Tag: M.W=200-350

Adebayo, Joshua Adeniyi published the artcileEfficacy of nifedipine versus hydralazine in the management of severe hypertension in pregnancy: A randomised controlled trial., HPLC of Formula: 21829-25-4, the main research area is Hydralazine; nifedipine; pregnancy; severe hypertension.

BACKGROUND: Despite the availability of effective antihypertensive drugs, the quality of evidence regarding the best antihypertensive agent for the treatment of hypertensive emergencies in pregnancy is still poor. AIM: The aim of this study was to compare the efficacy and side effects of oral nifedipine and intravenous hydralazine for control of blood pressure (BP) in severe hypertension in pregnancy. MATERIALS AND METHODS: An open-label, parallel, randomised, controlled trial of 78 pregnant women (â‰?8 weeks’ gestation) with severe hypertension was conducted. Severe hypertension was defined as systolic BP of 160 mmHg or above and/or diastolic BP of 110 mmHg or above. They were randomly (1:1 ratio) administered oral nifedipine 20 mg or intravenous hydralazine 10 mg every 30 min up to 5 doses or until the target BP of 140-150 mmHg systolic and 90-100 mmHg diastolic was achieved. Intravenous labetalol was given if the primary treatment failed. The primary outcome measure was the number of doses needed to achieve targeted BP. The secondary outcome measures were the time needed to achieve desired BP, maternal adverse effects and perinatal outcome. RESULTS: The sociodemographic characteristics did not differ between the two study groups. The average number of dosages (nifedipine; 1.4 ± 0.6 vs. hydralazine; 1.7 ± 0.5, P = 0.008) needed to control the BP was lower in the nifedipine arm. Time (min) taken to control the BP was similar between the groups (hydralazine; 43.7 ± 19.7 vs. nifedipine; 51.2 ± 18.9, P = 0.113). Adverse maternal and perinatal effects did not differ in the study groups. CONCLUSION: Oral nifedipine and intravenous hydralazine showed comparable efficacy in the BP control in the severe hypertensive disorders of pregnancy without significant difference in adverse maternal and perinatal outcomes. However, further studies are required to explore the role of these drugs in BP control during hypertensive emergencies in pregnancy. CLINICALTRIALS.GOV: (Identification number: NCT04435210).

The Nigerian postgraduate medical journal published new progress about Hydralazine; nifedipine; pregnancy; severe hypertension. 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

van de Vusse, Dylan published the artcilePharmacokinetics of the most commonly used antihypertensive drugs throughout pregnancy methyldopa, labetalol, and nifedipine: a systematic review, Category: pyridine-derivatives, the main research area is Hypertension; Hypertensive disorders of pregnancy; Labetalol; Methyldopa; Nifedipine; Pharmacokinetics; Pregnancy.

Abstract: Purpose: Antihypertensive drugs are among the most prescribed drugs during pregnancy. Methyldopa, labetalol, and nifedipine have been perceived safe to use during pregnancy and are therefore recommended in international guidelines for treatment of hypertension. In this review, we provide a complete overview of what is known on the pharmacokinetics (PK) of the antihypertensive drugs methyldopa, labetalol, and nifedipine throughout pregnancy. Methods: A systematic search was performed to retrieve studies on the PK of methyldopa, labetalol, and nifedipine used throughout pregnancy. The search was restricted to English and original studies. The systematic search was conducted on July 27, 2021, in Embase, Medline Ovid, Web of Science, Cochrane Library, and Google Scholar. Keywords were methyldopa, labetalol, nifedipine, pharmacokinetics, pregnancy, and placenta. Results: A total of 1459 unique references were identified of which title and abstract were screened. Based on this screening, 67 full-text papers were assessed, to retain 30 PK studies of which 2 described methyldopa, 12 labetalol, and 16 nifedipine. No fetal accumulation is found for any of the antihypertensive drugs studied. Conclusion: We conclude that despite decades of prescribing methyldopa, labetalol, and nifedipine throughout pregnancy, descriptions of their PK during pregnancy are hampered by a large heterogeneity in the low number of available studies. Aiming for evidence-based and personalized dosing of antihypertensive medication in the future, further studies on the relationship of both PK and pharmacodynamics (including the optimal blood pressure targeting) during pregnancy and pregnancy-related pathol. are urgently needed to prevent undertreatment, overtreatment, and side effects.

European Journal of Clinical Pharmacology published new progress about Hypertension; Hypertensive disorders of pregnancy; Labetalol; Methyldopa; Nifedipine; Pharmacokinetics; Pregnancy. 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, Category: pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Miller, Michael J published the artcileImplementation of a standardized nurse initiated protocol to manage severe hypertension in pregnancy., Product Details of C17H18N2O6, the main research area is Hypertension; hypertensive disorders of pregnancy; patient safety; quality improvement; standardization.

Objectives: Hypertensive disorders of pregnancy are a leading cause of maternal morbidity and mortality, studies have shown that standardized protocols for treating severe hypertension improves outcomes. Our goal was to examine the effects of a protocol for treating severe hypertension.Methods: Using quality improvement methodology, we developed an evidence-based nurse-initiated protocol for management of severe hypertension. We used a before and after study design, with the primary outcome of time to administration of antihypertensive medications and time to achieve blood pressure control. Secondary outcomes included medication usage, time to repeat blood pressure, and proportion of women receiving appropriate treatment. Statistical analysis was completed with Stata, using data medians, 95% confidence intervals and a rank-sum test.Results: Data was collected for 5 months before and 5 months after protocol implementation, with 67 patients included before and 125 patients after implementation. The median time to treatment of severe range blood pressure decreased from 25 min before to 11 min after protocol implementation, pâ€?.001. Twenty-four% of women were treated within 15 min before and 60.6% were treated within 15 min after protocol implementation. Median time required to regain sustained mild range blood pressure was reduced from 45 min before to 41 min after protocol implementation, p = .004. 67.5% of women regained mild range blood pressure within 60 min before and 81.9% achieved blood pressure control within 60 min after protocol implementation. These improved outcomes were evident within the first month after protocol implementation and remained stable throughout the follow-up period.Discussion: Implementation of an evidence-based nurse-initiated protocol for the treatment of severe hypertension in pregnancy decreases the time required to administer antihypertensive medication, time required to regain blood pressure control and nonbeneficial clinical variation. In addition, these benefits were achieved rapidly within a large hospital setting.

The journal of maternal-fetal & neonatal medicine published new progress about Hypertension; hypertensive disorders of pregnancy; patient safety; quality improvement; standardization. 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

Reddy, Snigdha published the artcileHypertension and Pregnancy: Management and Future Risks., Synthetic Route of 21829-25-4, the main research area is Hypertension; Preeclampsia; Pregnancy.

Pregnancy-induced hypertension is a major cause of maternal and fetal morbidity and mortality. The overall strategies of defining and managing these conditions are aimed at preventing cardiovascular and cerebrovascular complications in the mother without jeopardizing fetal well-being. Our understanding of the origin of these disorders is evolving. Women with chronic hypertension should undergo a prepregnancy evaluation and close monitoring during and after pregnancy to ensure medication safety and to prevent end-organ damage. Based on available data, the current recommendation is that antihypertensive therapy should be initiated only in women with severe hypertension (defined as systolic blood pressure â‰?60 mm Hg and/or diastolic blood pressure â‰?05 mm Hg). It is now becoming more and more clear that hypertensive complications during pregnancy are potentially linked to cardiovascular, kidney, and metabolic diseases later in life. This review discusses the spectrum of hypertensive disorders of pregnancy, general management principles, and the need to monitor for long-term cardiovascular sequelae for decades afterward.

Advances in chronic kidney disease published new progress about Hypertension; Preeclampsia; Pregnancy. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Synthetic Route of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Kawabata, Hideaki published the artcileIgG4-related Autoimmune Hepatitis with a Suspected Drug-induced Etiology., Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is IgG4; autoimmune hepatitis; drug-induced.

A 69-year-old man was referred to our department with acute hepatitis. He had been newly treated with benidipine hydrochloride for two months. His blood test results were as follows: aspartate aminotransferase, 1,614 IU/L; alanine aminotransferase, 1,091 IU/L and anti-smooth muscle antibody, ×80. Needle liver biopsy specimen showed interface hepatitis with mainly lymphocytic infiltration and bridging fibrosis in the periportal area. Immunohistochemistry revealed lymphocytic infiltration positive for IgG4. We diagnosed him with IgG4-related AIH with an etiology that was suspected of being drug-induced. Oral prednisolone was started and then tapered after achieving biochemical remission. Hepatitis recurred after the cessation of steroids; however, remission was achieved with ursodeoxycholic acid.

Internal medicine (Tokyo, Japan) published new progress about IgG4; autoimmune hepatitis; drug-induced. 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

Sikimic, Jelena published the artcilePossible New Strategies for the Treatment of Congenital Hyperinsulinism., Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is KATP channels; KCa3.1 channels; L-type Ca2+ channels; NN414; congenital hyperinsulinism; diazoxide.

Objective: Congenital hyperinsulinism (CHI) is a rare disease characterized by persistent hypoglycemia as a result of inappropriate insulin secretion, which can lead to irreversible neurological defects in infants. Poor efficacy and strong adverse effects of the current medications impede successful treatment. The aim of the study was to investigate new approaches to silence β-cells and thus attenuate insulin secretion. Research Design and Methods: In the scope of our research, we tested substances more selective and more potent than the gold standard diazoxide that also interact with neuroendocrine ATP-sensitive K+ (KATP) channels. Additionally, KATP channel-independent targets as Ca2+-activated K+ channels of intermediate conductance (KCa3.1) and L-type Ca2+ channels were investigated. Experiments were performed using human islet cell clusters isolated from tissue of CHI patients (histologically classified as pathological) and islet cell clusters obtained from C57BL/6N (WT) or SUR1 knockout (SUR1-/-) mice. The cytosolic Ca2+ concentration ([Ca2+]c) was used as a parameter for the pathway regulated by electrical activity and was determined by fura-2 fluorescence. The mitochondrial membrane potential (ΔΨ) was determined by rhodamine 123 fluorescence and single channel currents were measured by the patch-clamp technique. Results: The selective KATP channel opener NN414 (5 µM) diminished [Ca2+]c in isolated human CHI islet cell clusters and WT mouse islet cell clusters stimulated with 10 mM glucose. In islet cell clusters lacking functional KATP channels (SUR1-/-) the drug was without effect. VU0071063 (30 µM), another KATP channel opener considered to be selective, lowered [Ca2+]c in human CHI islet cell clusters. The compound was also effective in islet cell clusters from SUR1-/- mice, showing that [Ca2+]c is influenced by additional effects besides KATP channels. Contrasting to NN414, the drug depolarized ΔΨ in murine islet cell clusters pointing to severe interference with mitochondrial metabolism. An opener of KCa3.1 channels, DCEBIO (100 µM), significantly decreased [Ca2+]c in SUR1-/- and human CHI islet cell clusters. To target L-type Ca2+ channels we tested two already approved drugs, dextromethorphan (DXM) and simvastatin. DXM (100 µM) efficiently diminished [Ca2+]c in stimulated human CHI islet cell clusters as well as in stimulated SUR1-/- islet cell clusters. Similar effects on [Ca2+]c were observed in experiments with simvastatin (7.2 µM). Conclusions: NN414 seems to provide a good alternative to the currently used KATP channel opener diazoxide. Targeting KCa3.1 channels by channel openers or L-type Ca2+ channels by DXM or simvastatin might be valuable approaches for treatment of CHI caused by mutations of KATP channels not sensitive to KATP channel openers.

Frontiers in endocrinology published new progress about KATP channels; KCa3.1 channels; L-type Ca2+ channels; NN414; congenital hyperinsulinism; diazoxide. 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

Kaur, Prabhleen published the artcileA comparative study of transdermal nitroglycerine patch and oral nifedipine in preterm labor., Formula: C17H18N2O6, the main research area is Nifedipine; nitroglycerine patch; preterm labor.

Background: Currently, the main goal for the use of tocolytic therapy is to delay the birth so as to allow the use of corticosteroids for accelerating fetal lung maturity and maternal transfer to a tertiary care center and thereby reducing neonatal morbidity and mortality. Aims and Objectives: The aims amd objectives were to compare the safety and efficacy of transdermal nitroglycerine patch with oral nifedipine as a tocolytic agent to arrest preterm labor and prevent preterm birth. Materials and Methods: Based on the selection criteria, 50 patients were selected randomly in Group A and Group B. Group A women were given transdermal nitroglycerin patch, which delivered 10 mg Nitroglycerin (NTG) over 24 h and it was applied to the woman’s abdomen followed by another patch of 10 mg after 1 h if contractions persisted. After 24 h, it was replaced by a fresh patch. Group B women were given an oral loading dose of nifedipine 20 mg followed by a similar dose if contractions persisted after 1 h. A maintenance dose of 10 mg thrice daily was given if contractions were suppressed. Patients were monitored from the time of admission to the time of discharge. Results: The mean duration of prolongation of pregnancy in Group B (3.68 ± 1.91 days) was significantly more than Group A (2.78 ± 1.39 days). Headache was seen significantly more in Group A (42%) than group B (6%). Tachycardia, hypotension, and palpitation showed no statistically significant difference between them. There was no statistically significant difference in the birth weight of the babies in both the groups. Conclusion: Nifedipine is a safe and effective drug in prolonging preterm labor and has minimal maternal and neonatal side effects.

Annals of African medicine published new progress about Nifedipine; nitroglycerine patch; preterm labor. 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

Friedlander, Edwa published the artcileCumulative Risk of the Oxytocin Receptor Gene Interacts with Prenatal Exposure to Oxytocin Receptor Antagonist to Predict Children’s Social Communication Development., Quality Control of 21829-25-4, the main research area is OXTR; autism spectrum disorder; gene-environment interaction; oxytocin; oxytocin receptor antagonist; oxytocin receptor gene.

Compelling evidence for the far-reaching role of oxytocin (OT) in social cognition and affiliative behaviors set the basis for examining the association between genetic variation in the OT receptor (OXTR) gene and risk for autism spectrum disorder (ASD). In the current study, gene-environment interaction between OXTR and prenatal exposure to either OT or OXTR antagonist (OXTRA) in predicting early social communication development was examined. One hundred and fifty-three children (age: Mâ€?â€?.32, SD =â€?.07) were assigned to four groups based on prenatal history: children whose mothers prenatally received OXTRA and Nifedipine to delay preterm labor (nâ€?â€?7); children whose mothers received Nifedipine only to delay preterm labor (nâ€?â€?5); children whose mothers received OT for labor augmentation (nâ€?â€?6), and a no intervention group (nâ€?â€?5). Participants completed a developmental assessment of intelligence quotient (IQ), adaptive behavior, and social communication abilities. DNA was extracted via buccal swab. A genetic risk score was calculated based on four OXTR single nucleotide polymorphisms (rs53576, rs237887, rs1042778, and rs2254298) previously reported to be associated with ASD symptomatology. OXTRrisk-allele dosage was associated with more severe autism diagnostics observation schedule (ADOS) scores only in the OXTRA group. In contrast, in the Nifedipine, OT, and no intervention groups, OXTRrisk-allele dosage was not associated with children’s ADOS scores. These findings highlight the importance of both genetic and environmental pathways of OT in signaling early social development and raise the need for further research in this field. Autism Res 2019, 12: 1087-1100. © 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: In the current study, we examined if the association between prenatal exposure to an oxytocin receptor antagonist (OXTRA) and autism spectrum disorder (ASD) related impairments are dependent on an individual’s genetic background for the oxytocin receptor gene (OXTR). Children who carried a greater number of risk alleles for the OXTR gene and whose mothers received OXTRA to delay preterm labor showed more ASD-related impairments. The results highlight the importance of both genetic and environmental pathways of oxytocin in shaping early social development.

Autism research : official journal of the International Society for Autism Research published new progress about OXTR; autism spectrum disorder; gene-environment interaction; oxytocin; oxytocin receptor antagonist; oxytocin receptor gene. 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

Saraf, Isha published the artcileForced Solid-State Oxidation Studies of Nifedipine-PVP Amorphous Solid Dispersion, Safety of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is PVP chain length; amorphous solid dispersion; autoxidation; chemical stability.

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 PVP chain length; amorphous solid dispersion; autoxidation; chemical stability. 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

Kim, Sung Eun published the artcileComparison of calcium-channel blockers for long-term clinical outcomes in patients with vasospastic angina., COA of Formula: C17H18N2O6, the main research area is Calcium channel blockers; Coronary vasospasm; Patient outcome assessment.

BACKGROUND/AIMS: Calcium channel blockers (CCBs) are the most widely prescribed medication for patients with vasospastic angina (VA). However, few studies have compared the prognosis of VA patients who are prescribed different CCBs. METHODS: We enrolled 2,960 patients who received provocation test prospectively in 11 university hospitals in Korea. We divided 1,586 patients received four major CCBs into two groups: a first generation CCB (diltiazem and nifedipine) group and a second generation CCB (amlodipine and benidipine) group. Primary outcome was time to events of composite of death from any cause, acute coronary syndrome (ACS) and symptomatic arrhythmia during 3-year follow-up. We also compared the effect of each CCB on the control of angina symptoms. RESULTS: There was no difference of the primary outcome among the two groups with a cumulative incidence rate of 5.4%, 2.9%, and a person-month incidence rate of 2.33 and 1.26, respectively (hazard ratio [HR], 0.54; 95% confidence interval [CI], 0.25 to 1.17; p = 0.120, as reference with the 1st generation CCBs). The incidence of ACS was significantly lower in 2nd generation CCBs group with a person-month incidence rate of 1.66 vs. 0.35 (HR, 0.22; 95% CI, 0.05 to 0.89; p = 0.034). Use of benidipine showed a significant better control of angina symptom compared with diltiazem for 3 years (odds ratio, 0.17; 95% CI, 0.09 to 0.32; p < 0.0001 at 3rd year). CONCLUSION: The first and second generation CCB groups did not differ in terms of composite outcome occurrence. However, the ACS incidence rate was significantly lower in the users of the 2nd generation CCBs. The Korean journal of internal medicine published new progress about Calcium channel blockers; Coronary vasospasm; Patient outcome assessment. 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