Tag: M.W=200-350

Jeong, Heeseok published the artcilePreparation and drug release behavior of nifedipine-loaded poly(lactic acid)/polyethylene glycol microcapsules, Formula: C17H18N2O6, the main research area is nifedipine polylactic acid polyethylene glycol microcapsule drug release behavior.

Nifedipine (NF)-loaded poly(lactic acid) (PLA) and PLA/polyethylene glycol (PLA/PEG) microcapsules are synthesized using a high-speed agitator and a syringe pump with an oil-in-water emulsion-solvent evaporation technique to evaluate the effect of PLA/PEG ratio on morphol. and drug release behavior of the capsules. Fourier transform IR spectroscopy (FT-IR), differential scanning calorimeter (DSC), and X-ray diffraction (XRD) results indicate that PEG reacts successfully with PLA due to the ether bond between PEG and PLA. The drug release rate of PLA and PLA/PEG capsules increases dramatically from 0 to 5 min and then reaches a plateau within 15 to 20 min. Due to the high sp. surface area, the amount of NF released is raised by reducing the PLA concentration from 5 wt% to 2 wt%. Unlike PLA capsules, the drug release rate of PLA/PEG capsules increases due to the size effect by varying the PLA/PEG ratio from 10/0 to 6/4. Larger PLA/PEG capsules are attributed to higher amounts of encapsulated NF. The capsules show no evidence of cytotoxicity, suggesting that the PLA and PLA/PEG drug carriers are clin. safe.

Journal of Nanoscience and Nanotechnology published new progress about Cytotoxicity. 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

Haware, Rahul V. published the artcilePhysical properties and solubility studies of Nifedipine-PEG 1450/HPMCAS-HF solid dispersions, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is nifedipine polyethylene glycol 1450 hypromellose acetate succinateHF solid dispersion; Amorphization; DSC; FTIR; HPMCAS-HF; PEG 1450; PXRD; melt solvent method; nifedipine; solid dispersions; solubility.

Low-order high-energy nifedipine (NIF) solid dispersions (SDs) were generated by melt solvent amorphization with polyethylene glycol (PEG) 1450 and hypromellose acetate succinate (HPMCAS-HF) to increase NIF solubility while achieving acceptable phys. stability. HPMCAS-HF was used as a crystallization inhibitor. Individual formulation components, their phys. mixtures (PMs), and SDs were characterized by differential scanning calorimetry, powder X-ray diffraction, and Fourier transform IR spectroscopy (FTIR). NIF solubility and percent crystallinity (PC) were determined at the initial time and after 5 days stored at 25°C and 60% RH. FTIR indicated that hydrogen bonding was involved with the amorphization process. FTIR showed that NIF:HPMCAS-HF intermol. interactions were weaker than NIF:PEG 1450 interactions. NIF:PEG 1450 SD solubilities were significantly higher than their PM counterparts (p < 0.0001). The solubilities of NIF:PEG 1450:HPMCAS-HF SDs were significantly higher than their corresponding NIF:PEG 1450 SDs (p < 0.0001-0.043). All the SD solubilities showed a statistically significant decrease (p < 0.0001) after storage for 5 days. SDs PC were statistically lower than their comparable PMs (p < 0.0001). The PCs of SDs with HPMCAS-HF were significantly lower than SDs not containing only PEG 1450. All SDs exhibited a significant increase in PC (p < 0.0001-0.0089) on storage. Thermogravimetric anal. results showed that HPMCAS-HF bound water at higher temperatures than PEG 1450 (p < 0.0001-0.0039). HPMCAS-HF slowed the crystallization process of SDs, although it did not completely inhibit NIF crystal growth. Pharmaceutical Development and Technology published new progress about Amorphization. 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

Zhang, Joe Z. published the artcileEffects of Cryopreservation on Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes for Assessing Drug Safety Response Profiles, COA of Formula: C17H18N2O6, the main research area is cryopreservation human induced pluripotent stem cell cardiomyocyte; cardiac arrhythmia; cryopreservation; drug response; drug safety assessment; hiPSC-CMs; microelectrode arrays; recovery.

Burgeoning applications of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) in disease modeling, regenerative medicine, and drug screening have broadened the usage of hiPSC-CMs and entailed their long-term storage. Cryopreservation is the most common approach to store hiPSC-CMs. However, the effects of cryopreservation and recovery on hiPSC-CMs remain poorly understood. Here, we characterized the transcriptome, electro-mech. function, and drug response of fresh hiPSC-CMs without cryopreservation and recovered hiPSC-CMs from cryopreservation. We found that recovered hiPSC-CMs showed upregulation of cell cycle genes, similar or reduced contractility, Ca2+ transients, and field potential duration. When subjected to treatment of drugs that affect electrophysiol. properties, recovered hiPSC-CMs showed an altered drug response and enhanced propensity for drug-induced cardiac arrhythmic events. In conclusion, fresh and recovered hiPSC-CMs do not always show comparable mol. and physiol. properties. When cryopreserved hiPSC-CMs are used for assessing drug-induced cardiac liabilities, the altered drug sensitivity needs to be considered.

Stem Cell Reports published new progress about Cardiomyocyte. 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

Abramochkin, Denis V. published the artcileA characterization of the electrophysiological properties of the cardiomyocytes from ventricle, atrium and sinus venosus of the snake heart, Related Products of pyridine-derivatives, the main research area is acetylcholine atrium ventricle sinus venosus cardiomyocyte Python; Acetylcholine; Action potential; Heart; Ionic current; Pacemaker; Python molurus; Reptile; Sinus venosus.

A detailed description of the electrophysiol. features of cardiomyocytes in the various contractile chambers of the vertebrate heart is essential to understand the evolution of cardiac elec. activity, yet very little is known about reptiles. The present study characterizes major ionic currents (INa, ICaL, IKr, IK1 and IKACh) and action potential (AP) configuration in cardiomyocytes from the ventricle, the right atrium and the sinus venosus (SV) of Burmese pythons (Python molurus) using sharp microelectrode and patch clamp recordings. Special attention was given to SV, since it consists of myocardial cells and appears to contribute to right atrial filling in snakes. We demonstrate that most of the SV in pythons has a stable resting potential of – 82.3 ± 2.6 mV (n = 9) and lacks pacemaker activity. AP duration at 50% repolarization was similar in cells from SV and atria (350.2 ± 8.7 and 330.4 ± 17.2 ms, resp.; n = 7), but shorter than ventricular APs (557.6 ± 19.2 ms, n = 5) at 30°C. The densities of ionic currents, however, differed substantially between atrial and SV cells, where the latter had much lower densities of INa, ICaL and IKr than atrial and ventricular myocytes. IK1 in ventricle was ninefold greater than in atrial cells and 23-fold greater than in myocytes from SV. However, IKACh was absent in ventricular cells, while it was equally large in atrial and SV myocytes. Consistent with this observation, APs of atrium and SV, but not ventricle, were greatly shortened upon addition of acetylcholine (10-6 M). Thus, snake SV, right atrium and ventricle have distinct patterns of ionic currents, but the resulting elec. activity is similar in atrium and SV.

Journal of Comparative Physiology, B: Biochemical, Systems, and Environmental Physiology published new progress about Cardiomyocyte. 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

Lee, Jae-Rin published the artcileThe inhibition of chloride intracellular channel 1 enhances Ca2+ and reactive oxygen species signaling in A549 human lung cancer cells, HPLC of Formula: 21829-25-4, the main research area is lung cancer CLIC1 calcium reactive oxygen species signaling.

In this study, we investigated the function of CLIC1 in Ca2+ and ROS signaling in A549 human lung cancer cells. Depletion of CLIC1 via shRNAs in A549 cells increased DNA double-strand breaks both under control conditions and under treatment with the putative anticancer agent chelerythrine, accompanied by a concomitant increase in the p-JNK level. CLIC1 knockdown greatly increased basal ROS levels, an effect prevented by BAPTA-AM, an intracellular calcium chelator. Intracellular Ca2+ measurements clearly showed that CLIC1 knockdown significantly increased chelerythrine-induced Ca2+ signaling as well as the basal Ca2+ level in A549 cells compared to these levels in control cells. Suppression of extracellular Ca2+ restored the basal Ca2+ level in CLIC1-knockdown A549 cells relative to that in control cells, implying that CLIC1 regulates [Ca2+]i through Ca2+ entry across the plasma membrane. Consistent with this finding, the L-type Ca2+ channel (LTCC) blocker nifedipine reduced the basal Ca2+ level in CLIC1 knockdown cells to that in control cells. Taken together, our results demonstrate that CLIC1 knockdown induces an increase in the intracellular Ca2+ level via LTCC, which then triggers excessive ROS production and consequent JNK activation. Thus, CLIC1 is a key regulator of Ca2+ signaling in the control of cancer cell survival.

Experimental & Molecular Medicine published new progress about Cell membrane. 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

Takahashi, Tamayo published the artcileComponent of nicotine-induced intracellular calcium elevation mediated through α3- and α5-containing nicotinic acetylcholine receptors are regulated by cyclic AMP in SH-SY 5Y cells, Quality Control of 21829-25-4, the main research area is nicotine nAChR cyclic AMP SH SY 5Y cell.

The pathway from the medial habenular nucleus to the interpeduncular nucleus, in which nicotinic acetylcholine receptor (nAChR) including the α3 and α5 subunits (α3 * and α5 * nAChRs) are expressed, is implicated in nicotine dependence. We investigated whether α3 * and α5 * nAChRs are regulated by cAMP using SH-SY5Y cells to clarify the significance of these receptors in nicotine dependence. We analyzed the nicotine-induced elevation of intracellular Ca2+ ([Ca2+]i). Nicotine induces a concentration-dependent increase in [Ca2+]i. The elimination of Ca2+ from extracellular fluid or intracellular stores demonstrated that the nicotine-induced [Ca2+]i elevation was due to extracellular influx and intracellular mobilization. The effects of tubocurarine on nicotine-induced [Ca2+]i elevation and current suggest that intracellular mobilization is caused by plasma membrane-permeating nicotine. The inhibition of α3 *, α5 *, α7 nAChR and voltage-gated Ca2+ channels by using siRNAs and selective antagonists revealed the involvement of these nAChR subunits and channels in nicotine-induced [Ca2+]i elevation. To distinguish and characterize the α3 * and α5 * nAChR-mediated Ca2+ influx, we measured the [Ca2+]i elevation induced by nonmembrane-permeating acetylcholine when muscarinic receptors, α7nAChR and Ca2+ channels were blocked. Under this condition, the [Ca2+]i elevation was significantly inhibited with a 48-h treatment of dibutyryl cAMP, which was accompanied by the downregulation of α3 and β4 mRNA. These findings suggest that α3 * and α5 * nAChR-mediated Ca2+ influx is possibly regulated by cAMP at the transcriptional level.

PLoS One published new progress about Cell membrane. 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

Xu, Lu published the artcilePLA-PEG Micelles Loaded with a Classic Vasodilator for Oxidative Cataract Prevention, Application In Synthesis of 21829-25-4, the main research area is polylactic acid PEG micelle nifedipine cataract eye; calcium channel blocker; cataract treatment; eye drop; micelles; oxidative stress.

The only treatment for cataract in clinic is the clouded lens removal combined with artificial lens implantation. In this study, nifedipine (NFP), a classic vasodilator, was loaded in a U.S. FDA-approved polymer PLA-PEG to form NFP-loaded PLA-PEG micelles as a novel eye drop to prevent oxidative cataract formation and progression at the early stage. The NFP-loaded PLA-PEG micelles not only showed satisfactory biocompatibility and bioavailability, but also efficiently improved the anticataract ability through the inhibition of extracellular calcium ions influx. This study may provide a new insight into the development of cataract treatment.

ACS Biomaterials Science & Engineering published new progress about Antioxidants. 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

Oraebosi, M. I. published the artcileDiurnal efficacy of alpha-lipoic acid/nifedipine/glimepiride combination mitigates diabetic neuropathies in rats, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is diabetic neuropathy nifedipine glimepiride; Acide alpha-lipoïque; Alpha-lipoic acid; Circadian rhythm; Diabetic neuropathies; Glimepiride; Glimépiride; Neuropathies diabétiques; Nifedipine; Nifédipine; Rythme circadien.

Time-dependent effects of alpha-lipoic acid/nifedipine/glimepiride combination on diabetic neuropathies were investigated in rats. 7 groups (n = 9) of rats were used.First and second groups were apparently normal and diabetic rats resp., and were administered 1 mL/kg distilled water. The rest of the groups were diabetic and administered 10 mg/kg glimepiride at night-time (8:00 pm). Groups 4-7 were administered addnl. 20 mg/kg nifedipine at morning-time (8:00 am), while groups 5-7 were also administered 100 mg/kg alpha-lipoic acid (ALA) in the morning, afternoon and night-time resp. (8:00 am, 2:00 pm and 8:00 pm). During the 28 days of oral treatment, paw pressure, tail immersion and motor coordination tests were conducted. The rats were euthanized on the 29th day after a charcoal meal. The small intestines were excised to determine intestinal transit while the brain was collected, homogenised and used to determine levels of oxidative stress.Data show that treatment with ALA at 8:00 am or 2:00 pm significantly (P ≤ 0.01) produced a delay in the onset and improved prognosis of neuropathies. Treatment with ALA at 8:00 pm prevented manifestation of neuropathies throughout the study with pos. antioxidant effects.Time-dependent ALA treatment in combination with nifedipine and glimepiride should be studied in humans with an approx. similar circadian timing. This may provide addnl. clin. therapeutic options for diabetic neuropathies.

Annales Pharmaceutiques Francaises published new progress about Antioxidants. 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

Oraebosi, Michael Ikechukwu published the artcileChronopharmacology of the alpha-lipoic acid/nifedipine/glimepiride combination in the amelioration of retinopathy in rats, Related Products of pyridine-derivatives, the main research area is nifedipine glimepiride antioxidant diabetic retinopathy; Chronopharmacolgy; alpha-lipoic acid; diabetic retinopathy; diurnal variation; glimepiride; nifedipine.

Time of drug administration affects both the kinetics and dynamics of medications. This study investigated diurnal efficacy of alpha-lipoic acid (ALA), nifedipine, and glimepiride combination in the treatment of diabetic retinopathy. The study design comprised seven groups of rats, with groups 1 and 2 serving as non-diabetic and diabetic controls, resp., receiving 1 mL/kg distilled water. All other groups were diabetic, and received 10 mg/kg glimepiride at 20:00 h. Groups 4-7 also received 20 mg/kg nifedipine at 08:00 h. In addition, groups 5-7 received 100 mg/kg ALA at 08:00 h, 14:00 h, and 20:00 h, resp. Oral drug administration was for 28 days during which fasting and random blood glucose sampling were done weekly at 07:30 h and 13:30 h, resp. On the 29th day, rats were euthanized; blood was collected via the jugular veins for determination of serum ocular markers like magnesium, cholesterol, and triglyceride. Furthermore, the eyes were excised and their relative organ/body weight ratios determined The right eyes were persevered in phosphate buffer for homogenization and determination of retina antioxidant profile (MDA, SOD, CAT, GSH), while the left eyes were preserved in formalin for histol. examination Results showed that treatment with ALA and glimepiride at 20:00 h along with nifedipine at 08:00 h resulted in better prognosis than other treatment groups and with improved glycemic control. Also, all their serum markers for retinopathy, organ weight, and histol. did not differ significantly from that of the non-diabetic rats. Findings imply that diurnal efficacy in alpha-lipoic acid, nifedipine and glimepiride combination ameliorates diabetic retinopathy in rats and may be beneficial in the treatment of diabetic retinopathy.

Chronobiology International published new progress about Antioxidants. 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

Wang, Zhangting published the artcileLiquorice extract and 18β-glycyrrhetinic acid protect against experimental pyrrolizidine alkaloid-induced hepatotoxicity in rats through inhibiting cytochrome P450-mediated metabolic activation, Quality Control of 21829-25-4, the main research area is nifidepine glycyrrhetinic acid hepatoprotectant CYP450 liver injury; 18β-glycyrrhetinic acid; competitive inhibition; cytochrome P450; metabolic activation; pyrrolizidine alkaloid.

Misuse of pyrrolizidine alkaloid (PA)-containing plants or consumption of PA-contaminated foodstuffs causes numerous poisoning cases in humans yearly, while effective therapeutic strategies are still limited. PA-induced liver injury was initiated by cytochrome P 450 (CYP)- mediated metabolic activation and subsequent formation of adducts with cellular proteins. Liquorice, a hepato-protective herbal medicine, is commonly used concurrently with PA-containing herbs in many compound traditional Chinese medicine formulas, and no PA-poisoning cases have been reported with this combination. The present study aimed to investigate hepato-protective effects of liquorice aqueous extract (EX) and 18β-glycyrrhetinic acid (GA, the primary bioactive constituent of liquorice) against PA-induced hepatotoxicity and the underlying mechanism. Histopathol. and biochem. anal. demonstrated that both single- and multiple-treatment of EX (500 mg/kg) or GA (50mg/kg) significantly attenuated liver damage caused by retrorsine (RTS, a representative hepatotoxic PA). The formation of pyrrole-protein adducts was significantly reduced by single- (30.3% reduction in liver; 50.8% reduction in plasma) and multiple- (32.5% reduction in liver; 56.5% reduction in plasma) treatment of GA in rats. Single- and multiple-treatment of EX also decreased the formation of pyrrole-protein adducts, with 30.2 and 31.1% reduction in rat liver and 51.8 and 53.1% reduction in rat plasma, resp. In addition, in vitro metabolism assay with rat liver microsomes demonstrated that GA reduced the formation of metabolic activation-derived pyrrole-glutathione conjugate in a dose-dependent manner with the estimated IC50 value of 5.07μM. Further mechanism study showed that GA inhibited activities of CYPs, especially CYP3A1, the major CYP isoform responsible for the metabolic activation of RTS in rats. Enzymic kinetic study revealed a competitive inhibition of rat CYP3A1 by GA. In conclusion, our findings demonstrated that both EX and GA exhibited significant hepato-protective effects against RTS-induced hepatotoxicity, mainly through the competitive inhibition of CYP-mediated metabolic activation of RTS.

Frontiers in Pharmacology published new progress about Detoxification. 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