Category: 21829-25-4

Kim, Min Jun published the artcileHeme oxygenase-1 gene delivery for altering high mobility group box-1 protein in pancreatic islet, Synthetic Route of 21829-25-4, the publication is Journal of Controlled Release (2022), 326-337, database is CAplus and MEDLINE.

Pancreatic islet transplantation is a promising strategy for the treatment of type I diabetes. High-mobility group box-1 (HMGB1), highly expressed in islet cells, is a potent immune stimulator in immune rejection. Heme oxygenase-1 (HO1) gene therapy can modulate the release of HMGB1 by altering intracellular mols. for successful cell transplantation. After delivery of the heme oxygenase-1 (HO1) gene to islet cells using an adeno-associated viral vector (AAV), it was evaluated the changes in cytoplasmic Ca2+ ions and calcineurin activity as well as histone acetyltransferase (HAT) and Poly(ADP) ribose polymerase-1 (PARP-1). Inhibition of HMGB1 release was evaluated through altering these intracellular mols. Then, after transplantation of HO1-transduced islets, the therapeutic effect of them was evaluated through measuring blood glucose level to diabetic mice and through immunohistochem. anal. The transduced HO1 gene significantly inhibited HMGB1 release in islets that was under the cell damage by hypoxia exposure. It was confirmed that this result was initially due to the decrease in cytoplasmic Ca2+ ion concentration and calcineurin activity. In addition, the delivered HO1 gene simultaneously reduced the activity of HAT and PARP-1, which are involved in the translocation of HMGB1 from the nucleus to the cytoplasm. As a result, when the HO1 gene-transduced islets were transplanted into diabetic mice, the treatment efficiency of diabetes was effectively improved by increasing the survival rate of the islets. Collectively, these results suggest that HO1 gene transfer can be used for successful islet transplantation by altering the activity of intracellular signal mols. and reducing HMGB1 release.

Journal of Controlled Release 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

Takeya, Mitsue published the artcilePDGFRα⁺ subepithelial interstitial cells act as a pacemaker to drive smooth muscle of the guinea pig seminal vesicle, Quality Control of 21829-25-4, the publication is Journal of Physiology (Oxford, United Kingdom) (2022), 600(7), 1703-1730, database is CAplus and MEDLINE.

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 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 C13H9FO2, Quality Control of 21829-25-4.

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

Zhou, Min published the artcileFingerprinting pharmaceuticals of multiple sources at a provincial watershed scale, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Science of the Total Environment (2022), 153356, database is CAplus and MEDLINE.

Pharmaceutical residues in the aquatic environment have increasingly attracted public concerns but their fingerprint of sources remain unclear at a watershed scale. This study systematically explored pharmaceutical residues in effluent of 8 different type of sources in a provincial watershed in China using a multi-category protocol of pharmaceutical quantification. Seventy-seven out of 94 target compounds from 6 categories were quantified in effluent, up to 71,318 ng L^-1 in total from urban hospital sources with 20 antibiotics and 32 others. The spectrum of the quantified compounds in effluent significantly differentiated the urban (hospitals, domestic sewages, and WWTPs), rural (health centers and domestic sewages), and agricultural production sources (poultry and swine breeding yards, aquaculture ponds, and paddy fields). Compounds of non-steroidal anti-inflammation drugs (NSAIDs), cardiovascular drugs (CVs), and central nervous drugs (CNs) could fingerprint the three groups of sources. However, the three categories contributed 7 out of 10 compounds with high risk (risk quotient >1.0) to the aquatic environment identified by the eco-environmental risk assessment. No high-risk compounds were identified in effluent of urban WWTPs. Findings of this study suggest source identification and compound spectrum fingerprinting are crucial for studies on pharmaceutical residues in the aquatic environment, especially the complexity of pharmaceutical residues in source effluents for exploring source-sink dynamics at a watershed scale.

Science of the Total Environment 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 C9H12O, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

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

Drumm, Bernard T. published the artcileCa²⁺ signaling in interstitial cells of Cajal contributes to generation and maintenance of tone in mouse and monkey lower oesophageal sphincters, Related Products of pyridine-derivatives, the publication is Journal of Physiology (Oxford, United Kingdom) (2022), 600(11), 2613-2636, database is CAplus and MEDLINE.

The lower oesophageal sphincter (LES) generates tone and prevents reflux of gastric contents. LES smooth muscle cells (SMCs) are relatively depolarised, facilitating activation of Ca_v1.2 channels to sustain contractile tone. We hypothesised that i.m. interstitial cells of Cajal (ICC-IM), through activation of Ca²⁺-activated Cl^– channels (ANO1), set membrane potentials of SMCs favorable for activation of Ca_v1.2 channels. In some gastrointestinal muscles, ANO1 channels in ICC-IM are activated by Ca²⁺ transients, but no studies have examined Ca²⁺ dynamics in ICC-IM within the LES. Immunohistochem. and qPCR were used to determine expression of key proteins and genes in ICC-IM and SMCs. These studies revealed that Ano1 and its gene product, ANO1, are expressed in c-Kit ⁺cells (ICC-IM) in mouse and monkey LES clasp muscles. Ca²⁺ signalling was imaged in situ, using mice expressing GCaMP6f specifically in ICC (Kit-KI-GCaMP6f). ICC-IM exhibited spontaneous Ca²⁺ transients from multiple firing sites. Ca²⁺ transients were abolished by cyclopiazonic acid or caffeine but were unaffected by tetracaine or nifedipine. Maintenance of Ca²⁺ transients depended on Ca²⁺ influx and store reloading, as Ca²⁺ transient frequency was reduced in Ca²⁺ free solution or by Orai antagonist. Spontaneous tone of LES muscles from mouse and monkey was reduced ∼80% either by Ani9, an ANO1 antagonist or by the Ca_v1.2 channel antagonist nifedipine. Membrane hyperpolarisation occurred in the presence of Ani9. These data suggest that intracellular Ca²⁺ activates ANO1 channels in ICC-IM in the LES. Coupling of ICC-IM to SMCs drives depolarisation, activation of Ca_v1.2 channels, Ca²⁺ entry and contractile tone.

Journal of Physiology (Oxford, United Kingdom) 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

Romano, Sonia published the artcileDrug shortages in community pharmacies: Impact on patients and on the health system, Quality Control of 21829-25-4, the publication is Journal of the American Pharmacists Association (2022), 62(3), 791-799.e2, database is CAplus and MEDLINE.

Worldwide, drug shortages are a critical public health concern. Consequences range from inconvenience and distress to more serious concerns related to neg. clin., humanistic and economic outcomes. This study aimed to investigate the impact of drug shortages at the community pharmacies on patients and on the health system in Portugal. A national, cross-sectional, multicenter study was conducted in Portuguese community pharmacies during Apr. 2019. The proportion of patients reporting drug shortages, types of drugs affected and consequent economic burden to patients and the health system were estimated Regional and urban setting stratification was performed.A total of 71.1% of pharmacies participated in the study and 22,830 patient surveys were retrieved. About 52.2% of patients experienced a drug shortage in the past 12 mo; 21.5% had to see a physician to change the prescription and 5.7% declared treatment discontinuation because of this shortage. The estimated economic impact of shortages related to addnl. physician appointments varied between euro2.1-euro4.4 million for patients and euro35.3-euro43.8 million for the National Health Service. Drug shortages were mostly felt in rural and inner regions and least felt in the islands. This national study showed that community pharmacy drug shortages are a national problem with neg. consequences on patients and the health system, which need to be tackled and mitigated.

Journal of the American Pharmacists Association 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, Quality Control of 21829-25-4.

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

Hohmann, Urszula published the artcileNimodipine Exerts Time-Dependent Neuroprotective Effect after Excitotoxical Damage in Organotypic Slice Cultures, Computed Properties of 21829-25-4, the publication is International Journal of Molecular Sciences (2022), 23(6), 3331, database is CAplus and MEDLINE.

During injuries in the central nervous system, intrinsic protective processes become activated. However, cellular reactions, especially those of glia cells, are frequently unsatisfactory, and further exogenous protective mechanisms are necessary. Nimodipine, a lipophilic L-type calcium channel blocking agent is clin. used in the treatment of aneurysmal subarachnoid hemorrhage with neuroprotective effects in different models. Direct effects of nimodipine on neurons amongst others were observed in the hippocampus as well as its influence on both microglia and astrocytes. Earlier studies proposed that nimodipine protective actions occur not only via calcium channel-mediated vasodilatation but also via further time-dependent mechanisms. In this study, the effect of nimodipine application was investigated in different time frames on neuronal damage in excitotoxically lesioned organotypic hippocampal slice cultures. Nimodipine, but not nifedipine if pre-incubated for 4 h or co-applied with NMDA, was protective, indicating time dependency. Since blood vessels play no significant role in our model, intrinsic brain cell-dependent mechanisms seems to strongly be involved. We also examined the effect of nimodipine and nifedipine on microglia survival. Nimodipine seem to be a promising agent to reduce secondary damage and reduce excitotoxic damage.

International Journal of Molecular Sciences 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

Scott, Georgia published the artcileGuidelines-similarities and dissimilarities: a systematic review of international clinical practice guidelines for pregnancy hypertension, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is American Journal of Obstetrics and Gynecology (2022), 226(2_Suppl.), S1222-S1236, database is CAplus and MEDLINE.

A review. This study aimed to review pregnancy hypertension clin. practice guidelines to inform international clin. practice and research priorities. Relevant national and international clin. practice guidelines, 2009-19, published in English, French, Dutch or German. Following published methods and prospective registration (CRD42019123787), a literature search was updated. CPGs were identified by 2 authors independently who scored quality and usefulness for practice (Appraisal of Guidelines for Research and Evaluation II instrument), abstracted data, and resolved any disagreement by consensus. Of note, 15 of 17 identified clin. practice guidelines (4 international) were deemed “clin. useful” and had recommendations abstracted. The highest Appraisal of Guidelines for Research and Evaluation II scores were from government organizations, and scores have improved over time. The following were consistently recommended: (1) automated blood pressure measurement with devices validated for pregnancy and preeclampsia, reflecting increasing recognition of the prevalence of white-coat hypertension and the potential usefulness of home blood pressure monitoring; (2) use of dipstick proteinuria testing for screening followed by quant. testing by urinary protein-to-creatinine ratio or 24-h urine collection; (3) key definitions and most aspects of classification, including a broad definition of preeclampsia (which includes proteinuria and maternal end-organ dysfunction, including headache and visual symptoms and laboratory abnormalities of platelets, creatinine, or liver enzymes) and a recognition that it can worsen after delivery; (4) preeclampsia prevention with aspirin; (5) treatment of severe hypertension, most commonly with i.v. labetalol, oral nifedipine, or i.v. hydralazine; (6) treatment for nonsevere hypertension when undertaken, with oral labetalol (in particular), methyldopa, or nifedipine, with recommendations against the use of renin-angiotensin-aldosterone inhibitors; (7) magnesium sulfate for eclampsia treatment and prevention among women with “severe” preeclampsia; (8) antenatal corticosteroids for preterm birth but not hemolysis, elevated liver enzymes, and low platelet count syndrome; (9) delivery at term for preeclampsia; (10) a focus on usual labor and delivery care but avoidance of ergometrine; and (11) an apprecia. Lack of uniformity was seen in the following areas: (1) the components of a broad preeclampsia definition (specifically respiratory and gastrointestinal symptoms, fetal manifestations, and biomarkers), what constitutes severe preeclampsia, and whether the definition has utility because at present what constitutes severe preeclampsia by some guidelines that mandate proteinuria now defines any preeclampsia for most other clin. practice guidelines; (2) how preeclampsia risk should be identified early in pregnancy, and aspirin administered for preeclampsia prevention, because multivariable models (with biomarkers and ultrasonog. added to clin. risk markers) used in this way to guide aspirin therapy can substantially reduce the incidence of preterm preeclampsia; (3) the value of calcium added to aspirin for preeclampsia prevention, particularly for women with low intake and at increased risk of preeclampsia; (4) emerging recommendations to normalize blood pressure with antihypertensive agents even in the absence of comorbidities; (5) fetal neuroprotection as an indication for magnesium sulfate in the absence of “severe” preeclampsia; and (6) timing of birth for chronic and gestational hypertension and preterm preeclampsia. Consistent recommendations should be implemented and audited. Inconsistencies should be the focus of research.

American Journal of Obstetrics and Gynecology 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 C13H18BBrO3, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

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

Spring Walsh, Breeanna published the artcileA Cohort Comparison Study on Women in Threatened Preterm Labor Given Nifedipine or Nifedipine and Salbutamol Tocolysis in Air Medical Retrieval., HPLC of Formula: 21829-25-4, the publication is Air medical journal (2022), 41(3), 298-302, database is MEDLINE.

OBJECTIVE: Women with threatened preterm labor in remote Australia often require tocolysis in the prevention of in-flight birth during air medical retrieval. However, debate exists over the tocolytic choice. METHODS: A retrospective analysis was undertaken on data containing women who required air medical retrieval for threatened preterm labor within Western Australia between the years 2013 and 2018. RESULTS: A total number of 236 air medical retrievals were deemed suitable for inclusion; 141 received nifedipine, and 95 women received salbutamol + nifedipine. Tocolytic efficaciousness was reported in 151 cases, proportionally more (P < .05) from the women who received salbutamol + nifedipine (n = 68, 71.6%) compared with the women who received nifedipine only (n = 83, 58.9%). Those receiving salbutamol + nifedipine were more likely to suffer maternal tachycardia (n = 87 [91.6%] vs. n = 62 [44.0%]), fetal tachycardia (n = 26 [27.4%] vs. n = 13 [9.2%]), nausea (n = 17 [17.9] vs. n = 5 [3.55%]), and vomiting (n = 12 [12.6%] vs. n = 2 [1.4%]). Three women who received salbutamol + nifedipine had serious side effects including echocardiographic changes, chest pain, and metabolic and lactic acidosis. CONCLUSION: Salbutamol + nifedipine tocolysis was proven to be more effective than nifedipine only. Although salbutamol + nifedipine had increased temporary side effects, most were nonsevere and managed in-flight.

Air medical journal 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 C9H5FO2, HPLC of Formula: 21829-25-4.

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

Yart, Lucile published the artcileDual effect of nifedipine on pregnant human myometrium contractility: Implication of TRPC1, HPLC of Formula: 21829-25-4, the publication is Journal of Cellular Physiology (2022), 237(3), 1980-1991, database is CAplus and MEDLINE.

Nifedipine, an L-type voltage-gated Ca²⁺ channel (L-VGCC) blocker, is one of the most used tocolytics to treat preterm labor. In clin. practice, nifedipine efficiently decreases uterine contractions, but its efficacy is limited over time, and repeated or maintained nifedipine-based tocolysis appears to be ineffective in preventing preterm birth. We aimed to understand why nifedipine has short-lasting efficiency for the inhibition of uterine contractions. We used ex vivo term pregnant human myometrial strips treated with cumulative doses of nifedipine. We observed that nifedipine inhibited spontaneous myometrial contractions in tissues with high and regular spontaneous contractions. By contrast, nifedipine appeared to increase contractions in tissues with low and/or irregular spontaneous contractions. To investigate the mol. mechanisms activated by nifedipine in myometrial cells, we used the pregnant human myometrial cell line PHM1-41 that does not express L-VGCC. The in vitro measurement of intracellular Ca²⁺ showed that high doses of nifedipine induced an important intracellular Ca²⁺ entry in myometrial cells. The inhibition or downregulation of the genes encoding for store-operated Ca²⁺ entry channels from the Orai and transient receptor potential-canonical (TRPC) families in PHM1-41 cells highlighted the implication of TRPC1 in nifedipine-induced Ca²⁺ entry. In addition, the use of 2-APB in combination with nifedipine on human myometrial strips tends to confirm that the pro-contractile effect induced by nifedipine on myometrial tissues may involve the activation of TRPC channels.

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 C28H29NO4, HPLC of Formula: 21829-25-4.

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

Adel Madbouly, Neveen published the artcileIn vitro and in vivo impacts of nifedipine and diltiazem on praziquantel chemotherapy in murine Schistosoma mansoni, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Experimental Parasitology (2022), 108256, database is CAplus and MEDLINE.

This study was planned to evaluate the in vitro and in vivo antischistosomal effects of the widely used antihypertensive drugs, nifedipine (NIF) and diltiazem (DTZ), and their combinations with praziquantel (PZQ) on early and late Schistosoma (S.) mansoni infections 21- and 45- days old stages. In the In vitro study, Calcium channel blockers (CCBs), NIF and DTZ were added to schistosomula and adult worm cultures in different concentrations 10, 20 and 30 mg/mL. The mortality percentage was calculated 1, 12 and 24 h after incubation. In vivo, NIF and DTZ either alone or combined with PZQ were used to treat male albino mice. The parasitol. and total Ig (Ig) G and IgM anti-soluble egg antigen (SEA) were assessed to demonstrate the disease severity. In the In vitro study, 10 mg/mL NIF induced 100% mortality percentage of both schistosomula and adult worms after 24 h incubation, while DTZ induced similar mortality percentage at 30 mg/mL concentration In vivo results showed that early or late combination of 30 mg/kg of NIF, but not DTZ, significantly (P <0.05) enhanced the reductive efficacy of PZQ based on the parasitol. data. The maximal reduction (P <0.05) of anti-SEA IgM and IgG levels was developed during NIF-PZQ administration 21- (1.12 ± 0.06 and 1.09 ± 0.04, resp.) or 45- (1.00 ± 0.03 and 0.8 ± 0.06, resp.) days post infection (PI), compared to either PZQ or NIF individual treatments. The decreased concentration of anti-SEA antibodies was correlated with the diminished granulomatous diameter and disease severity. Nifedipine improved PZQ chemotherapy targeting either early or late S. mansoni infection in mice compared to the PZQ mono-therapy. Administering NIF can be considered as a promising drug candidate for schistosomiasis chemotherapy.

Experimental Parasitology 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, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

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