Tag: M.W=350-400

Hu, Jing published the artcileA fluorogenic assay for screening Sirt6 modulators, SDS of cas: 380315-80-0, the publication is Organic & Biomolecular Chemistry (2013), 11(32), 5213-5216, database is CAplus and MEDLINE.

A fluorogenic high-throughput assay suitable for screening Sirt6 modulators is developed based on the recently discovered efficient activity of Sirt6 to hydrolyze myristoyl lysine. Sirt6 modulators will be useful in investigating the function of Sirt6 and protein lysine fatty acylation.

Organic & Biomolecular Chemistry published new progress about 380315-80-0. 380315-80-0 belongs to amides-buliding-blocks, auxiliary class Apoptosis,p53, name is N-((4-Acetamidophenyl)carbamothioyl)-4-(tert-butyl)benzamide, and the molecular formula is C20H23N3O2S, SDS of cas: 380315-80-0.

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

Rausch, Keiko published the artcileScreening Bioactives Reveals Nanchangmycin as a Broad Spectrum Antiviral Active against Zika Virus, HPLC of Formula: 380315-80-0, the publication is Cell Reports (2017), 18(3), 804-815, database is CAplus and MEDLINE.

Zika virus is an emerging arthropod-borne flavivirus for which there are no vaccines or specific therapeutics. We screened a library of 2,000 bioactive compounds for their ability to block Zika virus infection in three distinct cell types with two different strains of Zika virus. Using a microscopy-based assay, we validated 38 drugs that inhibited Zika virus infection, including FDA-approved nucleoside analogs. Cells expressing high levels of the attachment factor AXL can be protected from infection with receptor tyrosine kinase inhibitors, while placental-derived cells that lack AXL expression are insensitive to this inhibition. Importantly, we identified nanchangmycin as a potent inhibitor of Zika virus entry across all cell types tested, including physiol. relevant primary cells. Nanchangmycin also was active against other medically relevant viruses, including West Nile, dengue, and chikungunya viruses that use a similar route of entry. This study provides a resource of small mols. to study Zika virus pathogenesis.

Cell Reports published new progress about 380315-80-0. 380315-80-0 belongs to amides-buliding-blocks, auxiliary class Apoptosis,p53, name is N-((4-Acetamidophenyl)carbamothioyl)-4-(tert-butyl)benzamide, and the molecular formula is C20H23N3O2S, HPLC of Formula: 380315-80-0.

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

Pontiki, Eleni published the artcileHistone deacetylase inhibitors (HDACIs). Structure-activity relationships: history and new QSAR perspectives, HPLC of Formula: 380315-80-0, the publication is Medicinal Research Reviews (2012), 32(1), 1-165, database is CAplus and MEDLINE.

A review. Histone deacetylase (HDAC) inhibition is a recent, clin. validated therapeutic strategy for cancer treatment. HDAC inhibitors (HDACIs) block angiogenesis, arrest cell growth, and lead to differentiation and apoptosis in tumor cells. In this article, a survey of published quant. structure-activity relationships (QSARs) studies are presented and discussed in the hope of identifying the structural determinants for anticancer activity. Secondly a two-dimensional QSAR study was carried out on biol. results derived from various types of HDACIs and from different assays using the C-QSAR program of Biobyte. The QSAR anal. presented here is an attempt to organize the knowledge on the HDACIs with the purpose of designing new chem. entities with enhanced inhibitory potencies and to study the mechanism of action of the compounds This study revealed that lipophilicity is one of the most important determinants of activity. Addnl., steric factors such as the overall molar refractivity (CMR), molar volume (MgVol), the substituent’s molar refractivity (MR) (linear or parabola), or the sterimol parameters B₁ and L are important. Electronic parameters indicated as σ_p, are found to be present only in one case. © 2010 Wiley Periodicals, Inc. Med Res Rev 32:1-165, 2012.

Medicinal Research Reviews published new progress about 380315-80-0. 380315-80-0 belongs to amides-buliding-blocks, auxiliary class Apoptosis,p53, name is N-((4-Acetamidophenyl)carbamothioyl)-4-(tert-butyl)benzamide, and the molecular formula is C20H23N3O2S, HPLC of Formula: 380315-80-0.

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

Matsunuma, Satoru published the artcileHigh concentration of oxaliplatin may be a risk factor for vascular pain, SDS of cas: 169590-42-5, the publication is Journal of Clinical Pharmacy and Therapeutics (2022), 47(4), 462-468, database is CAplus and MEDLINE.

Oxaliplatin (L-OHP) is an antineoplastic agent that frequently causes vascular pain. However, the risk factors for vascular pain are unclear, and prevention methods have not been established. We retrospectively investigated patients who were treated with L-OHP to examine the influence of patient characteristics and concomitant analgesic use on the incidence of vascular pain. We collected information about the presence or absence of vascular pain, age, sex, treatment dose and analgesic use of patients who received L-OHP at Tokyo Medical University Hachioji Medical Center. We analyzed the relevance of each factor between the vascular pain onset and non-onset groups. Thirty-two patients (average age: 68.6 years; 69.8% and 30.2% men and women, resp.) were classified into the vascular pain onset (n = 64) and non-onset groups (n = 68). The multivariate logistic regression anal. revealed that L-OHP concentration (>358.5 mg/L) was an independent determinant of vascular pain development (odds ratio: 2.422, 95% CI: 1.117-5.252). Intergroup differences in age, sex, body mass index, non-steroidal anti-inflammatory drug use, and underlying pain from cancer and other comorbidities were not significant. High L-OHP concentration was identified as a significant risk factor for L-OHP-induced vascular pain. Our results indicate that the dilution of L-OHP may reduce the incidence of vascular pain.

Journal of Clinical Pharmacy and 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, SDS of cas: 169590-42-5.

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

Grigoreva, Yu S published the artcile[The role of p53 in the regulation of proliferation and differentiation of the neural progenitors in mouse hippocampal organotypic culture]., Product Details of C20H23N3O2S, the publication is Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova (2013), 99(10), 1160-74, database is MEDLINE.

In the present work we have studied the effects of p53 on the proliferation and differentiation of neural progenitor cells (NPC) in mouse hippocampal organotypic culture. To study the role of p53 the selective p53 inhibitor pifithrin-alpha (PFT) and activator tenovin 1 (TEN) were used in the experiments. Obtained data demonstrated that the injections of PFT did not affect on the amount of phospho-H3 positive cells in the subgranular zone of hippocampus. This data revealed that p53 inhibition does not change the proliferation level of the NPC. In opposite, at the TEN treatments we observed increased of the proliferation activity. Analysis of Pim-1 and Phb 1, which regulate cell cycle progression, demonstrated that p53 activation led to increased level of Pim-1 as well as the proliferation. Thus, our data correlate with published ones and proposed that Pim-1 positively regulates NPC cell cycle progression. In opposite to Pim-1, Phb 1 has anti-proliferative action. Our obtained data demonstrated that TEN diminished Phb 1 expression. Primarily PFT injections led to the increasing Phbl level, but then dramatically decreased it that accompanied with unchanged proliferation level. In other words, increased proliferation level after TEN treatments, which we observed, can be partly depend from the inhibition of anti-proliferative activity of Phb. In our study we demonstrated that both TEN and in a greater degree PFT stimulates neuronal differentiation by activation of CRMP-2 expression, but do not affect on gliogenesis. Thus, obtained data revealed that p53 is an important factor of neuronal differentiation and, probably, p53 action is mediated by cell cycle regulator protein such as Pim-1 and Phbl.

Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova published new progress about 380315-80-0. 380315-80-0 belongs to amides-buliding-blocks, auxiliary class Apoptosis,p53, name is N-((4-Acetamidophenyl)carbamothioyl)-4-(tert-butyl)benzamide, and the molecular formula is C20H23N3O2S, Product Details of C20H23N3O2S.

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

Cecil, Denise L. published the artcileCOX-2 inhibitors decrease expression of PD-L1 in colon tumors and increase the influx of type I tumor-infiltrating lymphocytes, Category: amides-buliding-blocks, the publication is Cancer Prevention Research (2022), 15(4), 225-231, database is CAplus and MEDLINE.

Colon cancer is initiated under inflammatory conditions associated with upregulation of immune checkpoint proteins. We evaluated immune modulation induced by nonsteroidal anti-inflammatory agents used for colon cancer prevention. Both celecoxib and naproxen inhibited polyp growth in APC Min mice. Treatment of mice with either drug significantly decreased PD-L1 expression on polyps in a dose-dependent manner (P < 0.0001 for both). The decrease in PD-L1 was associated with an influx of CD8⁺ T cells into polyps (P < 0.0001, celecoxib; P = 0.048, naproxen) compared with lesions from untreated animals and correlated with disease control. Naproxen is a nonselective inhibitor of both COX-1 and COX-2, and we questioned the role of the different cyclooxygenases in PD-L1 regulation. Silencing either COX-2 or COX-1 RNA in the murine colon cancer cell line MC38, reduced PD-L1 expression by 86% in COX-2-silenced cells (P < 0.0001) while there was little effect with COX-1 siRNA compared with control. Naproxen could inhibit the growth of MC38 in vivo. Naproxen-treated mice demonstrated a significant reduction in MC38 growth as compared with control (P < 0001). Both Tbet⁺ CD4 and CD8 tumor-infiltrating lymphocytes (TIL) were significantly increased (P = 0.04 and P = 0.038, resp.) without a concurrent increase in GATA3+ TIL (P > 0.05). CD8⁺ TIL highly expressed the activation marker, CD69. Not only was PD-L1 expression decreased on tumors, but LAG3⁺CD8⁺ T cells and PD-1 and LAG3 expression on regulatory T cells was also reduced (P = 0.008 and P = 0.002, resp.). These data demonstrate COX-2 inhibitors significantly decrease PD-L1 in colonic lesions and favorably impact the phenotype of tumor-infiltrating lymphocytes to control tumor growth.

Cancer Prevention Research 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, Category: amides-buliding-blocks.

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

Ma, Yan-Na published the artcilePalladium-Catalyzed Regioselective B(9)-Amination of o-Carboranes and m-Carboranes in HFIP with Broad Nitrogen Sources, Recommanded Product: 4-(5-(p-Tolyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide, the publication is Journal of the American Chemical Society (2022), 144(18), 8371-8378, database is CAplus and MEDLINE.

Amination of carboranes has a good application prospect in organic and pharmaceutical synthesis. However, the current methods used for this transformation suffer from limitations. Herein, the authors report a practical method for a highly regioselective formation of a B-N bond by Pd(II)-catalyzed B(9)-H amination of o- and m-carboranes in hexafluoroisopropanol (HFIP) with different N sources under air atm. The Ag salt and HFIP solvent play critical roles in the present protocol. The mechanistic study reveals that the Ag salt acts as a Lewis acid to promote the electrophilic palladation step by forming a heterobimetallic active catalyst PdAg(OAc)₃; the strong H-bond-donating ability and low nucleophilicity of HFIP enhance the electrophilic ability of Pd(II). It is believed that these N-containing carboranes are potentially of great importance in the synthesis of new pharmaceuticals.

Journal of the American Chemical Society 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

Gutierrez-Seijo, Alba published the artcileActivin A Sustains the Metastatic Phenotype of Tumor-Associated Macrophages and Is a Prognostic Marker in Human Cutaneous Melanoma, Category: amides-buliding-blocks, the publication is Journal of Investigative Dermatology (2022), 142(3_Part_A), 653-661.e2, database is CAplus and MEDLINE.

Tumor cells attract and dynamically interact with monocytes/macrophages to subvert their differentiation into tumor-associated macrophages (TAMs), which mainly promote immune suppression and neoplastic progression, but the pathways and microenvironmental cues governing their protumoral deviation are not completely understood. To identify the mol. pathways responsible for TAM differentiation, we screened the biomarkers secreted during melanoma-macrophage interactions using Quantibody microarrays and RNA sequencing of macrophages. We found that activin A, a member of the transforming GF family, plays an instrumental role in the cross-talk between melanoma cells and monocytes/macrophages, which results in the upregulation of distinct tumor-sustaining genes and the achievement of proinvasive and immunosuppressive functions of TAMs. Blockade of activin reduces the upregulation of part of these genes and prevents the acquisition of protumoral functions, facilitating human melanoma rejection by transferred human lymphocytes in a xenograft mouse model. Remarkably, screening of two independent cutaneous primary melanoma collections showed that activin A is enriched in TAMs and melanoma cells from patients with worse outcomes and constitutes a new and independent prognostic marker. Thus, we identify activin A as a key intermediary in the protumoral and immunosuppressive functions of TAMs, with significant potential as a disease biomarker as well as an immunotherapeutic target.

Journal of Investigative Dermatology 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, Category: amides-buliding-blocks.

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

Singh, Chandra K published the artcileNovel downstream molecular targets of SIRT1 in melanoma: a quantitative proteomics approach., Computed Properties of 380315-80-0, the publication is Oncotarget (2014), 5(7), 1987-99, database is MEDLINE.

Melanoma is one of the most lethal forms of skin cancer and its incidence is continuing to rise in the United States. Therefore, novel mechanism and target-based strategies are needed for the management of this disease. SIRT1, a NAD(+)-dependent class III histone deacetylase, has been implicated in a variety of physiological processes and pathological conditions. We recently demonstrated that SIRT1 is upregulated in melanoma and its inhibition by a small-molecule, tenovin-1, inhibits cell proliferation and clonogenic survival of melanoma cells, possibly via activating p53. Here, we employed a gel free quantitative proteomics approach to identify the downstream effectors and targets of SIRT1 in melanoma. The human malignant melanoma, G361 cells were treated with tenovin-1 followed by protein extraction, in liquid trypsin digestion, and peptide analyses using nanoLC-MS/MS. A total of 1091 proteins were identified, of which 20 proteins showed significant differential expression with 95% confidence interval. These proteins were subjected to gene ontology and Ingenuity Pathway Analysis (IPA) to obtain the information regarding their biological and molecular functions. Real-Time qRT-PCR validation showed that five of these (PSAP, MYO1B, MOCOS, HIS1H4A and BUB3) were differentially expressed at mRNA levels. Based on their important role in cell cycle regulation, we selected to focus on BUB family proteins (BUB3, as well as BUB1 and BUBR1) for subsequent validation. The qRT-PCR and immunoblot analyses showed that tenovin-1 inhibition of SIRT1 resulted in a downregulation of BUB3, BUB1 and BUBR1 in multiple melanoma cell lines. Since tenovin-1 is an inhibitor of both SIRT1 and SIRT2, we employed lentivirus mediated silencing of SIRT1 and SIRT2 in G361 cells to determine if the observed effects on BUB family proteins are due to SIRT1- or SIRT2- inhibition. We found that only SIRT1 inhibition resulted in a decrease in BUB3, BUB1 and BUBR1. Our study identified the mitotic checkpoint regulator BUB family proteins as novel downstream targets of SIRT1. However, further validation is needed in appropriate models to confirm our findings and expand on our observations.

Oncotarget published new progress about 380315-80-0. 380315-80-0 belongs to amides-buliding-blocks, auxiliary class Apoptosis,p53, name is N-((4-Acetamidophenyl)carbamothioyl)-4-(tert-butyl)benzamide, and the molecular formula is C10H6F17N, Computed Properties of 380315-80-0.

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

Lucera, Mark B. published the artcileHIV signaling through CD4 and CCR5 activates Rho family GTPases that are required for optimal infection of primary CD4+ T cells, Product Details of C20H23N3O2S, the publication is Retrovirology (2017), 4/1-4/13, database is CAplus and MEDLINE.

Background: HIV-1 hijacks host cell machinery to ensure successful replication, including cytoskeletal components for intracellular trafficking, nucleoproteins for pre-integration complex import, and the ESCRT pathway for assembly and budding. It is widely appreciated that cellular post-translational modifications (PTMs) regulate protein activity within cells; however, little is known about how PTMs influence HIV replication. Previously, we reported that blocking deacetylation of tubulin using histone deacetylase inhibitors promoted the kinetics and efficiency of early postentry viral events. To uncover addnl. PTMs that modulate entry and early post-entry stages in HIV infection, we employed a flow cytometric approach to assess a panel of small mol. inhibitors on viral fusion and LTR promoterdriven gene expression. Results: While viral fusion was not significantly affected, early post-entry viral events were modulated by drugs targeting multiple processes including histone deacetylation, methylation, and bromodomain inhibition. Most notably, we observed that inhibitors of the Rho GTPase family of cytoskeletal regulators-including RhoA, Cdc42, and Rho-associated kinase signaling pathways-significantly reduced viral infection. Using phosphoproteomics and a biochem. GTPase activation assay, we found that virion-induced signaling via CD4 and CCR5 activated Rho family GTPases including Rac1 and Cdc42 and led to widespread modification of GTPase signaling-associated factors. Conclusions: Together, these data demonstrate that HIV signaling activates members of the Rho GTPase family of cytoskeletal regulators that are required for optimal HIV infection of primary CD4+ T cells.

Retrovirology published new progress about 380315-80-0. 380315-80-0 belongs to amides-buliding-blocks, auxiliary class Apoptosis,p53, name is N-((4-Acetamidophenyl)carbamothioyl)-4-(tert-butyl)benzamide, and the molecular formula is C20H23N3O2S, Product Details of C20H23N3O2S.

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