational hypertension and 48 patients with preeclampsia. The patients received no drug or an antihypertensive drug, such as metoprolol, methyldopa, or nifedipine, between 20 and 24 wk of gestation. The number of EPCs and circulating endothelial cells (CECs) in the blood was measured by flow cytometry. Moreover, colony formation and migration assays were performed on the isolated EPCs. Both the systolic and diastolic blood pressure (BP) increased, while the percentage of flow-mediated vasodilatation (FMD) decreased in patients with gestational hypertension and preeclampsia, compared to the healthy controls at 20 wk of gestation. CEC number increased in the patients, whereas EPC counts decreased. Furthermore, EPC colony formation and migration abilities were also impaired in the patients. However, administration of metoprolol, methyldopa, or nifedipine effectively restored the systolic and diastolic BP, FMD%, EPCs, and CEC numbers, as well as EPC migration capacity. Endothelial progenitor cells colony formation ability selectively improved with methyldopa and nifedipine. In patients receiving no drugs, most of these indexes worsened within 4 wk (study duration).

Clinical and Experimental Pharmacology and Physiology published new progress about Aging, animal. 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

Fu, Edouard L. published the artcileComparative Effectiveness of Renin-Angiotensin System Inhibitors and Calcium Channel Blockers in Individuals With Advanced CKD: A Nationwide Observational Cohort Study, Synthetic Route of 72509-76-3, the main research area is RAS inhibitor calcium channel blocker chronic kidney disease; Angiotensin-converting enzyme inhibitors (ACEi); CKD progression; advanced CKD; amlodipine; angiotensin receptor blockers (ARB); antihypertensive; calcium channel blockers (CCB); chronic kidney disease (CKD); comparative effectiveness; enalapril; end-stage kidney disease (ESKD); major adverse cardiovascular events (MACE); mortality; renoprotection.

It is unknown whether initiating renin-angiotensin system (RAS) inhibitor therapy in patients with advanced chronic kidney disease (CKD) is superior to alternative antihypertensive agents such as calcium channel blockers (CCBs). We compared the risks for kidney replacement therapy (KRT), mortality, and major adverse cardiovascular events (MACE) in patients with advanced CKD in routine nephrol. practice who were initiating either RAS inhibitor or CCB therapy. Observational study in the Swedish Renal Registry, 2007 to 2017.2,458 new users of RAS inhibitors and 2,345 CCB users with estimated glomerular filtration rates < 30 mL/min/1.73 m2 (CKD G4-G5 without KRT) who were being followed up by a nephrologist. As a pos. control cohort, new users of the same drugs with CKD G3 (estimated glomerular filtration rate, 30-60 mL/min/1.73 m2) were evaluated. RAS inhibitor vs. CCB therapy initiation. Initiation of KRT (maintenance dialysis or transplantation), all-cause mortality, and MACE (composite of cardiovascular death, myocardial infarction, or stroke). HRs with 95% CIs were estimated using propensity score-weighted Cox proportional hazards regression adjusting for demog., clin., and laboratory covariates. Median age was 74 years, 38% were women, and median follow-up was 4.1 years. After propensity score weighting, there was significantly lower risk for KRT after new use of RAS inhibitors compared with new use of CCBs (adjusted HR, 0.79 [95% CI, 0.69-0.89]) but similar risks for mortality (adjusted HR, 0.97 [95% CI, 0.88-1.07]) and MACE (adjusted HR, 1.00 [95% CI, 0.88-1.15]). Results were consistent across subgroups and in as-treated analyses. The pos. control cohort of patients with CKD G3 showed similar KRT risk reduction (adjusted HR, 0.67 [95% CI, 0.56-0.80]) with RAS inhibitor therapy compared with CCBs. Potential confounding by indication. Our findings provide evidence from real-world clin. practice that initiation of RAS inhibitor therapy compared with CCBs may confer kidney benefits among patients with advanced CKD, with similar cardiovascular protection. American Journal of Kidney Diseases published new progress about Aging, animal. 72509-76-3 belongs to class pyridine-derivatives, name is 3-Ethyl 5-methyl 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C18H19Cl2NO4, Synthetic Route of 72509-76-3.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Wicher, Sarah A. published the artcileAging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle, Product Details of C17H18N2O6, the main research area is calcium signaling ECM deposition human airway smooth muscle aging.

Lung function declines as people age and their lungs become stiffer. With an increasing elderly population, understanding mechanisms that contribute to these structural and functional changes in the aging lung is important. Part of the aging process is characterized by thicker, more fibrotic airways, and senile emphysema caused by changes in lung parenchyma. There is also senescence, which occurs throughout the body with aging. Here, using human airway smooth muscle (ASM) cells from patients in different age groups, we explored senescence pathways and changes in intracellular calcium signaling and extracellular matrix (ECM) deposition to elucidate potential mechanisms by which aging leads to thicker and stiffer lungs. Senescent markers p21, δH2AX, and β -gal, and some senescence-associated secretory proteins (SASP) increased with aging, as shown by staining and biochem. analyses. Agonist-induced intracellular Ca2+ responses, measured using fura-2 loaded cells and fluorescence imaging, increased with age. However, biochem. anal. showed that expression of the following markers decreased with age: M3 muscarinic receptor, TRPC3, Orai1, STIM1, SERCA2, MMP2 and MMP9. In contrast, collagen III, and fibronectin deposition increased with age. These data show that senescence increases in the aging airways that is associated with a stiffer but surprisingly greater intracellular calcium signaling as a marker for contractility. ASM senescence may enhance fibrosis in a feed forward loop promoting remodeling and altered calcium storage and buffering.

PLoS One published new progress about Aging, animal. 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

Lazcano-Perez, Fernando published the artcileA Sea Anemone Lebrunia neglecta Venom Fraction Decreases Boar Sperm Cells Capacitation: Possible Involvement of HVA Calcium Channels, Product Details of C17H18N2O6, the main research area is Lebrunia venom calcium channel boar sperm cell capacitation; HVA calcium channels; Lebrunia neglecta; boar sperm; capacitation; chromaffin cells; sea anemone.

Sea anemones produce venoms characterized by a complex mixture of low mol. weight compounds, proteins and peptides acting on voltage-gated ion channels. Mammal sperm cells, like neurons, are characterized by their ion channels. Calcium channels seem to be implicated in pivotal roles such as motility and capacitation. In this study, we evaluated the effect of a low mol. weight fraction from the venom of the sea anemone Lebrunia neglecta on boar sperm cells and in HVA calcium channels from rat chromaffin cells. Spermatozoa viability seemed unaffected by the fraction whereas motility and sperm capacitation were notoriously impaired. The sea anemone fraction inhibited the HVA calcium current with partial recovery and no changes in chromaffin cells’ current kinetics and current-voltage relationship. These findings might be relevant to the pharmacol. characterization of cnidarian venoms and toxins on voltage-gated calcium channels.

Toxins published new progress about Agglutination. 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