Category: 347174-05-4

Delehouze, Claire; Comte, Arnaud; Leon-Icaza, Stephen Adonai; Cougoule, Celine; Hauteville, Marcelle; Goekjian, Peter; Bulinski, Jeannette Chloe; Dimanche-Boitrel, Marie-Therese; Meunier, Etienne; Rousselot, Morgane; Bach, Stephane published the artcile< Nigratine as dual inhibitor of necroptosis and ferroptosis regulated cell death>, Safety of Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is nigratine dual inhibitor necroptosis ferroptosis cell death.

Nigratine (also known as 6E11), a flavanone derivative of a plant natural product, was characterized as highly specific non-ATP competitive inhibitor of RIPK1 kinase, one of the key components of necroptotic cell death signaling. We show here that nigratine inhibited both necroptosis (induced by Tumor Necrosis Factor-α) and ferroptosis (induced by the small mols. glutamate, erastin, RSL3 or cumene hydroperoxide) with EC50 in the μM range. Taken together, our data showed that nigratine is a dual inhibitor of necroptosis and ferroptosis cell death pathways. These findings open potential new therapeutic avenues for treating complex necrosis-related diseases.

Scientific Reports published new progress about Cell death. 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

Shi, Qing; Liu, Rui; Chen, Li published the artcile< Ferroptosis inhibitor ferrostatin-1 alleviates homocysteine-induced ovarian granulosa cell injury by regulating TET activity and DNA methylation>, Safety of Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is ferrostatin1 cytoprotectant ferroptosis DNA methylation ovarian granulosa cell injury; apoptosis; ferroptosis; ferrostatin‑1; oxidative stress; polycystic ovary syndrome.

Polycystic ovary syndrome is one of the most common endocrine and metabolic gynecol. disorders, of which dysfunction of ovarian granulosa cells is a key contributing factor. The aim of the present study was to explore the role of ferrostatin-1 (Fer-1), a ferroptosis inhibitor, in a cell injury model established by homocysteine (Hcy)-induced ovarian granulosa KGN cell line and the potential underlying mechanism. Cell viability was measured using Cell Counting Kit-8 assay in the presence or absence of Hcy and Fer-1. Cell apoptosis was assessed using TUNEL staining and the expression levels of apoptosis-related proteins were measured using western blotting. To explore the effects of Fer-1 on oxidative stress in Hcy-treated ovarian granulosa cells, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), lactate dehydrogenase (LDH) and glutathione (GSH) were measured using their corresponding kits. Furthermore, Fe2+ levels were assessed using Phen Green SK labeling and western blotting was performed to measure the protein expression levels of ferroptosis-associated proteins GPX4, SLC7A11, ASCL4 and DMT1. Subsequently, DNA methylation and ten-eleven translocation (TET) 1/2 demethylase levels were also detected to evaluate the extent of overall DNA methylation in ovarian granulosa cells after Hcy treatment. The TET1/2 inhibitor Bobcat339 hydrochloride was applied to treat ovarian granulosa cells before evaluating the possible effects of Fer-1 on TET1/2 and DNA methylation. Fer-1 was found to markedly elevate ovarian granulosa cell viability following Hcy treatment. The apoptosis rate in Fer-1-treated groups was also markedly decreased, which was accompanied by downregulated Bax and cleaved caspase-3 expression and upregulated Bcl-2 protein expression. In addition, Fer-1 treatment reduced the levels of ROS, MDA and LDH while enhancing the levels of GSH. Fe2+ levels were significantly decreased following Fer-1 treatment, which also elevated glutathione peroxidase 4 expression while reducing solute carrier family 7 member 11, achaete-scute family BHLH transcription factor 4 and divalent metal transporter 1 protein expression. Fer-1 significantly inhibited DNA methylation and enhanced TET1/2 levels, which were reversed by treatment with Bobcat339 hydrochloride. Subsequent experiments on cell viability, oxidative stress, Fe2+ content, ferroptosis- and apoptosis-related proteins levels revealed that Bobcat339 hydrochloride reversed the effects of Fer-1 on ovarian granulosa Hcy-induced cell injury. These results suggest that Fer-1 may potentially protect ovarian granulosa cells against Hcy-induced injury by increasing TET levels and reducing DNA methylation.

Molecular Medicine Reports published new progress about Basic helix-loop-helix transcription factors Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (ASCL4). 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

Wan, Yiting; Gu, Cancan; Kong, Jueying; Sui, Jin; Zuo, Ling; Song, Yanhua; Chen, Jing published the artcile< Long noncoding RNA ADAMTS9-AS1 represses ferroptosis of endometrial stromal cells by regulating the miR-6516-5p/GPX4 axis in endometriosis>, Name: Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is ADAMTS9 AS1 miR65165p GPX4 ferroptosis endometriosis.

Endometriosis (EMs) is one of the most frequent diseases of reproductive-age women and is characterized by the growth of endometrial tissues beyond the uterus. The enhanced proliferative and migratory potential of endometrial stromal cells (ESCs) plays an important role in the progression of EMs. Mounting studies have demonstrated that long noncoding RNAs (lncRNAs) exert an important role in regulating the development and progression of EMs. Given the aberrant expression of lncRNA ADAMTS9-AS1 in ectopic endometrium (ecEM), we investigated the biol. effect of ADAMTS9-AS1 on ESC proliferation and migration and explored the underlying mechanism. The current data showed that ADAMTS9-AS1 expression was significantly upregulated in ecEM compared with eutopic endometrium (euEM) in patients with EMs and in a murine model of EMs. Functionally, ADAMTS9-AS1 knockdown in ectopic ESCs (EESCs) decreased cell viability and migration, whereas ADAMTS9-AS1 overexpression in normal ESCs (NESCs) enhanced cell viability and migration. More importantly, the effect of ADAMTS9-AS1 inhibition on decreasing ESC viability was significantly blocked by ferrostatin-1 (Fer-1, a ferroptosis inhibitor), and ADAMTS9-AS1 overexpression repressed erastin (a ferroptosis activator)-induced cell death. Furthermore, the regulatory role of ADAMTS9-AS1 in ferroptosis was defined and evidenced by increased reactive oxygen species (ROS) levels and malonyl dialdehyde (MDA) content and decreased expression of glutathione peroxidase 4 (GPX4) after ADAMTS9-AS1 inhibition. Mechanistically, ADAMTS9-AS1 functioned as a competing endogenous RNA (ceRNA) by sponging miR-6516-5p to derepress the expression of GPX4, the critical repressor of ferroptosis. Taken together, these results demonstrate that upregulated ADAMTS9-AS1 accelerates ESC proliferation and migration by regulating miR-6516-5p/GPX4-dependent ferroptosis and may be a potential target for the treatment of EMs.

Scientific Reports published new progress about Apoptosis. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Name: Ethyl 3-amino-4-(cyclohexylamino)benzoate.

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

Sun, Chaofeng; Peng, Fang; Li, Jianfei; Cui, Xudong; Qiao, Xin; Zhu, Wangliang published the artcile< Ferroptosis-specific inhibitor ferrostatin-1 relieves H2O2- induced redox imbalance in primary cardiomyocytes through the Nrf2/ARE pathway>, Application of C15H22N2O2, the main research area is ferrostatin 1 ferroptosis redox imbalance cardiomyocyte Nrf2 ARE pathway.

Ischemic heart disease (IHD) has always been the focus of attention of many researchers in cardiovascular disease, and its pathogenesis is also very complicated. Ferroptosis may be involved in the occurrence and development of IHD. First, primary cardiomyocytes were treated with H2O2 to simulate the IHD in vitro model. After pretreatment with different concentrations of ferrostatin-1, cell survival rate was detected by MTT method, cell apoptosis was detected by TUNEL staining and flow cytometry, and the expression of oxidative stress, ferroptosis, and related mols. of Nrf2/ARE pathway was detected by Western blotting (WB) and quant. real-time polymerase chain reaction (qRT-PCR). The mortality of primary cardiomyocytes in the H2O2 group was obviously increased. Ferrostatin-1 treatment can effectively inhibit cell death, improve antioxidant enzyme activity, inhibit the expression of ferroptosis-related mols., and activate Nrf2/ARE pathway expression. Ferroptosis-specific inhibitor ferrostatin-1 relieves H2O2-induced redox imbalance in primary cardiomyocytes through the Nrf2/ARE pathway, inhibits ferroptosis, and thereby slows cardiomyocyte death.

Disease Markers published new progress about Antioxidant enzymes Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 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

Chen, Yue; Yi, Xin; Huo, Bo; He, Yi; Guo, Xian; Zhang, Zihao; Zhong, Xiaoxuan; Feng, Xin; Fang, Ze-Min; Zhu, Xue-Hai; Wei, Xiang; Jiang, Ding-Sheng published the artcile< BRD4770 functions as a novel ferroptosis inhibitor to protect against aortic dissection>, SDS of cas: 347174-05-4, the main research area is gene expression BRD4770 ferroptosis inhibitor aortic dissection smooth musclecell; Aortic dissection; BRD4770; Ferroptosis; Histone methylation; Inflammation; Smooth muscle cell.

Smooth muscle cell (SMC) loss is the characteristic feature in the pathogenesis of aortic dissection (AD), and ferroptosis is a novel iron-dependent regulated cell death driven by the excessive lipid peroxidation accumulation. However, whether targeting ferroptosis is an effective approach for SMC loss and AD treatment remains unclear. Here, we found that the iron level, ferroptosis-related mols. TFR, HOMX1, ferritin and the lipid peroxidation product 4-hydroxynonenal were increased in the aorta of AD. Then, we screened several inhibitors of histone methyltransferases and found that BRD4770 had a protective effect on cystine deprivation-, imidazole ketone erastin- or RSL3-induced ferroptosis of SMCs. The classic ferroptosis pathways, System Xc–GPX4, FSP1-CoQ10 and GCH1-BH4 pathways which were inhibited by ferroptosis inducers, were re-activated by BRD4770 via inhibiting mono-, di- and tri- methylated histone H3 at lysine 9 (H3K9me1/2/3). RNA-sequencing anal. revealed that there was a pos. feedback regulation between ferroptosis and inflammatory response, and BRD4770 can reverse the effects of inflammation activation on ferroptosis. More importantly, treatment with BRD4770 attenuated aortic dilation and decreased morbidity and mortality in a β-Aminopropionitrile monofumarate-induced mouse AD model via inhibiting the inflammatory response, lipid peroxidation and ferroptosis. Taken together, our findings demonstrate that ferroptosis is a novel and critical pathol. mechanism that is involved in SMC loss and AD development. BRD4770 is a novel ferroptosis inhibitor and has equivalent protective effect to Ferrostatin-1 at the optimal concentration Translating insights into the anti-ferroptosis effects of BRD4770 may reveal a potential therapeutic approach for targeting SMC ferroptosis in AD.

Pharmacological Research published new progress about Animal gene, CXCL1 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, SDS of cas: 347174-05-4.

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

Zhong, Meiyan; Huang, Yuanting; Zeng, Bo; Xu, Lihui; Zhong, Chunsu; Qiu, Jiahao; Ye, Xunjia; Chen, Mingye; Hu, Bo; Ouyang, Dongyun; He, Xianhui published the artcile< Induction of multiple subroutines of regulated necrosis in murine macrophages by natural BH3-mimetic gossypol>, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is bone marrow macrophage necrosis BH3 gossypol; BH3-mimetic; gossypol; macrophages; necroptosis; pyroptosis; secondary necrosis.

Macrophages are critical sentinel cells armed with multiple regulated necrosis pathways, including pyroptosis, apoptosis followed by secondary necrosis, and necroptosis, and are poised to undergo distinct form(s) of necrosis for tackling dangers of pathogenic infection or toxic exposure. The natural BH3-mimetic gossypol is a toxic phytochem. that can induce apoptosis and/or pyroptotic-like cell death, but what exact forms of regulated necrosis are induced remains largely unknown. Here we demonstrated that gossypol induces pyroptotic-like cell death in both unprimed and lipopolysaccharide-primed mouse bone marrow-derived macrophages (BMDMs), as evidenced by membrane swelling and ballooning accompanied by propidium iodide incorporation and lactic acid dehydrogenase release. Notably, gossypol simultaneously induces the activation of both pyroptotic and apoptotic (followed by secondary necrosis) pathways but only weakly activates the necroptosis pathway. Unexpectedly, gossypol-induced necrosis is independent of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, as neither inhibitor for the NLRP3 pathway nor NLRP3 deficiency protects the macrophages from the necrosis. Furthermore, necrotic inhibitors or even pan-caspase inhibitor alone does not or only partly inhibit such necrosis. Instead, a combination of inhibitors composed of pan-caspase inhibitor IDN-6556, RIPK3 inhibitor GSK’872 and NADPH oxidase inhibitor GKT137831 not only markedly inhibits the necrosis, with all apoptotic and pyroptotic pathways being blocked, but also attenuates gossypol-induced peritonitis in mice. Lastly, the activation of the NLRP3 pathway and apoptotic caspase-3 appears to be independent of each other. Collectively, gossypol simultaneously induces the activation of multiple subroutines of regulated necrosis in macrophages depending on both apoptotic and inflammatory caspases.

Acta Biochimica et Biophysica Sinica published new progress about Apoptosis. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate.

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

Zhang, Zhenzhou; Tang, Jianqiong; Song, Jiawei; Xie, Mengshi; Liu, Ying; Dong, Zhaojie; Liu, Xiaoyan; Li, Xueting; Zhang, Miwen; Chen, Yihang; Shi, Hongyu; Zhong, Jiuchang published the artcile< Elabela alleviates ferroptosis, myocardial remodeling, fibrosis and heart dysfunction in hypertensive mice by modulating the IL-6/STAT3/GPX4 signaling>, Synthetic Route of 347174-05-4, the main research area is elabela gene transcription ferroptosis heart fibrosis dysfunction hypertension mouse; IL6 STAT3 GPX4 signaling elabela drug target; Cardiac microvascular endothelial cells; Elabela; Ferroptosis; Hypertension; Myocardial remodeling.

Hypertension-mediated pathol. cardiac remodeling often progresses to heart failure. Elabela, mainly expressed in the cardiac microvascular endothelial cells (CMVECs), functions as a new endogenous ligand for apelin receptor. However, the exact roles of elabela in hypertension remain largely unclear. In this study, 10-wk-old male C57BL/6 mice were randomly subjected to infusion of angiotensin (Ang) II (1.5 mg/kg/d) or saline for 2 wk. Ang II infusion led to marked increases in systolic blood pressure levels and reduction of elabela levels in hypertensive mice with augmented myocardial hypertrophy and fibrosis. Furthermore, administration of elabela or ferroptosis inhibitor ferrostatin-1 significantly prevented Ang II-mediated pathol. myocardial remodeling, dysfunction, and ultrastructural injury in hypertensive mice with downregulated expression of inflammation-, hypertrophy-, and fibrosis-related genes. Notably, elabela strikingly alleviated Ang II-induced upregulation of iron levels and lipid peroxidation in hypertensive mice by suppressing cardiac interleukin-6 (IL-6)/STAT3 signaling and activating the xCT/glutathione peroxidase (GPX4) signaling. In cultured CMVECs, exposure to Ang II resulted in a marked decrease in elabela levels and obvious increases in cellular ferroptosis, proliferation, inflammation, and superoxide production, which were rescued by elabela or ferrostatin-1 while were blocked by co-treatment with rhIL-6. Furthermore, knockdown of elabela by siRNA in CMVECs contributed to Ang II-mediated augmentations in cellular proliferation, migration, and oxidative stress in cultured cardiac fibroblasts and cardiomyocytes, resp. In conclusion, elabela antagonizes Ang II-mediated promotion of CMVECs ferroptosis, adverse myocardial remodeling, fibrosis and heart dysfunction through modulating the IL-6/STAT3/GPX4 signaling pathway. Targeting elabela-APJ axis serves as a novel strategy for hypertensive heart diseases.

Free Radical Biology & Medicine published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (ANP). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Synthetic Route of 347174-05-4.

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

Zhang, Xiyu; Zheng, Cuiting; Gao, Zhenqiang; Chen, Hongyu; Li, Kai; Wang, Lingling; Zheng, Yuanyuan; Li, Chunjia; Zhang, Hongjia; Gong, Ming; Zhang, Hongbing; Meng, Yan published the artcile< SLC7A11/xCT Prevents Cardiac Hypertrophy by Inhibiting Ferroptosis>, Name: Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is slc7a11 xCT cardiac hypertrophy ferroptosis; Angiotensin II; Cardiac hypertrophy; Ferroptosis; xCT.

Systemic hypertension may induce adverse hypertrophy of the left cardiac ventricle. Pathol. cardiac hypertrophy is a common cause of heart failure. We investigated the significance of ferroptosis repressor xCT in hypertrophic cardiomyopathy. XCT expression in angiotensin II (Ang II)-treated mouse hearts and rat cardiomyocytes was determined using qRT-PCR and Western blotting. Cardiac hypertrophy was induced by Ang II infusion in xCT knockout mice and their wildtype counterparts. Blood pressure, cardiac pump function, and pathol. changes of cardiac remodeling were analyzed in these mice. Cell death, oxidative stress, and xCT-mediated ferroptosis were examined in Ang II-treated rat cardiomyocytes. After Ang II infusion, xCT was downregulated at day 1 but upregulated at day 14 at both mRNA and protein levels. It was also decreased in Ang II-treated cardiomyocytes, but not in cardiofibroblasts. Inhibition of xCT exacerbated cardiomyocyte hypertrophy and boosted the levels of ferroptosis biomarkers Ptgs2, malondialdehyde, and reactive oxygen species induced by Ang II, while overexpression of xCT opposed these detrimental effects. Furthermore, knockout of xCT aggravated Ang II-mediated mouse cardiac fibrosis, hypertrophy, and dysfunction. Ferrostatin-1, a ferroptosis inhibitor, alleviated the exacerbation of cardiomyocyte hypertrophy caused by inhibiting xCT in cultured rat cells or ablating xCT in mice. XCT acts as a suppressor in Ang II-mediated cardiac hypertrophy by blocking ferroptosis. Pos. modulation of xCT may therefore represent a novel therapeutic approach against cardiac hypertrophic diseases.

Cardiovascular Drugs and Therapy published new progress about Animalia. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Name: Ethyl 3-amino-4-(cyclohexylamino)benzoate.

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

Zhang, Xinhao; Jiang, Liping; Chen, Huangben; Wei, Sen; Yao, Kun; Sun, Xiance; Yang, Guang; Jiang, Lijie; Zhang, Cong; Wang, Ningning; Wang, Yan; Liu, Xiaofang published the artcile< Resveratrol protected acrolein-induced ferroptosis and insulin secretion dysfunction via ER-stress-related PERK pathway in MIN6 cells>, Category: esters-buliding-blocks, the main research area is endoplasmic reticulum stress ferroptosis PERK resveratrol insulin; Acrolein; Endoplasmic reticulum stress; Ferroptosis; MIN6 cells; Resveratrol.

Acrolein is a typical food and environmental pollutant and a risk factor for diabetes. The primary pathogenesis of diabetes is insulin deficiency and resistance. Ferroptosis is an iron-dependent cell death type, accompanying by lipid peroxide accumulation. Here, 25μM acrolein-induced ferroptosis is observed in mouse pancreatic β-cell MIN6 cells as indicated by ferroptosis-related indicators, including GPX4 exhaustion, lipid peroxides accumulation, and insulin secretion impairment. Addnl., acrolein-induced ferroptosis could be reversed by Ferrostatin-1. Furthermore, endoplasmic reticulum stress (ER stress) is involved in acrolein-induced ferroptosis. The ER stress inhibits the expression of PPARγ, an essential gene in glucose and lipid metabolism, and facilitates lipid peroxide accumulation, leading to MIN6 cells ferroptosis and dysfunction. Moreover, resveratrol, an antioxidant natural product, may relieve ER stress and upregulate PPARγ expression, thereby inhibiting acrolein-induced ferroptosis. Thus, this study demonstrated a new perspective for the cytotoxic mechanism of acrolein on pancreatic β-cell and the protective effect of resveratrol.

Toxicology published new progress about Activating transcription factor 4 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Category: esters-buliding-blocks.

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

Zhou, Pan; Zhang, Xican; Xin, Xiaoqian; Yang, Jinpei; Pan, Qiaofei; Liu, Chao; Liu, Yang; Yu, Xiang; Li, Zhizhong; Jiao, Genlong; Liu, Xiaowen published the artcile< Click chemistry-conjugated protein-drug micelles with anti-ferroptotic and anti-inflammatory properties promote regeneration in spinal cord injury>, Quality Control of 347174-05-4, the main research area is protein drug micelle delivery system antiinflammatory spinal cord injury.

Spinal cord injury (SCI) can disrupt neural circuitry and connectivity, leading to neurol. and motor disabilities. Functional recovery relies on neuroplasticity and injured axon regeneration to rebuild connections and circuits. Current drugs with potential neuropharmacol. effects are rapidly metabolized after systemic administration, reducing their pharmaceutical activity. Thus, efficient treatment of SCI remains a challenge. In this study, we designed click chem.-conjugated protein-drug micelles (FPAaF) by the conjugation of insoluble ferrostatin-1 (Fer-1) and dibenzocyclooctyne (DBCO) modules to amphiphilic polymers, followed by click chem. assembly with pH-responsive azido linker-modified acidic fibroblast growth factor (aFGF). SCI rats receiving systemic administration of FPAaF showed improved blood circulation and enhanced accumulation in the spinal cord. In vitro and in vivo studies showed the anti-ferroptotic and anti-inflammatory effects of FPAaF micelles. Moreover, significant improvements in neural and motor recovery were achieved upon the release of Fer-1 and aFGF in the acidic SCI microenvironment, which resulted in anti-ferroptotic and anti-inflammatory activities. This study shows that Fer-1 and aFGF conjugated micelles may exert their synergistic pharmacol. effects on SCIs, suggesting that this is a promising strategy for the treatment of as-yet-incurable diseases.

Chemical Engineering Journal (Amsterdam, Netherlands) published new progress about Anti-inflammatory agents. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Quality Control of 347174-05-4.

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