Category: 132-20-7

On November 30, 2019, Silverblatt, Joshua A.; Ziff, Oliver J.; Dancy, Luke; Daniel, Allen; Carter, Ben; Scott, Paul; Sado, Daniel M.; Shah, Ajay; Bromage, Daniel I. published an article.Synthetic Route of 132-20-7 The title of the article was Therapies to limit myocardial injury in animal models of myocarditis: a systematic review and meta-analysis. And the article contained the following:

Meta-anal. of current myocarditis guidelines do not advocate treatment to prevent myocardial injury and scar deposition in patients with myocarditis and normal left ventricular ejection fraction. We aimed to ascertain the utility of beta blockers, calcium channel blockers and antagonists of the renin-angiotensin system in ameliorating myocardial injury, scar formation and calcification in animal in vivo models of myocarditis. The project was prospectively registered with the PROSPERO database of systematic reviews (CRD42018089336). Primary outcomes (necrosis, fibrosis and calcification) were meta-analyzed with random-effects modeling. 52 Studies were systematically reviewed. Meta-anal. was performed compared with untreated controls. In each study, we identified all independent comparisons of treatment vs. control groups. The pooled weighted mean difference (WMD) indicated treatment reduced necrosis by 16.9% (71 controlled analyses, 95% CI 13.2-20.7%; P < 0.001), however there was less evidence of an effect after accounting for publication bias. Treatment led to a 12.8% reduction in fibrosis (73 controlled analyses, 95% CI 7.6-18.0%; P < 0.001). After accounting for publication bias this was attenuated to 7.8% but remained significant. Treatment reduced calcification by 4.1% (28 controlled analyses, 95% CI 0.2-8.0%; P < 0.0395). We observed significant heterogeneity in effect size in all primary endpoints, which was predominantly driven by differences between drug categories. Beta blockers and angiotensin-converting enzyme (ACE) inhibitors were the only agents that were effective for both necrosis and fibrosis, while only ACE inhibitors had a significant effect on calcification. This study provides evidence for a role for ACE inhibitors and beta blockers to prevent myocardial injury and scar deposition in in vivo models of myocarditis. There is a need for further well-designed studies to assess the translational application of these treatments. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Synthetic Route of 132-20-7

The Article related to meta analysis myocardial injury myocarditis beta calcium channel blocker, calcification, drug treatment, fibrosis, meta-analysis, myocarditis, necrosis, remodelling, systematic review and other aspects.Synthetic Route of 132-20-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Padivitage, Nilusha L.; Smuts, Jonathan P.; Breitbach, Zachary S.; Armstrong, Daniel W.; Berthod, Alain published an article in 2015, the title of the article was Preparation and Evaluation of HPLC Chiral Stationary Phases Based on Cationic/Basic Derivatives of Cyclofructan 6.Category: pyridine-derivatives And the article contains the following content:

The cyclofructan 6 (CF6) macrocyclic-oligosaccharide was derivatized with five different substituents able to bear pos. charges: Pr imidazole, Me benzimidazole, di-Me aminopropyl, pyridine, and di-Me aminophenyl. The derivatized cyclofructans were reacted with triethoxysilyl-propylisocyanate as a linker to bond them to 5μm spherical silica gel particles and then used to prepare liquid chromatog. columns. The bonded silica particles were analyzed to establish the bonding densities. A set of 34 chiral compounds including acids, neutral compounds, and bases was tested with nine different mobile phase compositions including two reverse phase (RP) acetonitrile/pH 4 buffer, three polar organic (PO) acetonitrile/methanol, and four normal phase (NP) heptane/ethanol mobile phases. No compounds could be separated in the RP mode. Eight compounds only could be enantiosepd. in the PO mode and 21 compounds in the NP mode. The most effective chiral stationary phase was the Pr imidazole derivatized CF6 phase, provided no more than six imidazole substituents and two linkers are attached per CF6 unit. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Category: pyridine-derivatives

The Article related to cyclofructan cationic derivative hplc chiral stationary phase enantiomer separation, liquid chromatography, cationic derivatives, chiral separation, cyclofructan, enantiomer separation and other aspects.Category: pyridine-derivatives

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

On September 5, 2013, Musdal, Yaman; Hegazy, Usama M.; Aksoy, Yasemin; Mannervik, Bengt published an article.Reference of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate The title of the article was FDA-approved drugs and other compounds tested as inhibitors of human glutathione transferase P1-1. And the article contained the following:

Glutathione transferase P1-1 (GST P1-1) is often overexpressed in tumor cells and is regarded as a contributor to their drug resistance. Inhibitors of GST P1-1 are expected to counteract drug resistance and may therefore serve as adjuvants in the chemotherapy of cancer by increasing the efficacy of cytostatic drugs. Finding useful inhibitors among compounds used for other indications would be a shortcut to clin. applications and a search for GST P1-1 inhibitors among approved drugs and other compounds was therefore conducted. We tested 1040 FDA-approved compounds as inhibitors of the catalytic activity of purified human GST P1-1 in vitro. We identified chlorophyllide, merbromine, hexachlorophene, and ethacrynic acid as the most effective GST P1-1 inhibitors with IC50 values in the low micromolar range. For comparison, these compounds were even more potent in the inhibition of human GST A3-3, an enzyme implicated in steroid hormone biosynthesis. In distinction from the other inhibitors, which showed conventional inhibition patterns, the competitive inhibitor ethacrynic acid elicited strong kinetic cooperativity in the glutathione saturation of GST P1-1. Apparently, ethacrynic acid serves as an allosteric inhibitor of the enzyme. In their own right, the compounds investigated are less potent than desired for adjuvants in cancer chemotherapy, but the structures of the most potent inhibitors could serve as leads for the synthesis of more efficient adjuvants. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Reference of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

The Article related to recombinant glutathione transferase p11 inhibitor adjuvant chemotherapy, adjuvant chemotherapeutics, enzyme inhibition, ethacrynic acid, fda-approved drugs, glutathione transferase p1-1 and other aspects.Reference of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

On September 15, 2014, Gouda, Ayman A.; Hashem, Hisham; Jira, Thomas published an article.Recommanded Product: 132-20-7 The title of the article was Development and validation of a rapid stability indicating HPLC-method using monolithic stationary phase and two spectrophotometric methods for determination of antihistaminic acrivastine in capsules. And the article contained the following:

Simple, rapid and accurate high performance liquid chromatog. (HPLC) and spectrophotometric methods are described for determination of antihistaminic acrivastine in capsules. The first method (method A) is based on accurate, sensitive and stability indicating chromatog. separation method. Chromolith Performance RP-18e column, a relatively new packing material consisting of monolithic rods of highly porous silica, was used as stationary phase applying isocratic binary mobile phase of ACN and 25 mM NaH2PO4 pH 4.0 in the ratio of 22.5:77.5 at flow rate of 5.0 mL/min and 40 °C. A diode array detector was used at 254 nm for detection. The elution time of acrivastine was found to be 2.080 ± 0.032. The second and third methods (methods B and C) are based on the oxidation of acrivastine with excess N-bromosuccinimide (NBS) and determination of the unconsumed NBS with, metol-sulfanilic acid (λmax: 520 nm) or amaranth dye (λmax: 530 nm). The reacted oxidant corresponds to the drug content. Beer’s law is obeyed over the concentration range 1.563-50, 2.0-20 and 1.0-10 μg mL-1 for methods A, B and C, resp. The limits of detection and quantitation were 0.40, 0.292 and 0.113 μg mL-1 and 0.782, 0.973 and 0.376 μg mL-1 for methods A, B and C, resp. The HPLC method was validated for system suitability, linearity, precision, limits of detection and quantitation, specificity, stability and robustness. Stability tests were done through exposure of the analyte solution for four different stress conditions and the results indicate no interference of degradants with HPLC-method. The proposed methods was favorably applied for determination of acrivastine in capsules formulation. Statistical comparison of the obtained results from the anal. of the studied drug to those of the reported method using t- and F-tests showed no significant difference between them. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Recommanded Product: 132-20-7

The Article related to chromatog monolithic stationary phase spectrophotometry antihistaminic acrivastine capsule, acrivastine, capsules, monolithic columns, n-bromosuccinimide, spectrophotometry, stability indicating lc-method and other aspects.Recommanded Product: 132-20-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

On September 15, 2014, Gouda, Ayman A.; Hashem, Hisham; Jira, Thomas published an article.Recommanded Product: 132-20-7 The title of the article was Development and validation of a rapid stability indicating HPLC-method using monolithic stationary phase and two spectrophotometric methods for determination of antihistaminic acrivastine in capsules. And the article contained the following:

Simple, rapid and accurate high performance liquid chromatog. (HPLC) and spectrophotometric methods are described for determination of antihistaminic acrivastine in capsules. The first method (method A) is based on accurate, sensitive and stability indicating chromatog. separation method. Chromolith Performance RP-18e column, a relatively new packing material consisting of monolithic rods of highly porous silica, was used as stationary phase applying isocratic binary mobile phase of ACN and 25 mM NaH2PO4 pH 4.0 in the ratio of 22.5:77.5 at flow rate of 5.0 mL/min and 40 °C. A diode array detector was used at 254 nm for detection. The elution time of acrivastine was found to be 2.080 ± 0.032. The second and third methods (methods B and C) are based on the oxidation of acrivastine with excess N-bromosuccinimide (NBS) and determination of the unconsumed NBS with, metol-sulfanilic acid (λmax: 520 nm) or amaranth dye (λmax: 530 nm). The reacted oxidant corresponds to the drug content. Beer’s law is obeyed over the concentration range 1.563-50, 2.0-20 and 1.0-10 μg mL-1 for methods A, B and C, resp. The limits of detection and quantitation were 0.40, 0.292 and 0.113 μg mL-1 and 0.782, 0.973 and 0.376 μg mL-1 for methods A, B and C, resp. The HPLC method was validated for system suitability, linearity, precision, limits of detection and quantitation, specificity, stability and robustness. Stability tests were done through exposure of the analyte solution for four different stress conditions and the results indicate no interference of degradants with HPLC-method. The proposed methods was favorably applied for determination of acrivastine in capsules formulation. Statistical comparison of the obtained results from the anal. of the studied drug to those of the reported method using t- and F-tests showed no significant difference between them. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Recommanded Product: 132-20-7

The Article related to chromatog monolithic stationary phase spectrophotometry antihistaminic acrivastine capsule, acrivastine, capsules, monolithic columns, n-bromosuccinimide, spectrophotometry, stability indicating lc-method and other aspects.Recommanded Product: 132-20-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

On March 2, 2022, Cai, Bicheng; Gong, Liang; Zhu, Yiying; Kong, Lingmei; Ju, Xiaoman; Li, Xue; Yang, Xiaodong; Zhou, Hongyu; Li, Yan published an article.Recommanded Product: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate The title of the article was Identification of Gossypol Acetate as an Autophagy Modulator with Potent Anti-tumor Effect against Cancer Cells. And the article contained the following:

Autophagy, an evolutionarily conserved process, is intricately involved in many aspects of human health and a variety of human diseases, including cancer. Discovery of small-mol. autophagy modulators with potent anticancer effect would be of great significance. To this end, a natural product library consisting of 170 natural compounds were screened as autophagy modulators with potent cytotoxicity in our present study. Among these compounds, gossypol acetate (GAA), the mostly used medicinal form of gossypol, was identified. GAA effectively increased the number of autophagic puncta in GFP-LC3B-labeled 293T cells and significantly decreased cell viability in different cancer cells. In A549 cells, GAA at concentrations below 10 μM triggered caspase-independent cell death via targeting autophagy, as evidenced by elevated LC3 conversion and decreased p62/SQSTM1 levels. Knocking down of LC3 significantly attenuated GAA-induced cell death. Mechanistically, GAA at low concentrations induced autophagy through targeting AMPK-mTORC1-ULK1 signaling. Interestingly, high concentrations of GAA induced LC3 conversion, p62 accumulation, and yellow autophagosome formation, indicating that GAA at high concentrations blocked autophagic flux. Mechanistically, GAA decreased intracellular ATP level and suppressed lysosome activity. Exogenous ATP partially reversed the inhibitory effect of GAA on autophagy, suggesting that decreased ATP level and lysosome activity might be involved in the blocking of autophagy flux by GAA. Collectively, our present study reveals the mechanisms by which GAA modulates autophagy and illustrates whether autophagy regulation by GAA is functionally involved in GAA-induced cancer cell death. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Recommanded Product: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

The Article related to drug screening gossypol acetate autophagy cancer, atp, adenosine 5′-monophosphate (amp)-activated protein kinase (ampk), apoptosis, autophagy, cancer cell death, gossypol acetate, lysosome, mammalian target of rapamycin complex-1 (mtorc1), unc-51-like autophagy-activating kinase 1 (ulk1) and other aspects.Recommanded Product: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

On March 2, 2022, Cai, Bicheng; Gong, Liang; Zhu, Yiying; Kong, Lingmei; Ju, Xiaoman; Li, Xue; Yang, Xiaodong; Zhou, Hongyu; Li, Yan published an article.Recommanded Product: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate The title of the article was Identification of Gossypol Acetate as an Autophagy Modulator with Potent Anti-tumor Effect against Cancer Cells. And the article contained the following:

Autophagy, an evolutionarily conserved process, is intricately involved in many aspects of human health and a variety of human diseases, including cancer. Discovery of small-mol. autophagy modulators with potent anticancer effect would be of great significance. To this end, a natural product library consisting of 170 natural compounds were screened as autophagy modulators with potent cytotoxicity in our present study. Among these compounds, gossypol acetate (GAA), the mostly used medicinal form of gossypol, was identified. GAA effectively increased the number of autophagic puncta in GFP-LC3B-labeled 293T cells and significantly decreased cell viability in different cancer cells. In A549 cells, GAA at concentrations below 10 μM triggered caspase-independent cell death via targeting autophagy, as evidenced by elevated LC3 conversion and decreased p62/SQSTM1 levels. Knocking down of LC3 significantly attenuated GAA-induced cell death. Mechanistically, GAA at low concentrations induced autophagy through targeting AMPK-mTORC1-ULK1 signaling. Interestingly, high concentrations of GAA induced LC3 conversion, p62 accumulation, and yellow autophagosome formation, indicating that GAA at high concentrations blocked autophagic flux. Mechanistically, GAA decreased intracellular ATP level and suppressed lysosome activity. Exogenous ATP partially reversed the inhibitory effect of GAA on autophagy, suggesting that decreased ATP level and lysosome activity might be involved in the blocking of autophagy flux by GAA. Collectively, our present study reveals the mechanisms by which GAA modulates autophagy and illustrates whether autophagy regulation by GAA is functionally involved in GAA-induced cancer cell death. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Recommanded Product: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

The Article related to drug screening gossypol acetate autophagy cancer, atp, adenosine 5′-monophosphate (amp)-activated protein kinase (ampk), apoptosis, autophagy, cancer cell death, gossypol acetate, lysosome, mammalian target of rapamycin complex-1 (mtorc1), unc-51-like autophagy-activating kinase 1 (ulk1) and other aspects.Recommanded Product: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem