Category: 347174-05-4

Zhang, Weinan; Wang, Chen; Zhu, Wenfeng; Liu, Fan; Liu, Yake published the artcile< Ferrostatin-1 alleviates cytotoxicity of cobalt nanoparticles by inhibiting ferroptosis>, COA of Formula: C15H22N2O2, the main research area is ferroptosis fibroblast cell viability ferrostatin 1 cobalt nanoparticle cytotoxicity; Cobalt nanoparticles; Ferrostatin-1; ferroptosis; hip arthroplasty; lipid peroxidation.

Cobalt is the main component of metal prostheses in hip arthroplasty. Studies have shown that metal particles mainly composed of cobalt nanoparticles (CoNPs) can cause systemic and local toxic reactions due to various phys. and chem. factors. Therefore, elucidating the underlying mechanisms of metal prosthesis action, coupled with identification of effective detoxification drugs are imperative to minimizing postoperative complications and prolonging the service life of these clin. tools. In this study, we treated Balb/3T3 mouse fibroblast cell line with CoNPs and ferrostatin-1, then measured cell viability via the CCK-8 assay. Next, we determined levels of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), cobalt and iron contents, as well as glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11) expression in each group. Finally, we employed transmission electron microscopy (TEM) to detect changes in the ultrastructure of each group of cells. Exposure of cells to CoNPs significantly suppressed their viability, and downregulated expression of GSH, GPX4, and SLC7A11 proteins. Conversely, this treatment mediated a significant increase in ROS, MDA, cobalt, and iron levels in the cells. TEM images revealed a marked increase in d. of the mitochondrial membrane of cells in the CoNPs group, while the outer membrane was broken. Notably, treatment with ferroptosis inhibitor Ferrostatin-1 alleviated the cytotoxic response caused by CoNPs. These findings suggest that CoNP-induced cytotoxicity may be closely related to ferroptosis, indicating that inhibition of ferroptosis is a potential therapeutic strategy for reducing CoNP toxicity.

Bioengineered published new progress about Cell survival. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, COA of Formula: C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Tang, Xuyuan; Li, Xiuyi; Zhang, Dongyan; Han, Wei published the artcile< Astragaloside-IV alleviates high glucose-induced ferroptosis in retinal pigment epithelial cells by disrupting the expression of miR-138-5p/Sirt1/Nrf2>, Reference of 347174-05-4, the main research area is ferroptosis astragaloside IV Sirt1 Nrf2 mitochondrial damage; AS-IV; DR; RPE; astragaloside-IV; diabetic retinopathy; retinal pigment epithelial.

Astragaloside-IV (AS-IV) (C41H68O14) is a high-purity natural product extracted from Astragalus, which has demonstrated biol. activities. However, the effect of AS-IV on retinal pigment epithelial (RPE) cells in diabetic retinopathy (DR) remains unclear. In this study, high glucose (HG) was shown to promote ARPE-19 RPE cell death, increase the contents of reactive oxygen species (ROS) and oxidized glutathione (GSSG), and enhance lipid peroxidation d. of mitochondrial membrane. In contrast, AS-IV decreased glutathione (GSH) content, mitochondria size and ridge. Addition of iron death inhibitor Ferrostatin-1 (Fer-1) to RPE cells decreased cell dead rate, thus indicating that HG-induced mitochondrial damage occurred due to ferroptosis. AS-IV alleviated HG-induced RPE cell damage. Furthermore, HG decreased levels of silent information regulator 1 (Sirt1) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in the nucleus of RPE cells; AS-IV could alleviate these effects and increased expression of glutathione peroxidase 4 (GPX4), glutamate cysteine ligase (GCLM) and glutamate cysteine ligase catalytic subunit (GCLC), which are Nrf2 downstream genes. Mechanistically, AS-IV was shown to alleviate the effects of HG by increasing mir-138-5p expression in RPE cells and promoting expression of Sirt1 and Nrf2 in the nucleus. Transfection of mir-138-5p agonist inhibited the regulatory effects of AS-IV on Sirt1 and Nrf2, accompanied by decreased GPX4, GCLM and GCLC levels, and restoration of ferroptosis-related changes. Collectively, HG increased ferroptosis rate in RPE cells. In addition, AS-IV inhibited miR-138-5p expression, subsequently increasing Sirt1/Nrf2 activity and cellular antioxidant capacity to alleviate ferroptosis, resulting decreased cell death, which potentially inhibits the DR pathol. process.

Bioengineered published new progress about Antioxidants. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Reference of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Pardieu, Bryann; Pasanisi, Justine; Ling, Frank; Dal Bello, Reinaldo; Penneroux, Justine; Su, Angela; Joudinaud, Romane; Chat, Laureen; Wu, Hsin Chieh; Duchmann, Matthieu; Sodaro, Gaetano; Chauvel, Clementine; Castelli, Florence A.; Vasseur, Loic; Pacchiardi, Kim; Belloucif, Yannis; Laiguillon, Marie-Charlotte; Meduri, Eshwar; Vaganay, Camille; Alexe, Gabriela; Berrou, Jeannig; Benaksas, Chaima; Forget, Antoine; Braun, Thorsten; Gardin, Claude; Raffoux, Emmanuel; Clappier, Emmanuelle; Ades, Lionel; de The, Hugues; Fenaille, Francois; Huntly, Brian J.; Stegmaier, Kimberly; Dombret, Herve; Fenouille, Nina; Lobry, Camille; Puissant, Alexandre; Itzykson, Raphael published the artcile< Cystine uptake inhibition potentiates front-line therapies in acute myeloid leukemia>, Reference of 347174-05-4, the main research area is cystine acute myeloid leukemia therapy.

By querying metabolic pathways associated with leukemic stemness and survival in multiple AML datasets, we nominated SLC7A11 encoding the xCT cystine importer as a putative AML dependency. Genetic and chem. inhibition of SLC7A11 impaired the viability and clonogenic capacity of AML cell lines in a cysteine-dependent manner. Sulfasalazine, a broadly available drug with xCT inhibitory activity, had anti-leukemic activity against primary AML samples in ex vivo cultures. Multiple metabolic pathways were impacted upon xCT inhibition, resulting in depletion of glutathione pools in leukemic cells and oxidative stress-dependent cell death, only in part through ferroptosis. Higher expression of cysteine metabolism genes and greater cystine dependency was noted in NPM1-mutated AMLs. Among eight anti-leukemic drugs, the anthracycline daunorubicin was identified as the top synergistic agent in combination with sulfasalazine in vitro. Addition of sulfasalazine at a clin. relevant concentration significantly augmented the anti-leukemic activity of a daunorubicin-cytarabine combination in a panel of 45 primary samples enriched in NPM1-mutated AML. These results were confirmed in vivo in a patient-derived xenograft model. Collectively, our results nominate cystine import as a druggable target in AML and raise the possibility to repurpose sulfasalazine for the treatment of AML, notably in combination with chemotherapy.

Leukemia published new progress about Acute myeloid leukemia. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Reference of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Yamane, Daisuke; Hayashi, Yuri; Matsumoto, Moe; Nakanishi, Hiroki; Imagawa, Haruka; Kohara, Michinori; Lemon, Stanley M.; Ichi, Ikuyo published the artcile< FADS2-dependent fatty acid desaturation dictates cellular sensitivity to ferroptosis and permissiveness for hepatitis C virus replication>, Safety of Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is HCV replication FADS fatty acid desaturation ferroptosis cellular sensitivity; FADS2; Mead acid; direct-acting antivirals; ferroptosis; hepatitis C virus; lipid peroxidation; polyunsaturated fatty acid.

The metabolic oxidative degradation of cellular lipids severely restricts replication of hepatitis C virus (HCV), a leading cause of chronic liver disease, but little is known about the factors regulating this process in infected cells. Here we show that HCV is restricted by an iron-dependent mechanism resembling the one triggering ferroptosis, an iron-dependent form of non-apoptotic cell death, and mediated by the non-canonical desaturation of oleate to Mead acid and other highly unsaturated fatty acids by fatty acid desaturase 2 (FADS2). Genetic depletion and ectopic expression experiments show FADS2 is a key determinant of cellular sensitivity to ferroptosis. Inhibiting FADS2 markedly enhances HCV replication, whereas the ferroptosis-inducing compound erastin alters conformation of the HCV replicase and sensitizes it to direct-acting antiviral agents targeting the viral protease. Our results identify FADS2 as a rate-limiting factor in ferroptosis, and suggest the possibility of pharmacol. manipulating the ferroptosis pathway to attenuate viral replication.

Cell Chemical Biology published new progress about Albumins Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Safety of Ethyl 3-amino-4-(cyclohexylamino)benzoate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Ye, Yang; Li, Xue; Feng, Guoquan; Ma, Ying; Ye, Fen; Shen, Haijun; Sun, Kang; Lu, Rongzhu; Miao, Shuhan published the artcile< 3,3'-Diindolylmethane induces ferroptosis by BAP1-IP3R axis in BGC-823 gastric cancer cells>, Formula: C15H22N2O2, the main research area is BAP1 IP3R anticancer agent gastric cancer.

To investigate the effect and potential mechanism of 3,3-diindolylmethane (DIM) on ferroptosis against gastric cancer, cells proliferation, lipid reactive oxygen species (ROS) and GSH level were measured in the BGC-823 gastric cancer cells after DIM treatment. Western blotting was used to detect the expression of SLC7A11, GPX4, IP3R and BAP1. Results showed that DIM could induce ferroptosis in the BGC-823 gastric cancer cells via upregulating lipid-ROS level and decreasing GSH generation. Besides, DIM also significantly reduced the protein level of SLC7A11 and GPX4, which was an important regulator of ferroptosis. In addition, DIM promoted the protein level of BAP1 and IP3R in a concentration-dependent manner in the BGC-823 gastric cancer cells. The knockdown of BAP1 could reduce IP3R level and DIM-induced ferroptosis of gastric cancer cells. Taken together, these results indicated that DIM could induce ferroptosis to exert anti-cancer effects via BAP1-IP3R axis, suggesting its effective therapeutic potential in gastric cancer.

Anti-Cancer Drugs published new progress about Antitumor agents. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Formula: C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Flores-Romero, Hector; Hohorst, Lisa; John, Malina; Albert, Marie-Christine; King, Louise E.; Beckmann, Laura; Szabo, Tamas; Hertlein, Vanessa; Luo, Xu; Villunger, Andreas; Frenzel, Lukas P.; Kashkar, Hamid; Garcia-Saez, Ana J. published the artcile< BCL-2-family protein tBID can act as a BAX-like effector of apoptosis>, Application of C15H22N2O2, the main research area is tBID BAX BCL2 BCL2A1 TRAIL immunity Shigella necrosulfonamide apoptosis; BCL-2 proteins; apoptosis; mitochondrial permeabilization; pore formation.

During apoptosis, the BCL-2-family protein tBID promotes mitochondrial permeabilization by activating BAX and BAK and by blocking anti-apoptotic BCL-2 members. Here, we report that tBID can also mediate mitochondrial permeabilization by itself, resulting in release of cytochrome c and mitochondrial DNA, caspase activation and apoptosis even in absence of BAX and BAK. This previously unrecognized activity of tBID depends on helix 6, homologous to the pore-forming regions of BAX and BAK, and can be blocked by pro-survival BCL-2 proteins. Importantly, tBID-mediated mitochondrial permeabilization independent of BAX and BAK is physiol. relevant for SMAC release in the immune response against Shigella infection. Furthermore, it can be exploited to kill leukemia cells with acquired venetoclax resistance due to lack of active BAX and BAK. Our findings define tBID as an effector of mitochondrial permeabilization in apoptosis and provide a new paradigm for BCL-2 proteins, with implications for anti-bacterial immunity and cancer therapy.

EMBO Journal published new progress about Ablation (genetic ablation). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Application of C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Zhao, Xin; Cui, Lijuan; Zhang, Yushan; Guo, Chao; Deng, Lijiao; Wen, Zhitong; Lu, Zhihong; Shi, Xiaoyuan; Xing, Haojie; Liu, Yunfeng; Zhang, Yi published the artcile< Screening for potential therapeutic agents for non-small cell lung cancer by targeting ferroptosis>, COA of Formula: C15H22N2O2, the main research area is NSCLC ferroptosis therapeutic agent screening target.

Ferroptosis is a form of non-apoptotic and iron-dependent cell death originally identified in cancer cells. Recently, emerging evidence showed that ferroptosis-targeting therapy could be a novel promising anti-tumor treatment. However, systematic analyses of ferroptosis-related genes for the prognosis of non-small cell lung cancer (NSCLC) and the development of antitumor drugs exploiting the ferroptosis process remain rare. This study aimed to identify genes related to ferroptosis and NSCLC and to initially screen lead compounds that induce ferroptosis in tumor cells. We downloaded mRNA expression profiles and NSCLC clin. data from The Cancer Genome Atlas database to explore the prognostic role of ferroptosis-related genes. Four prognosis-associated ferroptosis-related genes were screened using univariate Cox regression anal. and the lasso Cox regression anal., which could divide patients with NSCLC into high- and low-risk groups. Then, based on differentially expressed risk- and ferroptosis-related genes, the neg. correlated lead compound flufenamic acid (FFA) was screened through the Connective Map database. This project confirmed that FFA induced ferroptosis in A549 cells and inhibited growth and migration in a dose-dependent manner through CCK-8, scratch, and immunofluorescence assays. In conclusion, targeting ferroptosis might be a therapeutic alternative for NSCLC.

Frontiers in Molecular Biosciences published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (CISD1). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, COA of Formula: C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Zhao, Xin; Cui, Lijuan; Zhang, Yushan; Guo, Chao; Deng, Lijiao; Wen, Zhitong; Lu, Zhihong; Shi, Xiaoyuan; Xing, Haojie; Liu, Yunfeng; Zhang, Yi published the artcile< Screening for potential therapeutic agents for non-small cell lung cancer by targeting ferroptosis>, COA of Formula: C15H22N2O2, the main research area is NSCLC ferroptosis therapeutic agent screening target.

Ferroptosis is a form of non-apoptotic and iron-dependent cell death originally identified in cancer cells. Recently, emerging evidence showed that ferroptosis-targeting therapy could be a novel promising anti-tumor treatment. However, systematic analyses of ferroptosis-related genes for the prognosis of non-small cell lung cancer (NSCLC) and the development of antitumor drugs exploiting the ferroptosis process remain rare. This study aimed to identify genes related to ferroptosis and NSCLC and to initially screen lead compounds that induce ferroptosis in tumor cells. We downloaded mRNA expression profiles and NSCLC clin. data from The Cancer Genome Atlas database to explore the prognostic role of ferroptosis-related genes. Four prognosis-associated ferroptosis-related genes were screened using univariate Cox regression anal. and the lasso Cox regression anal., which could divide patients with NSCLC into high- and low-risk groups. Then, based on differentially expressed risk- and ferroptosis-related genes, the neg. correlated lead compound flufenamic acid (FFA) was screened through the Connective Map database. This project confirmed that FFA induced ferroptosis in A549 cells and inhibited growth and migration in a dose-dependent manner through CCK-8, scratch, and immunofluorescence assays. In conclusion, targeting ferroptosis might be a therapeutic alternative for NSCLC.

Frontiers in Molecular Biosciences published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (CISD1). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, COA of Formula: C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Wiernicki, Bartosz; Maschalidi, Sophia; Pinney, Jonathan; Adjemian, Sandy; Vanden Berghe, Tom; Ravichandran, Kodi S.; Vandenabeele, Peter published the artcile< Cancer cells dying from ferroptosis impede dendritic cell-mediated anti-tumor immunity>, Product Details of C15H22N2O2, the main research area is cancer ferroptosis impede dendritic cell antitumor immunity.

Immunogenic cell death significantly contributes to the success of anti-cancer therapies, but immunogenicity of different cell death modalities widely varies. Ferroptosis, a form of cell death that is characterized by iron accumulation and lipid peroxidation, has not yet been fully evaluated from this perspective. Here we present an inducible model of ferroptosis, distinguishing three phases in the process-‘initial’ associated with lipid peroxidation, ‘intermediate’ correlated with ATP release and ‘terminal’ recognized by HMGB1 release and loss of plasma membrane integrity-that serves as tool to study immune cell responses to ferroptotic cancer cells. Co-culturing ferroptotic cancer cells with dendritic cells (DC), reveals that ‘initial’ ferroptotic cells decrease maturation of DC, are poorly engulfed, and dampen antigen cross-presentation. DC loaded with ferroptotic, in contrast to necroptotic, cancer cells fail to protect against tumor growth. Adding ferroptotic cancer cells to immunogenic apoptotic cells dramatically reduces their prophylactic vaccination potential. Our study thus shows that ferroptosis neg. impacts antigen presenting cells and hence the adaptive immune response, which might hinder therapeutic applications of ferroptosis induction.

Nature Communications published new progress about Adaptive immunity. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Product Details of C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

I-Ju Leu, Julia; Murphy, Maureen E.; George, Donna L. published the artcile< Targeting ErbB3 and cellular NADPH/NADP+ abundance sensitizes cutaneous melanomas to ferroptosis inducers>, Computed Properties of 347174-05-4, the main research area is drug targeting ErbB3 NADPH NADP tachyphylaxis melanoma ferroptosis.

Melanoma is a serious health challenge. Ferroptosis is a regulated form of oxidative cell death that shows varied efficacy in melanoma. We aimed to better understand the mol. basis for this differential ferroptosis sensitivity. We find that elevated expression of ErbB3 (V-Erb-B2 Avian Erythroblastic Leukemia Viral Oncogene Homolog 3) associates with ferroptosis resistance and that ErbB3 knockdown sensitizes to ferroptosis inducers. ErbB3 depletion also promotes a marked reduction in the cellular ratio of GSH/GSSG (reduced/oxidized glutathione) and that of NADPH/NADP+ (reduced/oxidized NADP), together with an increase in the abundance of the lipid peroxidation product malondialdehyde (MDA). We identify several small mol. inhibitors targeting ErbB3 signaling pathways that also reduce the NADPH/NADP+ and GSH/GSSG ratios, concomitantly sensitizing the melanomas to ferroptosis activators. These findings point to a previously unrecognized role of ErbB3 in ferroptosis sensitivity and provide new insight into pathways that regulate this cell death process.

ACS Chemical Biology published new progress about Antioxidants. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Computed Properties of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics