Category: 518303-20-3

Min, Kyueng-Whan published the artcileHigh polymerase ε expression associated with increased CD8+T cells improves survival in patients with non-small cell lung cancer, Category: alcohols-buliding-blocks, the publication is PLoS One (2020), 15(5), e0233066, database is CAplus and MEDLINE.

DNA replicase polymerase ε (POLE) is critical in proofreading and correcting errors of DNA replication. Low POLE expression plays a pivotal role in accumulation of mutations and onset of cancer, contributing to development and growth of tumor cells. The aim of this study is to reveal the survival, alternative genes and antitumoral immune activities in non-small cell lung cancer (NSCLC) patients with low POLE expression and provide treatment strategies that can increase their survival rates. This study investigated the clinicopathol. parameters, various tumor-infiltrating lymphocytes (TILs), endogenous retrovirus, mol. interactions and in vitro drug screen according to POLE mutation/expression in 168 and 1,019 NSCLC patients from the Konkuk University Medical Center (KUMC) and the Cancer Genome Atlas, resp. We identified mutations of 75 genes in the sequencing panels, with POLE frame shift p.V1446fs being the most frequent (56.8%) in KUMC based on 170 targeted sequencing panels. Mutant and high expression of POLE correlated with favorable prognosis with increased TILs and tumor mutation burden, compared with wild type and low expression of POLE. We found specific mol. interactions associated with cell cycle and antigen presentation. An in vitro drug screen identified dasatinib that inhibited growth of the NSCLC cell line with low POLE expression. POLE could contribute to the future development of anticancer drugs for patients with NSCLC.

PLoS One published new progress about 518303-20-3. 518303-20-3 belongs to alcohols-buliding-blocks, auxiliary class Apoptosis,Bcl-2, name is 2-((4-(4-Bromophenylsulfonamido)-1-hydroxynaphthalen-2-yl)thio)acetic acid, and the molecular formula is C18H14BrNO5S2, Category: alcohols-buliding-blocks.

Referemce:
https://en.wikipedia.org/wiki/Alcohol,
Alcohols – Chemistry LibreTexts

Wang, Haolan published the artcileTargeting MCL-1 in cancer: current status and perspectives, Recommanded Product: 2-((4-(4-Bromophenylsulfonamido)-1-hydroxynaphthalen-2-yl)thio)acetic acid, the publication is Journal of Hematology & Oncology (2021), 14(1), 67, database is CAplus and MEDLINE.

A review. Myeloid leukemia 1 (MCL-1) is an antiapoptotic protein of the BCL-2 family that prevents apoptosis by binding to the pro-apoptotic BCL-2 proteins. Overexpression of MCL-1 is frequently observed in many tumor types and is closely associated with tumorigenesis, poor prognosis and drug resistance. The central role of MCL-1 in regulating the mitochondrial apoptotic pathway makes it an attractive target for cancer therapy. Significant progress has been made with regard to MCL-1 inhibitors, some of which have entered clin. trials. Here, we discuss the mechanism by which MCL-1 regulates cancer cell apoptosis and review the progress related to MCL-1 small mol. inhibitors and their role in cancer therapy.

Journal of Hematology & Oncology published new progress about 518303-20-3. 518303-20-3 belongs to alcohols-buliding-blocks, auxiliary class Apoptosis,Bcl-2, name is 2-((4-(4-Bromophenylsulfonamido)-1-hydroxynaphthalen-2-yl)thio)acetic acid, and the molecular formula is C7H7ClN2, Recommanded Product: 2-((4-(4-Bromophenylsulfonamido)-1-hydroxynaphthalen-2-yl)thio)acetic acid.

Referemce:
https://en.wikipedia.org/wiki/Alcohol,
Alcohols – Chemistry LibreTexts

Cen, Xufeng published the artcilePharmacological targeting of MCL-1 promotes mitophagy and improves disease pathologies in an Alzheimer’s disease mouse model, Formula: C18H14BrNO5S2, the publication is Nature Communications (2020), 11(1), 5731, database is CAplus and MEDLINE.

There is increasing evidence that inducing neuronal mitophagy can be used as a therapeutic intervention for Alzheimer’s disease. Here, we screen a library of 2024 FDA-approved drugs or drug candidates, revealing UMI-77 as an unexpected mitophagy activator. UMI-77 is an established BH3-mimetic for MCL-1 and was developed to induce apoptosis in cancer cells. We found that at sub-LDs, UMI-77 potently induces mitophagy, independent of apoptosis. Our mechanistic studies discovered that MCL-1 is a mitophagy receptor and directly binds to LC3A. Finally, we found that UMI-77 can induce mitophagy in vivo and that it effectively reverses mol. and behavioral phenotypes in the APP/PS1 mouse model of Alzheimer’s disease. Our findings shed light on the mechanisms of mitophagy, reveal that MCL-1 is a mitophagy receptor that can be targeted to induce mitophagy, and identify MCL-1 as a drug target for therapeutic intervention in Alzheimer’s disease.

Nature Communications published new progress about 518303-20-3. 518303-20-3 belongs to alcohols-buliding-blocks, auxiliary class Apoptosis,Bcl-2, name is 2-((4-(4-Bromophenylsulfonamido)-1-hydroxynaphthalen-2-yl)thio)acetic acid, and the molecular formula is C18H14BrNO5S2, Formula: C18H14BrNO5S2.

Referemce:
https://en.wikipedia.org/wiki/Alcohol,
Alcohols – Chemistry LibreTexts

Jackson, Mark R. published the artcileMesothelioma Cells Depend on the Antiapoptotic Protein Bcl-xL for Survival and Are Sensitized to Ionizing Radiation by BH3-Mimetics, Computed Properties of 518303-20-3, the publication is International Journal of Radiation Oncology, Biology, Physics (2020), 106(4), 867-877, database is CAplus and MEDLINE.

The incidence of mesothelioma continues to rise and prognosis remains dismal owing to resistance to conventional therapies and few novel treatment options. Failure to activate apoptotic cell death is a resistance mechanism that may be overcome using BH3-mimetic drugs. We investigated the role of antiapoptotic proteins in the radioresistance of mesothelioma, identifying clin. relevant targets for radiosensitization and evaluating the activity of BH3-mimetics alone and in combination with radiation therapy in preclin. models. Mesothelioma cell lines 211H, H2052, and H226 exposed to BH3-mimetics demonstrated Bcl-xL dependence that correlated with protein expression and was confirmed by genetic knockdown. The Bcl-xL inhibitor A1331852 exhibited cytotoxic (EC₅₀, 0.13-1.42μmol/L) and radiosensitizing activities (sensitizer enhancement ratios, 1.3-1.8). Cytotoxicity was associated with induction of mitochondrial outer membrane permeabilization and caspase-3/7 activation. Efficacy was maintained in a 3-dimensional model in which combination therapy completely eradicated mesothelioma spheroids. Clin. applicability was confirmed by immunohistochem. anal. of Bcl-2 proteins in patient samples and radiosensitizing activity of A1331852 in primary patient-derived mesothelioma cells. Mesothelioma cells exhibit addiction to the antiapoptotic protein Bcl-xL, and their intrinsic radioresistance can be overcome by small mol. inhibition of this novel therapeutic target.

International Journal of Radiation Oncology, Biology, Physics published new progress about 518303-20-3. 518303-20-3 belongs to alcohols-buliding-blocks, auxiliary class Apoptosis,Bcl-2, name is 2-((4-(4-Bromophenylsulfonamido)-1-hydroxynaphthalen-2-yl)thio)acetic acid, and the molecular formula is C18H14BrNO5S2, Computed Properties of 518303-20-3.

Referemce:
https://en.wikipedia.org/wiki/Alcohol,
Alcohols – Chemistry LibreTexts

Burrer, Christine M. published the artcileMcl-1 small-molecule inhibitors encapsulated into nanoparticles exhibit increased killing efficacy towards HCMV-infected monocytes, Category: alcohols-buliding-blocks, the publication is Antiviral Research (2017), 40-46, database is CAplus and MEDLINE.

Human cytomegalovirus (HCMV) spreads and establishes a persistent infection within a host by stimulating the survival of carrier myeloid cells via the upregulation of Mcl-1, an antiapoptotic member of the Bcl-2 family of proteins. However, the lack of potent Mcl-1-specific inhibitors and a targetable delivery system has limited the ability to exploit Mcl-1 as a therapeutic strategy to eliminate HCMV-infected monocytes. In this study, we found a lead compound from a novel class of Mcl-1 small-mol. inhibitors rapidly induced death of HCMV-infected monocytes. Moreover, encapsulation of Mcl-1 antagonists into myeloid cell-targeting nanoparticles was able to selectively increase the delivery of inhibitors into HCMV-activated monocytes, thereby amplifying their potency. Our study demonstrates the potential use of nanotechnol. to target Mcl-1 small-mol. inhibitors to HCMV-infected monocytes.

Antiviral Research published new progress about 518303-20-3. 518303-20-3 belongs to alcohols-buliding-blocks, auxiliary class Apoptosis,Bcl-2, name is 2-((4-(4-Bromophenylsulfonamido)-1-hydroxynaphthalen-2-yl)thio)acetic acid, and the molecular formula is C18H14BrNO5S2, Category: alcohols-buliding-blocks.

Referemce:
https://en.wikipedia.org/wiki/Alcohol,
Alcohols – Chemistry LibreTexts