Category: 21829-25-4

Mahajan, Abhishek published the artcileInterplay mechanisms between progesterone and endocannabinoid receptors in regulating bull sperm capacitation and acrosome reaction, Synthetic Route of 21829-25-4, the publication is Journal of Cellular Physiology (2022), 237(7), 2888-2912, database is CAplus and MEDLINE.

After ejaculation, sperm show a limited capacity for transcription and translation. In the oviduct, most of the signalling in sperm is nongenomic and is mediated through membrane receptors. Studies have shown that the cation channel of sperm (CatSper), cAMP, cGMP, protein kinases, and tyrosine phosphorylation are involved in the nongenomic signalling of progesterone (P4) in sperm. However, it is not known whether there is an interplay between P4 and cannabinoid receptors 1 and 2 (CB1 and CB2), transient receptor potential vanilloid 1 (TRPV1), CatSper channels, cAMP, inositol trisphosphate receptor (IP3R), and mitogen-activated protein kinase (MAPK); these potential regulators are involved in the regulation of capacitation and the acrosome reaction. In the present study, selective blockers of CB1, CB2, TRPV1, CatSper channels, cAMP, protein kinase A (PKA), IP3R, and MAPK were used to identify their involvement in P4-mediated bull sperm capacitation and the acrosome reaction. Selective blocking of any one of the mols. caused a significant reduction in P4 signalling (p < 0.05). Interestingly, blocking these mols. in combination followed by treatment with P4 resulted in the complete absence of capacitation and the acrosome reaction. Blocking a single receptor was not able to eliminate the P4-induced capacitation and the acrosome reaction. In addition to the CB1 and CB2 receptors, there may be other signalling pathways that mediate P4 signalling. In conclusion, P4 signalling exhibited interplay with the cannabinoid receptors. The regulation of sperm capacitation and the acrosome reaction also involved cAMP, PKA, L-type and T-type calcium channels, TRPV1, inositol trisphosphate, and MAPK.

Journal of Cellular Physiology published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Cheng, Ivy published the artcileEffects of pharmacological agents for neurogenic oropharyngeal dysphagia: A systematic review and meta-analysis, Related Products of pyridine-derivatives, the publication is Neurogastroenterology & Motility (2022), 34(3), e14220, database is CAplus and MEDLINE.

This systematic review and meta-anal. aimed to evaluate the effects of pharmacol. agents for neurogenic oropharyngeal dysphagia based on evidence from randomized controlled trials (RCTs). Electronic databases were systematically searched between Jan. 1970 and March 2021. Two reviewers independently extracted and synthesized the data. The outcome measure was changed in (any) relevant clin. swallowing-related characteristics. Data from 2186 dysphagic patients were collected from 14 RCT studies across a range of pharmacotherapies. The pooled effect size of transient receptor potential (TRP) channel agonists was large compared to placebo interventions (SMD[95%CI] =1.27[0.74,1.80], p < 0.001; I2 = 79%). Data were limited for other pharmacol. agents and the overall pooled effect size of these agents was non-significant (SMD [95% CI] =0.25 [-0.24, 0.73]; p = 0.31; I2 = 85%). When analyzed sep., large effect sizes were observed with Nifedipine (SMD[95%CI] =1.13[0.09,2.18]; p = 0.03) and Metoclopramide (SMD[95%CI] =1.68[1.08,2.27]; p < 0.001). By contrast, the effects of angiotensin-converting enzyme (ACE) inhibitors (SMD[95%CI] = -0.67[-2.32,0.99]; p = 0.43; I2 = 61%), Physostigmine (SMD[95%CI] = -0.05[-1.03,0.93]; p = 0.92) and Glyceryl Trinitrate (GTN) (SMD [95% CI] = -0.01 [-0.11, 0.08]; p = 0.78) were non-significant. Within stroke patients, subgroup anal. showed that TRP channel agonists had a moderate pooled effect size (SMD[95%CI] =0.74[0.10,1.39]; p = 0.02; I2 = 82%) whereas the effects of other agents were non-significant (SMD[95%CI] =0.40[-0.04,0.84]; p = 0.07; I2 = 87%). Our results showed that TRP channel agonists, Nifedipine and Metoclopromide may be beneficial for neurogenic dysphagic patients. Large scale, multicenter clin. trials are warranted to fully explore their therapeutic effects on swallowing.

Neurogastroenterology & Motility published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Anant, Arjun published the artcileAn analytical review for the estimation of montelukast sodium, Related Products of pyridine-derivatives, the publication is Separation Science plus (2022), 5(5), 120-137, database is CAplus.

A review. Montelukast is a highly potent and selective receptor antagonist of cysteinyl leukotrienes (CysLT1) used in chronic asthma and vasoconstriction reduction and also used in allergies, swelling, hay fever, and shortness of breath. For the measurement of montelukast sodium in biol. and pharmaceutical samples, there are different asynchronous and concurrent anal. methods, such as high-performance thin layer chromatog., UV spectroscopy, capillary electrophoresis, high-performance liquid chromatog., and liquid chromatog.-mass spectrometry, have been developed. The pathogenesis of asthma, mechanism of action, and various anal. methods for the detection of montelukast sodium and its combination of dosage forms and biol. samples have been described in the present review. Ranjan et al. suggested the reverse phase high-performance liquid chromatog. approach for estimating montelukast in rabbit plasma and found the best limit of detection result of 1.0 ng/mL. Ezzeldin et al. developed a liquid chromatog. with tandem mass spectrometry system for the simultaneous detection of combinations of montelukast, gliclazide, and nifedipine. The authors conclude that the studies described in the present manuscript will assist researchers in choosing a simple, rapid, and responsive method for the anal. of montelukast sodium and its combinations.

Separation Science plus published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Narimani, Saeedeh published the artcileMicrowave-assisted facile synthesis of N, P co-doped fluorescent carbon dot probe for the determination of nifedipine., Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Analytical sciences : the international journal of the Japan Society for Analytical Chemistry (2022), 38(2), 393-399, database is MEDLINE.

A simple and fast microwave synthesis method was applied for the preparation of several carbon dots (CDs) from various combinations of urea, phosphoric acid, and B-alanine as nitrogen, phosphorus, and carbon precursors. The maximum quantum yield (44%) was obtained for nitrogen and phosphorus co-doped carbon dots (N, P-CDs) prepared from urea, B-alanine, and phosphoric acid. Furthermore, N, P-CDs were exploited to synthesize a simple and sensitive fluorometric probe to determine nifedipine (NFD). We determined that the analytical response of the designed sensor could be affected by the kind of dopant and synthesis precursors. It is worth mentioning that the fluorescence intensity of N, P-CDs was weakened by NFD, and no fluorescence quenching was observed for other prepared CDs. The NFD-developed sensor demonstrated a linear response range of 3.3 ×â€?0^-8-3.2 ×â€?0^-5 mol/L, with the detection limit of 1.0 ×â€?0^-8 mol/L. The sensor was successfully applied to measure NFD in human biological fluids.

Analytical sciences : the international journal of the Japan Society for Analytical Chemistry published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Saraf, Isha published the artcileForced Solid-State Oxidation Studies of Nifedipine-PVP Amorphous Solid Dispersion, Computed Properties of 21829-25-4, the publication is Molecular Pharmaceutics (2022), 19(2), 568-583, database is CAplus and MEDLINE.

In the present study, the oxidative degradation behavior of nifedipine (NIF) in amorphous solid dispersions (ASDs) prepared with poly(vinyl pyrrolidone) (PVP) with a short (K30) and a long (K90) chain length was investigated. The ASDs were prepared via dry ball-milling and analyzed using Fourier transform IR (IR) spectroscopy, X-ray scattering, and differential scanning calorimetry. The ASDs were exposed to accelerated thermal-oxidative conditions using a pressurized oxygen headspace (120 °C for 1 day) and high temperatures at atm. pressure (60-120 °C for a period of 42 days). Addnl., solution-state oxidative degradation studies showed that pure NIF degrades to a greater extent than in the presence of PVP. Electronic structure calculations were performed to understand the impact of drug-polymer intermol. interactions on the autoxidation of drugs. While no drug degradation was observed in freshly prepared ASD samples, alkyl free radicals were detected via ESR (EPR) spectroscopy. The free radicals were found to be consumed to a greater extent by PVP K30- than PVP K90-based ASDs upon exposure to high oxygen pressures. This was consistent with the greater solid-state oxidative degradation of NIF observed in ASDs with PVP K30 than with PVP K90. As no drug recrystallization occurred during this study period, the lower glass-transition temperature and presumed greater mol. mobility of PVP K30 and its ASD as compared to the PVP K90 system appear to contribute to the greater drug degradation in PVP-K30-based ASDs. The extent and the rate of oxidative degradation were higher in the case of PVP-K30-based ASD as compared to that in PVP-K90-based ASD, and the overall degradation increased with an increase in temperature IR spectral anal. of drug-polymer interactions supports the electronic calculations of the oxidation process. We infer that, apart from the initial free radical content, the difference in the extent of drug-polymer intermol. interactions in ASDs and amorphous stabilization during the forced oxidation experiments contribute to the observed differences in the autoxidative reactivity of the drug in ASDs with different PVP chain lengths. Overall, the chem. degradation of NIF in ASDs with two PVP chain lengths obtained from accelerated solid-state oxidation studies was in qual. agreement with that obtained from long-term (3 years) storage under ambient conditions. The study highlights the ability of accelerated processes to determine the oxidative degradation behavior of polymeric ASDs and suggests that the polymer chain length could factor into chem. as well as phys. stability considerations.

Molecular Pharmaceutics published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Ravasenga, Tiziana published the artcileSpatial regulation of coordinated excitatory and inhibitory synaptic plasticity at dendritic synapses, SDS of cas: 21829-25-4, the publication is Cell Reports (2022), 38(6), 110347, database is CAplus and MEDLINE.

The induction of synaptic plasticity at an individual dendritic glutamatergic spine can affect neighboring spines. This local modulation generates dendritic plasticity microdomains believed to expand the neuronal computational capacity. Here, we investigate whether local modulation of plasticity can also occur between glutamatergic synapses and adjacent GABAergic synapses. We find that the induction of long-term potentiation at an individual glutamatergic spine causes the depression of nearby GABAergic inhibitory synapses (within 3 μm), whereas more distant ones are potentiated. Notably, L-type calcium channels and calpain are required for this plasticity spreading. Overall, our data support a model whereby input-specific glutamatergic postsynaptic potentiation induces a spatially regulated rearrangement of inhibitory synaptic strength in the surrounding area through short-range heterosynaptic interactions. Such local coordination of excitatory and inhibitory synaptic plasticity is expected to influence dendritic information processing and integration.

Cell Reports published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Feiteiro, Joana published the artcilePathways involved in the human vascular Tetrabromobisphenol A response: Calcium and potassium channels and nitric oxide donors, Category: pyridine-derivatives, the publication is Toxicology (2022), 153158, database is CAplus and MEDLINE.

Tetrabromobisphenol A (TBBPA) is a flame retardant that can contaminate the environment and human being, acting as an endocrine disruptor. Several studies propose a correlation between TBBPA exposure and adverse health outcomes, however, at vascular level TBBPA effects are still poorly understood. Thus, considering that the vascular tonus is regulated by vasoactive substances (serotonin and histamine) which are involved in some pathol. processes, this work aimed to analyze the direct effects and the 24 h exposure of TBBPA on the human umbilical artery (HUA) and to investigate its signalling pathway. Using organ bath technique, endothelium-denuded HUA rings were contracted with serotonin (5-HT, 1 μM), histamine (His, 10 μM) and potassium chloride (KCl, 60 mM), and the exposure (0-24 h) of different concentrations of TBBPA (1, 10 and 50 μM) were evaluated. Besides, the vascular mode of action of TBBPA was studied through the anal. of cyclic guanosine monophosphate and calcium channels activity, pathways involved in relaxation and contraction of HUA, resp. Our results demonstrated that the direct effects of TBBPA induce a vasorelaxation of HUA. The maximum relaxant effect was observed at 100 μM of TBBPA with 63.74%, 64.24% and 30.05%, for 5-HT-, His- or KCl-contracted arteries resp. The 24 h TBBPA exposure altered the vasorelaxant response pattern of sodium nitroprusside and nifedipine. This effect is due to the involvement of TBBPA with the NO/sGC/cGMP/PKG pathway and the interference in calcium influx. Furthermore, using the real-time quant. polymerase chain reaction, TBBPA clearly modulates -type calcium and large-conductance Ca2+ 1.1 α- and β1 -subunit channels, and soluble guanylyl cyclase and protein Kinase G. So, at vascular level TBBPA induces changes in HUA after TBBPA exposure.

Toxicology published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Category: pyridine-derivatives.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Gunaratne, Gihan S. published the artcileIdentification of a dihydropyridine scaffold that blocks ryanodine receptors, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is iScience (2022), 25(1), 103706, database is CAplus and MEDLINE.

Ryanodine receptors (RyRs) are large, intracellular ion channels that control Ca²⁺ release from the sarco/endoplasmic reticulum. Dysregulation of RyRs in skeletal muscle, heart, and brain has been implicated in various muscle pathologies, arrhythmia, heart failure, and Alzheimer′s disease. Therefore, there is considerable interest in therapeutically targeting RyRs to normalize Ca²⁺ homeostasis in scenarios involving RyR dysfunction. Here, a simple invertebrate screening platform was used to discover new chemotypes targeting RyRs. The approach measured Ca²⁺ signals evoked by cyclic ADP ribose, a second messenger that sensitizes RyRs. From a 1,534-compound screen, FLI-06 (currently described as a Notch “inhibitor”) was identified as a potent blocker of RyR activity. Two closely related tyrosine kinase inhibitors that stimulate and inhibit Ca²⁺ release through RyRs were also resolved. Therefore, this simple screen yielded RyR scaffolds tractable for development and revealed an unexpected linkage between RyRs and trafficking events in the early secretory pathway.

iScience published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Novais, Teddy published the artcilePotentially inappropriate medications and anticholinergic and sedative burden in older patients with haemophilia or von Willebrand disease: The M’HEMORRH-AGE study, Category: pyridine-derivatives, the publication is Journal of Clinical Pharmacy and Therapeutics (2022), 47(6), 783-791, database is CAplus and MEDLINE.

In older patients, multiple chronic conditions lead to the intake of multiple medications and a higher risk of adverse drug events. The exposure to inappropriate medications in older patients with bleeding disorders is poorly explored. The aim of this study was to describe the exposure to potentially inappropriate medications (PIMs) and medications with anticholinergic and sedative properties in older community-dwelling patients with haemophilia or von Willebrand Disease (VWD). The M’HEMORRH-AGE study (Medication in AGEd patients with HAEMORRHagic disease) is a multicentre prospective observational study. Community-dwelling patients over 65 years with haemophilia or VWD were included in the study. PIMs were identified using the EU(7)-PIM list, and the anticholinergic and sedative drug exposure was measured using the Drug Burden Index. In 142 older community-dwelling patients with haemophilia (n = 89) or VWD (n = 53) were included (mean age: 72.8 ± 5.8 years). PIMs were used by 45.8% of older patients and were mainly represented by cardiovascular (34.9%), nervous systems (26.7%) and alimentary tract and metabolism PIMs (25.6%). Regarding anticholinergic and/or sedative medications, 37.3% of older patients were exposed mainly due to nervous system medications (68.3%), for example analgesics. The MHEMORRH-AGE study showed the exposure to PIMs and anticholinergic/sedative medications was high in older community-dwelling patients with haemophilia or VWD. Interventions focusing on deprescription of these inappropriate medications should be conducted in this specific population.

Journal of Clinical Pharmacy and Therapeutics published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Category: pyridine-derivatives.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Macedo, Cicero Andre Ferreira published the artcileLippia origanoides essential oil induces tocolytic effect in virgin rat uterus and inhibits writhing in a dysmenorrhea mouse model, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Journal of Ethnopharmacology (2022), 115099, database is CAplus and MEDLINE.

The species Lippia origanoides Kunth, popularly known as “salva-de-marajo”, is used in Brazilian traditional “quilombola” communities to treat menstrual cramps and uterine inflammation. Evaluate the spasmolytic activity of Lippia origanoides essential oil (LOO) on exptl. models of uterine conditions related to menstrual cramps and investigate its mechanism of action. Virgin rat-isolated uterus was mounted in the organ bath apparatus to evaluate the spasmolytic effect of LOO on basal tonus and contractions induced by carbachol, KCl, or oxytocin. We used pharmacol. agents to verify the relaxation mechanism of LOO. The evaluation of uterine contractility in virgin rats, after treatment with LOO for three consecutive days, was carried out by the construction of a concentration-response curve with oxytocin or carbachol. The primary dysmenorrhea animal model was replicated with an injection of estradiol cypionate in female mice for three consecutive days, followed by i.p. application of oxytocin. LOO relaxed the rat uterus precontracted with 10-2 IU/mL oxytocin (logEC50 = 1.98 ± 0.07), 1μM carbachol (logEC50 = 1.42 ± 0.07) or 60 mM KCl (logEC50 = 1.53 ± 0.05). It was also able relax uterus on spontaneous contractions (logEC50 = 0.41 ± 0.05). Preincubation with glibenclamide, propranolol, phentolamine or L-NAME in contractions induced by carbachol did not alter significantly the relaxing effect of LOO. However, in the presence of 4-aminopyridine, CsCl or tetraethylammonium there was a reduction of LOO potency, whereas the blockers methylene blue, ODQ, aminophylline and heparin potentiated the LOO relaxing effect. Preincubation with LOO in a Ca2+ free medium at concentrations of 27μg/mL or 81μg/mL reduced the contraction induced by carbachol. The administration of LOO for 3 days did not alter uterus contractility. The treatment with LOO at 30 or 100 mg/kg i.p., or 100 mg/kg orally, inhibited writhing in female mice. The association of LOO at 10 mg/kg with nifedipine or mefenamic acid potentiated writhing inhibition in mice.The essential oil of L. origanoides has tocolytic activity in rat isolated uterus pre-contracted with KCl, oxytocin, or carbachol. This effect is possibly related to the opening of potassium channels (Kir, KV, and KCa), cAMP increase, and diminution of intracellular Ca2+. This relaxant effect, probably, contributed to reduce the number of writhings in an animal model of dysmenorrhea being potentiated by nifedipine or mefenamic acid. Taken together, the results here presented indicate that this species has a pharmacol. potential for the treatment of primary dysmenorrhea, supporting its use in folk medicine.

Journal of Ethnopharmacology published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, 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:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem