Month: November 2022

Lee, Bo Bin published the artcileMetformin and tenovin-6 synergistically induces apoptosis through LKB1-independent SIRT1 down-regulation in non-small cell lung cancer cells, HPLC of Formula: 1011557-82-6, the publication is Journal of Cellular and Molecular Medicine (2019), 23(4), 2872-2889, database is CAplus and MEDLINE.

Sirtuin 1 (SIRT1) is known to play a role in a variety of tumorigenesis processes by deacetylating histone and non-histone proteins; however, antitumor effects by suppressing SIRT1 activity in non-small cell lung cancer (NSCLC) remain unclear. This study was designed to scrutinize clinicopathol. significance of SIRT1 in NSCLC and investigate effects of metformin on SIRT1 inhibition. This study also evaluated new possibilities of drug combination using a SIRT1 inhibitor, tenovin-6, in NSCLC cell lines. It was found that SIRT1 was overexpressed in 300 (62%) of 485 formalin-fixed paraffin-embedded NSCLC tissues. Its overexpression was significantly associated with reduced overall survival and poor recurrence-free survival after adjusted for histol. and pathol. stage. Thus, suppression of SIRT1 expression may be a reasonable therapeutic strategy for NSCLC. Metformin in combination with tenovin-6 was found to be more effective in inhibiting cell growth than either agent alone in NSCLC cell lines with different liver kinase B1 (LKB1) status. In addition, metformin and tenovin-6 synergistically suppressed SIRT1 expression in NSCLC cells regardless of LKB1 status. The marked reduction in SIRT1 expression by combination of metformin and tenovin-6 increased acetylation of p53 at lysine 382 and enhanced p53 stability in LKB1-deficient A549 cells. The combination suppressed SIRT1 promoter activity more effectively than either agent alone by up-regulating hypermethylation in cancer 1 (HIC1) binding at SIRT1 promoter. Also, suppressed SIRT1 expression by the combination synergistically induced caspase-3-dependent apoptosis. The study concluded that metformin with tenovin-6 may enhance antitumor effects through LKB1-independent SIRT1 down-regulation in NSCLC cells.

Journal of Cellular and Molecular Medicine published new progress about 1011557-82-6. 1011557-82-6 belongs to amides-buliding-blocks, auxiliary class Epigenetics,Sirtuin, name is 4-(tert-Butyl)-N-((4-(5-(dimethylamino)pentanamido)phenyl)carbamothioyl)benzamide, and the molecular formula is C25H34N4O2S, HPLC of Formula: 1011557-82-6.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Fier, Patrick S. published the artcileA Multifunctional Reagent Designed for the Site-Selective Amination of Pyridines, Computed Properties of 1453-82-3, the publication is Journal of the American Chemical Society (2020), 142(19), 8614-8618, database is CAplus and MEDLINE.

The development of a multifunctional reagent for the direct conversion of pyridines to Boc-protected 2-aminopyridines such as I [R = H, 3-Br, 4-Ph, etc.] with exquisite site selectivity and chemoselectivity was reported. The novel reagent was prepared on 200g scale in a single step, reacted in title reaction under mild conditions without precautions toward air or moisture, and is tolerant of nearly all common functionality. Exptl. and in situ spectroscopic monitoring techniques provided detailed insights and unexpected findings for the unique reaction mechanism.

Journal of the American Chemical Society published new progress about 1453-82-3. 1453-82-3 belongs to amides-buliding-blocks, auxiliary class Pyridine,Amine,Amide, name is Isonicotinamide, and the molecular formula is C6H6N2O, Computed Properties of 1453-82-3.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Chou, Richard C. published the artcileLipid-Cytokine-Chemokine Cascade Drives Neutrophil Recruitment in a Murine Model of Inflammatory Arthritis, Safety of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Immunity (2010), 33(2), 266-278, database is CAplus and MEDLINE.

A large and diverse array of chemoattractants control leukocyte trafficking, but how these apparently redundant signals collaborate in vivo is still largely unknown. We previously demonstrated an absolute requirement for the lipid chemoattractant leukotriene B₄ (LTB₄) and its receptor BLT1 for neutrophil recruitment into the joint in autoantibody-induced arthritis. We now demonstrate that BLT1 is required for neutrophils to deliver IL-1 into the joint to initiate arthritis. IL-1-expressing neutrophils amplify arthritis through the production of neutrophil-active chemokines from synovial tissue cells. CCR1 and CXCR2, two neutrophil chemokine receptors, operate nonredundantly to sequentially control the later phase of neutrophil recruitment into the joint and mediate all neutrophil chemokine activity in the model. Thus, we have uncovered a complex sequential relationship involving unique contributions from the lipid mediator LTB₄, the cytokine IL-1, and CCR1 and CXCR2 chemokine ligands that are all absolutely required for effective neutrophil recruitment into the joint.

Immunity published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Safety of [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Kwon, Kee Woong published the artcileHost-directed anti-mycobacterial activity of colchicine, an anti-gout drug, via strengthened host innate resistance reinforced by the IL-1β/PGE₂ axis, Recommanded Product: 4-(5-(p-Tolyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide, the publication is British Journal of Pharmacology (2022), 179(15), 3951-3969, database is CAplus and MEDLINE.

To diversify and expand possible tuberculosis (TB) drug candidates and maximize limited global resources, we investigated the effect of colchicine, an FDA-approved anti-gout drug, against Mycobacterium tuberculosis (Mtb) infection because of its immune-modulating effects. We evaluated the intracellular anti-Mtb activity of different concentrations of colchicine in murine bone marrow-derived macrophages (BMDMs). To elucidate the underlying mechanism, RNA sequencing, biol. and chem. inhibition assays, and Western blot, quant. real-time PCR, ELISA (ELISA), and immunohistochem. analyses were employed. Finally, type I interferon-dependent highly TB-susceptible A/J mice were challenged with virulent Mtb H37Rv, and the host-directed therapeutic effect of oral colchicine administration on bacterial burdens and lung inflammation was assessed 30 days post-infection (2.5 mg·kg-1 every 2 days). Colchicine reinforced the anti-Mtb activity of BMDMs without affecting cell viability, indicating that colchicine facilitated macrophage immune activation upon Mtb infection. The results from RNA sequencing, NLRP3 knockout BMDM, IL-1 receptor blockade, and immunohistochem. analyses revealed that this unexpected intracellular anti-Mtb activity of colchicine was mediated through NLRP3-dependent IL-1β signalling and Cox-2-regulated PGE2 production in macrophages. Consequently, the TB-susceptible A/J mouse model showed remarkable protection, with decreased bacterial loads in both the lungs and spleens of oral colchicine-treated mice, with significantly elevated Cox-2 expression at infection sites. The repurposing of colchicine against Mtb infection in this study highlights its unique function in macrophages upon Mtb infection and its novel potential use in treating TB as host-directed or adjunctive therapy.

British Journal of Pharmacology published new progress about 169590-42-5. 169590-42-5 belongs to amides-buliding-blocks, auxiliary class Sulfamide,Immunology/Inflammation,COX, name is 4-(5-(p-Tolyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide, and the molecular formula is C17H14F3N3O2S, Recommanded Product: 4-(5-(p-Tolyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Jo, Woohyun published the artcileTransition-Metal-Free Regioselective Alkylation of Pyridine N-Oxides Using 1,1-Diborylalkanes as Alkylating Reagents, Formula: C10H14N2O, the publication is Angewandte Chemie, International Edition (2016), 55(33), 9690-9694, database is CAplus and MEDLINE.

Reported herein is an unprecedented base-promoted deborylative alkylation of pyridine N-oxides using 1,1-diborylalkanes as alkyl sources. The reaction proceeds efficiently for a wide range of pyridine N-oxides and 1,1-diborylalkanes with excellent regioselectivity. The utility of the developed method is demonstrated by the sequential C-H arylation and methylation of pyridine N-oxides. The reaction also can be applied to the direct introduction of a Me group to 9-O-methylquinine N-oxide; thus it can serve as a powerful method for late-stage functionalization.

Angewandte Chemie, International Edition published new progress about 530-40-5. 530-40-5 belongs to amides-buliding-blocks, auxiliary class Pyridine,Amine,Amide, name is N,N-Diethylisonicotinamide, and the molecular formula is C10H14N2O, Formula: C10H14N2O.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Lee, Wongyu published the artcilePhotoinduced α-C-H Amination of Cyclic Amine Scaffolds Enabled by Polar-Radical Relay, SDS of cas: 169590-42-5, the publication is Angewandte Chemie, International Edition (2022), 61(25), e202202971, database is CAplus and MEDLINE.

Herein, a polar-radical relay strategy for α-C-H amination of cyclic amines with N-chloro-N-sodio-carbamates is reported. The relay is initiated by in situ generation of a cyclic iminium intermediate using N-iodosuccinimide oxidant as an initiator, which then operates through a series of polar (addition and elimination) and radical (homolysis, hydrogen- and halogen atom transfer) reactions to enable the challenging C-N bond formation in a controlled manner. A broad range of α-amino cyclic amines were readily accessed with excellent regioselectivity, and the superb applicability was further demonstrated by functionalization of biol. relevant compounds

Angewandte Chemie, International Edition published new progress about 169590-42-5. 169590-42-5 belongs to amides-buliding-blocks, auxiliary class Sulfamide,Immunology/Inflammation,COX, name is 4-(5-(p-Tolyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide, and the molecular formula is C17H14F3N3O2S, SDS of cas: 169590-42-5.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Noei, Jalil published the artcileTiCl₃OTf-[bmim]Br, a novel and efficient catalyst system for chemoselective one-pot synthesis of thioamides from arylaldoximes, Product Details of C8H9NOS, the publication is Tetrahedron Letters (2008), 49(49), 6969-6971, database is CAplus.

The combination of TiCl₃OTf with 1-butyl-3-methylimidazolium bromide is an efficient and novel catalytic system for chemoselective one-pot transformation of arylaldoximes to their corresponding thioamides in high to excellent yields.

Tetrahedron Letters published new progress about 64559-06-4. 64559-06-4 belongs to amides-buliding-blocks, auxiliary class Amine,Benzene,Amide,Ether, name is 3-Methoxybenzothioamide, and the molecular formula is C8H9NOS, Product Details of C8H9NOS.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Aziz, Faisal published the artcilePartners in crime: The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer, Computed Properties of 169590-42-5, the publication is Pharmacology & Therapeutics (2022), 107994, database is CAplus and MEDLINE.

A review. Helicobacter pylori (H. pylori) is a major causative agent of chronic gastritis, gastric ulcer and gastric carcinoma. H. pylori cytotoxin associated antigen A (CagA) plays a crucial role in the development of gastric cancer. Gastric cancer is associated with glycosylation alterations in glycoproteins and glycolipids on the cell surface. H. pylori cytotoxin associated antigen A (CagA) plays a significant role in the progression of gastric cancer through post-translation modification of fucosylation to develop gastric cancer. The involvement of a variety of sugar antigens in the progression and development of gastric cancer has been investigated, including type II blood group antigens. Lewis Y (LeY) is overexpressed on the tumor cell surface either as a glycoprotein or glycolipid. LeY is a difucosylated oligosaccharide, which is catalyzed by fucosyltransferases such as FUT4 (α1,3). FUT4/LeY overexpression may serve as potential correlative biomarkers for the prognosis of gastric cancer. We discuss the various aspects of H. pylori in relation to fucosyltransferases (FUT1-FUT9) and its fucosylated Lewis antigens (LeY, LeX, LeA, and LeB) and gastric cancer. In this review, we summarize the carcinogenic effect of H. pylori CagA in association with LeY and its synthesis enzyme FUT4 in the development of gastric cancer as well as discuss its importance in the prognosis and its inhibition by combination therapy of anti-LeY antibody and celecoxib through MAPK signaling pathway preventing gastric carcinogenesis.

Pharmacology & Therapeutics published new progress about 169590-42-5. 169590-42-5 belongs to amides-buliding-blocks, auxiliary class Sulfamide,Immunology/Inflammation,COX, name is 4-(5-(p-Tolyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide, and the molecular formula is C17H14F3N3O2S, Computed Properties of 169590-42-5.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Ahmadi, Abbas published the artcileSynthesis and Investigating Hypoglycemic and Hypolipidemic Activities of Some Glibenclamide Analogues in Rats, Recommanded Product: 2,4-Dichlorobenzamide, the publication is Mini-Reviews in Medicinal Chemistry (2014), 14(2), 208-213, database is CAplus and MEDLINE.

Glibenclamide (5-chloro-N-(4-[N-(cyclohexylcarbamoyl) sulfamoyl] phenethyl)-2-methoxybenzamide, Glyburide, E) is a well-known and potent second-generation of sulfonylurea oral hypoglycemic drug which is most widely used in type 2 diabetes recently. It acts upon pancreatic β -cells by stimulating insulin secretion in glucose and lipid-lowering activities. So far, many derivatives of E have been synthesized by adding new structural moieties to its structure while preserving its binding affinity to the receptor before their anti-hyperglycemic and anti hyperlipidemic activities being evaluated. In this study, new analogs of E after changing lipophilic side chain (5-chloro-2-methoxy benzamide) with 4- bromo-3, 5-dimethoxy benzamide and 2, 4-dichloro benzamide were synthesized. Also, their glucose and lipid-lowering activities were evaluated and compared to E and Tolbutamide (a famous first-generation of sulfonylurea oral hypoglycemic drug) by the known procedures. Findings showed that chloride substitution on lipophilic side chain of Glibenclamide could possibly increase the affinity of drug for receptor/or its half life time that resulted in more lasting anti-hyperglycemic and anti lipidemic activities in diabetic rats. However, bromide substitution with addnl. methoxy groups in benzamide ring could slightly improve the anti-hyperglycemic potency of the new drug compared to the root drug (E).

Mini-Reviews in Medicinal Chemistry published new progress about 2447-79-2. 2447-79-2 belongs to amides-buliding-blocks, auxiliary class Chloride,Amine,Benzene,Amide, name is 2,4-Dichlorobenzamide, and the molecular formula is C7H5Cl2NO, Recommanded Product: 2,4-Dichlorobenzamide.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Sobh, Eman A. published the artcileNew benzothienopyrimidine derivatives as dual EGFR/ARO inhibitors: Design, synthesis, and their cytotoxic effect on MCF-7 breast cancer cell line, Application of 2-Chloroacetamide, the publication is Drug Development Research, database is CAplus and MEDLINE.

New cytotoxic agents based on benzothienopyrimidine scaffold were designed, synthesized, and evaluated against the MCF-7 breast cancer line in comparison to erlotinib and letrozole as reference drugs. Eight compounds demonstrated up to 20-fold higher anticancer activity than erlotinib, and five of these compounds were up to 11-fold more potent than letrozole in MTT assay. The most promising compounds were evaluated for their inhibitory activity against EGFR and ARO enzymes. Compound 12, which demonstrated potent dual EGFR and ARO inhibitory activity with IC₅₀ of 0.045 and 0.146 μM, resp., was further evaluated for caspase-9 activation, cell cycle anal., and apoptosis. The results revealed that the tested compound 12 remarkably induced caspase-9 activation (IC₅₀ = 16.29 ng/mL) caused cell cycle arrest at the pre-G₁/G₁ phase and significantly increased the concentration of cells at both early and late stage of apoptosis. In addition, it showed a higher safety profile on normal MCF-10A cells, and higher antiproliferative activity on cancer cells (IC₅₀ = 8.15 μM) in comparison to normal cells (IC₅₀ = 41.20 μM). It also revealed a fivefold higher selectivity index than erlotinib towards MCF-7 cancer cells. Docking studies were performed to rationalize the dual inhibitory activity of compound 12.

Drug Development Research published new progress about 79-07-2. 79-07-2 belongs to amides-buliding-blocks, auxiliary class Chloride,Amine,Aliphatic hydrocarbon chain,Amide,Inhibitor, name is 2-Chloroacetamide, and the molecular formula is C5H10Cl3O3P, Application of 2-Chloroacetamide.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics