Day: December 6, 2022

Alhalaweh, Amjad published the artcileMolecular drivers of crystallization kinetics for drugs in supersaturated aqueous solutions, Recommanded Product: 3-Ethyl 5-methyl 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is drug crystallization kinetics supersaturated aqueous solution; crystallization; glass; in silico modeling; physicochemical properties; precipitation; supersaturation.

In this study, we explore mol. properties of importance in solution-mediated crystallization occurring in supersaturated aqueous drug solutions Furthermore, we contrast the identified mol. properties with those of importance for crystallization occurring in the solid state. A literature data set of 54 structurally diverse compounds, for which crystallization kinetics from supersaturated aqueous solutions and in melt-quenched solids were reported, was used to identify mol. drivers for crystallization kinetics observed in solution and contrast these to those observed for solids. The compounds were divided into fast, moderate, and slow crystallizers, and in silico classification was developed using a mol. K-nearest neighbor model. The topol. equivalent of Grav3 (related to mol. size and shape) was identified as the most important mol. descriptor for solution crystallization kinetics; the larger this descriptor, the slower the crystallization Two electrotopol. descriptors (the atom-type E-state index for -Caa groups and the sum of absolute values of pi Fukui(+) indexes on C) were found to sep. the moderate and slow crystallizers in the solution The larger these descriptors, the slower the crystallization With these 3 descriptors, the computational model correctly sorted the crystallization tendencies from solutions with an overall classification accuracy of 77% (test set).

Journal of Pharmaceutical Sciences (Philadelphia, PA, United States) published new progress about Crystallization. 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, Recommanded Product: 3-Ethyl 5-methyl 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

El-Masry, Soha Mahmoud published the artcilePharmacokinetic and Tolerability Comparison of Sustained and Immediate Release Oral Formulations of Nifedipine Tablet Formulations: A Single-Dose, Randomized, Open-Label, Two-Period, Two-Way Crossover Study in Healthy, Fasting Egyptian Male Volunteers, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is nifedipine tablet oral formulation pharmacokinetics safety tolerability Egypt.

Sustained-release formulation of nifedipine is available in Egyptian community and administered twice daily. This study aimed to to compare pharmacokinetics and safety profiles of a 20 mg SR and IR formulation of nifedipine after single-dose administration in healthy Egyptian subjects. Randomized, crossed open-label two- way clin. trial, in 16 healthy adult volunteers, of 24.75±5.20 years, with BMI 23.26±1.756 were assessed. Blood samples were collected at predefined times for 48 h and analyzed for Nifedipine plasma concentrations using validated reversed phase liquid chromatog. method with UV detection. Pharmacokinetics was determined using non- compartmental model pharmacokinetics and analyzed using one-way ANOVA (P≤0.05). Following a single oral administration, SR formulation had a lower C max, compared to IR formulation (54.46±17.75 , 107.45±29.85 ng/mL, resp.), and T maxwas significantly longer (2.97 vs. 1.13 h) for the SR and IR formulation, resp. There was no significant difference between SR and the IR formulations for AUC 0-lastand AUC 0-∞(326.7±98.28 vs. 309.27±105.53 ng·h·mL -1and 380.9 ± 105.24 vs. 334.36±108.1 ng·h·mL -1, resp.). SR formulation of nifedipine showed similar pharmacokinetics to the IR Formulation (F%=1.049), but it addnl. allows a less frequent administration. Therefore, nifedipine SR and IR formulations were well tolerated and displayed comparable safety profiles.

Drug Research (Stuttgart, Germany) published new progress about Clinical trials. 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

Li, Yan published the artcileHydrogen sulfide relaxes human uterine artery via activating smooth muscle BKCa channels, Quality Control of 21829-25-4, the main research area is uterine artery dilation BKca channel hydrogen sulfide smooth muscle; BKCa channels; hydrogen sulfide; smooth muscle; uterine artery; women.

Opening of large conductance calcium-activated and voltage-dependent potassium (BKCa) channels hyperpolarizes plasma membranes of smooth muscle (SM) to cause vasodilation, underling a key mechanism for mediating uterine artery (UA) dilation in pregnancy. Hydrogen sulfide (H2S) has been recently identified as a new UA vasodilator, yet the mechanism underlying H2S-induced UA dilation is unknown. Here, we tested whether H2S activated BKCa channels in human UA smooth muscle cells (hUASMC) to mediate UA relaxation. Multiple BKCa subunits were found in human UA in vitro and hUASMC in vitro, and high β1 and γ1 proteins were localized in SM cells in human UA. Baseline outward currents, recorded by whole-cell and single-channel patch clamps, were significantly inhibited by specific BKCa blockers iberiotoxin (IBTX) or tetraethylammonium, showing specific BKCa activity in hUASMC. H2S dose (NaHS, 1-1000μM)-dependently potentiated BKCa currents and open probability. Co-incubation with a Ca2+ blocker nifedipine (5μM) or a chelator (ethylene glycol-bis (β-aminoethyl ether)-N,N,N’,N’-tetraacetic acid (EGTA), 5 mM) did not alter H2S-potentiated BKCa currents and open probability. NaHS also dose-dependently relaxed phenylephrine pre-constricted freshly prepared human UA rings, which was inhibited by IBTX. Thus, H2S stimulated human UA relaxation at least partially via activating SM BKCa channels independent of extracellular Ca2+.

Antioxidants published new progress about Cell activation. 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

Takeya, Mitsue published the artcilePDGFRα+ subepithelial interstitial cells act as a pacemaker to drive smooth muscle of the guinea pig seminal vesicle, Category: pyridine-derivatives, the main research area is PDGFR alpha subepithelial interstitial pacemaker smooth muscle seminal vesicle; PDGFRα; electrical slow wave; interstitial cell; mucosa; seminal vesicle; spontaneous Ca2+ transient.

Smooth muscle cells (SMCs) of the guinea pig seminal vesicle (SV) develop spontaneous phasic contractions, Ca2+ flashes and elec. slow waves in a mucosa-dependent manner, and thus it was envisaged that pacemaker cells reside in the mucosa. Here, we aimed to identify the pacemaker cells in SV mucosa using intracellular microelectrode and fluorescence Ca2+ imaging techniques. Morphol. characteristics of the mucosal pacemaker cells were also investigated using focused ion beam/SEM tomog. and fluorescence immunohistochem. Two populations of mucosal cells developed spontaneous Ca2+ transients and elec. activity, namely basal epithelial cells (BECs) and subepithelial interstitial cells (SICs). Pancytokeratin-immunoreactive BECs were located on the apical side of the basement membrane (BM) and generated asynchronous, irregular spontaneous Ca2+ transients and spontaneous transient depolarisations (STDs). The spontaneous Ca2+ transients and STDs were not diminished by 10μM nifedipine but abolished by 10μM cyclopiazonic acid (CPA). Platelet-derived growth factor receptor α (PDGFRα)-immunoreactive SICs were distributed just beneath the basal side of the BM and developed synchronous Ca2+ oscillations and elec. slow waves, which were suppressed by 3μM nifedipine and abolished by 10μM CPA. In SV mucosal preparations in which some smooth muscle bundles remained attached, SICs and residual SMCs developed temporally correlated spontaneous Ca2+ transients. Neurobiotin injected into SICs spread not only to neighboring SICs but also to neighboring SMCs or vice versa. These results suggest that PDGFRα+ SICs electrotonically drive the spontaneous contractions of SV smooth muscle. Key points : In many visceral smooth muscle organs, spontaneous contractions are elec. driven by non-muscular pacemaker cells. In guinea pig seminal vesicles (SVs), as yet unidentified mucosal cells appear to drive neighboring smooth muscle cells (SMCs). Two populations of spontaneously active cells are distributed in the SV mucosa. Basal epithelial cells (BECs) generate asynchronous, irregular spontaneous Ca2+ transients and spontaneous transient depolarisations (STDs). In contrast, subepithelial interstitial cells (SICs) develop synchronous Ca2+ oscillations and elec. slow waves. Pancytokeratin-immunoreactive (IR) BECs are located on the apical side of the basement membrane (BM), while platelet-derived growth factor receptor α (PDGFRα)-IR SICs are located on the basal side of the BM. Spontaneous Ca2+ transients in SICs are synchronised with those in SV SMCs. Dye-coupling between SICs and SMCs suggests that SICs act as pacemaker cells to drive the spontaneous contractions of SV smooth muscle.

Journal of Physiology (Oxford, United Kingdom) published new progress about Cavia porcellus. 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

Chen, Yuan-Yuan published the artcileParacetamol inhibits Ca2+ permeant ion channels and Ca2+ sensitization resulting in relaxation of precontracted airway smooth muscle, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is paracetamol nifedipine acetylcholine analgesic antipyretic agent asthma; Airway smooth muscle; Ca(2+) sensitization; Canonical transient receptor potential channel; L-type voltage dependent Ca(2+) channel; Paracetamol; Store-operated Ca(2+) channel.

The purpose of this study was to screen a bronchodilator from old drugs and elucidate the underlying mechanism. Paracetamol (acetaminophen) is a widely used analgesic and antipyretic drug. It has been reported that it inhibits the generation of prostaglandin and histamine, which play roles in asthma. These findings led us to explore whether paracetamol could be a potential bronchodilator. Paracetamol inhibited high K+- and acetylcholine (ACH)-induced precontraction of mouse tracheal and bronchial smooth muscles. Moreover, the ACH-induced contraction was partially inhibited by nifedipine (selective blocker of LVDCCs), YM-58483 (selective inhibitor of store-operated Ca2+ entry (SOCE), canonical transient receptor potential 3 (TRPC3) and TRPC5 channels) and Y-27632 (selective blocker of ROCK, a linker of the Ca2+ sensitization pathway). In single airway smooth muscle cells, paracetamol blocked the currents sensitive to nifedipine and YM-58483, and inhibited intracellular Ca2+ increases. In addition, paracetamol inhibited ACH-induced phosphorylation of myosin phosphatase target subunit 1 (MYPT1, another linker of the Ca2+ sensitization pathway). Finally, in vivo paracetamol inhibited ACH-induced increases of mouse respirator system resistance. Collectively, we conclude that paracetamol inhibits ASM contraction through blocking LVDCCs, SOCE and/or TRPC3 and/or TRPC5 channels, and Ca2+ sensitization.

Journal of Pharmacological Sciences (Amsterdam, Netherlands) published new progress about Bronchodilators. 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 of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Qiu, Jun-Ying published the artcileFolium Sennae and emodin reverse airway smooth muscle contraction, Product Details of C17H18N2O6, the main research area is folium Sennae emodin airway smooth muscle contraction; Ca2+ sensitization; Folium Sennae; L-type voltage-dependent Ca2+ channels; emodin; respiratory system resistance; store-operated Ca2+ entry.

The objective of this project was to find a bronchodilatory compound from herbs and clarify the mechanism. We found that the ethanol extract of Folium Sennae (EEFS) can relax airway smooth muscle (ASM). EEFS inhibited ASM contraction, induced by acetylcholine, in mouse tracheal rings and lung slices. High-performance liquid chromatog. assay showed that EEFS contained emodin. Emodin had a similar reversal action. Acetylcholine-evoked contraction was also partially reduced by nifedipine (a selective inhibitor of L-type voltage-dependent Ca2+ channels, LVDCCs), YM-58483 (a selective inhibitor of store-operated Ca2+ entry, SOCE), as well as Y-27632 (an inhibitor of Rho-associated protein kinase). In addition, LVDCC- and SOCE-mediated currents and cytosolic Ca2+ elevations were inhibited by emodin. Emodin reversed acetylcholine-caused increases in phosphorylation of myosin phosphatase target subunit 1. Furthermore, emodin, in vivo, inhibited acetylcholine-induced respiratory system resistance in mice. These results indicate that EEFS-induced relaxation results from emodin inhibiting LVDCC, SOCE, and Ca2+ sensitization. These findings suggest that Folium Sennae and emodin may be new sources of bronchodilators.

Cell Biology International published new progress about Bronchodilators. 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

Zhao, Feifei published the artcileChanges and clinical significance of serum inflammatory factors in the treatment of pregnancy hypertension syndrome with magnesium sulfate combined with nifedipine, Application In Synthesis of 21829-25-4, the main research area is serum inflammatory factors pregnancy hypertension syndrome magnesium sulfate; magnesium sulfate; nifedipine; pregnancy-induced hypertension; serum inflammatory factors.

Curative effect of magnesium sulfate combined with nifedipine on pregnancy-induced hypertension and the effect of serum inflammatory factors were investigated. A total of 188 cases of patients were collected as the research subjects. They all had pregnancy-induced hypertension, and were admitted to The First People’s Hospital of Yunnan Province hospital from June 2016 to Feb. 2018. There were, 94 patients treated with magnesium sulfate in the control group, and further 94 patients treated with magnesium sulfate combined with nifedipine in the study group. ELISA was used to detect the expression levels of suppressors of cytokine signaling-3 (SOCS-3), interleukin-10 (IL-10) and interleukin 18 (IL-18), and the relationship between serum inflammatory factors and efficacy was analyzed. The curative effect and eutocia rate in the study group were significantly higher than those in the control group (P<0.05), and the cesarean section rate was lower than that of the control group (P<0.05). In the study group, the adverse reactions were significantly lower than those in the control group (P<0.05). After treatment, the expression levels of serum SOCS-3 and IL-10 in the study group were significantly higher than those in the control group (P<0.05), while the expression level of serum IL-18 was significantly lower than that in the control group (P<0.05). The area under the curve (AUC) of the predictive value of SOCS-3, IL-10 and IL-18 in pregnancy-induced hypertension was 0.717, 0.727 and 0.725, resp. The best specificity was 76.19, 52.98 and 61.90%, resp., when the cut-off value was <0.553 ng/l, 48.06 ng/mL and 269.46 ng/mL, and their sensitivity was 70.00, 94.74 and 85.00%, resp. In conclusion, magnesium sulfate combined with nifedipine significantly improved the disease course of pregnancy-induced hypertension. The levels of SOCS-3, IL-10 and IL-18 in patients are correlated with the curative effect of pregnancy-induced hypertension, suggesting that they have important value in the treatment and monitoring of gestational hypertension. Experimental and Therapeutic Medicine published new progress about Body mass index. 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

Villegas, Daniela published the artcileActivation of TRPV4 channels leads to a consistent tocolytic effect on human myometrial tissues, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is iberiotoxin TRPV4 channel tocolytic agent myometrial reactivity; BKCa, Ca2+-activated large conducting potassium channels; Calcium conductance; Cell signaling; IbTX, Iberiotoxin; MLC, Myosin light chain; MLCP, Myosin light chain phosphatase; PLC, Phospholipase C; PTB, Preterm birth; TRP, Transient Receptor Potential proteins; TRPV channels; TRPV, Transient Receptor Potential of the vanilloid family; Tocolytic effect; USMC, Uterine Smooth Muscle Cells; Uterine contractions.

Human myometrium is a therapeutic target for labor induction and preterm labor. This study aimed to assess the physiol. role of alternative calcium conductance on contractions triggered by uterotonic drugs in human myometrium. Membrane conductances, supported by TRPV channels, may provide alternative pathways to control either free intracellular and/or submembrane Ca2+-concentration, which in turn will modulate membrane polarization and contractile responses. Uterine biopsies were obtained from consenting women undergoing elective caesarean delivery at term without labor (N = 22). Isometric tension measurements were performed on uterine smooth muscle strips (n = 132). Amplitude, frequency, and area under the curve (AUC) of phasic contractions, as well as resting tone, were measured under various exptl. conditions. Immuno histo- and cyto-chem., as well as Western blot analyses, have been performed with specific antibodies against TRPV1, TRPV3, and TRPV4 proteins. TRPV4 agonists; GSK1016790A, 4αPDD, and 5,6-EET were used to assess the role of TRPV4 channels on rhythmic activity triggered by 30-300 nM oxytocin. 5μM of ruthenium red was used as an efficient blocker of ionic current through TRPV4 channels. Nanomolar concentrations of iberiotoxin (IbTX) were also used to confirm the downstream involvement of BKCa channels in controlling uterine reactivity and contractility. The expression of TRPV3 and TRPV4 isoforms has now been demonstrated in human myometrial tissue and cell culture. Nanomolar concentrations of the TRPV4 agonists, (either GSK1016790A or 4αPDD) abolished the rhythmic contractions, resulting in a rapid and consistent tocolytic effect. While 5μM of ruthenium reversed this tocolytic effect. The addition of IbTX (a BKCa channel blocker) reversed the effects of GSK1016790A. Carvacrol, a TRPV3 agonist, had similar tocolytic effects on rhythmic contractions albeit at higher concentrations This inhibitory effect was also reversed by ruthenium red. Collectively, these data suggest that activation of TRPV4 leads to a Ca2+ entry and subsequent BKCa channel activation (increase in open state probability), which in turn hyperpolarizes the myometrial cell membrane, inactivating L-type Ca2+ channels and efficiently abrogates contractile activity. Consequently, alternative Ca2+ conductance supported by TRPV4 plays a physiol. role in the modulation of myometrial reactivity.

European Journal of Obstetrics & Gynecology and Reproductive Biology: X published new progress about Body mass index. 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

Yu, Weiqun published the artcileReviving Cav1.2 as an attractive drug target to treat bladder dysfunction, COA of Formula: C17H18N2O6, the main research area is review Cav1 2 drug target therapy bladder dysfunction; calcium channel blockers; overactive bladder; smooth muscle.

Inhibition of bladder contraction with antimuscarinics is a common approach to treat bladder hyperactivity, and the L-type voltage-gated calcium channel α1C (Cav1.2) is crucial for bladder contractility. Therefore, strategies aimed at inhibiting Cav1.2 appear warranted. However, multiple clin. trials that attempted to treat bladder overactivity with calcium channel blockers (CCBs) have been unsuccessful, creating an unsolved mystery. In contrast, cardiologists and epidemiologists have reported strong associations between CCB use and bladder hyperactivity, opposing expectations of urologists. Recent findings from our lab offer a potential explanation. We have demonstrated that ketamine which can cause cystitis, functions, like nifedipine, as a Cav1.2 antagonist. We also show that a Cav1.2 agonist which potentiates muscle contraction, rather than antagonizing it, can increase the volume of voids and reduce voiding frequency. This perspective will discuss in detail the unsuccessful urol. trials of CCBs and the promise of Cav1.2 agonists as potential novel therapies for bladder dysfunctions.

FASEB Journal published new progress about Bladder disease. 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

Ines Silva, Maria published the artcileSmall scale in vitro method to determine a potential bioequivalent equilibrium solubility range for fed human intestinal fluid, Application of 3-Ethyl 5-methyl 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is human intestinal fluid potential bioequivalent equilibrium solubility; BCS; DCS; aprepitant; bioavailability; bromocriptine; carvedilol; fed intestinal fluid; felodipine; fenofibrate; ibuprofen; indomethacin; itraconazole; phenytoin; probucol; solubility; tadalafil; valsartan; zafirlukast.

Intestinal drug solubility is a key parameter controlling oral absorption but varies both intra and inter individuals and between the fasted and fed states, with food intake known to alter the bioavailability of many compounds Intestinal solubility can be measured in vitro either using sampled fed human intestinal fluid (FeHIF) or simulated fed intestinal fluid (SIF) but neither approach is optimal. FeHIF is difficult to obtain and variable, while for fed SIF multiple recipes are available with no consensus on the ideal version. A recent study characterised FeHIF aspirates using a multidimensional approach and calculated nine simulated media recipes that covered over ninety percent of FeHIF compositional variability. In this study the equilibrium solubility of thirteen drugs have been measured using the nine simulated media recipes and compared to multiple previous design of experiment (DoE) studies, which have examined the impact of fed SIF media components on solubility The measured nine media solubility data set is only statistically equivalent to the large scale 92 media DoE in 4 out of 13 drug comparisons, but has improved equivalence against small scale DoEs (9 or 10 media) with 6 out of 9 or 10 out of 12 (9 and 10 media resp.) equivalent Selective removal of non-biorelevant compositions from the 92 media DoE improves statistical equivalence to 9 out of 13 comparisons. The results indicate that solubility equivalence is linked to media component concentrations and compositions, the nine media system is measuring a similar solubility space to previous systems, with a narrower solubility range than the 92 point DoE but equivalent to smaller DoE systems. Phenytoin and tadalafil display a narrow solubility range, a behavior consistent with previous studies in fed and fasted states and only revealed through the multiple media approach. Custom DoE anal. of the nine media results to determine the most statistically significant component influencing solubility does not detect significant components. Indicating that the approach has a low statistical resolution and is not appropriate if determination of media component significance is required. This study demonstrates that it is possible to assess the fed intestinal equilibrium solubility envelope using the nine media recipes obtained from a multi-dimensional anal. of fed HIF. The derivation of the nine media compositions coupled with the results in this study indicate that the solubility results are more likely to reflect the fed intestinal solubility envelope than previous DoE studies and highlight that the system is worthy of further investigation.

European Journal of Pharmaceutics and Biopharmaceutics published new progress about Bioavailability. 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 of 3-Ethyl 5-methyl 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem